Ida F. Dancyger, Ida F. Dancyger, Victor M. Fornari - Evidence Based Treatments For Eating Disorders - Children, Adolescents, and Adults-Nova Kroshka Books (2009)

EVIDENCE-BASED TREATMENTS FOR
EATING DISORDERS: CHILDREN,

ADOLESCENTS AND ADULTS
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EVIDENCE-BASED TREATMENTS FOR
EATING DISORDERS: CHILDREN,
ADOLESCENTS AND ADULTS
IDA F. DANCYGER AND

VICTOR M. FORNARI
EDITORS
Nova Science Publishers, Inc.

New York
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Library of Congress Cataloging-in-Publication Data

Evidence-based treatment for eating disorders : children, adolescents, and adults / Ida F.
Dancyger, Victor M. Fornari (editors). p. ; cm.
Includes bibliographical references and index.
ISBN: (eBook)
1. Eating disorders. 2. Evidence-based medicine. I. Dancyger, Ida F. II. Fornari, Victor M.
[DNLM: 1. Eating Disorders--therapy. 2. Evidence-Based Medicine. WM 175 E93 2009]
RC552.E18E95 2009
616.85'26--dc22 2008041221
Published by Nova Science Publishers, Inc.  New York

Contents
Foreword A Book Reflecting the Kaleidoscopic Nature of the Treatment of

Eating Disorders vii
Walter Vandereycken
Preface ix
Acknowledgments xiii
List of Contributors xv
Chapter I Overview of the Biopsychosocial Risk Factors Underlying
Anorexia Nervosa 1
Anita Federici and Allan S. Kaplan
Chapter II Overview of Evidence on the Underpinnings of
Bulimia Nervosa 19
Timothy D. Brewerton
Chapter III Overview of Evidence on the Underpinnings of Binge Eating
Disorder and Obesity 53
Massimo Cuzzolaro and Giuseppe Vetrone
Chapter IV Research and Clinical Practice: A Dynamic Tension in the
Eating Disorder Field 71
Judith D. Banker and Kelly L. Klump
Chapter V Inpatient Psychiatric Treatment of Adolescents and Adults
with Eating Disorders 87
Parinda Parikh, Dara Bellace and Katherine Halmi
Chapter VI Day Treatment for Anorexia Nervosa 101
Ida F. Dancyger, Victor M. Fornari and Jack L. Katz
Chapter VII Medical and Nutritional Treatment of Children, Adolescents
and Young Adults with Eating Disorders 119
Martin Fisher
vi Contents
Chapter VIII Evidence-Informed Care of Children with Eating Disorders 137

Sloane Madden
Chapter IX Evidence-Guided Treatment for Males with Eating Disorders 155
Fernando Fernández-Aranda and Susana Jiménez-Murcia
Chapter X Treatment Resistance: Persuasion, Perceived Coercion
and Compulsion 171
Angela S. Guarda and Janelle W. Coughlin
Chapter XI Cognitive Behavioral Therapy for Anorexia Nervosa 187
Kathleen M. Pike and Marisa A. Yamano
Chapter XII Cognitive Behavioral Therapy for Bulimia Nervosa 207
Devra Lynn Braun
Chapter XIII Evidence-Informed Strategies for Binge Eating Disorder
and Obesity 231
Kimberly A. Brownley, Jennifer R. Shapiro and
Cynthia M. Bulik
Chapter XIV Interpersonal Psychotherapy (IPT) for Eating Disorders 257
Rebecca Murphy, Suzanne Straebler, Zafra Cooper
and Christopher G. Fairburn
Chapter XV Using Dialectical Behavioral Therapy for the Treatment of
Eating Disorders: A Model for DBT Enhanced CBT 275
Lucene Wisniewski, Kelly Bhatnagar and Mark Warren
Chapter XVI Evidenced-Based Approaches to Family-Based Treatment
for Anorexia Nervosa and Bulimia Nervosa 291
James Lock and Kathleen Kara Fitzpatrick
Chapter XVII Emotion, Eating Disorders, and Integrative Cognitive-
Affective Therapy 307
Scott G. Engel, Andrea Wadeson, Chad M. Lystad,
Heather K. Simonich and Steve A. Wonderlich
Chapter XVIII Pharmacological Therapies for Anorexia Nervosa 331
James L. Roerig, Kristine J. Steffen, James E. Mitchell
and Scott J. Crow
Chapter XIX Pharmacological Therapies for Bulimia Nervosa 351
Amanda Joelle Brown, Lisa A. Kotler and B. Timothy Walsh
Index 369
Foreword
A Book Reflecting the Kaleidoscopic

Nature of the Treatment of
Eating Disorders
Walter Vandereycken
Symptoms associated with food avoidance or overeating varied considerably over time.
In view of this historical variability, eating disorders apparently belong to those disorders
whose features show a remarkable susceptibility over the span of centuries to prevailing
economic and sociocultural conditions as well as to developing medical knowledge. The
current constellations of symptoms comprising anorexia nervosa and bulimia nervosa are to
be considered the latest – and conceivably not the last – variants in an ever-existing, but
constantly changing pattern of disordered eating behavior. Preoccupations with weight and
shape and the use of weight control strategies like dieting and self-induced vomiting, have
acquired popular and medical attention relatively recently and predominantly in Western or
westernized countries. Hence, in medicine, the specific syndromes of anorexia nervosa and
bulimia nervosa appear to be relatively "modern" clinical entities. Our diet-culture started
more than a century ago and it is going to be with us for many years to come, probably
together with eating disorders, "old" or "new" ones...
More than a century after the first systematic clinical observations, eating disorders still
induce quite opposite reactions in clinicians: their "therapeutic appetite" may be either
stimulated or suppressed. A considerable number of health care professionals do not want to
treat patients with eating disorders, mainly because of feelings of frustration and lack of
empathy with these patients. Others devote their entire professional career to the research
and/or treatment of eating disordered patients. Why are these disorders so fascinating for
some and so frustrating for others?
An ever-recurring pitfall in writings about one particular diagnostic category is the
"uniformity myth", i.e. the assumption of homogeneity. Such a myth can easily be detected
when one asks a clinician to briefly describe the major characteristics of anorexia nervosa.
We all have a prototype in our mind, a kind of typical model which has been imprinted in our
viii Walter Vandereycken
memory when first hearing or learning of the disorder. A common anorectic prototype is the
"skinny teenage girl refusing to eat". If that picture becomes the leading image in our
perception, we are likely not only to miss the diagnosis in several cases, but to mistreat many
patients. Regardless of its diagnostic simplification into a DSM code, each person with an
eating disorder reflects a complexity of biopsychosocial issues. This book bears witness to
that kaleidoscopic picture. An impressive list of leading international experts presents a
comprehensive review of the evidence supporting the best practices in the field.
Nowhere in a medical discipline is the plurality of opinion as great as in psychiatry. Does
this diversity reflect the appealing richness of the discipline or is it symptomatic for a hybrid
professional identity? This colorful picture is even more striking in the management of eating
disordered patients, including the whole spectrum of professionals and the most diverse
therapeutic arsenal in health care. But what treatment,by whom is the best for which patient?
A book like this can be compared to a global positioning system tracing a variety of roads –
the easiest, the fastest, and the most scenic – toward the desired goal. But for navigation in
daily clinical practice, can science be the only reliable and useful guide?
Treatment for serious eating disorders can last many years and still its long-term outcome
remains difficult to predict. So, how long should one go on with treatment trials? When does
the disorder become chronic or "recalcitrant"? And what should we do for those patients who
have "chosen" a life as an abstainer or a bulimic? Challenged by the reality of health care
costs, be it in varying degrees depending on the health care system of the country involved,
therapists dealing with seriously ill patients have to face some difficult decisions, both
clinically and ethically, for which no clear-cut evidence-based guidelines exist.
Evidence-based medicine, in general, uses the double blind randomized controlled trial
as the gold standard for judging the effectiveness of an intervention. The outcome of this type
of research is then translated in algorithmic guidelines and manual-based treatments. For an
increasing number of clinicians, only this approach can guarantee the scientific status of their
work and safeguard the quality of care for a diversity of patients. For others, this scientific
mainstreaming is experienced as the ultimate straitjacket squeezing their professional
creativity into some form of pre-programmed practice. In recent years, the most challenging
task in health care appears to be the fruitful merging of an evidence-based and an
experienced-based approach. As in general medicine, this is the case in the field of eating
disorders. Indeed, daily practice of working with eating disorder patients is not summarizable
to some simple “do’s and don'ts”. Therefore, a book like this cannot offer easy-to-use recipes.
However, Evidence Based Treatments of Eating Disorders: Children, Adolescents and Adults
proposes a rich variety of methods and ingredients for the creative clinician who faces the
challenges of caring for these individuals, and wants to be able to integrate the best current
knowledge available.
Walter Vandereycken
Preface
This book represents the opportunity to bring together the currently available evidence
for the best practices in the treatment of the eating disorders (EDs). We feel privileged that
we have been able to assemble such a distinguished international group of experts in the field
of eating disorders research and treatment. We will be gratified if clinicians across the wide
range of disciplines treating individuals with eating disorders find the chapters in this book
helpful to them in their work with patients, whether in treatment facilities, in the community,
or in private practice. The chapters describe evidence-based or evidence-informed practices
for the full range of eating disorders- including anorexia nervosa, bulimia nervosa, binge
eating disorder, and obesity, and cover the full range of individuals with EDs seen across the
life cycle: from childhood through adolescence and into adulthood, including a special
section on males as well.
The topics are organized into four sections: (I) Overview of the evidence on the
underpinnings of anorexia nervosa, bulimia nervosa, binge eating disorder, and obesity, as
well as the tension in the field between research and clinical practice (Chapters 1-4); (II)
Intensive treatments of eating disorders, including particular attention to treatment resistance
(Chapters 5-10); (III) Evidence based and informed approaches to the psychotherapy of
eating disorders, including cognitive behavioral, interpersonal, dialectical behavioral, family-
based, and integrative cognitive-affective therapies (Chapters 11-17); and (IV)
Pharmacological therapies for anorexia and bulimia nervosa (Chapter 18 and 19). Authors
share with the reader their vast clinical experience and provide clinical vignettes in order to
highlight important treatment considerations.
The book begins with Federici and Kaplan in Chapter 1 providing an informative
overview of the bio-psycho-social risk factors underlying anorexia nervosa (AN). This
chapter reviews the breadth of empirical evidence regarding neuro-biological, socio-cultural,
familial, and psychological variables.
Brewerton in Chapter 2 presents the underpinnings of bulimia nervosa (BN) as it results
from the dynamic interplay between biological, psychological, and social dimensions that
operate along a developmental continuum. The research evidence is comprehensively
examined as it relates to predisposing, precipitating, and perpetuating factors underlying BN,
as there is no single etiology.
x Ida F. Dancyger and Victor M. Fornari
Cuzzularo and Vetrone in Chapter 3 provide an overview of the evidence for the
underpinnings of binge eating disorder (BED) and obesity. BED is the most distinct subgroup
in the eating disorder not otherwise specified (EDNOS) category. An account of the current
knowledge on the epidemiology of BED and obesity is given along with the nosological
status of this possible new diagnostic category.
Banker and Klump in Chapter 4 offer the reader an exciting review of the dynamic
tension in the eating disorder field between research and clinical practice. The “research
practice gap” is evidenced by discrepancies between the rate at which research results are re-
produced and the rate at which the results are utilized in practice. The factors underlying the
gap are explored and the authors provide a “road map” for closing this gap.
The second section begins with Parikh, Bellace, and Halmi in Chapter 5 describing the
inpatient psychiatric treatment of adolescents and adults with an eating disorder. There are no
standardized, universally accepted, evidence based criteria for the inpatient treatment of
patients with EDs, but the multidisciplinary team approach for the inpatient care of
individuals with AN and BN is emphasized.
Together with Katz, in Chapter 6 we examine the emergence of day treatment in the
spectrum of care for AN. The evidence for its utility is reviewed, including the unique
challenges and pitfalls with the different care options.
Fisher in Chapter 7 clearly summarizes the four key areas in the medical and nutritional
care of children, adolescents, and young adults with EDs. This includes several consensus
statements from professional associations describing a team approach as well as the clinical
experience of the author.
Chapter 8 by Madden focuses on the challenge of the care of children with EDs where
the evidence base for treatment remains weak. Developmental issues and their impact on
treatment provide a framework to clinicians for identifying and managing the care of these
young children.
An increasing incidence of males with EDs has been observed in recent years,
specifically BN and EDNOS as described by Fernandez-Aranda and Jimenez-Murcia in
Chapter 9. Therapy for males with EDs has received relatively little attention in the literature
to date; however, description of a specific therapy program for males is fully presented.
Guarda and Coughlin in Chapter 10 discuss the critically important issue of ambivalence
towards treatment and treatment resistance, both characteristics of patients with EDs,
particularly AN. The matters of persuasion, perceived coercion, and treatment refusal,
including competency and capacity to give or refuse consent, are among the many challenges
facing clinicians and are thoroughly examined.
Section three begins with Pike and Yamano’s up-to-date description of cognitive
behavioral therapy (CBT) for AN in Chapter 11. There is an emerging data base that CBT has
the potential to be an effective psychotherapy, particularly for individuals with weight-
restored AN.
Chapter 12 by Braun offers a detailed overview of the impressive data on CBT in treating
BN, with a brief description of underlying related brain functioning.
Brownley, Shapiro, and Bulik in Chapter 13 review current evidence-based treatment for
obesity and BED. Topics include novel therapies that have shown promise in limited clinical
studies, available pharmacological treatments, and effective behavioral therapies.
Preface xi
Interpersonal psychotherapy to treat patients with EDs is described by Murphy, Straebler,

Cooper, and Fairburn in Chapter 14. The authors provide a detailed rationale for how helping
patients identify and resolve current interpersonal difficulties can lead to recovery from
deviant eating behaviors.
Chapter 15 by Wisniewski, Bhatnagar, and Warren presents a promising model for
Dialectical Behavioral Therapy (DBT) enhanced CBT for the treatment of EDs. This chapter
describes DBT, reviews relevant literature, and offers a novel approach for fusing principles
of CBT with those of DBT.
Lock offers clinicians the latest advancements in an evidence based approach to family
treatment for AN and BN in Chapter 16. An evaluation of existing research on family-based
treatments, as well as skills necessary to implement this model, is provided.
Empirical research on emotions and EDs, the neurobiology of emotion, and a new
treatment for BN called Integrative Cognitive-Affective Therapy (ICAT) are discussed in
Chapter 17 by Engel, Wadeson, Lystad, Simonich, and Wonderlich.
The concluding two chapters present the empirical evidence for pharmacological
therapies for AN in Chapter 18 by Roerig, Steffen, Mitchell, and Crow and for BN in Chapter
19 by Brown, Kotler, and Walsh. Randomized, double-blind, placebo controlled trials are
emphasized.
We are delighted that so many of the leading international experts in the field of eating
disorders have provided in this volume a compendium of the best studied treatments currently
available. This book is thus intended to serve as a framework to the clinician searching for
guidance on how to proceed with treatment when caring for an individual with an eating
disorder. We are grateful to the authors for their generosity in sharing their clinical expertise,
insights, and wisdom. We hope that the reader will appreciate and benefit from these
contributions. Ultimately, patient care relies on the artful therapist who can integrate the best
available evidence to inform his or her practice while tailoring the treatment for each
individual. We sincerely hope that readers will find this book a useful reference, whether they
are beginning or seasoned clinicians.
Acknowledgments
We are particularly delighted to have the opportunity to co-edit this book together. We
are very fortunate to have collaborated these past ten years in our clinical and academic work
with children, adolescents and adults with an eating disorder. We dedicate this volume to the
many individuals and families with whom we have had the privilege to work with, and who
have taught us about the complexities of caring for those struggling with these challenging
disorders.
It has been an immense honor to work with our outstanding group of contributors; the
researchers, clinicians and scholars who have so generously contributed not only their
knowledge, but also their passion to the treatment of those with eating disorders. Several of
the authors have been not only our teachers, but also international leaders in this field.
This book would not have been possible without the administrative help, dedication,
intelligence and commitment from Nicole Taylor at North Shore University Hospital, who
helped with the early organization of the project; and Marie Stercula at Long Island Jewish
Medical Center, who helped with the preparation of the manuscript.
Finally, we would like to thank our families, for their continued support and enthusiasm
throughout this lengthy project. To my husband, Ken, an extremely gifted and prodigious
writer, your constant belief in me and your loving input whenever requested made this dream
of mine come true. To my wife Alice, for your continuous love and encouragement.
In memory of our parents, Mendel and Malka Flint and Ermanno and Alice Notrica
Fornari.
List of Contributors
Judith D. Banker, MA, LLP, FAED

Center for Eating Disorders, Ann Arbor, Michigan
Dara Bellace, PhD

Eating Disorders Program, New York Presbyterian Hospital-Payne Whitney Westchester
Department of Psychiatry, Cornell Weill School of Medicine, White Plains, New York
Kelly Bhatnagar, MA
The Cleveland Center for Eating Disorders and Case Western Reserve University,
Cleveland, Ohio
Devra Lynn Braun, MD

Weill Cornell Medical College, New York, New York
Integrative Medicine and Psychotherapy of Greenwich, LLC, Connecticut
Timothy D. Brewerton, MD, DFAPA, FAED

Department of Psychiatry and Behavioral Sciences,
Medical University of South Carolina, Charleston, South Carolina
Amanda Joelle Brown, BA

The New York State Psychiatric Institute, New York, New York
Kimberly A. Brownley, PhD

Department of Psychiatry, University of North Carolina at Chapel Hill, North Carolina
Cynthia M. Bulik, PhD

Departments of Psychiatry and Nutrition,
University of North Carolina at Chapel Hill, North Carolina
Zafra Cooper, DPhil, DipPsych

Department of Psychiatry, University of Oxford, United Kingdom
xvi List of Contributors
Janelle W. Coughlin, PhD

Department of Psychiatry and Behavioral Sciences, The Johns Hopkins School of Medicine,
Baltimore, Maryland
Scott J. Crow, MD
Department of Psychiatry, University of Minnesota Medical School, Minneapolis, Minnesota
Massimo Cuzzolaro, MD
Eating and Weight Disorders Unit, Department of Medical Physiopathology,
University of Rome, Sapienza, Roma, Italy
Ida F. Dancyger, PhD

Department of Psychiatry, The Zucker Hillside Hospital,
North Shore-Long Island Jewish Health System, Glen Oaks, New York
Clinical Associate Professor of Psychology in Psychiatry,
New York University School of Medicine, New York, New York
Scott G. Engel, PhD

Neuropsychiatric Research Institute, Fargo, North Dakota
University of North Dakota, Grand Forks, North Dakota
Christopher G. Fairburn, DM, FMedSci, FRCPsych

Anita Federici, MSc

Department of Psychology, York University, Toronto, Ontario, Canada
Fernando Fernández-Aranda, PhD, FAED

Eating Disorder Unit and Research Group
Department of Psychiatry, University Hospital of Bellvitge and
CIBER Fisiopatología de la Obesidad y Nutrición (CIBEROBN),
Instituto Carlos III, Barcelona, Spain
Martin Fisher, MD
Division of Adolescent Medicine, Schneider Children’s Hospital,
North Shore-Long Island Jewish Health System, New Hyde Park, New York
Kathleen Kara Fitzpatrick, PhD

Department of Psychiatry, Stanford University School of Medicine, Stanford, California
List of Contributors xvii
Victor M. Fornari, MD
Director, Division of Child and Adolescent Psychiatry, Department of Psychiatry,
The Zucker Hillside Hospital, North Shore-Long Island Jewish Health System,
Glen Oaks, New York
Professor of Psychiatry, New York University School of Medicine, New York, New York
Angela S. Guarda, MD
Department of Psychiatry and Behavioral Sciences, The Johns Hopkins School of Medicine,
Baltimore, Maryland
Katherine Halmi, MD
New York Presbyterian Hospital-Payne Whitney Westchester
Cornell Weill School of Medicine, White Plains, New York
Susana Jiménez-Murcia, PhD

Department of Psychiatry, University Hospital of Bellvitge and CIBER Fisiopatología de la
Obesidad y Nutrición (CIBEROBN), Instituto Carlos III, Barcelona, Spain
Allan S. Kaplan, MD FRCP(C)

Eating Disorders, Toronto General Hospital
Department of Psychiatry, University of Toronto, Ontario, Canada
Jack L. Katz, MD
Department of Psychiatry, The Zucker Hillside Hospital,
North Shore-Long Island Jewish Health System, Glen Oaks, New York
Lisa A. Kotler, MD
Columbia University College of Physicians and Surgeons, New York, New York
Kelly L. Klump, PhD, FAED

Department of Psychology, Michigan State University, East Lansing, Michigan
James Lock, MD, PhD

Division of Child Psychiatry and Pediatrics, Department of Psychiatry and
Behavioral Sciences, Stanford University School of Medicine, Stanford, California
Chad M. Lystad, MS
Sloane Madden, MB BS (Hons) FRANZCP

Child and Adolescent Eating Disorder Program, Psychiatry,
The Children's Hospital at Westmead, Sydney, Australia
xviii List of Contributors
James E. Mitchell, MD
Department of Clinical Neuroscience, University of North
Dakota School of Medicine and Health Sciences, Fargo, North Dakota
Rebecca Murphy, DClinPsych

Parinda Parikh, MD
Child and Adolescent Eating Disorder Program,
New York Presbyterian Hospital-Payne Whitney Westchester
Cornell Weill School of Medicine, White Plains, New York
Kathleen M. Pike, PhD

Temple University, Japan
James D. Roerig, PharmD, BCPP

Department of Clinical Neuroscience, University of North Dakota School of Medicine and
Health Sciences, Fargo, North Dakota
Jennifer Shapiro, PhD

Department of Psychiatry, University of North Carolina at Chapel Hill, North Carolina
Heather K. Simonich, MA
Kristine Steffen, PharmD

Suzanne Straebler, APRN-Psychiatry, MSN

Walter Vandereycken, MD, PhD

Department of Psychiatry, Catholic University Leuven, Belgium
Giuseppe Vetrone, MD
Department of Philosophical Research, University of Rome Tor Vergata, Roma, Italy
Andrea Wadeson, BA
North Dakota State University, Fargo, North Dakota
List of Contributors xix
B. Timothy Walsh, MD
Columbia University College of Physicians and Surgeons, New York, New York
Mark Warren, MD, MPH

Cleveland, Ohio
Lucene Wisniewski, PhD, FAED

Cleveland, Ohio
Steve A. Wonderlich, PhD

University of North Dakota, Grand Forks, North Dakota
Marisa A. Yamano, BA
In: Evidence-Based Treatments for Eating Disorders ISBN 978-1-60692-310-8
Author: Ida F. Dancyger and Victor M. Fornari © 2009 Nova Science Publishers, Inc.
Chapter I
Overview of the Biopsychosocial Risk

Factors Underlying Anorexia Nervosa
Anita Federici1 and Allan S. Kaplan2

1
York University, Toronto, Ontario, Canada
2
University of Toronto, Ontario, Canada
Abstract
Historically, anorexia nervosa has been a poorly understood and difficult to treat
psychiatric illness. With the advent of more sophisticated medical technology, enhanced
research methodology, and widespread international interest, current conceptualizations
of the disorder have become increasingly more refined and advanced. The goal of this
chapter is to review the breadth of empirical evidence regarding risk factors for the
development of anorexia nervosa, spanning neuro-biological, sociocultural, familial, and
psychological domains.
Introduction
Developing an evidence based theory regarding the etiological underpinnings of anorexia
nervosa (AN) is an important yet challenging task. Many variables have been hypothesized to
be risk factors for AN, however, their relative contribution and specificity to the development
of the disorder is unknown (Fairburn, Cooper, Doll, and Welch, 1999; Pike, 1998). In
addition, there are relatively few longitudinal studies with adequate cohort sizes to allow
proper examination and identification of potential risk factors in AN. Nevertheless, there is
evidence in the published literature that certain biological, personality, and familial variables
appear to contribute to the development of AN. We will attempt to comprehensively review
these risk factors in this chapter.
Phenomenologically, AN is characterized by a refusal to maintain a body weight at or
above what is considered a minimal normal weight for age and height. Individuals with AN
2 Anita Federici and Allan S. Kaplan
exhibit intense fears of becoming fat despite being underweight and display severe
disturbances in the way their bodies are perceived and experienced (DSM -IV, American
Psychiatric Association (APA), 2000). The presence of amenorrhea is also part of the current
diagnostic criteria, although the necessity of this feature is currently under review (Garfinkel
et al., 1996). Depending on symptom presentation, the illness may be further nosologically
characterized as a restricting subtype (e.g., absence of any binging or purging behaviour
during the course of the illness) or a binge-purge subtype (e.g., regular occurrence of binge
eating and/or purging behaviours). AN is prevalent in approximately 0.5 % of the female
population and the long-term prognosis of the disorder is poor (APA, 2000; Steinhausen,
2002). In comparison to other psychiatric conditions, AN is considered to be one of the most
severe and life-threatening as it confers a standardized mortality rate that is 12 times higher
than the general population of females aged 15-24 (Sullivan, 1995). Mortality rates as high as
22% have been reported (Lowe, Zipfel, Dupont, Reas and Herzog, 2001; Birmingham, Su,
Hlynsky, Goldner, and Gao, 2005). Identifying and elucidating the factors that contribute to
the development and maintenance of AN are paramount to our ability to effectively treat the
disorder.
While early descriptions of the origins of AN typically focused on discreet causal factors
(e.g., maturational fears, familial difficulties, repressed sexual conflicts), modern theoretical
accounts are predominately multifactorial in nature. Most theorists agree that a single
etiological cause of AN does not sufficiently address the complexities of the illness
(Garfinkel and Garner, 1982). AN is best understood using a more sophisticated,
multidimensional model. From this perspective, the disorder is likely a manifestation of
biological, psychological and sociocultural risk factors (Anderson, Bowers and Evans, 1997;
Jacobi, Hayward, de Zwaan, Kraemer, Agras, 2004).
I. Biological Factors
There is increasing evidence for the importance of neurobiological factors in potentiating
the vulnerability to anorexia nervosa. These include genetic factors, changes in brain
structure/blood flow, neurotransmitter/ neuropeptides, and pre- and perinatal factors.
Genetic Factors
Family and twin studies have shown that genes contribute substantially more than 50%
of the risk for AN (Klump, Kaye, and Strober, 2001). Over the past decade, a number of
association and linkage studies have identified specific genetic diatheses contributing to the
development of AN. Association studies have examined genes responsible for the regulation
of various neurotransmitter systems. The most well studied is the serotonin system. A meta-
analysis of the studies examining the 5HT2a receptor gene found a very significant
association between AN and the AA genotype, suggesting a role for the 5HT2a receptor in
the genetic risk for AN (Gorwood, Kipman, and Foulon, 2003). Other neurotransmitter and
neuropetide systems have been examined, including the opioid, dopamine, neuropeptide Y,
Overview of the Biopsychosocial Risk Factors Underlying Anorexia Nervosa 3
leptin and agouti related protein genes, with largely negative results, possibly related to
inadequate sample sizes ( Klump and Gobrogge, 2005.) Linkage studies emanating from a
large multi-site consortium have shown modest evidence of linkage on chromosomes 1, 4 11,
13 and 165 and much stronger linkage on chromosome 1 when only restrictor anorexics were
included in the analyses (Grice et al., 2002). Candidate genes such as the delta opioid
receptor (OPRD1) and serotonin 1 D receptor ( 5HTR1D) genes were also associated with
AN in this cohort (Bergen et al., 2003). These studies point to significant genetic effects in
the risk for AN but require replication.
Changes in Brain Structure/Cerebral Blood Flow
Structural neuroimaging studies have demonstrated enlarged ventricles and loss of gray
matter in underweight subjects with AN, changes which are thought to be related to the state
of emaciation and starvation and to reverse with refeeding and weight gain. (Wagner et al.,
2006). However, more recent studies suggest that these changes may persist in the recovered
state (Mühlau et al., 2007). Regional blood flow changes utilizing SPECT (single photon
emission computed tomography) have been reported in adolescents with AN (Lask et al.,
2005). These studies have found unilateral reduction in blood flow in the temporal lobe in
about 75% of subjects studied. There was no association between this reduced blood flow
and nutritional state, length of illness, associated comorbidity, or eating disorder
psychopathology, suggesting a primary phenomenon independent of starvation. This reduced
blood flow was associated with impaired visual processing and memory and enhanced
information processing, suggesting altered cognitive functioning in AN. These findings are
intriguing and require further research.
Neurotransmitter/Neuropeptide Systems
Many changes in monamines described in the past among individuals with AN are
virtually all due to either the starvation state or emaciation and correct with nutritional
rehabilitation and weight gain (Kaplan, 1990). Recent functional neuroimaging studies have
implicated several of the neurotransmitters and neuropeptides in the etiology of AN. These
studies have found that recovered subjects with AN had reduced 5HT2a receptor activity in
the cingulate and other cortical areas and normal 5HT1A activity (Frank et al., 2002).
Observed abnormalities in serotonergic functioning could contribute to the symptoms seen in
AN, such as changes in appetitive behaviors, and increased anxiety and obsessionality (Kaye,
Frank, Bailer, and Henry, 2005). In addition, abnormalities of the dopaminergic system found
in recovered restricting anorexics could contribute to other symptoms seen in AN such as
hyperactive motor behavior and abnormalities in reward and behavioral inhibition (Kaye,
Frank, and McConaha, 1999).
Prenatal and Perinatal Factors
Several Swedish investigators have demonstrated the importance of perinatal risk factors
in increasing the risk for AN by as much as 3.6%, (Lindberg and Hjern, 2003). These factors,
which include prematurity, especially associated with small for gestational age and the
presence of cephalohematoma, increases the risk for AN later in life (Cnattingius, Hultman,
Dahl, and Sparén, 1999). These factors appear to be independent of sociodemographic
variables. It is quite possible that such prematurity and small for gestational age are
secondary effects of nutritional deficiencies that occur during pregnancy in mothers with
eating disorder symptoms (Bulik, Reba, Siega-Riz, and Reichborn-Kjennerud, 2005). Finally,
recent investigations have suggested that the intrauterine exposure to sex steroid hormones
might influence neurodevelopment and increase the risk for AN in adult life, especially in
females (Procopio and Marriott, 2007).
II. Psychological Factors

Personality Features
Certain personality factors have been hypothesized to play a significant role in the
development and maintenance of AN. Two characterological traits that have been widely
studied among individuals with AN are perfectionism and obsessionality (Bastiani, Rao,
Weltzin, and Kaye, 1995; Klump et al., 2004). Compared to non-clinical control groups,
individuals with AN demonstrate high levels of perfectionism, inflexibility, and constraint
during both acute and remitted phases of the illness, suggesting that such traits are not state-
dependent; rather, they are considered enduring features that predispose an individual to
specific eating pathology (Casper, 1990; Fairburn et al., 1999; Halmi et al., 2000; Klump et
al., 2004). In line with these findings, investigations using neuropsychological tests have
provided compelling data showing that individuals with AN have difficulty with set-shifting
and cognitive flexibility, indicating more rigid approaches to problem-solving and difficulties
adapting to novel stimuli (for a review see Tchanturia, Campbell, Morris, and Treasure,
2005)
Obsessive and/or compulsive features are also common among AN populations and have
been shown to persist post-recovery (Serpell, Livingstone, Neiderman, and Lask, 2002;
Srinivasagam et al., 1995). A significant proportion of patients with AN also report pre-
morbid obsessional traits which have been found to be predictive of subsequent eating
disorder development (Anderluh, Tchanturia, Rabe-Hesketh, and Treasure, 2003; Halmi et
al., 2005). More broadly speaking, anxiety disorders in general tend to precede the onset of
AN; therefore it has been suggested that childhood anxiety may be a risk factor in the
development of the illness (Bulik, 2002). Many studies have reported a lifetime prevalence of
an anxiety disorder in more than half of the female subjects who meet criteria for AN, with
obsessive compulsive disorder and social phobia being most common (Bulik, 2004).
Similarities between AN and OCD or OCPD have sparked much debate in recent years with
some researchers speculating that the two disorders are etiologically related (for a review see
Serpell et al., 2002).
Other identified personality traits include neuroticism, negative emotionality, harm
avoidance, compulsivity, social inhibition, emotional restraint, compliance, and low self-
esteem (Geller, Cockell, Hewitt, Goldner, and Flett, 2000; Vervaet, van Heeringen, and
Audenaert, 2004; Vitousek and Manke, 1994; Zaitsoff, Geller, Srikameswaran, 2002).
Problems with identity formation, issues with autonomy, maturity fears, and negative self-
evaluation are also common in AN sufferers (de Groot and Rodin, 1994; Fairburn et al.,
1999; Stein and Nyguist, 2001).
There is also some empirical support for characterological differences between AN
subtypes. For example, individuals with the binge-purge subtype are more likely to score
higher on measures of impulsivity and sensation-seeking (Claes, Vandereycken, and
Vertommen, 2005; Lacey and Evans; 1986; Rossier, Bolognini, Plancherel, and Halfan,
2000; Vervaet et al., 2004). In contrast, individuals with the restricting type of AN are more
likely to be compulsive, constricted, and neurotic (Wonderlich, Lilenfeld, Riso, Engel, and
Mitchell, 2005).
With regard to specific Axis II pathology, Cluster C disorders, particularly obsessive
compulsive and avoidant personality disorder, are more commonly observed among the
restricting subtype of AN while Cluster B pathologies are more frequently associated with
patients who engage in binging and purging behaviours (Bornstein, 2001; Cassin and von
Ranson, 2005; Rastam, 1992). Borderline personality disorder (BPD) is considered to be the
most common Axis II disorder among this latter population (Dennis and Sansone, 1997).
Data from epidemiological studies consistently show that a significant subgroup of ED
patients meet criteria for BPD (Skodol et al., 1993; Vitousek and Manke, 1994). Sansone,
Levitt, and Sansone (2005) reported that BPD was prevalent in 35% of patients with AN
(25% with the binge/purge subtype and 10% with the restricting subtype). Individuals with
comorbid AN and BPD have significantly greater difficulty regulating internal emotional
states and are more likely to engage in self-injurious behaviours, substance abuse, and other
impulsive and reckless acts; thus, they represent a more challenging and complex patient
population. Impulsivity has been associated with a more protracted course of illness, poor
treatment outcome, premature dropout, and higher rates of relapse (Agras et al., 2000;
Johnson-Sabine, Reiss, and Dayson, 1992; Finfgeld, 2002; Sansone, Sansone, and Levitt,
2004).
Emotion Dysregulation
Deficits in the ability to recognize, integrate, and express emotion are hypothesized to
play a central role in the development and maintenance of AN (Bruch, 1978). As early as the
1960s, conceptualization of AN included a pervasive inability to identify and describe
internal emotional states and many researchers have since described eating disorder
symptoms (e.g., self-starvation, binging, vomiting) as maladaptive attempts to regulate
intense negative emotions (Bruch, 1988). Certainly, it is not uncommon for individuals with
AN to report feeling disconnected from their feelings or to feel confused and overwhelmed
by emotion. Numerous studies have shown that the most commonly cited trigger for
symptomatic behaviours is stress or negative affect. Eating disorder patients have consistently
reported that symptoms provide relief from emotions that are perceived as threatening,
overwhelming, or that exceed their existing coping abilities (Cockell, Zaitsoff, and Geller,
2004). Identifying, tolerating, and expressing negative affect has also been identified as an
essential component in the recovery process (Federici and Kaplan, 2007).
Some researchers have speculated that alexithymia (referring to the inability to identify
and describe feelings, difficulty discriminating between physical sensations and emotions,
and a concrete, externalized orientation) may be an important predisposing factor in the
development of AN (Schmidt, Jiwany, and Treasure, 1993; Zonnevijlle-Bendek, van Goozen,
Cohen-Kettenis, van Elburg, and van Engeland, 2002). Studies using the Toronto
Alexithymia Scale (TAS) provide consistent evidence that alexithymia is, in fact, more
prevalent in eating disorder populations (Bydlowski et al., 2005; Schmidt et al., 1993).
Compared to control groups, where the prevalence of alexithymia ranged from 6.7% to 26%,
Bourke, Taylor, Parker, and Bagby (1992) reported prevalence rates as high as 77% in female
AN patients, 56% in patients with BN, and 64% in patients with BED. Zonnevijlle-Bendek et
al. (2002) demonstrated that, compared to a control group, patients with AN and BN have
greater difficulty recognizing and labelling affective states. In addition, Bydlowski et al.
(2005) demonstrated lower levels of emotional awareness among individuals with AN
compared to those with BN, highlighting a more pronounced deficit in the ability to
recognize and accurately label affective states. It is not uncommon for patients with AN to
report that the onset of their symptoms were preceded by a pervasive sense of ineffectiveness,
feelings of shame or worthlessness, a feeling of being internally flawed, and strong fears of
criticism and rejection. One of the identified functions of severe food restriction and binge
eating or purging behaviours, is to regulate, dismiss, or reduce aversive mood states.
Similarly, a significant subgroup of patients with AN engage in recurrent episodes of self-
harm and self-mutilation, often in an attempt to regulate intense negative affect. In a meta-
analysis of studies conducted between 1986 and 2000 examining self harm and suicidal acts
in patients with an ED, Sansone and Levitt (2004) found that 11% of outpatients with AN
reported a history of attempted suicide and 22% of outpatients with AN reported engaging in
self injurious behaviours.
The significant and pervasive problems with affect observed in those with AN has
prompted clinicians to incorporate emotion regulation strategies into existing treatment
protocols (Corstorphine, 2006; Fairburn, Cooper, and Shafran, 2003). In addition, alternative
treatment approaches that focus on the processing of emotional experience (e.g., Emotion
Focused Therapy) and teaching specific affect regulation skills (e.g., Dialectical Behaviour
Therapy) are currently being adapted for use in clients with eating disorders (Telch, 1997;
Telch, Agras, and Linehan, 2001).
Cognitive Factors
Cognitive models have been particularly influential in providing a theoretical framework

for the conceptualization of disordered eating. Such models posit that eating disorders are the
result of core disturbances in thinking, perception, and memory. Individuals with AN

demonstrate maladaptive, rigid, and idiosyncratic schemas involving food, weight, and shape
which directly influence their thoughts, feelings, and subsequent behaviours (Green,
McKenna, and De Silva, 1994; Sackville, Schotte, Touyz, Griffiths, and Beaumont, 1998;
Vitousek and Hollon, 1990). Obsessive thoughts about eating and body weight, overly rigid,
dichotomous, and perfectionist styles of thinking, and body size overestimation are all well
documented phenomena in the literature on AN. In addition, investigators have recently
found evidence to support the presence of thought-action fusion (TAF) or thought-shape
fusion (TSF) in patients with AN (Shafran, Teachman, Kerry, and Rachman, 1999). Typically
used to describe a cognitive distortion common among patients with OCD, TAF refers to the
belief that a thought about something aversive occurring can increase the likelihood of a
negative event happening and/or is equivalent to having actually carried out the negative
event. Radomsky, de Silva, Todd, Treasure and Murphy (2002) found that the act of writing
an aversive sentence (e.g., “I am eating cake”) significantly increased anxiety, depression,
guilt, and increased subjective ratings of fatness among individuals with AN. Notably, 75%
of the sample chose to act on urges to neutralize or correct the statement (e.g., crossed
out/modified/covered the sentence). The presence of such ingrained and dysfunctional
cognitive patterns serves to direct, organize, and classify incoming information in such a way
as to reinforce the core assumptions and beliefs.
In their seminal paper exploring the role of schematic processing in eating disordered
individuals, Vitousek and Hollon (1990) argued that eating disorders are maintained and
intensified by particular attentional biases to weight and body-related stimuli. People with
eating disorders are expected to detect food and weight-based cues more quickly, and to
attach greater meaning and be more attentive to schema-related information in their
environment. Vitousek and Hollon (1990) further proposed that anorexic and bulimic
sufferers would exhibit selective memory for schema-consistent information, be resistant to
details perceived as schema-inconsistent, and perceive ambivalent stimuli as weight, shape,
or food-related, thus differentiating them from non-eating disordered individuals.
There is some empirical evidence for the presence of specific memory and attentional
biases for food and weight-related stimuli in AN. Hermans, Pieters and Eelen (1998) reported
that patients with AN showed a pattern of selective recall of anorexia-related words on a task
of explicit memory compared to a control group. Modified versions of the Stroop colouring
naming task have demonstrated that individuals with AN and BN are slower to colour-name
the ink in which food or body-related words are
written (Fairburn, Cooper, Cooper, McKenna, and Anastasiades, 1991; Cooper,
Anastasiades, and Fairburn, 1992). Using the dot probe visual detection task, Rieger et al.
(1998) found that, compared to unrestrained eaters (e.g., non-dieters) individuals with AN
and BN detected target probes faster when they appeared in the same location as negative
body shape/weight words (e.g. fat). Differences in response patterns have also been detected
between patients with AN and BN, with the former group having greater difficulty colour
naming food–related words and the latter group responding more slowly to body shape and
weight words (Ben-Tovim and Walker, 1991; Channon, Hemsley, and de Silva, 1988; Cooper
and Todd, 1997). Observed colour-naming latencies and interference effects are thought to be
the result of difficulties attending to emotionally salient and highly evocative stimuli. These
data provide compelling evidence that patients with AN selectively attend to, and prioritize,
schema-congruent stimuli. It is unclear, however, whether these cognitive patterns are
etiological in nature or a by-product of chronic hunger and starvation. Some data have shown
that hunger alone is not sufficient to account for these observed effects. For example,
Placanica, Faunce, and Job (2002) examined the effect of hunger on attention in a sample of
female undergraduate students. While fasting increased the detection of high-calorie food
words across the entire sample, individuals with elevated drive for thinness and body
dissatisfaction scores processed food words significantly faster than participants with low
scores. More research is needed to further understand the nature of the relationship between
cognitive biases and the development of AN.
Sociocultural Factors
While the association between disordered eating and socio-cultural influences are
commonly acknowledged in the literature, the degree to which such factors play a causal role
in AN is widely debated (Keel and Klump, 2003; Striegel-Moore and Smolak, 2002).
Feminist and sociological theories of the etiology of AN have long proposed that cultural
ideals of beauty, sex-role stereotypes, and the increasing demands on women to occupy
multiple roles have oppressed women and presented them with conflicting messages about
their bodies and their relationships with food (Szmukler and Patton, 1995; Stice, 2002).
Given the disproportionately greater prevalence of AN among Caucasian women in
Westernized societies, many have suggested that the emphasis and value placed on
slenderness in modern society (and the concurrent hostility toward overweight body types)
facilitate and reinforce the internalization of a “thinness ideal”, particularly among women
(Harrison and Cantor, 1997; Mills, Polivy, Herman, and Tiggerman, 2002). Internalization of
the thinness ideal occurs when an individual accepts and integrates societal norms and
expectations about body weight and shape into her developing self concept. As a result, self-
esteem and self-worth become dependent upon one’s perceived ability to approximate and
successfully achieve such standards. The inherent paradox, however, (i.e., that cultural
standards for weight and shape are virtually unattainable and unrealistic for the majority of
women) tends to foster body dissatisfaction, cultivate a drive for thinness, and promote
dieting behaviour; factors that have each been identified as prominent risk factors for the
development of disordered eating.
In lab settings, with both clinical and non-clinical populations, exposure to thin media
images is associated with greater negative affect and body dissatisfaction. Yamamiya, Cash,
Melnyk, Posavac and Posavac (2005) found that degree of internalization moderated the
effect on mood and body shape concerns among a sample of 123 college females exposed to
a five-minute display of thin fashion models. The impact of the messages espoused by
industrialized countries on non-industrialized societies has also been studied. Investigations
evaluating the influence of television exposure among a sample of female adolescents from
Fiji found that exposure to Western media was related to an increased desire to reshape the
body, identification with female television characters as role models, and greater eating
disordered attitudes and behaviours (Becker, 2004; Becker, Burwell, Gilman, Herzog, and
Hamburg, 2002). Similarly, the degree to which one’s peer group ascribes to culturally
sanctioned weight ideals is correlated with a greater likelihood of body dissatisfaction and
low self-esteem. For example, Mills and Miller (2007) reported that restrained eaters (i.e,
chronic dieters) were more likely to rate themselves as heavier, less attractive, and more
depressed when a same-sex peer (e.g., a fellow undergraduate student), compared to a same-
sex non-peer (e.g., a PhD student), guessed their weight to be 15 pounds heavier than their
actual weight. Peer influences appear to play an important role in the promotion of body
dissatisfaction, social comparison, and dieting behaviours (Grigg, Bowman, and Redman,
1996; Schutz, Paxton, and Wertheim, 2002; Stice, Maxfield, and Wells, 2003). Individuals
suffering from AN have identified weight and shape-based teasing and pressures to be thin by
female peers as contributory factors in the development of their disorder (Nilsson
Abrahamsson, Torbiornsson, and Hagglof, 2007; Tozzi, Sullivan, Fear, McKenzie, and Bulik,
2002).
While these findings paint a compelling picture of the detrimental effects of sociocultural
ideas linking beauty and success with thinness, these particular influences alone fail to
account for the relatively low base rate of AN in the general population. In contrast to the
increasing incidence rates of BN over the past several decades, rates of AN have remained
relatively stable over time (Willi, Giacometti, and Limacher, 1990) . Given the pervasiveness
of the media and the fact that significant numbers of adolescents (McVey, Tweed, and
Blackmore, 2004) and adult women are dieting at any one point in time, one would expect to
observe a much greater prevalence of AN in Westernized societies. In contrast, only a small
proportion of individuals exposed to the noxious influence of the media go on to develop the
disorder. It is best to conceptualize societal pressures and cultural influences as
environmental risk factors that promote dieting behaviours and poor body image and interact
with genetic factors in biologically vulnerable individuals to produce the illness; i.e., gene-
environment correlation (Bulik et al., 2005). It is important to clearly distinguish the severe
psychiatric illness of AN which has genetic and psychopathological determinants from the
type of body dissatisfaction and aberrant eating beahviour which is ubiquitous among young
women in most Westernized societies.
Furthermore, there is increasing evidence that AN exists in non-industrialized societies
where the influence of Western culture is either unlikely or non-existent. In their review of
the literature, Keel and Klump (2003) identified cases of AN in India, Malaysia, Nigeria,
Hong Kong, and Pakistan. Documented cases of self-starvation, sometimes leading to death,
also date back to the 12th century, and possibly earlier (Lacey 1982). Such evidence calls into
question the notion that modern Westernized views of the female body are necessary for the
development of AN. In addition, there are important historical and cross-cultural variations of
the illness which suggest that dominant cultural norms tend to shape and influence the
outward expression of the syndrome as opposed to directly causing the disorder. For
example, the current conceptualization of AN considers weight and shape concerns to be a
defining feature of the illness and a necessary diagnostic criterion. Such concerns, however,
are endorsed with far less frequency in historical writings and in non-industrialized societies
among individuals who otherwise meet diagnostic criteria (e.g., Hong Kong; Lee, Ho, and
Hsu, 1993). It appears as though the presentation of AN and the specific motivations for food
refusal (e.g., religious devotion, gastric discomfort) is culturally dependent but that the
disorder itself is not culture-bound.
Family Systems and Environmental Risk Factors

Family dysfunction and negative childhood experiences have consistently been
implicated as significant contributory factors (Beresin, Gordon, and Herzog, 1989; Button
and Warren, 2001; Tozzi et al., 2002). Much has been written over the decades regarding the
role of family dynamics as a contributory factor in the development of AN (Bruch, 1978;
Minuchin, Rosman, Baker, and Lester, 1978). Hilde Bruch (1978) proposed that several
characteristic traits of the disorder (e.g. emotional distress, low self-esteem, a sense of
ineffectiveness) were partially the result of insufficiently met needs in childhood and
inadequate maternal validation. Individuals with AN consistently describe their early home
environments as controlling and emotionally invalidating. In their qualitative study exploring
causes of AN, Tozzi et al. (2002) reported that the most frequently cited etiological factor
was a dysfunctional family environment. Families are often described as intrusive, enmeshed,
overbearing, and adverse to the emotional and psychological needs of the developing child
(Beresin et al., 1989; Garfinkel and Garner, 1982; Polivy and Herman, 2002). Research has
also demonstrated that AN families have more difficulty resolving conflict and are less
communicative with one another (Lattimore, Wagner and Gowers, 2000). Less secure, and
more avoidant /anxious attachment styles have also been implicated as salient predisposing
factors (Latzer, Hochdorf, Bacher and Canetti, 2002; Ward and Gowers, 2003). Marital
discord, high parental expectations, expressed value on thinness, and chronic dieting
behaviours in the home have also been hypothesized to exacerbate body dissatisfaction and
disordered eating. Given that AN typically develops during adolescence, these data
underscore the importance of understanding the relative contribution that dysfunctional
family dynamics play in the pathogenesis the illness. Having said this, much of the
disturbance in family dynamics seen in the families of individuals with AN is more likely the
result of having a child who is tenaciously pursuing thinness and engaged in self starvation
rather than being directly causative of the disorder.
Recent research has also identified that having a mother with either an active eating
disorder or a past history of one is an environmental risk factor for AN (Mazzeo, Zucker,
Gerke, Mitchell, and Bulik, 2005). Disturbed feeding practices (Russell, Treasure, and Eisler,
1998), disturbed attitudes towards feeding and weight (Stice, Agras, Hammer, 1999),
conflictual mealtime interactions (Stein, Woolley, Cooper, and Fairburn, 1994) interference
with parenting and meeting the child’s needs (Stein and Woolley, 1996), and difficulties with
interpersonally relating to their children ( Franzen and Gerlinghoff, 1997) have all been
reported to contribute to this risk.
Patients with AN have also reported an association between symptom onset and stressful
life transitions. Advancing from high school to university, moving to a new home, losing a
close friend, or experiencing difficulties in intimate relationships have frequently been
identified as precipitating factors (Beresin et al., 1989; Nilsson et al., 2007; Tozzi et al.,
2003). Childhood sexual abuse has also been implicated as a risk factor for the development
of AN. While trauma histories are not uncommon among individuals with AN and continue
to be an important focus of research and treatment, the empirical evidence to date does not
support a direct, causal link between trauma exposure and the development of the illness
(Brewerton, 2005; Wonderlich, Brewerton, Jocic, Dansky, and Abbott, 1997). At this time,
there is a stronger association between sexual abuse and the development of BN rather than
AN (see Fallon and Wonderlich, 1997 and Brewerton, 2005 for review).
Conclusion
Notable advances have been made in recent years with respect to our understanding of
the risk factors that contribute to the development of AN. The goal of this chapter was to
provide a comprehensive overview of the etiological factors that have been empirically
identified to date. While the precise mechanisms and associations between these risk factors
are yet to be determined, the data presented in this chapter highlight that AN is a distinct and
multi-determined serious clinical disorder. The precise interactional effects between
predisposing biological, social, and psychological determinants is unique to each individual
and understanding these interactions is key to our ability to effectively treat this complex and
debilitating illness.
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Chapter II
Overview of Evidence on the

Underpinnings of Bulimia Nervosa
Timothy D. Brewerton
Medical University of South Carolina
Charleston, South Carolina, USA
Abstract
There is no single etiology or basis for any of the eating disorders, including bulimia
nervosa, but similar to other mental disorders, bulimia results from the dynamic interplay
between biological, psychological and social factors that operate along a developmental
continuum. In this chapter these factors are further subdivided into predisposing,
precipitating and perpetuating factors (the “3 P’s), which creates nine categories of
underpinnings from which to examine the evidence as it relates to bulimia nervosa.
Latent vulnerability theory suggests strong genetic predisposing factors linked to anxiety,
harm avoidance, obsessive-compulsiveness and drive for thinness, which are exposed,
triggered and/or exacerbated by behaviors geared toward weight loss. Among a host of
psychosocial factors, traumatic experiences often play important roles in predisposing,
precipitating and perpetuating bulimic disorders, especially when there is psychiatric
comorbidity.
Introduction
This chapter will review the underpinnings of bulimia nervosa (BN). In essence,
underpinnings refer to the underlying foundations or bases of a condition. Such an
understanding is a complex one that encompasses multiple levels or layers interacting over
time. At the outset it is important to unequivocally state that there is no single cause or basis
of any of the eating disorders (EDs), including BN. Nevertheless, one traditional approach to
this etiological conundrum is to think of BN, like any other mental illness, as a result of a
dynamic interplay between biological, psychological and social factors. Because these factors
20 Timothy D. Brewerton
interact along a developmental continuum in which nature and nurture interact, for the sake
of this discussion we can further subdivide these layers into the “3 P’s,” i.e., predisposing,
precipitating and perpetuating factors. This creates nine categories of underpinnings from
which to examine the evidence as it relates to BN. In the previous chapter the underpinnings
of anorexia nervosa (AN) are reviewed, and in the following chapter those of binge eating
disorder (BED) are reviewed. Many, but not all of these underpinnings, may also be relevant
for BN. This chapter will seek to highlight those underpinnings that are more specific for BN
(and to some extent the binge-purge type of AN).
Although Russell is often given credit for first reporting BN, which he described as “an
ominous variant of anorexia nervosa” (1979), it was Boskind-Lodahl (1978) who described
bingeing and purging in normal weight women first, a phenomenon she called bulimarexia.
She perceived this condition as a Western culture-bound syndrome that developed from
society’s preoccupation with female thinness as well as its patriarchal oppressive restrictions
of female gender roles. The Diagnostic and Statistical Manual of Mental Disorders (DSM)
included bulimia for the first time in 1980 (American Psychiatric Association, 1980) and the
term was changed to bulimia nervosa in DSM-III-R in 1987 (American Psychiatric
Association, 1987).
Latent vulnerability theory provides an overarching, interactive perspective for
understanding the underpinnings of BN. It goes a long way toward answering the question of
why so many young women begin dieting but only a small minority of these go on to develop
the illness of BN. In short, dieting, bingeing, purging and exercise all alter neurochemistry,
which then expose a genetically mediated latent vulnerability. In other words, “genetics loads
the gun and environment pulls the trigger.” The remainder of this chapter will seek to
illuminate these processes or underpinnings in more detail.
Predisposing Biological Underpinnings

Gender
Gender is an indisputable characteristic of BN. One of the most consistent findings in

epidemiological studies is that BN occurs significantly more frequently in females than
males. Depending on the study the ratio of females to males ranges from 10:1 (American
Psychiatric Association, 2004; Hsu, 1996; Lewinsohn, Hops, Roberts, Seeley and Andrews,
1993; Neilsen, 1990; Schotte and Stunkard, 1987; Paton, Selzer, Coffey, Carlin and Wolfe,
1999; Vollrath, Koch and Angst, 1992; Whitaker, Johnson, Shaffer, et al., 1990) to 3:1
(Hudson, Hiripi, Pope, Kessler, 2007). Since gender is an unchangeable characteristic and
uneven gender distributions have been found for several other mental disorders, female status
appears to be a non-specific risk factor for BN.
Overview of Evidence on the Underpinnings of Bulimia Nervosa 21
Genetics
There is indisputable evidence from well-controlled twin and family studies that BN (like
all EDs) runs in families. Twin studies with large sample sizes indicate that as much as 60%
to 83% of bulimia’s etiological variance is due to genetic factors (Bulik, Sullivan and
Kendler, 1998). In a major family history study involving 504 probands and over 1800
relatives, the risk that a first degree relative of a bulimic proband also had BN was four times
greater than a first degree relative of a non-bulimic proband (p < 0.05) (Strober, Freeman,
Lampert, Diamond and Kaye, 2000). In summary, heritability estimates for BN have been
reported to be on the order of 0.5-0.8 (Bulik, Sullivan, Wade and Kendler, 1998; Fichter and
Noegel 1990; Holland, Hall, Murray, Russell and Crisp, 1984; Holland, Sicotte and Treasure,
1988; Hsu, et al 1990; Kendler et al 1991, 1995; Klump et al, 2002; Treasure and Holland
1990; Walters and Kendler, 1995).
One might ask what exactly is heritable. How is this genetic transmission accomplished?
Studies indicate that not only are EDs inherited, but other related disorders that may
predispose the individual to develop BN are also genetically mediated. These include anxiety
and mood disorders as well as temperament and the personality traits of perfectionism,
obsessionality, compulsivity, novelty seeking, sensation seeking and impulsivity. In addition,
low self esteem, a trait quite common in BN and all eating disorders, been shown to be due in
large part to genetic factors, a finding that is contrary to conventional social wisdom
(Kendler, Gardner and Prescott, 1998).
In summary, AN, BN, EDNOS diagnoses and symptoms are transmitted in families. In
addition, AN and BN are cross transmitted, and AN and BN are highly heritable. Family
members have similar mood and temperament traits. Suspect genes have been identified. In
particular, chromosome 10 has been implicated in BN (Bulik, Devlin, Bacanu, et al., 2003).
Trait-Related Biological Differences
Biological differences that appear to be related to specific personality traits linked to BN

have been noted in the literature (Brewerton and Steiger, 2004). In comparison to healthy age
matched controls, persistent alterations in serotonergic activity have been reported in women
following long-term recovery from BN (> 1 year), including increased cerebrospinal fluid
(CSF) concentrations of 5-hydroxyindoleacetic acid (5-HIAA), the major metabolite of 5-
hydroxytryptamine or serotonin (Kaye, Greeno, Moss, et al., 1998), reduced 5-HT2A receptor
activity on positron emission topography (PET) scanning (Kaye, Frank, Meltzer, et al., 2001),
and reduced platelet [(3)H]paroxetine binding (Steiger, Richardson, Israel, et al., 2005).
Furthermore, as in AN, these CSF 5-HIAA alterations have been found to correlate with
obsessive-compulsive personality traits, perfectionism and behavioral inhibition, which are
associated with a hypothetical tendency towards a hyper-serotonergic status. Given these
results in recovered bulimic patients, it could be hypothesized that a disturbance of 5-HT
activity may be part of the genetically determined biological vulnerability for the
development of an ED including BN. However, whether these findings represent a true
premorbid biological liability or a consequence of the ED itself cannot be definitively
determined from these results. To tease out this issue studies of transmitter function in at-risk
pre-morbid individuals as well as non-affected identical and fraternal twins, siblings, and
other first-degree relatives of ED patients, could begin to confirm trait related disturbances
(Brewerton and Steiger, 2004). To this end, Steiger, Gauvin, Joober, et al. (2006) studied
paroxetine binding in the unaffected mothers and sisters of recovered patients with BN and
found that they too had reduced platelet [(3)H]paroxetine binding compared to healthy
controls and their mothers and sisters. Furthermore, there were significant within family
correlations for Bmax, which indicates a heritable trait or endophenotype possibly linked to
serotonin function and passed on by those with BN and their first degree relatives.
Age
In both clinical and population-based surveys, the peak incidence of EDs has been found
in the age range from adolescence to early adulthood (Woodside and Garfinkel, 1992). BN
typically begins later in life than AN, usually between the ages of 18 and 23 years, although
onset may be variable. Clinical samples report earlier onset whereas representative and
community samples report later onset (Dansky, Brewerton, O’Neal and Kilpatrick, 1997).
Ethnicity and Race
Eating disorders have been usually considered primarily Caucasian phenomena (Striegel-
Moore and Smolak, 1996), but more recent literature has seriously challenged this notion.
Results indicate that the ethnic distribution is much more complicated (Crago, Shisslak, and
Estes, 1996; Smith and Krejci, 1991) with Native Americans reported as having higher rates
of EDs than Caucasians, and Hispanics having comparable rates as Caucasians. Studies have
indicated lower rates of BN among Asians (Chen, Wong, Lee, Chan-Ho, Lau and Fung,
1993; Ohzeki, Hanaki, Motozumi, et al., 1990), while other studies have indicated
comparable rates of BN in Black women (Field, Colditz, and Peterson, 1997; Le Grange,
Telch, and Tibbs, 1998; Pumariega, Gustavson, Gustavson, Motes, and Ayers, 1994). Still
others report higher rates of laxative abuse, diuretic abuse, and/or self-induced vomiting in
young Black women (Emmons, 1992; Field et al., 1997).
Pregnancy and Perinatal Complications
In a large population-based study by Foley, Thacker, Aggen Neale and Kendler (2001)
complications of pregnancy were associated with a significantly increased risk for later
developing BN. It was notable that these complications were not associated with the other
psychiatric disorders but were specific for BN. Increased rates of perinatal complications
have been reported in the histories of patients with both AN and BN (Favaro, Tenconi and
Santonastaso, 2006). In this well-controlled study, patients with BN had significantly higher
odds ratios for a number of complications, including hyporeactivity, low birth weight for
gestational age, and early feeding problems. In addition, a highly significant odds ratio of 7.7
for developing BN was found for those patients with 2 or more complications (p < 0.001).
Seasonality of Birth
In a related area of research, Brewerton, Dansky, O’Neil, and Kilpatrick, (2007) reported
significant alterations in the season of birth of individuals who later developed BN. Using
results from the National Women’s Study women with BN were more likely to be born in the
fall and less likely to be born in the spring than women without BN. Similar seasonal findings
have been fruitful in schizophrenia research in which an excess of winter births led to the
identification of a relationship between intrauterine influenza and later onset of schizophrenia
(neurodevelopmental aspects).
BMI and Obesity
Obesity during childhood has been reported to be an important risk factor for the
subsequent development of BN and its symptoms. Fairburn, Welch, Doll, Davies and
O`Connor (1997) reported that 40% of the bulimics vs. 13% of psychiatric controls and 15%
of normal controls retrospectively reported childhood obesity. In addition, the bulimic
subjects reported more parental obesity than subjects in either of the comparison groups.
Childress, Brewerton, Hodges and Jarrell (1993) found that middle school children who
reported bulimic symptoms such as vomiting to lose weight were heavier than those children
without bulimic symptoms. Some longitudinal studies have also found that higher BMI or
body fat is predictive of disordered eating (Killen, Taylor, Hayward, et al., 1994; Patton,
Johnson-Sabine, Wood, Mann and Wakeling, 1990; Vollrath, Koch and Angst, 1992).
However, this has not been true for all studies (Killen, Taylor, Hayward, et al., 1994; Patton,
Selzer, Coffey, Carlin and Wolfe, 1999; Gowen, Hayward, Killen, Robinson and Taylor,
1999). Nevertheless, higher BMI appears to be an important risk factor for BN.
Pica and Early Digestive Problems
Marchi and Cohen (1990) found pica, early digestive problems, and weight reducing
efforts to be related to later bulimic symptoms. The risk of BN was found to be almost seven
times higher in those individuals with early childhood pica. However, this was not found in
another longitudinal study (Kotter, Cohen, Davies, et al., 2001
Family History of Psychopathology
Many, many studies report elevated rates of an array of psychiatric disorders in first-
degree relatives of patients with BN, including other EDs, anxiety disorders, mood disorders,
substance use disorders and cluster B personality disorders (Jacobi, Hayward, de Zwaan,
Kraemer, and Agras, 2004; Lilenfeld, 2004). Unfortunately, the temporal relationship of the
psychiatric disorders of patients’ family members in relationship to the onset of BN in the
patients was not addressed in any of these studies. However, selected parental psychiatric
disorders occurring prior to the onset of the child’s BN were assessed retrospectively in a
study by Fairburn, Welch, Doll, Davies and O`Connor (1997), who found that parental
depression, parental alcoholism, and parental drug abuse predating the onset of the BN were
significantly more frequent in patients compared to normal controls. Interestingly, parental
alcoholism was even more frequent in the relatives of BN patients compared to those of
psychiatric controls.
Predisposing Psychological Underpinnings
Perfectionism and Obsessive-Compulsive Personality Traits

In their retrospective assessment of reputed risk factors Fairburn, Welch, Doll, Davies
and O`Connor (1997) found that premorbid perfectionism was elevated in bulimic patients
when compared to healthy controls. However, measures in the BN group did not differ from
psychiatric controls. More recently, Halmi, Tozzi, Thornton, Crow, Fichter et al., (2005)
demonstrated that perfectionism and obsessionality are core features of EDs, regardless of
diagnosis. In a large sample of ED subjects, they found no differences across diagnostic
subtypes in the prevalence of obsessive-compulsive personality disorder (OCPD) and
obsessive-compulsive disorder (OCD), or with the association between OCPD and OCD.
Perfectionism was noted to be highest in individuals with OCPD with or without concomitant
OCD. The authors emphasized that our developing understanding of the relationship between
these traits and EDs may ultimately enhance our ability to identify pertinent behavioral
endophenotypes for EDs, but the combination of perfectionism with OCPD may be a
fundamental core behavioral feature underlying vulnerability to ED.
Establishing that perfectionism predates BN in longitudinal studies has been difficult. In
one study (Killen, Taylor, Hayward, et al., 1994; 1996) measures of perfectionism at time one
were not linked to subsequent disordered eating in multivariate analyses but did discriminate
between symptomatic and asymptomatic girls at baseline in univariate comparisons (Killen,
Taylor, Hayward, et al., 1994). In addition, studies by Leon, Fulkerson, Perry and Early-Zald
(1995) and Leon, Fulkerson, Perry, Keel and Klump (1999) did not find perfectionism to be
predictive in multivariate comparisons.
Low Self-esteem
The other side of perfectionism is low self-esteem. When one’s actions can “never be
good enough,” then one always “falls short” and feels badly about oneself. Low self-esteem
has been noted to be an important risk factor for the development of BN (Fairburn, Welch,
Doll, Davies and O`Connor, 1997). Although this is typically thought of as a purely
psychological phenomena twin studies show that self-esteem has a strong genetic component
with as much as 50% of the variance being accounted for by genetic factors (Kendler,
Gardner and Prescott, 1998). Patients with BN have consistently been found in the literature
to possess lower self-esteem than healthy controls (Jacobi, Paul, de Zwaan, Nutzinger and
Dahme, 2000). The retrospective assessment of self-concept and its temporal relation to onset
of the BN has been considered in two cross-sectional studies. Fairburn, Welch, Doll, Davies
and O`Connor (1997) found negative self-evaluation prior to onset of ED to be more common
in BN subjects than in healthy and psychiatric controls. Low self-esteem was also reported by
Raffi, Rondini, Grandi and Fava (2000) to be one of several prodromal symptoms of patients
with BN as compared to controls. Kendler, MacLean, Neale, Kessler, Heath and Eaves
(1991) also found that low self-esteem was a major risk factor for BN in a large group of
twins.
Measures of self-concept have been included in four longitudinal studies. In the studies
by Leon, Fulkerson, Perry, and Early-Zald (1995) and Calam and Waller (1998) they did not
prove to be important predictors. On the other hand, low self-esteem predicted elevated
Eating Attitudes Test (EAT) scores four years later in the study by Button, Sonuga-Barke,
Davies, and Thompson (1996). Girls in the lowest self-esteem range had an eightfold
increased risk for a high EAT score (≥ 20) compared to those with high self-esteem.
Similarly, Ghaderi and Scott (2001) reported significantly lower self-esteem at time one for
the group that developed an ED two years later.
Ineffectiveness
Early on Hilda Bruch noted a “profound sense of ineffectiveness” in patients with EDs
(1973). This hypothesis as applied to BN and bulimic symptoms was tested using the Eating
Disorder Inventory (EDI)-Ineffectiveness subscale in four longitudinal studies (Leon,
Fulkerson, Perry, Early-Zald, 1995; Leon, Fulkerson, Perry, Keel Klump, 1999; Taylor,
Hayward, Haydel, Wilson, et al., 1996). The EDI-Ineffectiveness scale score was found to be
predictive of disturbed eating patterns or bulimic caseness in one study using multivariate
analyses (Leon, Fulkerson, Perry, Keel Klump, 1999). Significant differences, however, were
found in the univariate comparisons of the subsequent symptomatic and the asymptomatic
groups (Killen, Taylor, Hayward, Wilson, Haydel, et al., 1994; Killen, Taylor, Hayward,
Haydel, Wilson, et al., 1996).
Anxiety and Mood Disorders

Psychiatric disorders, particularly anxiety and mood disorders have long been
hypothesized to play a primary role in the development of EDs, including BN. Bulik,
Sullivan, Fear and Joyce (1997) compared prevalence and onset of co-morbid childhood
anxiety disorders in anorexics, bulimics and clinical as well as healthy controls. They noted
the prevalence of social phobia to be highest in the bulimic group, and overanxious disorder
highest in both the bulimic and anorexic groups. In terms of chronology of onset, 94% of
women with BN with lifetime anxiety disorders reported that their anxiety disorder predated
the onset of their BN. Fornari et al (1992) reported anxiety disorders to be as prevalent as
depressive disorders in individuals with an ED. Brewerton, Lydiard, Herzog, Brotman, O'Neil
and Ballenger (1995) also reported high rates of anxiety disorders in a group of patients with
BN and that the anxiety disorders predated the onset of BN in 70% of cases. Social phobia
was the most common anxiety disorder noted in this sample. These and many other authors
have also noted higher rates of mood disorders, particularly major depressive disorder, among
subjects with BN (Brewerton, Lydiard, Herzog, Brotman, O'Neil and Ballenger, 1995;
Dansky, Brewerton, O’Neil and Kilpatrick, 1997; Lilenfeld, 2004). In addition, in a large
non-treatment seeking, representative sample of women in the United States, Dansky,
Brewerton, O’Neil and Kilpatrick (1997) found higher rates of both lifetime and current
posttraumatic stress disorder (PTSD) in subjects with BN as compared to non-bulimic
subjects. (see trauma below)
Raffi, Rondini, Grandi and Fava (2000) explored mood- and anxiety-related prodromal
symptoms of BN and found a number of symptoms to be significantly more common in BN
patients than controls six months prior to onset. These specifically included depressed mood,
anhedonia, low self-esteem, irritability, impaired work performance, generalized anxiety,
reactivity, phobic avoidance, guilt, pessimism and strict dieting. However, to what extent
these symptoms are a result of strict dieting was not addressed in this study. In a study of risk
factors for BN in a large group of twins, Kendler, MacLean, Neale, Kessler, Heath and Eaves
(1991) reported that an external locus of control and high levels of neuroticism were
predictive of BN.
Negative emotionality has also been found to predict eating disturbances and disorders in
a number of longitudinal studies (Attie and Brooks-Gunn, 1989; Graber, Brooks-Gunn,
Paikoff and Warren, 1994; Killen, Taylor, Hayward, et al., 1996; Leon, Fulkerson, Perry and
Early-Zald, 1995; Leon, Fulkerson, Perry, Keel and Klump, 1999; Patton, Johnson-Sabine,
Wood, Mann and Wakeling, 1990; Patton, Selzer, Coffey, Carlin and Wolfe, 1999). For
example, in the study by Patton et al. (1990) the change score in general psychiatric
morbidity was found to be the lone predictor of bulimic caseness. Psychiatric morbidity also
was found to predict the onset of EDs (apart from dieting status) in a subsequent study by
Patton et al. (1999). Subjects in the highest psychiatric morbidity category revealed a nearly
sevenfold increased risk of developing an ED. Leon et al. (1999) reported that negative
affectivity was the only statistically significant predictor of ED risk assessed three to four
years later. Finally, in the study by Killen et al. (1996), the temperament scales, distress and
fear, discriminated symptomatic from asymptomatic girls
Novelty Seeking, Sensation Seeking, and Impulsivity

The personality traits of novelty seeking, sensation seeking, and impulsivity, which
appear to be related to each other, have all been linked to BN by a variety of investigators
(Bailer, Price, Meltzer, et al., 2004; Berg, Crosby, Wonderlich, and Hawley, 2000; Bloks,
Hoek, Callewaert, van Furth, 2004; Brewerton, 1995; Brewerton et al., 1992; Brewerton,
Paolone, Soefje, 2002; Bulik, Sullivan, Weltzin, Kaye, 1995; Bulik, Sullivan, McKee,
Weltzin, and Kaye, 1994; Cassin and von Ranson, 2005; Fassino, Abbate-Daga, Amianto,
Leombruni, Boggio, and Rovera, 2002; Fassino, Amianto, Gramaglia, Facchini, and Abbate
Daga, 2004; Fernandez-Aranda, Jimenez-Murcia, Alvarez-Moya, Granero, Vallejo and Bulik,
2006; Kleifield, Sunday, Hurt, and Halmi, 1994; Klump, Strober, Bulik, et al. 2004;
Mizushima, Ono and Asai, 1998; Mulder, Joyce, Sullivan, Bulik and Carter, 1999; Schmeck
and Poustka, 2001; Steiger and Bruce, 2007; Tomotake and Ohmori, 2002; Vervaet and van
Heeringen, Audenaert, 2004; Wade, Bulik, Prescott and Kendler, 2004). Many clinical
researchers have conceptualized a number of bulimic symptoms and behaviors in terms of
impulsivity, including bingeing, purging, substance abuse, stealing, self-injury, suicide, and
sexual acting out. Lacey and Evans (1986) coined the phrase “multi-impulsive bulimia,”
which has been shown to carry a poor prognosis. In addition, Wonderlich, Crosby, Mitchell,
and colleagues (2001) found that impulsivity mediated the effects of childhood trauma on the
development of bulimic symptoms.
Girls who later turned out to be symptomatic in the study by Killen et al. (1994) showed
elevations on subscales of Aggressive and Unpopular in a personality inventory when
compared to asymptomatic girls. Girls who developed a partial syndrome in the study by
Killen et al. (1996) had higher 30-day prevalence of alcohol consumption. High use of
escape-avoidance coping as well as low perceived social support were found to be
prospective risk factors for subsequent EDs, primarily BN and BED, in the study by Ghaderi
and Scott (2001).
Trauma, Neglect and PTSD

Accumulating evidence indicates that BN, unlike restricting AN, is a trauma-related
disorder (Brewerton, 2003; 2004; 2005; 2007; Wonderlich, Brewerton, Jocic, Dansky and
Abbott, 1997). It is now well established that prior traumatic or victimization experiences are
nonspecific yet significant risk factors for the development of BN, especially when in
association with other comorbid psychopathology such as anxiety, mood, substance use and
personality disorders. Many, many studies now confirm this relationship as shown in meta-
analyses (Smolak and Murnen, 2002; Molinari, 2001) and major reviews (Jacobi, Hayward,
de Zwaan, Kraemer and Agras, 2004). However, despite the plethora of studies indicating
higher than expected rates of prior abuse experiences in BN patients, very few studies have
also examined for the presence of current and lifetime PTSD, which is a more powerful
predictor of BN than abuse per se (Brewerton, 2007; Dansky, Brewerton, O’Neil, and
Kilpatrick, 1997).
The National Women’s Study (NWS) remains the most comprehensive study of the
relationship of trauma history and PTSD to EDs and related comorbidity. Detailed histories
of crime victimization experiences (rape, molestation, attempted sexual assault, and
aggravated assault), PTSD, major depressive disorder, EDs, and substance abuse/dependence
were obtained using DSM-III-R and DSM-IV (BED) criteria (Dansky, Brewerton, O’Neil and
Kilpatrick, 1997). Rape and molestation was reported to have occurred approximately twice
as often in BN participants compared to non-bulimic participants, while aggravated assault
was three times as common. In the great majority of cases the age of victimization occurred
prior to the age of first binge. For example, the age of first rape occurred before the age of 1st
binge in 84% of all BN rape cases. These results provide substantial validity to the notion
that victimization is indeed a causative risk factor for BN, albeit a non-specific one.
However, the subsequent development of PTSD following victimization appears to incur the
greatest risk of developing BN. The age of first binge (in BN) was significantly earlier in
cases of rape resulting in PTSD compared to those with rape not resulting in PTSD or no
rape. In addition, prevalence rates for BN were significantly higher in subjects with rape
histories with PTSD (10.4%) compared to those with rape histories without PTSD (2.0%) or
those with no rape (2.0%). This strongly suggests that PTSD rather than prior abuse per se
best predicts the development of BN. In both the National Comorbidity Study and the
National Women’s Study, psychiatric comorbidity was highly associated with a history of
serious victimization and especially a lifetime history of PTSD (Kessler Sonnega, Bromet,
Hughes, Nelson, 1995). The odds ratios for several major axis I disorders have been reported
to be on the order of 2.4 to 4.5 in both the National Comorbidity Study and the National
Women’s Study in participants with PTSD compared to those without PTSD. In other words,
PTSD itself is a strong predictor of psychopathology including BN.
Besides a lifetime history of PTSD, other specific features of childhood sexual abuse
(CSA) have been found to be associated with the development of BN, including decreased
social competence, a poor maternal relationship, unreliable parenting, and greater severity of
CSA (Wonderlich, Brewerton, Jocic, Dansky and Abbott, 1997). Interestingly, most of these
features are also predictive of PTSD in the face of trauma.
Johnson, Cohen, Kasen and Brook (2002) conducted the most comprehensive
longitudinal study on childhood adversities (including CSA, physical abuse (PA), and
neglect), and the subsequent development of eating- or weight-related problems, including
EDs. The participants in this study included a large community-based sample of mothers and
their offspring (n = 782) who were followed over an 18-year period. This study further
established CSA as important predictor of BN and bulimic disorders. In addition, the role of
physical neglect in forecasting disturbed eating behaviors was demonstrated.
Alexithymia
Alexithymia is the inability to put one’s emotions into words, a psychological
characteristic originally described in patients with a variety of psychosomatic disorders. In
addition, alexithymia refers to a diminished fantasy life and confusion of physical sensations
often associated with emotions. Measures of alexithymia have been reported to be common in
individuals with EDs and/or related conditions, such as mood, anxiety, substance use and
dissociative disorders. Specifically, a number of investigators have described high rates of
alexithymia in patients with BN (Cochrane, Hodges, Brewerton, 1993; Jimerson, Wolfe,
Franko, Covino, and Sifneos, 1994). Interestingly, Espina (2003) reported that the parents of
daughters with EDs show higher scores on measures of alexithymia than the control parents.
These data suggest that alexithymia may be a familial condition which predisposes to the
development of eating and related disorders.
Predisposing Social Underpinnings

Cultural Pressures for Thinness
Notwithstanding the powerful biogenetic contributions to the development of EDs noted

previously, it is evident from a number of sources that sociocultural factors also predispose
toward the development of EDs, including BN. Cross-cultural studies indicate significant
variations in the prevalence rates of EDs, which have led investigators to conclude that
specific sociocultural factors are influential. Although EDs are found in all socioeconomic
status (SES) groups, they do occur more frequently in cultures and subcultures that promote
thinness and place a great deal of emphasis on the control of body shape and weight
(Anderson-Fye and Becker, 2004). Such cultures are typically those that are said to be
industrialized or “Westernized.” In a study of risk factors for BN in a large group of twins in

the U.S., Kendler, MacLean, Neale, Kessler, Heath and Eaves (1991) demonstrated that birth
after 1960 and a slim ideal body image were significant risk factors for bulimia. In addition,
to cultural ideals favoring thinness, other cultural factors that may predispose toward EDs
include exposure to TV and print media, cultural and social transition (see acculturation), and
modernization (Becker, Burwell, Gilman, Herzog, and Hamburg, 2002; Stice, Maxfield, and
Wells, 2003). Specific subcultures have also been reported to have higher prevalence rates of
EDs, such as homosexual men, and occupations or activities that place a high premium on
thinness, weight loss, beauty and physical appearance, such as models, actresses, dancers,
gymnasts, wrestlers, etc, or on food preparation (Hodges, Stellefson, Jarrell, Cochrane, and
Brewerton, 1999).
Acculturation
Acculturation is the process of adopting the cultural traits or social patterns of another
group. Several reports indicate a connection between the degree of acculturation within
ethnic minorities and the occurrence of eating disorder symptoms, including those of BN
(Davis and Katzman, 1999; Gowen, Hayward, Killen, Robinson and Taylor, 1999; Hooper
and Garner, 1986).
High Achievement and Athletic Competition
In a comprehensive survey of 522 female elite athletes from six different sport disciplines
(Sundgot-Borgen, 1994), 8% of the surveyed athletes met DSM-III-R criteria for BN.
Slightly more conservative results were obtained in a recent national survey by Johnson,
Powers and Dick (1999), in which 1.1% of the female and none of the male athletes met
DSM-IV criteria for BN, while 9.2% of the female and 0.005% of the male athletes were
reported as having subclinical bulimia
Family Dysfunction
In the majority of the cross-sectional studies on family interaction, functioning or

attachment style, bulimic patients describe various aspects of their family interaction as more
problematic or dysfunctional than healthy controls. Characterizations of “bulimic families:
have included being “less expressive, less cohesive, and experiencing more conflicts than
normal control families” (Hodges, Cochrane, and Brewerton, 1998; Johnson and Flach, 1985;
Laliberte, Boland, Leichner, 1999). In one study families of BN patients were reported to
exhibit significantly more lack of care, indifference, discord, and overall adversity than AN
patients and normal controls, but they did not differ from psychiatric patients with major
depression (Webster and Palmer, 2000). In the community-based study by Fairburn, Welch,
Doll, Davies and O`Connor (1997) parental variables such as low contact, high expectations,
and critical comments about body shape and weight by family members were reported to be
predictive of BN as compared to psychiatric controls. Hanna and Bond (2006) reported that,
even after controlling for BMI, the frequency of negative messages is an important
contributor to disordered eating symptomatology for both secondary school and university
students. In a study by Wade, Bergin, Martin, Gillespie, Nathan, and Fairburn (2006) the
number of lifetime eating disorder behaviors was associated with the degree of impaired
functioning, which in turn was associated with conflict reported between parents and
criticism from parents when growing up. In a survey of 210 undergraduate women at two
universities, Botta and Dumlao (2002) tested the hypothesis that father-daughter
communication and conflict resolution would be related to eating disordered behaviors.
Results indicated that a lack of skilled conflict resolution and open communication between
father and daughter could lead to disordered eating behaviors, and that the presence of such
skills might offset the development of EDs.
In a two-part study Laliberte, Boland, and Leichner (1999) investigated variables thought
to be more directly related to disturbed eating and bulimia as contributing to a "family
climate for eating disorders." In the first study a nonclinical sample of 324 women who had
recently left home for college and a sample of 121 mothers evaluated their families.
Principal-components analyses revealed with three factors loading together for both students
and mothers: Family Body Satisfaction, Family Social Appearance Orientation, and Family
Achievement Emphasis. These factors represented the hypothesized “family climate for
eating disorders” variable, while the rest of the variables loaded with more traditional family
process variables (expressiveness, cohesion, and conflict), which represented more general
family dysfunction. As hypothesized, the family climate for eating disorders factor score was
a more powerful predictor of disturbed eating. The second study tested this finding in a
clinical sample of bulimic patients (n = 40) and depressed patients (n = 17) and healthy
controls (n = 27). Again, the bulimic group scored significantly higher on family climate
variables than healthy controls as well as the depressed group after controlling for depression.
One of the major findings in a large twin study (Kendler, MacLean, Neale, Kessler, Heath
and Eaves, 1991) was that low paternal care was a risk factor for the later development of
BN. Similarly, in a comparison study between 40 women with BN and their non-eating
disordered sisters, insecure paternal attachment significantly predicted the risk for BN
(Lehoux and Howe, 2007).
Annus, Smith, Fischer, Hendricks, and Williams (2007) reported that a history of food-
related teasing from friends and family, negative maternal modeling, and friends' criticism of
eating all related to both adult disordered behavior and adult eating and thinness
expectancies.
Precipitating Biological Underpinnings

Dieting
Abundant evidence supports the contention that dieting is an important precursor of EDs,
including BN. The onset of BN has been observed to occur either during a period of
purposeful dieting (Mitchell, Hatsukami, Pyle and Eckert, 1986; Pyle, Mitchell and Eckert,
1981) or following weight loss (Garfinkel, Modolfsky, and Garner, 1980; Russell, 1979) for
the vast majority of cases (73%-91%). While the studies by Mitchell, Hatsukami, Pyle and
Eckert (1986) and Pyle, Mitchell and Eckert (1981) are rather nondescript about the
chronological sequence of dieting and bingeing, more recent studies have validated the
temporal precedence of dieting before bingeing in most BN subjects (Brewerton, Dansky,
Kilpatrick and O’Neil, 2000; Haiman and Devlin, 1999; Mussell, Mitchell, Fenna, Crosby,
Miller and Hoberman, 1997).
Experimental and laboratory-based studies on restrained eating and diet-induced binge
eating yield further evidence for the relevance of this factor. One of the earliest, albeit
uncontrolled studies demonstrating the effects of prolonged dieting in a non-clinical
population was reported by Keys, Brozek, Hentschel, Mickelsen and Taylor (1950). Besides a
variety of physical, emotional, and social changes following a prolonged period of semi-
starvation and average weight decrease of 25%, binge eating was one of the behavioral
changes reported, a phenomenon that had not been previously observed in the subjects before
the study. Taken together, the cross-sectional research provides strong evidence of the
temporal sequence of first dieting, then binge eating. In a study of risk factors for BN in a
large group of twins, Kendler, MacLean, Neale, Kessler, Heath and Eaves (1991) found that
risk factors for bulimia included a history of wide weight fluctuation, dieting, or frequent
exercise.
A number of longitudinal studies have confirmed that dieting behavior, along with its
associated weight concerns, such as negative body image and fear of weight gain, predicts the
development of bulimic behaviors (Attie and Brooks-Gunn, 1989; Ghaderi and Scott, 2001;
Graber, Brooks-Gunn, Paikoff, and Warren, 1994; Killen, Taylor, Hayward, et al., 1994;
1996; Leon, Fulkerson, Perry and Early-Zald, 1995; Leon, Fulkerson, Perry, Keel and
Klump, 1999; Patton, Johnson-Sabine, Wood, Mann and Wakeling, 1990; Patton, Selzer,
Coffey, Carlin and Wolfe, 1999; Vollrath, Koch and Angst, 1992). Patton, Johnson-Sabine,
Wood, Mann and Wakeling (1990) reported that subjects classified as "dieters" at the outset
were found to have nearly an 8 times higher risk of becoming "cases" than those originally
classified as non-dieters.
Puberty
Based on evidence published by Graber, Lewinsohn, Seeley and Brooks-Gunn (1997)

and Hayward, Killen, Wilson, et al. (1997), early sexual maturation or pubertal timing can be
regarded as a non-specific risk factor for BN. Although this association between EDs and
early sexual maturation has been hypothesized to be a function of increasing BMI (see
obesity/BMI section), some studies don’t support that relationship and some other aspect of
puberty may play a role. Killen, Hayward, Litt, Hammer, Wilson, et al., (1992) examined the
association between stage of sexual maturation and bulimic symptoms in a community-based
sample of 971 adolescent girls enrolled in the sixth- and seventh-grades. Girls manifesting
bulimic symptoms, while not older than their peers without such symptoms, were more
developmentally advanced as determined using Tanner self-staging. The odds ratio for the
association between sexual maturity and symptoms was 1.8 (95% confidence interval, 1.2 to
2.8), while the odds ratio for the association between BMI (adjusted for sexual maturity) and
symptoms was 1.02 (95% confidence interval, 1.0 to 1.05). In addition, there was no
independent statistical effect of age or of the interaction between age and sexual maturity
index. In another study, Field et al. (1999) reported that girls who were further along in their
maturational development were more likely than their less developed peers to begin purging
at least once a month in order to control their weight. Taken together these results suggest
that early puberty may be an important risk factor for the development of BN or bulimic
symptoms independent of age and BMI.
Precipitating Psychological Underpinnings

Life Stressors
In a population-based study Welch, Doll and Fairburn (1997) reported that BN patients
had more life events in the year preceding the onset of their disorder than age-matched
normal controls (18% vs. 5% for > 3 events). Adverse life events also differentiated eating
disordered patients (mixed anorexic and bulimic) from both healthy and psychiatric controls
(Horesh, Apter, Ishai, et al., 1996).
Schmidt, Slone, Tilley and Treasure (1993) reported that BN patients were significantly
more likely to experience a “major difficulty” as well as “pudicity” problems. Taken together,
there is some evidence that bulimic patients experience more severe life events than healthy
controls.
Trauma/neglect/PTSD
Just as traumatic experiences may predispose to the subsequent development of BN, so

can they also precipitate them acutely. The time period between traumatic experiences and
the subsequent development of bulimic symptoms is extremely variable, with onset occurring
anywhere from almost immediately in which vomiting may be in part a disgust reaction to
years later. What determines this timing is likely to be a function of the interaction of other
major risk factors for both BN and PTSD.
Precipitating Social Underpinnings

Peer Pressures
Both clinical experience and research reports indicate that some cases of BN begin with
teasing about weight or appearance. In a study reported by Lehoux and Howe (2007) the role
of perceived non-shared environmental influences in the risk of developing BN was
compared in 40 women with BN and their non-eating disordered sisters. Perceptions of
teasing distinguished bulimic women from their sisters. In a one year follow-up study of 6982
girls aged 9 to 14 years who denied vomiting, Field, Camargo, Taylor, Berkey, and Colditz
(1999) found that the importance of thinness to peers (OR = 2.3; 95% CI, 1.8-3.0) was
predictive of beginning to purge at least monthly. This finding was independent of age and
Tanner stage of pubic hair development and suggests that peers can clearly exert a negative
influence on girls’ weight control beliefs and behaviors.
Media Messages
In their follow-up study of 6982 girls, Field, Camargo, Taylor, Berkey, and Colditz
(1999) also demonstrated that trying to look like females on television, in movies, or in
magazines (OR = 1.9; 95% CI, 1.6-2.3) was strongly predictive of beginning to purge at least
monthly. This finding was also independent of age and Tanner stage of pubic hair
development. In a related study, Field, Cheung, Wolf, Herzog, Gortmaker, Colditz, (1999)
reported that the majority of preadolescent and adolescent girls studied in this school-based
study of 548 5th through 12th graders were unhappy with their body weight and shape and that
this discontentment was strongly related to the frequency of reading fashion magazines. The
authors observed that the frequency of reading fashion magazines was positively related with
the prevalence of dieting to lose weight, exercising to lose weight or improve body shape,
dieting because of a magazine article, and deciding to exercise because of a magazine article.
Family Dynamics
In a study by Okon, Green, and Smith (2003), 20 adolescent girls diagnosed with BN
completed questionnaires about bulimic symptoms and family “hassles” for one week, eight
times daily, whenever contacted by pager. Statistical regression analyses found that “potent
family hassles” were positive predictors of bulimic symptoms later that day, but this was only
true for girls who perceived their family as having high levels of conflict or low levels of
emotional expressiveness. Therefore, within the context of an apparent dysfunctional family
environment, potent family hassles can predict intraindividual and interindividual bulimic
symptoms that arise acutely for adolescent girls.
Perpetuating Biological Underpinnings
Starvation/Semi-Starvation
It is likely that disturbances in a number of neurotransmitters, neurohomones, peptides
and neuromodulators act as important biological perpetuating factors
CNS Neurotransmitter Changes

There is considerable evidence for an impaired serotonergic responsiveness during the
active phase of BN (Brewerton, 1995; Brewerton, Mueller, Lesem, et al., 1992; Goldbloom,
Garfinkel, Katz and Brown, 1990; Kaye, Gendall, Fernstrom, Fernstrom, McConaha and
Weltzin, 2000; Kaye, Greeno, Moss, et al., 1998; Jimerson, Wolfe, Metzger, et al., 1997;
Levitan, Kaplan, Joffe, Levitt and Brown, 1997; Monteleone, Brambilla, Bortolotti, Ferraro
and Maj, 1998; Oldman, Walsh, Salkovskis, Fairburn and Cowen, 1995; Smith, Fairburn and
Cowen, 1999; Weltzin, Fernstrom, Fernstrom, Neuberger and Kaye, 1995; Weltzin,
Fernstrom, McConaha and Kaye, 1994). Studies have shown an inverse relationship between
symptom severity and measures of serotonergic responsiveness (Jimerson, Lesem, Kaye and
Brewerton, 1992; Monteleone, Brambilla, Bortolotti and Maj, 2000). In addition, there is
evidence for an association between self-destructiveness, a history of sexual abuse,
impulsivity and reduced serotonin function (Steiger, Gauvin, Israel, et al., 2001; Steiger,
Koerner, Engelberg, et al., 2001; Steiger, Young, Ng Ying Kin, et al., 2001).
In addition to affecting eating behavior directly, alterations in CNS serotonin function
may contribute to other psychological symptoms associated with BN. The diminished CNS
serotonin could play a role in the high prevalence of depressive disorders in patients with BN.
An impulsive-aggressive behavioral style, which is frequently seen in bulimic patients, may
also be associated with diminished CNS serotonin function (Brewerton and Steiger, 2004).
Reduced CSF levels of the dopamine metabolite homovanillic acid (HVA) have been
reported in BN patients with frequent binge-purge episodes (Kaye, Ballenger, Lydiard, et al.,
1990; Jimerson, Lesem, Kaye and Brewerton, 1992) but not in those less severely ill.
Furthermore, binge frequency has been reported to be inversely correlated with CSF HVA
levels (Jimerson, Lesem, Kaye and Brewerton, 1992). Upon long-term recovery, normal
concentrations of CSF HVA have been reported to normalize in BN (Kaye, Gendall and
Strober, 1998). However, during the active phase of the illness these purported
neurotransmitter abnormalities may drive the expression and continuation of symptoms.
Neuropeptide and Hormonal Alterations

Other neurochemical systems have been reported to be significantly different from
controls in BN patients and may also contribute to the maintenance of symptoms. For
example, CSF levels of cholecystokinin (CCK) have been reported to be significantly lower
in BN patients, and levels were correlated with measures of anxiety (Lydiard, Brewerton,
Beinfeld, Laraia, Stuart and Ballenger, 1993). In another study, BN patients showed
significantly lower levels of beta-endorphin (B-END), which were correlated with measures
of depression (Brewerton, Lydiard, Laraia, 1992).
It has also been shown that bulimic patients have significantly lower serum leptin
concentrations in comparison to matched controls (Baranowska, Wolinska-Witort,
Wasilewska-Dziubinska, Roguski, and Chmielowska, 2001; Brewerton, Lesem, and Garvey,
2000; Jimerson, Mantzoros, Wolfe, and Metzger, 2000; Monteleone, Bortolotti, Fabrazzo, La
Rocca, Fuschino, Maj, 2000). Leptin levels appear to remain decreased even after sustained
recovery in comparison to controls with matched percent BMI. This finding suggests that
serum leptin levels may remain decreased and could be linked to decreased metabolic rate
and a tendency to gain weight that is characteristic of BN
Plasma ghrelin concentrations have been reported to be significantly higher in bulimic
patients as compared to healthy controls even though there was no difference between the
BMIs between the groups (Tanaka, Naruo, Muranaga, Yasuhara, Shiiya, et al., 2002). These
results suggest that not only BMI, but also disordered eating behavior characterized by
bingeing and purging can influence circulating ghrelin levels.
Actively bulimic individuals have significantly higher plasma cortisol levels in
comparison to controls (Brewerton et al, 1992; Brewerton, 1995). In addition, plasma cortisol
levels have also been shown to be inversely correlated to serotonin receptor sensitivity.
Therefore, the stresses of semi-starvation, bingeing and purging may lead
Perpetuating Psychological Underpinnings

Cognitive Distortions
One of the foremost clinical features of patients with EDs, including those with BN, is
the presence of prominent cognitive distortions, in particular distorted self-statements or
negative, self-deprecatory beliefs about oneself, e.g., “I am fat,” “I am ugly,” “I am
unworthy,” “I am inferior,” etc. The success of cognitive behavioral therapy (CBT) for the
treatment of BN, as well as many of its associated comorbid conditions, e.g., major
depression, anxiety disorders, and substance use disorders, attests to the importance of
addressing cognitive distortions. Failure to make an impact on this often resistant feature can
result in the perpetuation of symptoms and/or behaviors that are “driven” by these illogical
thoughts.
Interpersonal Problems
A related issue often associated with the maintenance of bulimic symptoms or

nonresponsiveness to treatment is the failure to fully process or resolve challenging
interpersonal issues. Such dynamics may often overlap or intersect with the cognitive
distortions and negative affects noted elsewhere. Patients with BN are reported to have
histories of more problematic social experiences, including histories of family dysfunction
and interpersonal stressors that often lead to feelings of low self-esteem, social isolation, lack
of perceived support, and poor coping and problem solving skills (Fairburn, Welch, Doll,
Davies and O’Connor, 1997; Ghaderi and Scott, 1999; Grissett and Norvell, 1992; Gual,
Perez-Gaspar, Martinez-Gonzalez, Lahortiga, Irala-Estevez and Cervera-Enguix, 2002;
Herzog, Keller, Lavori and Ott, 1987; O’Mahony and Hollwey, 1995; Rorty, Yager,
Buckwalter and Rossotto, 1999; Tiller, Sloane, Schmidt, Troop, Power and Treasure, 1997;
Troop, Holbrey, Trowler and Treasure, 1994; Tuschen-Caffier and Vogele, 1999).
Interpersonal Psychotherapy (IPT) seeks to enhance self-esteem, interpersonal functioning,
and negative affect as they relate to each other and to bulimic symptoms.
Trauma, Neglect and PTSD
Trauma-related disorders, such as BN, major depression, and PTSD, may share common
underlying factors that account for such interrelationships, including dysregulation in
neuropsychobiological mechanisms that are triggered by gene expression and resultant
underlying affective dysregulation, as well as common cognitive schemas involving issues of
self-esteem, control, guilt and shame (Brewerton, 2004; 2007). This perspective is supported
by several studies of mediating variables between previous abuse and later development of
BN, which demonstrate that impulsivity and fundamental beliefs involving self-esteem,
shame, and perceived control are important considerations in more completely understanding
etiological mechanisms as well as treatment approaches (Andrews,1997; Brady, Killeen,
Brewerton and Lucerini, 2000; Murray and Waller, 2002; Waller, 1998; Waller, Meyer,
Ohanian, Elliott, Dickson and Sellings, 2001; Wonderlich, Crosby, Mitchell, Thompson,
Redlin, Demuth and Smyth, 2001; Wonderlich, Crosby, Mitchell, et al., 2001). Rodriguez,
Perez and Garcia (2005) reported that the highest likelihood of poor outcome was found in
patients with sexual abuse and histories of other violent acts. In addition, this group of
patients was at greatest risk for dropout and relapse following treatment.
Likewise, Anderson, LaPorte, Brandt and Crawford (1997) reported that sexually abused
inpatients with BN exhibited higher levels of depression, anxiety, and eating disordered
attitudes at each assessment point relative to nonabused subjects and that abused subjects
were more likely to be re-hospitalized in the three month post-discharge period.
In another follow-up study of hospitalized bulimic patients, Fallon, Sadik, Saoud and
Garfinkel (1994) reported that childhood PA and a family environment characterized by low
cohesion and high control were significantly associated with poor outcome. The family
environment characteristics seemed to have greater influence on clinical outcome than abuse
per se. Gleaves and Eberenz (1994) also reported an association between sexual abuse history
and poor prognosis in 464 bulimic women in residential treatment.
Schmidt, Slone, Tiller and Treasure (1993) compared the defensive styles of anorexic
and bulimic patients and healthy female controls in an attempt to establish a link between
early childhood adversity and later adult defensive style. BN patients were found to have a
significantly less mature defense style than the other groups. In addition, excessive parental
control during childhood was a negative predictor of mature defenses and physical abuse a
positive predictor of immature defense style. The authors concluded that childhood adversity
may constitute a vulnerability factor for the later development of BN, mediated by
personality development.
Depression
There is some evidence that the presence of major depression or significant depressive
symptoms interfere with either the engagement in treatment or with response to treatment.
Maddocks and Kaplan (1991) studied 86 women with BN treated in a group program and
found that depression and core symptoms of eating disorder best discriminated “positive”
from “poor” treatment responders. In a one-year follow-up study of 100 bulimic patients who
completed a clinical trial of CBT, the presence of major depression predicted poor outcome
(Bulik, Sullivan, Joyce, Carter and McIntosh, 1998).
Personality Factors
A number of investigators have reported that bulimic patients with borderline personality
disorder or so-called borderline features have a relatively poorer response to treatment
(Herzog, Hartmann, Sandholz and Stammer, 1991).
Perpetuating Social Underpinnings

Cultural Effects
Western culture is a toxic environment for the individual recovering from BN. Pressures
to be thin, young and physically attractive are ubiquitous in our culture, while at the same
time exposure to highly palatable and readily available foods in large quantifies makes
attaining abstinence from bingeing and purging and subsequent recovery difficult.
Social Reinforcement
Observations from clinical practice indicate that positive reinforcement for weight loss
from others plays a powerful role in maintaining symptoms. Patients often irrationally fear
weight gain following cessation of bingeing and purging.
Family Dysfunction
Blouin, Carter, Blouin, et al. (1994) studied potential prognostic indicators of short-term
outcome in 69 women with BN who participated in a weekly 10-session structured CBT
outpatient group program. The only significant predictor of improvement in binge frequency
and bulimic cognitions was family environment. Controlling conflicted and over-organized
family environments appeared to hinder improvements in not only binge frequency but
bulimic cognitions as well. In an important study by Dancyger, Fornari, Scionti, Wisotsky,
Sunday (2005), the mothers of ED patients were found to rate family functioning as
significantly healthier and less chaotic than their daughters. Although there were fewer
significant differences between maternal and paternal views of family functioning, there were
no significant differences between fathers' and daughters' family perceptions. In addition,
increased levels of depressive symptoms as reported by the daughters were linked to the
perception of high family dysfunction. Differences in viewpoints between parents and
daughters regarding family environment may negatively impact on the course of treatment
and contribute to the continuation of dysfunctional family patterns.
FACTORS BIOLOGICAL PSYCHOLOGICAL SOCIAL

Pressures for
PREDISPOSING Genetics Perfectionism/OCP traits
Thinness
Gender Low self-esteem Acculturation
Trait-related diffs Ineffectiveness High achievement
Age Anxiety/mood D/O’s Athletic competition
Ethnicity/race Trauma/neglect/PTSD Family dysfunction
Prenatal/perinatal Novelty/sensation
probs seeking
Season of birth Impulsivity
BMI/Obesity Alexithymia
Pica/digestive
problems
Family history of psychopathology
PRECIPITATING Puberty Life stressors Peer pressures
Illness Interpersonal dynamics Media messages
Dieting/weight loss Trauma/neglect/PTSD Family dynamics
PERPETUATING Starvation effects Cognitive distortions Cultural effects
CNS changes Interpersonal problems Social Reinforcement
Peptide changes Trauma/neglect/PTSD Family dysfunction
Hormone changes Depression/Personality
Figure 1. THE 3 “P’s” across the bio-psycho-social spectrum.
Conclusion
In summary, there is no one cause of BN. Etiology is best seen using a biopsychosocial
model along a neurodevelopmental continuum. The three P’s are useful in thinking about
etiology in any given individual. Latent vulnerability theory suggests strong genetic
predisposing factors linked to anxiety, obsessive-compulsiveness which are exposed or
triggered by behaviors leading to weight loss. Traumatic experiences often play important
roles in predisposing, precipitating and perpetuating bulimic disorders, especially with
comorbidity. Future research will uncover interactions among genetic and environmental
factors (Caspi and Moffitt, 2006) in the tradition of newer integrative studies that assess
gene-environment interactions such as those performed by Caspi and colleagues for major
depression (Caspi, Sugden, Moffitt, Taylor, Craig, et al., 2003), antisocial behavior (Caspi,
McClay, Moffitt, Mill, Martin, et al., 2002) and substance abuse (Caspi, Moffitt, Cannon,
McClay, Murray, et al., 2005).
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Chapter III
Overview of Evidence on the

Underpinnings of
Binge Eating Disorder and Obesity
Massimo Cuzzolaro1 and Giuseppe Vetrone2

1
University of Rome Sapienza, Roma, Italy
2
University of Rome Tor Vergata, Roma, Italy
Abstract
Binge eating disorder (BED) is the most distinct subgroup in the diagnostic category
of eating disorders not otherwise specified (EDNOS) and it is already accepted as an
eating disorder (ED) in actual practice. However, it is not yet an approved DSM
(Diagnostic and Statistical Manual of Mental Disorders) or ICD (International
Classification of Diseases) diagnosis. Patients with both obesity and BED face many
tasks: controlling their eating patterns and acquiring beneficial lifestyle changes,
promoting and maintaining weight loss, improving their physical and psychological
health and their quality of life. BED may benefit from specialized interventions, either
psychosocial or pharmacological, in addition to standard behavioral weight control
treatment. BED treatment programs have attempted to address these goals sequentially or
in combination; they usually reduce binge eating, at least in the short term, but weight
loss is insufficient or absent in most cases. After a brief account of current knowledge on
epidemiology of BED, we will discuss in detail the nosological status of this possible
new diagnostic category and its diagnostic criteria.
Introduction
The concept of binge eating disorder (BED) was introduced in the early 1990s (Spitzer,
1991). This symptom cluster presentation was formally recognized as a possible new
diagnostic category only in 1994, in the fourth edition of the Diagnostic and Statistical
Manual of Mental Disorders (DSM-IV) (American Psychiatric Association, 1994).
54 Massimo Cuzzolaro and Giuseppe Vetrone
We enumerate three milestones that led to the proposal that BED should be added to the
current list of mental disorders:
I. The first description of recurrent compulsive overeating as a clinical phenomenon

probably dates back to 1932 (Stunkard, 1990; Wulff, 1932; Wulff, 2001) but the
expression “binge eating” was coined half a century ago by Hyman Cohen
(Stunkard, 1959). In the late 1950s the American psychiatrist Albert Stunkard
(Stunkard, 2002; Stunkard, 1959) proposed the name of “binge-eating syndrome” for
a possible new diagnostic category.
II. In 1979 the British psychiatrist Gerald Russell proposed naming “bulimia nervosa” (BN)
a syndrome which he considered an “ominous variant” of anorexia nervosa (AN)
(Russell, 1979). People with BN suffer from frequent binge eating attacks , regular
compensatory behaviors, and morbid fear of fatness. Most of them maintain their
weight within the normal range.
III. In the last two decades, clinicians increasingly reported on women and men who,
engaged in recurrent binge eating but without the regular compensatory behaviors
that characterize bulimia nervosa; most of these patients were overweight or obese.
On the basis of these observations Spitzer and colleagues advanced the proposal of
BED as a new diagnostic category (Spitzer, 1991; Spitzer, Devlin, Walsh, et al.,
1992; Spitzer, Yanovski, Wadden, et al., 1993) and DSM-IV agreed with the
suggestion.
We are now aware that binge eating as a symptom crosses the entire field of eating
disorders (ED) and the whole spectrum of body weights (Fairburn and Wilson, 1993; Russell,
1997). However, BED is the name of a syndrome that in the DSM-IV and in the DSM-IV-TR
(Text Revision) is defined as follows: “recurrent episodes of binge eating in the absence of
the regular use of inappropriate compensatory behaviors characteristic of bulimia nervosa”
(American Psychiatric Association, 1994; American Psychiatric Association, 2000). In the
DSM-IV-TR, BED is proposed as an example of an eating disorder not otherwise specified
(EDNOS) category. In addition, it is included in Appendix B (possible new diagnostic
categories requiring further study). The Eating Disorders Work Group of the DSM-IV task
force in conjunction with Spitzer and colleagues (1992) developed the provisional diagnostic
criteria for BED on the basis of those for BN (American Psychiatric Association, 2000). No
comparable diagnostic category related to BED exists in the tenth edition of the WHO
International Classification of Diseases (ICD-10) (World Health Organization, 1992). The
ICD-10 diagnosis for individuals who present with the clinical picture of BED may be
Atypical Bulimia Nervosa (code number F50.3) or Eating Disorder, unspecified (code
number F50.9) (World Health Organization, 1993). The DSM is one of the possible methods
of classification of mental disorders but, since the publication of its third edition (1980), the
taxonomy proposed by the American Psychiatric Association (APA) has become dominant.
This event has probably contributed to the acceptance of the diagnostic category of BED.
BED has connected the psychiatric field of EDs with the medical area of obesity. The
bridge drew more attention to the psychological and psychiatric aspects of obesity and
contributed to the development of a multidimensional team approach to the assessment and
Overview of Evidence on the Underpinnings of Binge Eating Disorder… 55
treatment of eating and weight disorders. According to many handbooks and practice
guidelines this approach appears now as the best therapeutic model for ED and obesity
(American Psychiatric Association, 2006; Basdevant and Guy-Grand, 2004; Bosello, 2008;
Fairburn and Brownell, 2002; Goldstein, 2005; Grilo, 2006; Lau, Douketis, Morrison, et al,
2007; Mitchell, Devlin, de Zwaan, et al., 2008; National Heart Lung and Blood Institute,
(NHLBI), North American Association for the Study of Obesity, et al, 2000; National
Institute for Clinical Excellence, 2004 January; Palmer and Norring, 2005; Wadden and
Stunkard, 2002; Yager and Powers, 2007).
Although the conceptual issues and the diagnostic criteria of BED have not yet met
sufficient agreement: in actual practice, BED is already accepted as an ED, and an increasing
number of scientific articles have been devoted to it since 1991. Figure 1 illustrates the
findings.
45
40
35
30
25
20
15
10
0
90
91
92
93
94
95
96
97
98
99
00
01
02
03
04
05
06
07
19
19
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19
19
19
19
19
19
19
20
20
20
20
20
20
20
20
Figure 1. Number of PubMed references (1990-2007) that contain in the title the expression binge
eating disorder (BED).
Epidemiological Research
Epidemiological research on BED has at least three major limitations: diagnostic status is
recent, provisional and uncertain; many studies have assessed the disorder by self-report
questionnaires rather than semi-structured clinical interviews; community-based
investigations have examined samples of convenience rather than representative samples. For
example, there is significant discrepancy in prevalence rates of BED as defined by self-report
and interview assessment methods, with the interview method yielding lower estimates of
prevalence (Varnado, Williamson, Bentz, et al., 1997).
Prevalence – International
BED seems to be significantly more prevalent than AN or BN, and is also almost as
prevalent in males as in females. This is certainly in contrast to the sex ratio of females to
males of 10:1 in AN. Studies based on community samples have indicated prevalence rates
between 0.7 and 4 % (Striegel-Moore and Franko, 2003). According to Spitzer (Spitzer,
Devlin, Walsh, et al., 1992; Spitzer, Yanovski, Wadden, et al., 1993), BED is probably 1.5
times more common in women than men. All EDs, including BED, are more common among
white women than among black women with low treatment rates in both groups (Striegel-
Moore, Dohm, Kraemer, et al, 2003).
The National Comorbidity Survey Replication (Hudson, Hiripi, Pope, et al., 2007) was a
face-to-face household study, conducted in 2001-2003 in a large representative sample (n =
9282). The results of this recent research indicated the following lifetime community
prevalence rates of DSM-IV-BED in USA: 3.5% in women and 2.0% in men; F to M ratio
was 1.75 to 1.0.
An Italian three-phase community-based study evaluated 2,355 subjects representative of
the population aged >14 years living in Sesto Fiorentino (Faravelli, Ravaldi, Truglia, et al.,
2006). The authors found an overall lifetime prevalence of BED considerably lower than the
American rate: 0.32%.
Lamerz and colleagues (Lamerz, Kuepper-Nybelen, Bruning, et al., 2005) conducted a
cross-sectional survey in a German urban population of 6-year-old children and their parents.
Episodes of binge eating were found in 2.0% of the children surveyed. There was a
significant relationship between binge eating and obesity, but not between night eating and
the child's weight. Furthermore, children's binge eating was strongly associated with eating
disturbances on the part of their mothers. BED may manifest itself differently in children than
adults. Shapiro and colleagues (Shapiro, Woolson, Hamer, et al., 2007) recently developed
the Children's Binge Eating Disorder Scale (C-BEDS), a brief, structured, interviewer-
administered scale to measure BED in children.
BED and Obesity: The Chicken or the Egg?
BED may especially be observed in overweight and obese individuals, and in Hudson et
al.’s research (Hudson, Hiripi, Pope, et al., 2007), lifetime BED was significantly associated
with current obesity class III (body mass index, BMI ≥ 40 kg/m2). BED is much more
frequent among treatment seeking obese subjects: up to 30% of participants in weight loss
programs meet DSM-IV-TR criteria for BED. In France, for example, Basdevant et al.
(Basdevant, Pouillon, Lahlou, et al., 1995) concluded that BED was very common (15%) in
women seeking help for weight control, but extremely rare in a community sample of women
(0.7%).
Subjects with obesity and BED, in an effort to feel better about themselves, often have
become trapped in a cycle of attempting to diet, then losing control, binge eating, and gaining
even more weight (Devlin, 2001; Polivy, 2001). However, it remains unclear which comes
first: bingeing or dieting?
Some authors consider dieting as a precondition for the development of binge eating
(Herman and Polivy, 1980; Herman and Polivy, 1990). It was recently suggested that a
distinction between intention to restrict food intake and actual restrictive behavior may be
useful to predict changes in overeating and BMI (Larsen, van Strien, Eisinga, et al., 2007).
Reas and Grilo examined a sample of 284 treatment-seeking adults with BED and found
that weight problems preceded dieting and binge eating behaviors for a majority of patients
(Reas and Grilo, 2007). In addition, proportionally more women than men reported that
dieting preceded overweight or binge eating.
BED and Diabetes
There is a significant relationship between BED and type 2 diabetes.

A German multi-center study (Herpertz, Albus, Wagener, et al., 1998) explored the
prevalence of ED (full and partial syndromes) in an inpatient and outpatient population of
men and women with type 1 and type 2 diabetes. The overall prevalence range of current ED
was 5.9-8.0% (lifetime prevalence 10.3-14.0%) without significant difference between the
two types. However, the distribution of the EDs was different, with a predominance of BED
in the type 2 diabetes sample. Patients with type 1 (5.9%) and type 2 (2.2%) diabetes,
reported deliberate omission of insulin or oral agents in order to lose weight. In this research,
BED seems to precede type 2 diabetes in most patients, and could be one of the causes of
their obesity.
According to Herpertz and colleagues, BED is likely a risk factor for an accelerated
weight gain, which often involves an increase of insulin resistance (Herpertz, Petrak, Kruse,
et al., 2006).
BED and Psychiatric Comorbidity
BED is usually accompanied by co-morbid psychiatric disorders, especially depression,

anxiety disorders, and substance abuse disorders (Guerdjikova, McElroy, Kotwal, et al.,
2007; Stunkard, 2002; Stunkard and Allison, 2003; Wilfley, Friedman, Dounchis, et a.l,
2000). Hudson et al.’s study recently confirmed that lifetime BED is significantly associated
with other psychopathology and role impairment (Hudson, Hiripi, Pope, et al., 2007).
Nosological Status of BED

May BED be Conceptualized as a Separate Syndrome?
BED is the most distinct EDNOS subgroup, however, it is currently not a diagnosis
approved in either DSM or ICD. According to the current DSM-IV-TR definition, BED is
characterized by repeated episodes of uncontrolled eating with excessive food intake and
subjective distress but without subsequent compensatory weight loss mechanisms. The
question remains, does BED represent a really separate diagnostic entity? In other words, is
the concept of BED a reliable and valid diagnosis? We will report on some relevant studies
that address this question.
In 1999 Williamson and Martin reviewed the first five years of research on BED and
concluded that questions about the definition of BED remained (Williamson and Martin,
1999). The authors reported that binge eating is a common symptom associated with obesity.
They also posited that BED may be conceptualized as a separate psychiatric syndrome, or it
may be viewed as a behavioral symptom associated with obesity in a large number of cases.
Other researches supported the distinction between BED and BN. In 2000, Fairburn et
al., published a paper on the relative course and outcome of BN and BED (Fairburn, Cooper,
Doll, et al., 2000). They prospectively studied over a five-year period, two community-based
cohorts of women, one with BN and the other with BED. BN and BED showed different
courses of illness, with little movement of participants across the two diagnostic categories.
The outcome of the BED cohort was better. Crow et al. examined a large sample of 385
women with full or partial AN, BN, or BED (Crow, Stewart Agras, Halmi, et al., 2002).
Discriminant analysis demonstrated clear differences between full AN, BN, and BED, and
this supported the distinction between BED and the other EDs.
However, Fichter et al. (Fichter, Quadflieg and Hedlund, 2008) recently found that
course, outcome and mortality were similar for BED and BN-P with a diagnostic shift
between them over time, “pointing to their nosological proximity”.
In 2003, Devlin et al. (Devlin, Goldfein and Dobrow, 2003) evaluated four models
relating to the nosological status of BED: a distinct disorder in itself; a variant of BN; a
behavioral subtype of obesity; and a behavior that reflects psychopathology among the
individuals with obesity (a psychopathological marker). According to the evidence, the
authors wrote that BED “differs importantly from purging BN” but not from non-purging
BN, and that BED “is not a strikingly useful behavioral subtype of obesity” because obese
individuals with BED do not differ greatly from similar obese patients without BED in their
response to obesity treatment. They concluded that it was not possible to determine the
validity of BED as a distinct ED.
Stunkard, who originally described binge eating (Stunkard, 1959), defended with Allison
a similar point of view in a thought-provoking article (Stunkard and Allison, 2003): the great
variability of BED limits the implications that can be drawn from its diagnosis and, in
particular, the presence or absence of BED is not a useful distinction in selecting treatment
for obese individuals. BED may be more useful as “a marker of psychopathology” than as a
new distinct diagnostic entity.
Walsh and Satir reviewing the literature published during the period 2002-2003
concluded that “a consensus does not yet appear to have formed in the field regarding the
wisdom of formally designating BED as an eating disorder” (Walsh and Satir, 2005).
Dingemans et al. (Dingemans, van Hanswijck de Jonge and van Furth, 2005) discussed the
empirical status of BED after a decade of research in the light of Pincus et al.’s (Pincus,
Frances, Davis, et al., 1992) general arguments for and against the inclusion of new
diagnostic categories in the DSM. Unlike Walsh and Satir they concluded that “... there is
evidence to suggest that BED represents a distinct eating disorder category” (p. 76).
More recently, Wilfley and colleagues, (Wilfley, Bishop, Wilson, et al, 2007) and
Striegel-Moore and Franko (Striegel-Moore and Franko, 2008) supported the same point of
view: BED should be made an official diagnosis in DSM-V.
It is probable that DSM-V will move some boundary lines in the section of ED. In
particular, BN non-purging subtype (BN-NP) and BED give the impression of clinical
pictures very close together. In 1998, Hay and Fairburn published the results of an interesting
study designed to assess the validity of the DSM-IV classification of recurrent binge eating
(Hay and Fairburn, 1998). They recruited a general population sample of 250 young women
with recurrent binge eating and studied their eating habits and associated psychopathology by
personal interviews. Subjects were reassessed one year later. The authors found that, on
present state features, it was not possible to distinguish BED from the non-purging subtype of
bulimia nervosa. However, these groups differed in their outcome at one year. Hay and
Fairburn concluded that “the data on outcome support retaining a distinction between non-
purging bulimia nervosa and binge eating disorder”. In their opinion, bulimic eating disorders
exist on a continuum of clinical severity, from BN purging type (most severe), through BN
non-purging type (intermediate severity), to BED (least severe).
Other authors (Mond, Hay, Rodgers, et al., 2006), however, called into question the
validity of subtyping of BN into purging and non-purging forms. In the opinion of
Ramacciotti et al. (Ramacciotti, Coli, Paoli, et al., 2005) differences between BED and BN-
NP seem to be more of degree than type and there seems little value in the separation
between BED and BN-NP based on weight-shape concerns that substantially impair self-
esteem. This construct seems core to both disorders and plays a substantial role in triggering
and maintaining the binge-eating cycle.
Wilfley et al. (Wilfley, Bishop, Wilson, et al., 2007), in evaluating the current ED
nosology on the basis of the available scientific evidence, concluded that in DSM-V it would
be better to remove the subtypes both for AN and for BN. They also suggested that ED
classification should be modified in DSM-V by retaining categories but adding a dimensional
component.
Concerning this subject, let us mention that EDs have been conceptualized as discrete
syndromes (or categories) and as dimensions that differ in degree among individuals.
Schlundt and Johnson proposed in 1990 a three-dimensional model for ED: binge eating, fear
of fatness, and body size (Schlundt and Johnson, 1990). Four years later, Beumont et al.
suggested a unitary approach to ED diagnosis and proposed a slightly different three-
dimensional model: binge eating, purging, and body size (Beumont, Garner and Touyz,
1994). However, which of these two models, categorical versus dimensional, is most valid?
Do the current classifications of EDs capture the natural clustering of eating-related

pathology?
Some recent studies have directly and empirically addressed these questions.
Bulik et al. examined 2163 Caucasian female twins from a population-based registry
(Virginia Twin Registry) and assessed bulimic and anorectic symptoms through personal
interviews (Bulik, Sullivan and Kendler, 2000). The authors applied latent class analysis to
nine symptoms of EDs; then they used demographic, personality, co-morbidity, and co-twin
diagnosis data to validate the resultant classes and found three classes which largely
correspond to the current diagnostic categories of AN, BN and BED. In particular,
individuals in the three ED classes displayed differences in co-twin risk for AN, BN, and
obesity.
Also Williamson et al. investigated “the question of whether the EDs vary along
dimensions, with normalcy defining one end of the continuum, or whether the EDs are
discrete categories” (Williamson, Womble, Smeets, et al., 2002). They explored the latent
structure of ED symptoms, as defined by DSM-IV, in a group of 341 women with and without
an ED diagnosis. The presence and severity of DSM-IV ED symptoms was assessed with a
semi-structured interview and the data were subjected to a factor analysis. The results
suggested that EDs may be conceptualized as having three primary features: binge eating,
fear of fatness/compensatory behaviors, and drive for thinness. In addition, women with an
ED diagnosis differed (at least partly) from women without an ED diagnosis “in kind rather
than simply in degree”. The three factors identified were then examined using taxometric
analyses (statistical procedures used to discover whether the three factors varied along a
continuum or detected the presence of latent classes). Taxometric tests found empirical
support for conceptualizing BN and BED as discrete syndromes.
Williamson et al. recently reviewed a series of taxometric studies related to the validity
of dimensional versus categorical models of ED and concluded that a conceptual
representation of ED may involve at least a latent taxon (a taxon is any distinct group
constituting a category within a system of classification), related to binge eating (and
possibly purging), and one or more dimensions (Williamson, Gleaves and Stewart, 2005).
In summary, at this time, we suggest that more studies are required with large samples to
empirically sort out which differences among the various EDs are qualitative and which
differences are only quantitative (dimensional).
Does BED Represent a Stable Syndrome?
A number of studies and, in particular, those on the fate of untreated subjects and those
on placebo responsiveness have raised concern about the diagnostic stability of BED and the
question is still controversial (Stunkard, 2002).
Fairburn et al., studied prospectively a community based cohort over a five-year period
and found that only 10% of subjects with BED at the beginning of the survey met criteria for
this diagnosis five years later. The authors wrote that BED “is an unstable state with a strong
tendency toward spontaneous remission” (Fairburn, Cooper, Doll, et al., 2000).
In contrast, Pope et al., in their retrospective research, found that BED is at least as
chronic as AN and BN (Pope, Lalonde, Pindyck, et al., 2006). They interviewed 888 first-
degree relatives of 300 overweight or obese probands (150 with BED and 150 with no
lifetime ED) and discovered that the mean lifetime duration of illness among relatives with
lifetime diagnoses of BED (N=131) was 14.4 years (SD=13.9). In the opinion of the authors,
these results suggest that BED likely represents a stable syndrome.
Jacobs-Pilipski et al. studied sibutramine hydrochloride in a randomized controlled trial
that included 451 participants (ages 19-63) with BED (Jacobs-Pilipski, Wilfley, Crow, et al.,
2007). The investigators found that placebo responders (32.6%) exhibited significantly less
symptom severity but, at follow-up, many of them reported continued symptoms. Therefore,
placebo response in BED may be transitory or incomplete and the results seem to imply
unpredictable stability in the BED diagnosis.
Diagnostic Criteria for BED

Should We Maintain DSM-IV Research Criteria for BED?
Diagnostic criteria are in a permanent state of revision and in the area of mental disorders
they probably should be regarded as useful concepts and guidelines rather than as separate
entities. In the last fifteen years, several authors have raised doubts about the DSM-IV
research criteria for BED.
Criterion A (recurrent episodes of binge eating), in the opinion of Dingemans et al., “as
currently defined should be maintained” (Dingemans, van Hanswijck de Jonge and van Furth,
2005). However, difficulties with diagnosis may arise from the precise identification of binge
eating episodes in obese people. Three remarks may illustrate this point. The phenomenon of
binge eating is described in DSM-IV-TR in the same way for BED and BN. Nevertheless,
there are some differences (Wilfley, Schwartz, Spurrell, et al., 2000): for example, in BN,
binge eating episodes usually happen in the context of overall dietary restraint and are easily
identifiable, whereas, in most cases of BED, they occur in the background of habitual
overeating and chaotic eating patterns. Raymond et al. recently compared energy intake in
obese women with and without BED when they were allowed to have a binge eating episode
in a laboratory setting (Raymond, Bartholome, Lee, et al, 2007). The BED obese group
consumed significantly more total food in kilocalories (but not significantly more total grams
of food) than the non-BED obese participants. Furthermore, the BED group consumed more
dairy products and, in general, more kilocalories of fat. Bartholome et al. (Bartholome,
Raymond, Lee, et al., 2006) evaluated multiple methods of assessing food intake in obese
women with BED: laboratory binge eating episodes, 24-hour dietary recalls, and the Eating
Disorder Examination (EDE) interview. The findings suggested only moderate agreement
among these different methods.
With regard to criterion B (features associated with the binge-eating episodes) we agree
with Dingemans et al.(Dingemans, van Hanswijck de Jonge and van Furth, 2005) who wrote
that it is superfluous because it overlaps A and C criteria.
According to the same authors, criterion C (marked distress) should be revised to

distinguish distress as an emotional state from distress as impairment in social or
occupational functioning (Dingemans, van Hanswijck de Jonge and van Furth, 2005).
In the present form, criterion D (binge eating occurs at least two days a week for six
months) may complicate the distinction between binge eating (acute and circumscribed attack
with manifest loss of control) and compulsive overeating (urge to eat that may last an entire
day). Therefore Dingemans et al. suggested “counting the number of binge-eating episodes
rather than counting the number of days” (Dingemans, van Hanswijck de Jonge and van
Furth, 2005).
Moreover, according to some researchers, it would be better to change the severity
criterion and to move the boundary line between full-syndrome BED and sub-threshold BED
(STBED). Striegel-Moore et al. (2000) compared 44 women with STBED and 44 women
with BED and 44 healthy controls. The two ED groups did not differ significantly on
measures of weight and shape concern, restraint, psychiatric distress, and history of seeking
treatment for an eating or weight problem. The authors concluded that, given the importance
of diagnostic status for access to treatment, the severity criterion specified for BED should be
revised (Striegel-Moore, Dohm, Solomon, et al, 2000).
Also Crow and colleagues, in a study of 385 women with full or partial (sub-threshold)
ED found that full and partial BED appear quite similar (Crow, Stewart Agras, Halmi, et al,
2002).
More recently, Friederich et al. compared eating-related and general psychopathology at
baseline and in response to a multimodal treatment program in obese people with full
syndrome BED, and STBED. They did not find differences between STBED and BED
participants with regard to eating-related and general psychopathology at baseline and with
regard to treatment outcome and concluded that a differentiation currently seems not to be of
clinical significance (Friederich, Schild, Wild, et al., 2007).
We thus agree with Wilfley et al. who included among their specific recommendations
for DSM-V, “unifying the frequency and duration cut-points for BN and BED to once per
week for three months” (Wilfley, Bishop, Wilson, et al., 2007).
Criterion E (no regular use of inappropriate compensatory behaviors) tolerates unsafe
compensatory behaviors on condition that they are infrequent (not “regular”). The
elimination of the term “regular” may ensure a clearer distinction between BN and BED
(Dingemans, van Hanswijck de Jonge and van Furth, 2005) but, on the other hand, this
choice may increase the cumbersome residual category of EDNOS that is the most common
diagnosis in clinical practice (Palmer and Norring, 2005).
Should New Diagnostic Criteria be Added for BED in DSM-V?
Body Image
The twentieth century has seen in Western countries, possible constant links between ED
and body image disturbances (Habermas, 1989; Janet, 1903; Wulff, 1932). Unlike AN and
BN, current diagnostic criteria for BED focus completely on eating behavior and feelings
about binge eating and do not include body image distortion and/or distress.
At this time, many studies have shown that obese individuals with BED present greater
uneasiness and dissatisfaction about their body appearance, weight and shape than obese
people without BED.
Marano et al. (Marano, Cuzzolaro, Vetrone, et al, 2007) recently investigated the
psychometric properties of the Body Uneasiness Test (BUT) (Cuzzolaro, Vetrone, Marano, et
al., 2006) in 1,812 adult subjects (18-65 years) with obesity seeking treatment, and evaluated
the influence of gender, age and BMI on body image distress. Concurrent validity with Binge
Eating Scale (BES) (Gormally, Black, Daston, et al., 1982) was evaluated, and the positive
correlation between BUT and BES scores appears noteworthy.
Wilfley et al. (Wilfley, Schwartz, Spurrell, et al., 2000) compared five groups of women:
patients with ED (AN, BN and BED), normal-weight and overweight control subjects. They
found that patients with BED had weight and shape concerns comparable to BN patients and
higher than AN patients.
More recently, Hrabosky et al. studied the excessive influence of shape or weight on self-
evaluation (shape/weight overvaluation) in 399 consecutive patients with BED (Hrabosky
and Grilo, 2007). Results showed that shape/weight overvaluation was unrelated to BMI but
was strongly associated with psychometric measures of eating-related psychopathology and
psychological functioning (higher depression and lower self-esteem). The authors concluded
that shape/weight overvaluation “warrants consideration as a diagnostic feature for BED”.
Some authors have compared males and females and have found that there are
predictable gender differences. Reas et al. (Reas, White and Grilo, 2006) found that obese
women with BED reported significantly greater levels of body checking than obese men with
BED. Among women, the frequency of checking was related to younger age, lower BMI,
body dissatisfaction, over evaluation of body shape and weight, greater depression, and lower
self-esteem.
These sex related differences support Guerdjikova et al.’s results (Guerdjikova, McElroy,
Kotwal, et al., 2007). The authors compared 44 obese males with BED with 44 age- and race-
matched obese females with BED seeking weight loss treatment. They found that obese men
and women with BED who presented for weight management were very similar in current
and lifetime prevalence of psychiatric disorders, and metabolic abnormalities, but males had
fewer previous attempts at weight loss or fewer help-seeking behaviors, possibly related to
their less pronounced body dissatisfaction.
Obesity
Another matter of primary importance is the relationship between BED and obesity. In
DSM-IV-TR obesity is not a criterion for the diagnosis of BED. Should obesity be included
as a criterion for BED in DSM-V in the same way as underweight is a criterion for the
diagnosis of AN? This question is still outstanding (Dingemans, van Hanswijck de Jonge and
van Furth, 2005).
With regard to the nosological status of obesity, it is important to remember that this
condition has traditionally been defined as a body-mass index (BMI) (the weight in kilograms
divided by the square of the height in meters) of 30 or more kg/m2. Excessive weight
increases morbidity (e.g., hypertension, hyperlipidemia, cardiovascular disease, type 2
diabetes mellitus, numerous types of cancer, gallstones, and osteoarthritis) and the risk of
death. For these reasons obesity has traditionally been classified among medical diseases.
However, Wooley and Garner’s provocative statements appear still truthful: “Although
millions seek treatments for obesity ... the majority of the obese struggle in vain to lose
weight and blame themselves for relapses ... Many therapists may be contributing to this
psychological damage by giving their patients false hope for success and by failing to
recognize that seeking treatment for obesity may be triggered by psychological problems that
are not addressed in obesity treatment” (Wooley and Garner, 1991). Furthermore, guidelines
for the assessment, treatment and prevention of obesity and public health recommendations
urge a focus not only on the degree of overweight and the obesity related medical
complications; but also on lifestyle, eating behavior, motivation, social stigma, and mental
health (Brownell, Puhl, Schwartz, et al., 2005; Herpertz, Kielmann, Wolf, et al., 2003; Lau,
Douketis, Morrison, et al., 2007; Mitchell and de Zwaan, 2005; Mitchell, Devlin, de Zwaan,
et al., 2008; National Heart Lung and Blood Institute, (NHLBI), North American Association
for the Study of Obesity, et al, 2000; National Institutes of Health, 1998; World Health
Organization, 2000).
On the other hand, considering obesity, or some aspect of obesity, as a mental (or
behavioral) disorder has some merits but also raises many problems. In 2007 Devlin
wondered if there is a place for obesity in DSM-V (Devlin, 2007). He divided into three
groups the possible models of nonhomeostastic overeating that result in obesity: eating
disorder models that stress the form of overeating; substance use disorder models that focus
on its consequences; and affect regulation or stress response models that consider especially
its function. The author concluded that to devise diagnostic criteria based on the above
models raises multiple difficulties because the phenomena central to each model are basically
dimensional. A more detailed understanding of the neurobiological relationships among
eating behavior, reward systems, and affect regulation systems is needed.
In summary we suggest that a negative body image and a BMI value > 25 should be
added as diagnostic criteria for BED in a future classification of ED.
Conclusion
In spite of many uncertainties, the concept of BED has been of increasing interest in the
last fifteen years to both researchers and clinicians. The close relationship of BED with
obesity has made it a field of study which has deeply involved and connected psychiatry,
clinical psychology and internal medicine.
Acknowledgement
In memory of Professor Giuseppe Vetrone.
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Chapter IV
Research and Clinical Practice:

A Dynamic Tension in the Eating
Disorder Field
Judith D. Banker1 and Kelly L. Klump2

1
Center for Eating Disorders
Ann Arbor, Michigan
2
Michigan State University
East Lansing, Michigan
Abstract
Recent research suggests that there is a “research-practice gap” in the field of eating
disorders, as evidenced by discrepancies between the rate at which research results are
produced and the rate at which the results are utilized in practice. Reasons for the gap,
however, remain unclear. Even more uncertain are strategies that can be used to bridge
this gap. Consequently, the purpose of the present chapter was to: 1) explore factors
underlying the persistent research-practice gap in the eating disorders field; and 2)
develop a “road map” for closing the gap. Data from an informal survey of members of
the Academy for Eating Disorders were used to answer both questions. In addition, the
learning and communication models of Innovation Diffusion Theory, Knowledge
Transfer Theory, and the Evidence-Based Medicine movement were used to develop
novel research-practice integration strategies for the eating disorders field. Findings from
these data sources revealed that the primary reasons for the gap include an institutional,
relational, and economically-driven separation between the research and practice
communities; a perceived lack of generalizability of current empirically supported
treatment (EST) research to clinical practice settings; the reliance on a one-directional
research dissemination model of information transfer; and a lack of research translation
training and education. To bridge the divide, it is recommended that the eating disorder
field implement a long-range strategy, or road map, that fosters reciprocal
communication and interaction between researchers and practitioners, institutional and
organizational support of research-practice partnerships, and integration of interactive,
rather than top-down, learning opportunities. Increased cross-talk and a respect for the
72 Judith D. Banker and Kelly L. Klump
value of research data and clinical observations will enhance efforts to close the research-
gap and ultimately advance the treatment, research, and prevention of eating disorders.
It were not best that we should all think alike; it is difference of opinion that makes horse
races.
– Mark Twain
Clinicians who treat people with eating disorders express frustration over pressure from
researchers to provide empirically supported treatments (ESTs). Researchers scratch their
heads over the seeming resistance of clinicians to stay current on the latest findings in
research. Clinicians feel their expertise is dismissed by researchers; researchers feel their
expertise is met with indifference from clinicians. We are witnessing, in the field of eating
disorders, the classic research-practice gap, a long-standing phenomenon spanning fields as
varied as medicine, engineering, education, public health, and even geography and library
science. Indeed, a quick Google search of “research-practice gap” yielded over 17,000 hits,
highlighting the universality of the gap in fields with both an applied and basic science
component.
The phrase “research-practice gap” is frequently used to describe a research
dissemination gap, i.e., the discrepancy between the rate at which research results are
produced and the rate at which the results are utilized (Fain, 2003; Demaerschalk, 2004).
Within this framework, solutions for bridging the gap focus on ways to enhance
dissemination from a top-down or one-way knowledge transfer perspective (Haddow and
Klobas, 2003; Schecter and Brunner, 2005). However, other references to the research-
practice gap describe a broader, multivariate tension between researchers and practitioners
that arises from a complicated array of factors, such as communication barriers (i.e., lack of
shared language), economic and political influences, professional culture differences and
“blindspots”, and ineffective educational strategies (Robinson, 1998; Herle and Martin, 2002;
McConnell, 2002; Botvin, 2004). It is into this latter group that we squarely place the
research-practice gap in the field of eating disorders--where all of the above factors converge
to create a rather sizeable “Bermuda Triangle”, where valuable research findings disappear
into the abyss along with the vital observations, techniques, and insights of experienced
clinicians.
The debate surrounding the use of empirically supported treatments (ESTs) is perhaps the
most glaring example of the gap that exists between research and practice in our field.
Despite empirical support for the use of cognitive behavior therapy (CBT) in the treatment of
eating disorders, in particular bulimia nervosa, research consistently shows that few clinicians
use CBT as their primary treatment approach (Wilson, 1998; Crow et al., 1999; Mussell et al.,
2000; Haas and Clopton, 2003; Von Ranson and Robinson, 2006; Tobin, Banker, Weisberg,
and Bowers, 2007). Previous attempts to increase dissemination of ESTs have focused on the
publication of treatment manuals (Agras and Apple, 1997; Lock, le Grange, Agras, and Dare,
2001; Fairburn, Marcus, and Wilson, 1993), conference workshops on treatment methods,
and treatment plenary lectures. Nonetheless, despite best efforts, these strategies have
generally failed, as the majority of clinicians do not use ESTs (Mussel et al., 2000).
Research and Clinical Practice 73
The failure of these attempts to increase the utilization of ESTs prompted discussion at a
recent international eating disorders research meeting that focused on how to improve our
methods of research dissemination. One suggestion was to deliver the message about the
importance of ESTs in a clearer way during joint meetings with practitioners. Clarifying and
honing the message may be constructive. However, before refining previously ineffective
methods and perhaps exacerbating the tension in the field, it seems ideal to take a step back
and evaluate the utility of this one-directional approach, and to explore other frameworks for
addressing research dissemination and the broader research-practice connection. Clearly, our
field, our patients, and their families, would be significantly better off if the clinicians and
researchers who are most invested in identifying effective treatments developed ways to
interface around these critical issues. In fact, it is possible that while we are busy debating the
best ways to disseminate ESTs, the adapted practices in the field may be as or even more
effective than ESTs alone. Or maybe not. In any case, bridging the gap between research and
practice by promoting a synthesis of research and clinical evidence could translate into
significant breakthroughs for our patients and our treatment, research, and prevention efforts.
With so much at stake, it is imperative that we, as a field, take stock of the factors that feed
the tension between researchers and practitioners and start identifying strategies for
constructing a much-needed bridge between these critical groups.
In this chapter, we hope to accomplish both of these goals by examining “data” from
both within and outside of our field. The data from within the field come from a decidedly
unscientific survey we conducted of the membership of the Academy for Eating Disorders
(AED) asking them to comment on reasons for the gap and ways to overcome it. We will
describe these “data” and the ways in which they can help us move forward in this age-old
debate. In addition, we will use “data” from the education field, and principles from
knowledge transfer, diffusion innovation theory, and the evidence-based practice (EBP)
movement to propose a road map for bridging the schism between researchers and
practitioners in the eating disorders field. We will end by discussing activities of the AED
Research-Practice Task Force, a work group formed specifically to address the gap in our
field.
The AED Survey

We start by looking within our own field to identify where and why tensions exist. We do
this by capitalizing on our affiliations with the AED. As an international, multidisciplinary
professional organization comprised of research scientists, clinicians, and various hybrids
thereof, the AED has seen the research-practice gap played out in its own membership.
Clinicians at times reported that they felt marginalized and unsupported, and researchers
expressed frustration over the underutilization of empirical data. Professionally, we are
representatives or even prototypes of these estranged groups. Kelly Klump is the 2007-2008
AED President and is a tenured faculty member at a major research university. She does not
treat patients. Judith Banker was the 2008-2009 AED President and is a clinician and the
founding director of an outpatient treatment center. She has only recently ventured into the
world of conducting formal research. We decided to build on the differences in our roles
within the AED and investigate the causes for, and possible solutions to, the research-practice
gap in our field. Instead of carrying out the usual review of the empirical literature, we chose
to do our own analysis by conducting an informal survey of our AED colleagues. This survey
was humbly unscientific; however, it provided us with information on why the gap persists in
our field, despite a long-standing literature on the topic (Arnow, 1999; Fairburn, 2005;
Wilson, 1998).
The “research” questions were straightforward:
1) There appears to be a researcher-clinician gap in our field. What do you think is the
main cause of this gap?
2) What is one step we can take to close the gap?
We emailed these questions to 32 AED colleagues from North America, Europe,

Australia, and the U.K., half of whom do both research and clinical work. Of the half
remaining, one quarter was strictly clinical practitioners and one quarter was strictly
researchers. The response to our survey was overwhelming. We received all of the responses
within one week. More importantly, the responses were uniformly thoughtful and united in
their concern about this issue and about the importance to our field of finding effective ways
to bridge the gap.
We reviewed these responses for common themes, but also for important differences that
likely underscore the persistent gap. These commonalities and specific points of departure are
delineated below, but we feel that we must make a “process” comment before proceeding.
With few exceptions, the tone of the responses differed between researchers and clinicians.
Clinicians clearly felt “under attack”, as their responses included references to “a faith-based
assault against clinicians” and the view that they are perceived as “unscientific charlatans”.
By contrast, the tone of responses from researchers was not of feeling attacked, but instead
reflected a feeling of resignation and a bit of hopelessness that the gap could be closed.
What should we make of these differences in tone? We think they reflect the perceived
power differential between clinicians and researchers and the tendency for researchers to be
more commonly at the podium espousing the need for clinicians to change (rather than the
reverse). Clinicians understandably feel attacked by this, while researchers feel hopeless, as
the researchers’ data fail to translate into new clinical practices. All of this points to a need to
change our dialogue – change how it takes place, where it takes place, and the nature of the
interchange. We will return to ideas about this change later. However, suffice it to say that
the feelings about the gap and the history between “camps” runs deep and affects how we
think and talk about the differences in our field.
Question #1: What Accounts for the Gap?
Commonalities
At least one structural obstacle to achieving optimal clinician-researcher collaboration
was cited with startling uniformity: a lack of time and resources. This was the most frequent
response for researchers and a common response for clinicians. Researchers noted that
providing clinical care is not valued or rewarded at their academic institutions where
publishing and grant funding are the standards by which they are evaluated. Likewise,
researchers and clinicians acknowledged that clinicians neither have the time nor the
resources to stay abreast of research in their practice where demands from managed care
and/or other clinical pressures take precedence. The lack of funding for studies that involve
clinician-researcher collaborations, as well as limited funding for translating research
findings into practice, were also noted. Finally, clinicians pointed out several resource-based
obstacles, including the lack of funding for long-term supervision for training in ESTs and
time and financial constraints that tend to lower motivation to apply research to practice.
In addition to a lack of resources, clinicians and researchers perceived the differential
“evidence” for good practice as key to the persisting gap. Respondents noted that researchers
value data from randomized controlled trials (RCTs), whereas clinicians value clinical data
from professional experience and observation. These different views about what is
considered “evidence” were perceived as contributing to each side devaluing and “talking
down” to the other rather than leading to an appreciation of the reasons why each side values
different data. The perception of practitioners that research lacks relevance to clinical
practice is a commonly cited factor contributing to a tension between research and practice in
our field.
A final common finding of the survey focused on training. Researchers and clinicians
both felt that they had received inadequate training to engage in integrated clinical-research
activities. Respondents felt that researchers were not trained in how to disseminate research
findings effectively and translate them into practice. Likewise, respondents felt that clinicians
were not adequately trained in how to interpret and apply empirical data to their work.
Deficits in each of these areas were thought to contribute to a resistance to change and a rigid
either/or mentality that inhibits the integration of clinical and empirical data.
Differences
Aside from these commonalities, there were also some striking differences in clinician
and researcher responses. While researchers overwhelmingly viewed a lack of resources and
the differences in “evidence” as the primary obstacles to clinical-research collaboration,
clinicians cited many more issues that needed to be addressed. This difference in the number
and type of factors viewed as causative underscores our earlier comments about the
differential experience of the gap in these two groups.
A number of clinicians reported feeling that the gap was due to a perception that most
research findings are irrelevant for the realities of clinical practice. Respondents reported that
exhortations from researchers to practice evidence-based treatment in the face of limited
effectiveness for all eating disorder patients (e.g., for those with anorexia nervosa and/or
extensive co-morbidity) leads to significant frustration and a sense of disconnect from the
usefulness of empirical data. Clinicians reported that it is often necessary to blend a variety of
treatment modalities in order to adapt to the shifting symptom picture and multiple disorders
they encounter in their patients; yet, clinicians felt that few empirical guidelines exist for
adapting ESTs to “real life” treatment and for changing course when ESTs are ineffective.
Importantly, one researcher agreed with these responses, saying that researchers must do a
better job of demonstrating generalizability of research findings to standard clinic
populations. Likewise, two additional researchers felt that most eating disorders research
lacks clinical relevance, as, in their view, the research focuses on issues that have little-to-no
bearing on day-to-day practice.
Question #2: What can we do to close the gap?
Fortunately, the responses to this question were almost wholly uniform! First and
foremost, our respondents believed that promoting institutional and organizational support for
clinician-researcher interaction and collaboration is key to bridging the research-practice gap.
Many suggestions centered on creating forums for open and honest discussions between
clinicians and researchers. The most commonly cited venue for such discussions was the
AED annual international conference. Both researchers and clinicians alike called for a
stronger fusion of clinical and research data at these conferences, where ideally, presenters of
empirical data would discuss clinical applications. Perhaps more importantly, respondents
reported a strong desire for a greater prominence of purely clinical presentations at
professional meetings. Finally, there was a desire for smaller, informal group discussions
where professionals could discuss the “evidence” they value, the reasons for their opinions,
and the ways in which the different forms of evidence inform, rather than contradict, each
other. This coming together of the “minds” (aptly described by one clinician as a “researcher-
clinician rapprochement”) on the same playing field would serve to mitigate any perceived
power differential or implied value placed on one type of evidence over another.
In addition to broadening the appeal of conferences, respondents felt that it would be
useful to have regular clinical commentaries on empirical data in scientific journals (e.g., the
International Journal of Eating Disorders) and professional newsletters (e.g., the AED
Forum). Respondents also called for a need to lobby for funding for clinician-researcher
collaborations and for translating research into patient care. Many felt that changes at the
level of academic institutions or managed care would only occur if there were funding
opportunities available for exploring clinical-research collaborations.
Respondents also felt that improvements in training could close the gap. Suggestions in
this area included: 1) encouraging the inclusion of evidence-based interventions in clinician
training to impart an appreciation for, rather than suspicion of, research; 2) changing training
expectations by creating and encouraging “clinician investigator” job profiles rather than
“clinician” OR “investigator” profiles; 3) providing refresher research design and statistics
courses at conferences; and 4) teaching scientists to think like clinicians and vice versa.
Finally, clinicians made several suggestions for ways to increase the clinical relevance of
research including testing treatments in randomized controlled trials (RCTs) and in “real life”
treatment settings. Clinicians also stressed the importance of studying what clinicians do in
their treatments rather than simply expecting clinicians to do what researchers study.
Developing a Road Map

It is clear from the responses of our survey that the dynamic tension between researchers
and clinicians in the field of eating disorders is a multilayered, complex interaction of
structural, institutional, relational and systemic factors. These “data” appear to strongly
corroborate empirical findings, both within and outside of our field. Within our field,
investigators have found that clinicians who treat individuals with eating disorders prefer to
make treatment decisions based on their clinical experience rather than on the empirical
literature (Haas and Clopton, 2003; Mussell et al., 2000; Von Ranson , 2005). Reasons cited
for this include; a lack of a research emphasis in graduate training, a lack of EST training
opportunities, inconsistency between ESTs and the clinician’s preferred clinical approach,
and the view that ESTs are not flexible enough to meet the treatment demands of patients
typically seen in clinical practice (i.e., those with extensive co-morbidity, complex social
histories, etc.). Overall, these findings are remarkably similar to the impressions of our AED
colleagues described above.
These same tensions have been observed in other fields. For example, in software
engineering, the underutilization of research findings in applied practice is reportedly due to:
1) an overemphasis on technology that lacks generalizability to applied settings; 2) a research
focus that is too specialized and not interdisciplinary or problem-focused; and 3) a lack of
incorporation of state-of-practice engineering into empirical research (Abrial, 2005). A
similar situation exists in education, where empirically supported programs are not routinely
implemented in schools because of a lack of training and support for teachers, competing
demands for staff, limited resources (e.g., time, financial resources), and a failure of the
programs to apply to the student populations they serve (Donovan, Brandsford, and
Pellegrino, 2007). Thus, the research-practice divide, and reasons underlying the divide,
appear to be universal phenomena. This means that effective strategies for overcoming the
gap are unlikely to be specific to the eating disorders field, but will instead need to be broad-
based efforts aimed at addressing core features underlying applied-research divides in all
fields.
Fortunately, there are fields that are ahead of us in addressing these issues from whom
we can borrow to develop our own road map. Three in particular, the education,
organizational development, and medicine fields, offer theoretical models that seem
especially relevant: Innovation Diffusion Theory, Knowledge Transfer Theory, and
Evidence-Based Medicine.
Innovation Diffusion Theory
A number of fields (including education) have incorporated principles from innovation

diffusion theory into their research-practice integration strategies. For the purposes of our
discussion, we will cull the literature on these approaches down to core tenets.
Innovation diffusion, outlined in Everett Rogers’ classic work The Diffusion of
Innovations (1995), is the “process by which an innovation (an idea or practice perceived to
be new) is communicated through certain channels over a period of time among the members
of a social system.” The communication in this process is based on mutual exchange and
understanding between all stakeholders within a given system or culture. Innovation
diffusion theorists stress that didactic, lecture-based presentations and lectures do very little
to facilitate this mutual understanding and learning (O’Brien et al., 2001). Indeed, practices
used to facilitate these key aspects of innovation diffusion tend to be highly experiential and
interactive, including simulation (i.e., role playing), paired work (i.e., small group or paired
training/discussion), guided experience or communities of practice (e.g., individual or peer
supervision, special interest groups), work shadowing (i.e., learner observation), and
narrative transfer (e.g., stories). Interestingly, in our field, we rarely utilize these interactive
strategies, but instead rely on didactic, lecture-based presentations. According to innovation
diffusion theory, these practices will do little to engender the effective learning and use of
new knowledge generated by ESTs.
The interactive learning strategies described above can increase the chances that users
will adopt the new innovation. During the learning process, users are theorized to progress
through five stages in deciding whether to use the innovation in their everyday work/practice
(Rogers, 1995):
1) Knowledge (awareness and basic understanding of the innovation)

2) Persuasion (the process of forming an attitude toward, or developing interest in, the
innovation)
3) Decision (activities leading to a choice to either adopt or reject the innovation)
4) Implementation (putting the innovation into practice)
5) Confirmation (cost/benefit evaluation of on-going full use of the innovation).
In our field, we tend to view the decision making process for using ESTs as a discrete
event, characterized primarily by stages 1 and 2. We have not moved forward in any
significant way to: 1) develop processes that promote the evaluation of empirical research
recommendations or clinical observational data (Stage 3); 2) develop guidelines for the
integration of empirical research into clinical practice; or 3) translate clinical observation into
treatment research (Stage 4). Clearly, as we embark on our attempts to integrate research and
practice in our field, it is critical that we appreciate that the dissemination of information as a
staged process, requiring a blend of experiential, collaborative, and interactive approaches.
Knowledge Transfer Theory
Organizational management guru Peter Drucker coined the terms “knowledge society”
and “knowledge workers” in 1994 (Drucker, 1994), marking the beginning of the
“knowledge field”. The knowledge movement soon led to the general conceptualization of
“knowledge transfer”, or the transfer of best practices within an organization or firm
(Szulanski, 2003). For our purposes, we will define knowledge transfer as the process of
transferring or conveying knowledge, skills, and competence from those who generate this
knowledge to those who will utilize the knowledge. What is important for us to note is that
within the framework of knowledge transfer, equal value is placed on the transfer of “explicit
knowledge” (i.e., research findings, hard facts, material for guidelines and protocols) and the
transfer of “tacit knowledge” (i.e., clinical “know-how”, expertise, unwritten, practical,
contextual knowledge) (Nonaka and Takeuchi, 1995). Currently, our field tends to view
explicit knowledge (e.g., ESTs) as the only knowledge, with a decidedly one-directional
pattern of knowledge transfer. However, theorists have highlighted several different models
of knowledge transfer that are not limited to this uni-directional pattern. For example,
Reardon, Lavis, and Gibson (2006) propose three models of knowledge transfer:
1) Producer Push: The producers of the knowledge explicitly plan and implement
strategies to push that knowledge towards audiences they identify as needing to
know.
2) User Pull: The users of the knowledge deliberately plan and implement strategies to
pull knowledge from sources they identify as producing information useful to their
own decision-making.
3) Exchange: Relationships are built and nurtured between those who produce the
knowledge and those who might use the knowledge, to facilitate the exchange of
information, ideas, and experience. Integral to the exchange are producers helping
users to build the capacity to integrate the knowledge and users helping producers’
work be more relevant.
To date, our field has primarily adhered to the “Producer Push” model of knowledge
transfer, with researchers encouraging and, at times, demanding clinicians to adopt ESTs. It
has been a stunningly ineffective model for research dissemination (see data on rates of EST
use above). By contrast, the exchange model appears to be ideal for our field, as relationships
foster the mutual dissemination of both explicit (research) and tacit (clinical) knowledge,
which should result in stronger alignment of research and practice. Research from a wide
range of fields supports this model in showing that knowledge is most effectively assimilated
and integrated when there is buy-in from key stakeholders (O’Brien et al., 2001; Donovan et
al., 2007; Reardon et al., 2006).
Evidence-Based Practice
The Evidence-Based Practice (EBP) movement, begun in the medical field in the U.K.,
has become ubiquitous in the field of medicine. EBP is defined as “the integration of best
research evidence with clinical expertise and patient values” which leads to optimized
clinical outcomes and quality of life (Sackett et al., 2000). The basic principles of EBP have
common-sense appeal. We include it here because EBP has frequently become synonymous
with the use of ESTs and, therefore, could be a tempting model for our field to turn to for
guidance on research dissemination.
Within this model, it is the responsibility of the clinician to seek the current, best
research evidence for their practice following five steps (Sackett et al., 2000):
1) Convert one’s need for information into an answerable question.

2) Track down the best clinical evidence to answer that question.
3) Critically appraise that evidence in terms of its validity, clinical significance, and
usefulness.
4) Integrate this critical appraisal of research evidence with one’s clinical expertise and
the patient’s values and circumstances.
5) Evaluate one’s effectiveness and efficiency in undertaking the four previous steps,
and strive for self-improvement.
Literature in the field of medicine emphasizes ways to streamline this process, educating
practitioners on how to access and streamline their literature research (Fain, 2003; Straus et
al., 2005). Although clinical judgment, expertise, and experience are taken into account in
EBP, this model places the brunt of the dissemination burden on the practitioner. Our current
one-directional, “Producer-Push” model of research dissemination fits with the EBP model,
i.e., researchers produce ESTs and provide descriptions and recommendations about them in
the form of papers in research journals and conference presentations. It is then incumbent
upon clinicians to seek out information about ESTs , avail themselves of expert training and
supervision on the use of ESTs, and successfully integrate these practices into their treatment
of patients. However, as we have seen, this approach has resulted in a research-practice
stalemate in our field. Clinicians continue to rely more on their own clinical experience and
judgment, and ESTs remain underutilized. Importantly, the American Psychological
Association (Levant, 2006) has developed guidelines for Evidence-Based Practice in
Psychology (EBPP) that offer an expanded definition of evidence and research designs that
reinforces the contribution of clinical expertise within the EBP model.
The Road Map

In order to organize the theories and principles reviewed above into our own road map,
we again look to the field of education to provide us with a unifying framework. This field
has been addressing its own research-practice gap for over a decade and has been a
forerunner in integrating knowledge transfer and innovation diffusion principles into its
strategies for overcoming research-practice gaps (Warford, 2005; Love, 1985). In their
seminal report, Donovan et al. (2007) present an extensive set of steps, strategies, and
directives that aim to promote dissemination within, and integration of research findings
with, applied practice. As we are at the beginning stages of this process, we must move in a
thoughtful, deliberate way to create a similarly layered, thematic map tailored to the
dynamics unique to our field. We selected three fundamental guidelines from the education
report to organize our initial phase of research-practice integration:
1) Research findings and clinical knowledge need to be organized and communicated in

a way that is easy to understand and integrate.
2) Implementation of a new model for research-practice integration must be viewed as a
long-term, five to ten year process.
3) Research-practice collaboration will require a fundamental change in the relationship

between the two groups.
All three steps include elements of innovation diffusion, knowledge transfer, and EBP
discussed above. Thus, these recommendations provide an excellent framework within which
to integrate what we have learned from our own field and others into a road map for moving
forward. We outline recommended guidelines below, accompanied by specific action items
and strategies. Notably, we describe these guidelines within the context of the AED, as we
feel this organization is in the best position to charter the implementation of the suggested
strategies.
The AED Research-Practice Integration Guidelines

Guideline #1. Research findings and clinical practice information need to be organized
and communicated to practitioners and researchers, respectively, in a way that is easy to
comprehend and to integrate into their thinking.
• Provide plain language summaries (similar to the practice of The Cochrane Library1)
for empirical articles in AED publications, including the International Journal of
Eating Disorders
• Form “clinical topics” committees to translate and describe clinical practices to
researchers. These committees can serve as liaisons between clinical and research
communities, promote the clinical practice of formulating and seeking answers to
“answerable questions”, and model writing up case studies, conducting single-case
experiments, and pioneering other ways to convey clinical or “tacit” knowledge.
• Create interactive learning opportunities for disseminating research as well as
clinical evidence These techniques should include those recommended by innovation
diffusion theory (see above), including mentoring, guided experience and
experimentation, simulation, work shadowing, paired work, communities of practice,
and narrative transfer.
• Support and encourage the development of AED conference workshops that
integrate participatory learning methods.
• Support and encourage translational research.
Guideline #2. Given that it will take five to ten years to build the bridge between research
and practice, we must remain consistent and persevere in our methods of approach.
1
The Cochrane Collaboration is a non-profit organization dedicated to improving healthcare decision-making
globally, through systematic review of the effects of healthcare interventions published in The Cochrane
Library (see www.cochrane.org)
• Sustain, augment, and ensure the quality of the “bridge” by maintaining a research-
practice oversight group to monitor and evaluate the process, to review the literature,
and to continue to strategize ways to further facilitate research-practice integration.
• Regularly review the AED Research-Practice Integration Guidelines on a member-
wide basis (through the AED general listserv, website, and/or Forum) to ensure
relevance and scope.
• Develop mechanisms that promote and strengthen full AED membership buy-in into
the research-practice integration process over time.
• Build on existing organizational infrastructure (e.g., AED Special Interest Groups,
committees, member listserv, publications, education and training programs) to
support and integrate research-practice linkages throughout the AED membership.
Guideline #3. Research-practice collaboration will require a fundamental change in the

relationship between the two groups.
• Expand definitions of current terminology to embrace the range of experience and

values of both partner groups.
• Support the American Psychological Association’s (see Levant, 2006) endorsement
of a) an expanded understanding of “research evidence” that includes multiple types
of evidence (e.g. efficacy, effectiveness, epidemiological, treatment utilization, etc.)
drawn from a range of potential sources (e.g., laboratory and clinical settings,
assessments, etc.); and b) the position that evidence-based practice is not confined to
RCTs alone, but rather multiple research designs contribute to effective treatment
• Support the recognition that clinical observation, judgment and experience (tacit
knowledge) contribute to the knowledge base in our field.
• Encourage research funding mechanisms that: 1) address what clinicians are doing in
their treatment practices; 2) provide resources for clinicians to learn and be
supervised in ESTs; 3) support researcher-clinician partnerships that field test ESTs
as well as clinical interventions derived solely from clinical practice; and 4) support
research conducted by practicing clinicians.
• Foster the development of a common language by discouraging the use of jargon.
• Develop AED conference sessions that foster researcher-practitioner dialogue and
collaborations.
• Create researcher-practitioner columns and news pieces in the AED Forum.
• Continue the researcher-practitioner model for AED conference plenaries and
keynote addresses.
Guideline Implementation
Given the scope, variety, and complexity of some of the strategies outlined above, it is
critical that the implementation of the guidelines is monitored, as described in the first
directive under Guideline #2. The formation of an oversight group would be the first step in
the implementation process. Members of this group should represent the domains of research
and practice, and should be professionals who share a long-term commitment to

strengthening the research-practice interface. Exposure to, and on-going education in, the
areas of knowledge transfer, diffusion theory, and interactive learning methods will be
necessary so that members of the group understand how to establish effective implementation
priorities, strategies, and methods for evaluating the process.
The AED, as a representative of the field, has taken this initial step by forming a
Research-Practice Task Force2. Comprised of an international, cross-section of seasoned
researchers, researcher-practitioners, and practitioners, the mandate of the task force is to
develop strategies (including those outlined above) to foster research-practice integration
within the AED and the field at large. Begun in 2007, the task force is implementing
preliminary steps by promoting researcher-clinician dialogue in interactive formats into the
AED International Conference on Eating Disorders. For example, the task force hosted the
2008 World Summit on Eating Disorders entitled “Let’s Talk: Advancing the Research-
Practice Partnership”. This summit session included researchers and clinicians from around
the globe who discussed their own perspectives for closing the gap. Several of the strategies
outlined above were described and beginning action plans were developed. In the future, the
task force will continue to oversee the implementation and on-going review of research-
practice integration within the AED, expanding on the guidelines outlined above.
Conclusion
In ending, it is clear that the research-practice gap is a universal phenomenon that exists
within virtually all professions that have an applied and basic science component. Given the
universality of the causes of the tension and the barriers to integration, it is likely that the
basis of the gap lies somewhere in human nature and somewhere in the character of
organizational systems (both quite daunting variables with which to tamper). Nonetheless, the
resounding enthusiasm of our colleagues for developing ways to address the research-practice
gap is heartening and, given the guidance and experience of other fields, it is incumbent upon
us to move forward in this direction. However, before we are able to enact the larger
structural changes described above, we must first focus on the fundamental steps involved in
establishing on-going opportunities for clinician-researcher dialogue and collaboration.
The AED Research-Practice Integration Guidelines set forth a range of actions we can
implement to strengthen the research-practice partnership in the AED. These guidelines are
by no means exhaustive or set in stone. Rather, they are intended to provide a work-in-
progress that will stimulate an on-going conversation between researchers and practitioners
about the sources and types of knowledge, tools, processes, and initiatives that will promote
the most effective practices in our field.
Despite our quite different professional experiences, we, the authors, developed mutual
trust and respect for each other through our AED opportunities to work closely and talk
together about our perspectives. Dialogue, shared experience, and support bridged any gap
that may have initially existed between us. The AED and professionals in our field can
similarly help close the gap by using dialogue, collaboration, mutual support, and respect to
bring researchers and clinicians together. In joining the richness of clinical observation with
the world of formal scientific investigation, the quality of our research and treatments will
improve. Our community of professionals and the quality of the lives of people with eating
disorders will be all the better for it.
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Chapter V
Inpatient Psychiatric Treatment of

Adolescents and Adults with
Eating Disorders
Parinda Parikh, Dara Bellace and Katherine Halmi

Weill Cornell Medical College
White Plains, New York, USA
Abstract
Although eating disorders (EDs) have been described in the literature for over a
millennium there are no standardized, universally accepted, evidence based criteria for
the inpatient treatment of patients with EDs. This may be due to the ethical conundrum
involved in enrolling medically compromised ED patients in randomized controlled trials
where urgent medical stabilization often takes precedence over conducting a regimented
research treatment protocol, as the latter may expose the patient to undue clinical risk.
Most clinicians specializing in EDs rely on their clinical training and experience along
with the treatment guidelines published by the American Psychiatric Association (2006)
in managing and determining the level of care needed for their patients. In the United
States, managed care companies and other health maintenance organizations use their
own heterogeneous cost-efficiency driven criteria in determining the level and length of
inpatient care, with mostly unknown but sometimes documented poor long-term
outcomes.
This chapter discusses the inpatient management of anorexia nervosa (AN) and
bulimia nervosa (BN) for adolescent and adult patients. Any reputable treatment program
should emphasize a multidisciplinary approach integrating comprehensive diagnostic
evaluation, medical management, pharmacotherapy, individual psychotherapy, group
psychotherapy, family therapy, nutritional counseling and comprehensive discharge
planning.
88 Parinda Parikh, Dara Bellace and Katherine Halmi
Introduction
Patients suffering from AN, BN, and ED Not Otherwise Specified (ED NOS) often
experience significant medical and psychiatric complications, in addition to having other co-
morbid psychiatric illnesses. This chapter will discuss the clinical manifestations and the
medical complications of EDs along with pertinent medico-legal issues and evidence in the
literature regarding treatment recommendations for the inpatient management of adolescents
and adults diagnosed with EDs.
General Issues for AN Patient Hospitalization
There is little research data comparing the efficacy of different inpatient treatment
protocols for AN. In determining a patient’s appropriateness for an inpatient level of care, it
is important to consider the patient’s overall medical condition, psychiatric symptoms,
psychological well-being, social support network, prior treatment response or failure, and the
patient’s commitment to treatment. Many of the symptoms of AN are ego-syntonic, which
often leads to complete denial of the illness and failure in seeking the proper treatment. As a
result, an emaciated, medically compromised AN patient will often continue to refuse
treatment for weight restoration. The dropout rate from voluntary inpatient treatment
programs is reported to be as high as 51%. (Woodside, Carter and Blackmore, 2004).
This the 12th inpatient hospitalization for Laura, a 16-year-old Caucasian female first
diagnosed with her ED 3 years ago. She usually gets readmitted at a BMI of 13 in a
severely emaciated state, with electrolyte imbalance from diuretic abuse and water
loading. During her inpatient stay, she complies with the weight restoration program and
reaches a BMI of 18.5 only to lose a significant amount of weight within 3 months after
discharge. There are multiple psychosocial stressors contributing to her disorder but
various treatment teams at different hospitals have been unsuccessful in resolving them.
During the last admission, Child Protective Services were involved because of concerns of
medical neglect and it was recommended that Laura enter a residential program away from
home. That was the first time Laura was able to maintain her weight for over a year. She
stated that she "always wanted to lose weight but could not do it" and "was waiting to get
out of there.” When she was given a Thanksgiving pass to come home for few hours, she
convinced her parents that she did not need to return to the residential program. At that
point, her case slipped through the cracks in the vast maze of Child Protective Services.
Laura lost 40 pounds in 2 months and was re-hospitalized for her ED.
Clinical presentations similar to Laura’s are no longer an exception. Increasingly,
young adolescents presenting with an earlier onset of ED’s have repeated hospitalizations
before they reach adulthood. In addition to weight restoration and pharmacological
management, we need to fully examine, identify and try to resolve any contributing
perpetuating psychological and social stressors.
Inpatient Psychiatric Treatment of Adolescents and Adults... 89
Jenny, a 35-year-old married female, had a prior history of an ED was taken to a nearby
emergency room after a family member called 911 stating that she had “passed out” at home.
Upon arrival at the hospital emergency department, the patient was noted to be severely
emaciated. She weighed only 69 pounds and was 5 feet 3 inches tall (BMI 12.2 kg/m2). Jenny
was found to be orthostatic, bradycardic (with pulse of 42), hypothermic and cognitively
compromised. After initiation of intravenous hydration and immediate stabilization, she was
admitted to a medical floor of the hospital for management of electrolyte abnormalities and
further cardiac monitoring. One week later, even though her condition improved, Jenny was
still unable to eat any food or accept any liquid supplements. When the internist discussed the
option of admission to an ED unit for weight restoration, Jenny attempted to get up from her
bed and threatened to walk out of the hospital against medical advice. A psychiatric
consultant was called in to assess Jenny’s judgment and her capacity to understand the risks
and benefits of undergoing treatment and the consequences of her treatment refusal. When
talking with her husband, the treatment team realized that he had made several attempts to
have her hospitalized for her ED with no success. An application for involuntary admission to
an inpatient ED unit at a psychiatric hospital was made by the treating psychiatrist. This
application was supported by assessments from three other independent psychiatrists, as
required by state law.
In the United States, patients can voluntarily consent to be admitted to a psychiatric unit.
When a patient is in imminent danger to herself or others, an involuntary commitment is
available when clinically necessary. Few studies have compared the rates and outcomes of
voluntary versus involuntary inpatient treatment of AN patients. Follow-up studies have
shown that involuntarily hospitalized patients were eventually thankful to the people who
intervened during the time of their initial treatment refusal (Russell, 2001).
Often a severely emaciated AN patient who presents to an emergency room with
electrolyte abnormalities, autonomic instability, and electrocardiogram changes requires
involuntary commitment.
Criteria for Inpatient Hospitalization for Patients with AN
For adults, the physiological parameters that are considered important for inpatient
admission include the rate and amount of weight loss, the presence of autonomic instability,
as well as the patient’s metabolic and electrolyte status. Generally, adult patients who weigh
significantly less than 85% of the weight recommended for their height and body frame (BMI
< 17.5) have tremendous difficulty gaining weight outside of a highly specialized and
intensely structured inpatient program. This is due to the poor insight and judgment, lack of
motivation (Ametller, Castro, Serrano, et al, 2005), and lack of physical and emotional
resources that tend to characterize this group of patients. At times, this type of inpatient
setting may also be medically and psychiatrically necessary for patients above 85% of their
targeted body weight, especially if they are having medical complications or are not
responding to outpatient treatment.
The clinician’s threshold for admitting an adolescent patient with AN is usually lower
than that for adults, regardless of the patient’s percent body weight and/or BMI, as research
has shown that early intervention in adolescents improves outcomes (Lindblad, Lindberg and
Hjern, 2006). For instance, an adolescent’s unexplained, rapid weight loss over a short period
of time (greater than 8-10 lbs every month), coupled with a refusal to eat, may necessitate a
brief inpatient stay for immediate stabilization.
For all AN inpatients, it is necessary to obtain a complete blood analysis including
complete blood count with differential; a metabolic panel including sodium, potassium,
chloride, bicarbonate, glucose, magnesium, phosphorus and calcium; a liver function panel;
thyroid function tests; iron studies; pregnancy test (for females); an electrocardiogram; and a
consultation with an inte rnist for medical clearance to rule out any organic etiology
contributing to symptoms of AN. Other co-morbid psychiatric conditions like worsening
depression, psychotic symptoms or serious suicidality are also likely to warrant
hospitalization. Patients with AN are candidates for inpatient admission if they show poor
progress in the outpatient setting or if they do not have access to a partial program or a day
treatment program. Other psychosocial factors supporting the decision for an inpatient
admission may include a chaotic family environment; substance abuse by the patient or other
family members; physical, sexual or emotional abuse; other family members with psychiatric
or medical problems; medical neglect; and lack of resources.
Table 1 and Table 2 outline some common medical indicators for inpatient admission and
common laboratory findings in AN, respectively.
Table 1. Common Medical Indicators for Inpatient Hospitalization for AN
Clinical Condition Features

Autonomic Instability Heart rate < 40bpm; BP < 90/60 mm Hg; blood glucose < 60 mg/dl;
uncontrolled diabetes; electrolyte imbalance
Weight (% of healthy In adults, < 85% and refusal to gain weight in outpatient setting;
body weight) In children and adolescents, rapid weight loss and/or refusal to eat,
regardless of % of healthy weight
Outpatient Compliance Poor
Behaviors Purging
Starvation
Dangerousness Refusal of treatment; Dangerousness to self and/or others
(Adapted from the American Psychiatric Association, (1))
Nutritional Rehabilitation and Medical Monitoring

of AN Inpatients
When an adult patient with AN is admitted to an inpatient ED unit, an appropriate target
weight range should be established. To do so, clinicians should take into consideration
factors such as the patient’s height, age-appropriate weight, current weight and menstrual
history (for females).
Table 2. Common Laboratory Findings Related to Restricting Behaviors/Starvation
• Hyponatremia
• Low T3 and T4 levels
• Low estrogen, low luteinizing and follicle-stimulating hormone, low testosterone
• Hyperadrenocortisolemia
• Leukopenia, anemia, thrombocytopenia
• Hypophosphatemia
• Elevated liver function tests (AST, ALT, GGT, Alkaline phosphatase)
• Elevated serum cholesterol
• Increased ventricular-brain ratio on brain imaging
• Sinus bradycardia, arrhythmias, prolonged QTc
• Hypoalbuminemia
(Parikh and Halmi, 2006).
To establish a target weight range for adolescent patients with AN, one should consider
the patient’s menstrual history (for females with secondary amenorrhea), mid-parental heights
(average of the heights of both parents), and skeletal frame. The Center for Disease Control
(CDC) growth charts can also be helpful in establishing a target weight range (Kuczmarski,
Ogden, Grummer-Strawn, et al, 2000). Patients must always be given a target weight range
rather than a specific target weight, as multiple factors including dehydration, vomiting,
laxative abuse, diuretic abuse and other causes of fluid shift may contribute to weight
fluctuations. Most multidisciplinary treatment programs have a registered dietitian who can
design each patient’s meal plans according to their caloric needs, and individual preferences.
Prior to discharge, the dietician can also prepare a structured meal plan that can ensure
nutritional adequacy once the patient begins treatment in an outpatient setting.
Published guidelines recommend a weight gain of 1.1 to 2.2 kg per week for hospitalized
AN patients (British-Psychological-Society, 2004). The weight restoration process typically
starts at 30–40 kcal/kg/day (i.e., approximately 1,000–1,600 kcal/day), however this rate may
need to be slowed in more severely ill patients who are below 70% of their ideal body
weight. Intake can then be progressively increased to 70–100 kcal/kg/day, while monitoring
their total daily intake, 24-hour urine output, vital signs, electrolytes (i.e., sodium, potassium,
phosphorus, magnesium, calcium), and liver function tests. AN patients should also be
monitored for any edema or electrocardiogram changes.
Studies have shown that it is more efficient, effective and easier for severely emaciated
patients to take high-calorie liquid supplements divided into six small feedings throughout
the day, rather than consuming the same amount of solid food calories, in order to maintain
the same rate of weight gain (Okamoto, Yamashita, Nagoshi, et al, 2002). As the patient’s
weight continues to increase, they can be gradually introduced to solid foods. This process
should start with ‘partial trays’ consisting of approximately 1,000 calories per day in solid
foods, accompanied by six small liquid feedings. When patients start achieving healthier
eating patterns, with better perceptions of hunger and satiety, and are improving medically,
they can progress to higher-calorie trays (up to 2,400 kcal per day) with liquid supplements at
snack time depending on their metabolic needs.
All inpatient feedings must be done in a supervised setting, monitored by trained nursing
staff who record each patient’s food and fluid intake. Bathrooms on the unit should be locked
at all times, except for 6 to 8 designated “commode times” during the day. During these
times, a nursing staff member should monitor each patient and record her urine output as well
as any bowel movements. Constipation is a major complication of restrictive eating as well as
laxative abuse, and often becomes problematic during the weight restoration process. Using a
gentle stool softener along with a fiber supplement may therefore be helpful. Occasionally a
patient may complain of impaction which requires immediate medical attention and possible
use of stronger laxatives or manual disimpaction to avoid further complications like
obstipation or more rarely colonic obstruction. Inpatients should be weighed daily in a
hospital gown prior to morning showers and after they have voided. Staff members should be
aware that many AN patients will frequently engage in behaviors to manipulate their weights,
such as hiding coins or weights in their gowns, intentionally retaining urine, or water loading.
Such possible behaviors must be monitored closely and addressed by the treatment team.
Each patient’s internist or pediatrician (for adolescent patients) should be consulted by
the inpatient treatment team and involved in the treatment process where appropriate.
Occasionally a cardiologist will need to be consulted for any unresolved electrocardiogram
changes. An orthopedist may need to be consulted when there are any concerns about
fractures and bone loss. It is important for clinicians treating these complicated patients to
realize that most abnormal laboratory findings will start improving gradually as nutritional
rehabilitation progresses. However, some complications such as severe osteoporosis may be
irreversible.
Inpatient nutritional rehabilitation programs should attempt to create a milieu that
incorporates emotional nurturance. Such programs should also implement a combination of
reinforcers that link each patient’s activity level and other unit privileges to appropriate
weight gain and desired improvement in negative behaviors, while avoiding power struggles
with patients. Daily feedback during morning rounds concerning any changes in weight,
privilege status and other observable parameters is also helpful for these patients.
Psychosocial Treatments for AN Inpatients

Individual, group and family therapy are all utilized within the inpatient setting.
Cognitive and behavior therapy principles can be applied in both inpatient and outpatient
settings. Individual behavior therapy has been reported to successfully restore weight in AN
patients (Halmi, 1985). In controlled inpatient studies of AN, behavior therapy was found to
be effective in inducing weight gain (Wulliemier, Rossel and Sinclair, 1975). Behavior
therapy is important in the treatment of AN patients as it can mitigate some of the symptoms
arising from the emaciated, malnourished state such as irritability, depression, preoccupation
with food, cognitive impairments and sleep disturbances. Individual cognitive therapy
focuses on severe cognitive distortions related to food and body image, although success with
this technique can be achieved only after some weight gain in a severely underweight patient
(Garner, 1986). More recent modifications of these therapies are well described in the
literature (Kleifield, Wagner and Halmi, 1996). Two techniques often used in cognitive
therapy are cognitive restructuring and problem solving. AN patients usually have a rigid
style of thinking and perceiving their world, characterized by dichotomous, “all-or-nothing”
thinking. These distorted thoughts are present primarily in relation to food and weight, but
also around issues of self-esteem and self-concept, with pervasive feelings of ineffectiveness
often accompanied with an extreme drive for perfectionism. These cognitive distortions are
best addressed in individual cognitive therapy.
Family therapy and family groups are also utilized on most inpatient units. As a general
rule, a family assessment should be done on all AN patients living with their families
regardless of the age the patient. For adolescent AN patients, family therapy is an essential
element of management (Eisler, Dare and Russell, 1997). Family support groups facilitated
by clinicians are also helpful in educating other family members regarding the illness.
During inpatient stay, the patient should participate in group therapy sessions, including
those geared toward body image and specific ED problems; self-esteem, self-confidence, and
self-expression; gender specific issues; nutrition; and medication education. These groups,
along with substance abuse counseling groups and controlled exercise groups, are all proven
to be helpful in educating patients about the different aspects of recovery from AN. Separate
body image groups and peer support groups for adolescent patients are especially useful in
addressing their age-specific issues.
Psychopharmacology for AN Inpatients

Pharmacotherapy is not the first line of treatment for AN. However, medications may be
helpful in treating the comorbid psychiatric conditions that many AN patients experience,
such as anxiety disorders, mood disorders, and psychotic symptoms. For further discussion on
this topic, please refer to the chapter by Mitchell and colleagues.
Discharge Planning for the Hospitalized AN Patient
To date, there are no studies to provide evidence-based discharge criteria for AN

patients. The ideal discharge criteria, if permitted by managed care, are as follows: 1)
achieving and maintaining normal weight range for at least one week in patients who are
repeatedly hospitalized for treatment of AN or attaining 90% of normal weight in patients
with first episode of inpatient hospitalization; 2) significant improvement in other ED
behaviors such as purging, over-exercising, laxative abuse, and binge eating; 3) medical
stability (e.g., stable vitas signs, normal electrocardiogram and lab work); and 4) no suicide
risk or overt psychiatric symptoms warranting continued inpatient stay. Discharge planning
should consider transition to a partial hospitalization program or a day treatment program
especially if the patient has had repeated relapses or in the case of an adolescent patient with
lack of structure at home. Comprehensive multifaceted treatment must be continued with
experienced professionals including an internist or a pediatrician for medical care, individual
cognitive psychotherapist, and a family therapist especially for patients under age 18.
Criteria for Inpatient Hospitalization for BN
The majority of BN patients can be treated effectively in an outpatient community

setting. The main clinical indications for inpatient hospitalization are often medical or
psychiatric instability. Medical hospitalization is usually a consequence of purging behaviors,
such as frequent vomiting, laxative abuse, and/or abuse of diet pills or diuretics, which can
create serious electrolyte imbalances and dehydration, as described in Table 3. These patients
are usually referred to an inpatient ED unit by their families or an emergency room clinician.
These patients may present with complaints of weakness and lethargy and are at risk for
developing cardiac arrhythmias. A serum potassium below 2.5 mEq/L requires medical
admission for electrolyte correction. Other situations that can present as medical emergencies
are severe abdominal pain, gastric dilation, intractable vomiting, bloody vomitus, and cardiac
problems from ipecac intoxication. The most serious consequence of gastric dilatation is
gastric rupture (Matikainen, 1979). Esophageal tears and rupture due to severe vomiting are
also life threatening complications (Mitchell, Pyle and Miner,1982).
Psychiatric symptoms requiring inpatient hospitalization for BN include a severe mood
disorder, substance abuse or dependence, and concerns of suicidal or repeated parasuicidal
behaviors. Over 30% of patients with BN have co-morbid depression, which is also
accompanied by suicidal ideation (Braun, Sunday and Halmi, 1994). Bulimic patients who
become dysfunctional in their work, social, or personal lives, and who spend most of their
income on financing their binges, will benefit from hospitalization. A course of intensive,
closely monitored inpatient treatment can help these patients to break the binge-purge cycle
and establish healthier routines.
Table 3. Medical Findings Related To Purging Behaviors (Vomiting And Laxative

Abuse)
• Dehydration (evident by elevated sodium)

• Hypokalemia (diagnosed by low potassium, can induce cardiac arrhythmias)
• Metabolic alkalosis (diagnosed by elevated serum bicarbonate, decreased chloride and
decreased potassium)
• Hypomagnesaemia, hypophosphatemia, hypochloremia,
• Hyperamylasemia (salivary or pancreatic amylase hypersecretion)
• Esophageal tears, gastric ruptures
• Pneumomediastinum
• Skeletal or cardiac myopathies (syrup of ipecac-induced)
• Metabolic seizures (from electrolyte abnormalities)
• Mild neuropathies
• Cognitive impairment
• Chronic constipation, loss of normal bowel functioning (may need colon resection and
colostomy in severe cases)
(Parikh and Halmi, 2006).
Although, the length of stay for a bulimic patient is now mainly dictated by the managed
care companies and health maintenance organizations, treatment based on expert clinical
consensus may be far more clinically advantageous for patients. Generally, an inpatient ED
hospital stay of 7-10 days is approved by insurance companies for bulimic patients
experiencing one or more of the above mentioned complications. Such approval is granted if
the patient was treated and failed multiple levels of care in the community setting (i.e.,
outpatient, partial hospitalization and day treatment programs).
A comprehensive psychiatric evaluation along with a thorough family assessment is
especially important for a bulimic adolescent or adult patient living at home. Vocational
assessment and training are also useful for a dysfunctional bulimic patient who has been
unable to cope with her home, work and social life.
Nutritional Rehabilitation and Medical Monitoring

of BN Inpatients
The first goal of treatment is to stop the binge-purge behaviors. This can be done by
providing maintenance calories in supervised meals, sometimes divided into six small meals
for breakfast, lunch, dinner, and three small snacks over the course of the day. Patients must
be observed during meals as well as for several hours after meals. This approach of
preventing a vomiting response to eating is known as response prevention behavior therapy
(Leitenberg, Rosen, Gross, et al, 1988). Because bulimic patients will tend to surreptitiously
vomit in their room, bathroom, or in any non-monitored place, it is important to supervise
their bathroom and room access. Frequent monitoring of serum amylase level, bicarbonate,
chloride, and potassium can be helpful in assessing their vomiting behaviors as well. Under
the guidance of a registered dietitian, patients are trained to identify their binge-inducing
foods and challenge their binge practices, learning to eat these foods in smaller amounts
while in a supervised setting. Once the BN patient is able to establish normal eating
behaviors in a supervised setting, she is given increasing freedom to select her own meals.
Weekly electrolyte assessment and electrocardiograms are helpful in monitoring and
correcting abnormal laboratory values. Positive urine toxicology upon admission must be
followed with a repeat drug and urine test to ensure that the patient has not been abusing any
illicit substances during their inpatient stay. Patients with a history of laxative abuse will
report constipation and constantly seek laxatives to relieve the unpleasant “feeling of
fullness”. This should be monitored by the bathroom log, medical examination and x-rays of
abdomen, if indicated. Using a stool softener and a fiber supplement may help these patients
regulate their bowels, while training them to stop abusing stimulant and osmotic laxatives.
Psychosocial Treatments for BN Inpatients

Among the different psychotherapy approaches that have been rigorously studied,
cognitive behavioral therapy has been shown to be the most effective for BN patients
(Fairburn, Kirk, O'Connor, et al, 1986). This approach to treatment helps these patients to
focus on personal psychological issues, interpersonal relationships, and development of
social skills, as well as stabilizing their eating behaviors. Common psychological issues that
tend to arise with this population are an inability to express anger and other feelings
appropriately; depression stemming from feelings of guilt, abandonment, losses and trauma;
and dependency and control issues.
Bulimic patients are often found to exhibit severe impulsivity, which includes engaging
in a range of antisocial behaviors (e.g., lying and shoplifting) complicated by substance abuse
and mood dysregulation. Even though a significant number of BN patients also meet criteria
for avoidant personality disorder (Braun, Sunday and Halmi, 1994), borderline personality
traits (e.g., splitting; projection) are more frequently observed in the inpatient setting. For
these patients, food often becomes an escape medium from the discomfort and dissatisfaction
they feel within their personal lives. In the inpatient unit, it is common to see these patients
“acting out” in other ways when their relationship with food is being supervised, monitored
and restructured. Frequently, patients will rebel and may at times leave the hospital
prematurely prior to completion of the treatment, resulting in frequent relapses and poorer
long-term prognosis. Concepts derived from skills training groups (Linehan, Heard and
Armstrong, 1993) are therefore used to enhance competence in regulating affect,
interpersonal relationships, problem solving, and distress tolerance – all of which can be
helpful in teaching these patients effective coping skills.
It is common to see adolescents with BN secretly engaging in bulimic behaviors,
frequently isolating themselves from the rest of their family. Family therapy and family
groups must be included for all adolescent and adult patients living at home (Eisler, Simic,
Russell, et al, 2007). This often helps to elucidate the precipitating and perpetuating factors
of their binge/purge behaviors. In addition, a “family contract” can be used effectively in
helping patients and families take responsibilities for their behaviors and adopt healthier
coping mechanisms.
Medication Treatments for BN Inpatients

Compared to AN, the pharmacological interventions for BN have been more extensively
studied and published in the literature. Various agents that have found to be useful are
antidepressant medications such as the tricylic antidepressants (TCAs), the serotonin specific
reuptake inhibitors (SSRIs) and other newer agents. For further discussion on this topic,
please refer to the chapter by Mitchell and colleagues.
Discharge Planning for the Hospitalized

BN Patient
In the absence of evidence-based studies evaluating discharge criteria, the ideal discharge
criteria, if permitted by managed care, are as follows: 1) achieving and maintaining a binge-
purge free period for at least a week, if this is the patient’s first inpatient hospitalization, and
longer for relapsing patients; 2) medical stability (e.g., stable vital signs, normal electro-
cardiogram and serum electrolytes); 3) successful pharmacological treatment of psychiatric
symptoms, and 4) no suicide risk or overt co-morbid psychiatric symptoms warranting a
continued inpatient hospital stay. Discharge planning should consider transition to a partial
hospitalization program or a day treatment program for adult BN patients who have had
repeated relapses, or for adolescent BN patients who lack structure at home.
Erika is a 21-year-old adult female who was transferred from a medical hospital for
further treatment of her ED on a ‘voluntary’ legal status. One week prior to her transfer,
she had walked into the emergency room with complaints of dizziness, light headedness
and palpitations. Metabolic panel revealed sodium and potassium of 129 and 2.6mg/dl
respectively. Erika admitted that she has been drinking 4-5 liters of water along with diet
sodas and coffee to suppress her appetite. She proudly reported that she managed to lose
20 lbs in just one month using this strategy. She was at BMI of 17.5 on admission. Later
she also admitted to purging behaviors (6-8 times daily) which started 4 weeks before
admission, when she was having feelings of gastric fullness while consuming large
amounts of fluids. She also endorsed symptoms of depression and anxiety, and admitted
that she had been binge drinking alcohol with friends on the weekends. She is currently a
second year law student who feels overwhelmed, juggling her studies and a part-time job at
a corporate law firm.
At the advice of her psychiatrist, Erica admitted herself voluntarily in an inpatient ED
unit once she was medically stabilized. However, she reported tha she “felt better” within
3 days and wanted to leave the hospital. The treating psychiatrist discussed with her the
possibility of staying for at least for 1 week to “interrupt the purging cycle” but Erika was
focused on not missing work and school. As she was not deemed to be psychotic, suicidal
or homicidal, she was discharged against medical advice with referral to an outpatient ED
program. Within a 6-month span, she was rehospitalized 3 times to different inpatient ED
units for similar symptoms of purging, physical complaints suggestive of electrolyte
abnormalities, bloody vomitus and refusal to eat adequately.
Conclusion
EDs including AN, BN and their variants are psychiatric disorders with high morbidity
and mortality from medical complications. The etiology of these disorders is mutifactorial,
with a prominent biologic diathesis interacting with environmental factors facilitating its
development and progression. As described earlier, certain patients do require an inpatient
level of care due to the severity of their symptoms. Even though the length of an inpatient
stay is primarily determined by the constraints of insurance limitations, clinicians should
utilize guidelines based on current expert clinical consensus. Despite considerable research in
the treatment of these disorders, a significant number of patients do not recover completely
and the course of their illness is marked by life long relapses and frequent inpatient
hospitalizations. Outcome is favorable in over 50 % of those treated. For an adolescent
patient, it is even more important to restore weight to a near-optimum level so as to restore
menses and ovulation in female patients and prevent long-term irreversible damage from
osteoporosis. Hospitalization for these patients provides them with numerous advantages
including: 1) rapid restoration of weight for an AN patient; 2) medical and psychiatric
stabilization for both AN and BN patients; 3) interruption of self-harming behaviors; and 4)
comprehensive evaluation and treatment of previously undiagnosed psychiatric co-

morbidities. Current good clinical practice recommendations include a multidisciplinary
approach integrating nutritional rehabilitation, medical stabilization, pharmacotherapy,
psychotherapy, various group therapies, with appropriate aggressive care in order to improve
outcome and prevent morbidity and mortality from the ED.
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Parikh P, Halmi KA. (2006). Anorexia Nervosa. Current Psychosis and Therapeutics
Reports, 4, 121-7.
Russell GF. (2001). Involuntary treatment in anorexia nervosa. The Psychiatric Clinics of
North America, 24(2), 337-49.
Woodside DB, Carter JC, Blackmore E. (2004). Predictors of premature termination of
inpatient treatment for anorexia nervosa. The American Journal of Psychiatry, 161(12),
2277-81.
Wulliemier F, Rossel F, Sinclair K. (1975). A comparison of two different treatments of
anorexia nervosa. Journal of Psychosomatic Research, 19(4), 267-72.
Chapter VI
Day Treatment for Anorexia Nervosa∗
Ida F. Dancyger, Victor M. Fornari and Jack L. Katz

New York University School of Medicine
New York, New York, USA
Abstract
This chapter examines the emergence during the past 25 years of day treatment as an
intensive therapeutic alternative to hospital inpatient care for patients with anorexia
nervosa. The scientific literature regarding the inpatient treatment of eating disorder
patients, whether on a general medical, general psychiatric, pediatric, or specialized
eating disorders unit, is reviewed. A summary of the research describing the use of a day
treatment model for anorexia nervosa is then provided. Criteria for admission or
exclusion and the unique challenges and pitfalls with the different care options, including
the authors’ own experience with eating disorder populations in various clinical settings,
are presented. Two cases of young women with anorexia nervosa are described to
highlight the complex clinical and pragmatic considerations in selecting a treatment
setting. It is noted that economic (that is., managed care) constraints have played an
increasingly important role in the decisions regarding level of care. Future research
efforts should help to provide an evidence-based framework to inform clinical decision-
making regarding the optimal treatment setting for individuals with anorexia nervosa at
different stages of their illness.
Introduction
When should a person with anorexia nervosa (AN) be treated in the hospital? How does
one decide what the suitable level of care is? When does one decide to end a certain level of
care and either transfer a patient to a less or more restrictive program or discharge her to
services in the community? How do mental health providers balance the often conflicting
∗ Parts of this chapter were previously published and are reprinted here with permission from NOVA Publishers.
102 Ida F. Dancyger, Victor M. Fornari and Jack L. Katz
viewpoints of patients and their families (not to mention managed care companies)? These
questions will be examined in this chapter as it addresses day treatment in the spectrum of
care for the treatment of AN. The clinical evaluation and care of individuals with AN is
sufficiently complex so as to present a major challenge for any practitioner treating these
patients. Families, many health professionals, and much of the lay public do not sufficiently
appreciate the serious nature of eating disorders (ED). Despite what is often viewed as simply
a self-imposed dietary restriction, EDs are serious conditions that carry a high rate of medical
complications and substantial risk of death.
Current Trends
Treating patients in a managed care environment has strongly influenced the site of
treatment in the continuum from inpatient to day treatment to outpatient care. Overall, a wide
range of treatment options is available on an outpatient level for those individuals who can
manage safely outside of an inpatient or partial hospitalization /day program setting (per
criteria to be discussed). Outpatient care for AN and/or bulimia nervosa can and often does
include some combination of the following modalities: individual or group psychotherapy,
family therapy, nutritional counseling, medical monitoring, and/or psychopharmacology.
Recently, treatment for many adolescents/ adults with EDs has shifted from an inpatient
setting to a more cost effective day hospital approach. But first we will examine the
parameters of inpatient care for EDs.
Inpatient Treatment of Anorexia Nervosa

on a General Psychiatric
or a Specialized Eating Disorders Unit
Introduction and Clinical Issues
While outpatient treatment represents the most commonly employed approach for the
management of AN (Robinson, 1993), there can occur circumstances that suggest or even
mandate treatment in an inpatient setting. Whether this will be on a medical (or adolescent)
unit, a general psychiatric unit, or a dedicated ED unit will reflect not only certain clinical
considerations but also facility availability and insurance constraints.
The clinical considerations in outpatient vs. inpatient treatment relate to the severity of
the symptoms of AN and their biological concomitants, co-morbidity concerns, the course of
the illness, and the degree of compliance with and response to prior treatment. The behavioral
aspects of the disorder, namely, the self-starvation, the eating rituals, the excessive exercise,
and the possible purging activities will typically fall along a spectrum of severity, as will the
consequent physiological aberrations. When the latter become potentially life threatening (see
section on treatment in a general medical or adolescent unit), the priority obviously exists for
biological intervention. When the behavioral issues are particularly prominent, admission to
Day Treatment for Anorexia Nervosa 103
an inpatient unit, whether general or specialized, becomes more logical (Vandereycken,

2003).
Indications for Psychiatric Admission
Probably the most clear cut indication of a need for psychiatric admission is the presence
of suicidality. As perhaps 50% of ED patients meet criteria for co-morbid major depression at
some time during the course of illness (Cooper, 1995; Halmi et al., 1991), suicidal ideation
can occur; the presence of intent, and certainly a plan, requires urgent psychiatric admission.
But more common are the other indications. These include: significant weight loss, either
gradually to below 75% of ideal body weight (IBW), or more acutely to 85% to 75% of IBW
(APA Guidelines, 2006); poor motivation to participate in outpatient treatment with
progressive overall downhill course; declining ability to function in activities of daily life
because of the patient’s preoccupation with her diet, weight, appearance, etc.; exercise that
has become so frenetic that the patient frequently borders on a state of exhaustion or is
unavailable for other obligations; purging with emetics, laxatives, or diuretics that has gotten
so out of hand as to threaten the patient’s physiological homeostasis; and, finally, family
turmoil consequent to the patient’s ED which in turn is further aggravating matters and from
which the patient must be extricated to have any chance of being stabilized. The presence of
co-morbid substance abuse, if severe enough in its own right, might also mandate inpatient
admission.
General Psychiatric Unit vs. Specialized Eating Disorder Unit
Because of the clinical expertise and formalized treatment protocols that characterize
most dedicated ED units, admission to such a setting might seem the obvious choice for
inpatient treatment. Nevertheless, there are considerations that can lead instead to admission
to a general psychiatry unit. The first of these is, quite simply, lack of availability. Not all
regions have a specialized ED unit, whereas general psychiatry units are more widely
distributed; moreover, admission waiting time may be shorter for a general unit because of
the more rapid turnover rate characteristic of acute inpatient services. The second
consideration is insurance coverage, as this might not be approved for an ED unit, which can
require a specific minimum length of stay to facilitate treatment protocols and thus optimize
outcome.
From a clinical standpoint, there is also a potential downside to an ED unit stay in that
younger patients may learn “anorectic techniques” (e.g., purging mechanisms, how to hide
one’s purging, methods to artificially elevate one’s weight, etc.) from their more seasoned
fellow patients. Furthermore, as mentioned above, active suicidality in an anorectic patient is
probably best treated on a general psychiatric unit because of the familiarity of such units
with this problem. Finally, general psychiatry units are typically locked while ED units may
or may not be. For the suicidal, uncooperative, or even psychotic AN patient, a locked unit
clearly has advantages.
Pitfalls and Exclusionary Criteria for a Psychiatric Unit Admission
While psychiatric admission is indicated by the above considerations, it should not be

assumed that it is without its own possible perils. Particularly noteworthy is the impact on
self-esteem. Moreover, if the hospitalization proves unsuccessful in reversing the patient’s
downward spiral, it may contribute to a sense of total hopelessness in patient and family
about possible recovery in the future.
Very young patients (e.g., those under 16 years of age) should probably not be admitted
to a general adult unit but rather to an adolescent medicine unit. The presence of highly
disturbed adults and the absence of age-appropriate peers would likely be deleterious to the
youthful patient’s course.
Finally, not all general psychiatric units are experienced in treating eating disordered
patients. Staff may be readily deceived by the anorectic (or bulimic) patient’s manipulations.
Angry countertransferences may develop in response to a starving anorectic patient’s
adamant refusal to eat. There may even be some staff envy of the seeming impenetrable will
power of the starving anorectic patient to continue dieting in the face of available food and
external pressure to resume normal eating.
The Advantages of Treatment on an Eating Disorders Unit
A specialty unit is obviously organized to deal with the special pathology to which it is
dedicated. An Eating Disorders Unit (EDU) staff is prepared to provide multi-modal
treatment that can address the multiple facets of AN. This will include such approaches as:
individual therapy, family therapy, group therapy, therapeutic activities, psychoeducation,
nutritional counseling, and pharmacotherapy. Moreover, behavior therapy that provides both
positive and negative reinforcers to promote weight gain, whether via access to or restrictions
from exercise, visitors, or off-unit privileges, is comfortably employed by an EDU staff. An
appropriate dietary schedule (often with small multiple feedings), use of liquid nutritional
supplements, and prevention of bathroom access by purgers after meals are also standard
operating procedures for an EDU. Similarly, the common weekly weight gain target (of 2.0 –
3.0 lbs) is well known to the staff and carefully monitored.
In addition, the availability of a full unit of eating-disordered patients facilitates group
therapy, both cognitive-behavioral and insight oriented. And a nutritionist, in light of the
serious nutritional needs of these patients, becomes a funded and visible member of the
permanent staff, a circumstance that would not exist on a general psychiatric unit.
Finally, the staff members of an EDU are savvy. They are sophisticated in their
knowledge of the tricks and maneuvers employed by anorectic patients to hide their weight
loss, non-eating, and purging. Patients are carefully weighed, watched, and monitored.
Pitfalls and Disadvantages of Treatment on an Eating Disorders Unit
If an EDU presents all of the above advantages, why is it not the perfect place for
treatment of AN (managed care considerations aside)? Ironically, it is precisely because the
unit contains perhaps one to two dozen ED patients housed together that problems occur.
Frequently, because of the resistance of AN patients to gain weight, there can be an “Us
vs. Them” atmosphere on the unit. If the staff is knowledgeable about deceptive techniques,
the patients are equally shrewd, often leading to a competition as to who is in charge and
more iron-willed.
Also, as stated above, patients learn anorectic techniques from each other. They can also
become competitive about their thinness with each other. Not surprisingly, some patients
prove treatment resistant and will eventually be discharged with negligible improvement in
any sphere, which can have a demoralizing effect on the other patients. Even amongst those
who have improved, there is no guarantee of sustained improvement. Indeed, Bruch argued
that patients who gain weight principally as a consequence of behavioral reinforcers are
particularly likely to relapse following discharge (Bruch, 1974).
Finally, because EDs are so pernicious and frustrating to treat, staff burnout can become
a problem on an EDU. The staff itself needs periodic “feeding” to maintain morale and
motivation in working with such resistant patients day after day.
Weight Gain Parameters
While severe weight loss need not be the only reason for inpatient admission, it is
commonly the most glaring concern and thus merits particular attention. Techniques for
promoting weight gain include: behavioral reinforcers, small but frequent feedings, use of
liquid nutritional supplements, and a structured daily meal plan. (Purgers are also not
permitted bathroom privileges for about two hours after meals.)
If the patient is fully uncooperative with the treatment regimen and her weight continues
to fall, the staff must be prepared to take more aggressive steps to insure adequate re-
nourishment. Two techniques are available: nasogastric feeding and total parenteral nutrition.
Neither is without its dangers (e.g., severe fluid retention with its consequences) and both
must be administered carefully, expertly, and only when urgently needed. (Nasogastric
feedings will have a secondary benefit in that the N-G tube discomfort provides a negative
reinforcer for ongoing avoidance of eating.) Also, additional electrolyte and mineral
supplements, particularly potassium and phosphorous, may be required in those who have
been extensive purgers (Halmi et al., 1991).
A goal weight restoration to at least 90% of ideal body weight (a percentage at which
regular menstruation is likely to resume) is typically set (Golden at al., 1997). The rate of
weight gain is usually targeted at no more than 2.0 – 3.0 lbs./week (Halmi et al., 1991). This
is to minimize the possibility of re-feeding edema and also to allow the patient to feel that her
weight restoration is not going to go out of control and that the treatment weight goal is not
one which will result in her now perceiving herself as being “fat.”
Research Findings
While there is a paucity of research on the efficacy of inpatient treatment for AN, a few
studies have examined certain aspects of this modality. At least two studies (Wiseman et al.,
2001; Baron et al., 1995) have described a greater rate of relapse among anorectic patients
who were discharged at lower than target weights. Lower weights were associated with
briefer hospital stays (often due to managed care pressures), rather than with more severe
presenting symptomatology. There is a virtual absence of controlled studies that examine the
effectiveness of treatment on an EDU vs. that on a general psychiatric inpatient unit.
A randomized controlled study of treatment efficacy for AN on ED inpatient units vs. in
outpatient settings could not establish a significant outcome difference between the two after
five years (Crisp et al., 1991). But such comparisons are difficult because of the possible
range of treatment modalities in both settings (individual, family, group, dynamic,
interpersonal, behavioral, cognitive-behavioral, pharmacologic, etc.), differing durations of
treatment, differences in treatment adherence, differences in pre-treatment symptoms, and
symptom severity and duration. Nevertheless, in life threatening situations, it would be
difficult to justify withholding or even delaying inpatient admission for the patient with AN.
Other Types of Inpatient Care: General Medicine

and Adolescent Medicine Units
Introduction
Individuals with EDs who require acute physiological stabilization, due to a variety of
serious complications, are generally admitted to medical units of general hospitals.
Interestingly, weight gain can vary dramatically between treatment sites (Goldberg et al.,
1980). However, closer analysis suggests that differences are linked primarily to prognostic
indicators in the patients admitted to each site. There is a lack of empirical data to support the
possibility that the type of unit the ED patient enters makes a difference in outcome. Except
for the Crisp and colleagues (1991) study referred to previously, there has not been any other
randomized controlled trials of inpatient versus outpatient treatment of AN (Meads, Gold and
Burns, 2001).
Clinical Considerations
The location of inpatient treatment in the spectrum of care for AN often depends more on
chance than scientifically validated data (Vandereycken, 2003). There is currently no clear-
cut clinical consensus regarding the major treatment questions, including that of when to
admit to an inpatient setting. The lack of controlled research limits the availability of
evidence-based practice in this regard. What is more evident is that economic restraints posed
by managed care limit the length of inpatient care, which leads to early discharge at lower
body weights and thus greater likelihood of relapse and chronicity. When comparing the
clinical experience among the United Kingdom, the United States, and Australia, variations
in clinical practice exist depending upon the health care system of the country. Therapists
dealing with the seriously ill anorectic patients have to face difficult decisions, ethically as
well as clinically.
Locus of Control: Whose Responsibility Is It Anyway?
The age of the patient may determine where the locus of responsibility lies. Refusal of
life saving care can become a clinical concern. Parents of minors must provide the
appropriate care for their dependent children and provide consent for treatment. Rarely, if
ever, do families refuse to co-operate. Only one report in the literature that we could find
addressed the role of parental medical neglect in two cases reported to the child protective
agency in that locale (Fornari et al., 2001). The situation with adult patients can be more
problematic but they usually have someone who is significantly involved with them. Parents,
siblings, and, when married, spouses are the ones to request and/or petition for care when
their ill family member refuses treatment and faces a life-threatening situation. On occasion,
it may be necessary to petition for emergency care even over the objection of the family
member when it appears that the family is not able to provide for the safe treatment for their
loved one. It may be that family members become fatigued after a long illness in their child
or sibling or spouse and relinquish hope. In certain situations, it may also be that the
identified patient is the victim of abuse and the family will not acknowledge this, but would
rather opt for allowing the patient to die. Thus, the clinical decision-making requires an
understanding of the history of the illness, as well as familiarity with the family structure,
history, and dynamics. Although some investigators question the role of the family in the
evaluation and treatment of adults with AN, in our experience, it is important for the
understanding and ultimate recovery of the patient (Dancyger et al., 2005).
Specialized Day Treatment for Eating Disorders

Emergence of Day Programs
There is support in the literature for the use of day treatment/partial hospitalization as an
alternative to inpatient hospitalization for patients with serious mental illnesses
(Orgrodniczuk and Piper, 2001). The first day hospital for general psychiatric illnesses was
founded in 1937 (Dzhagarov, 1937) and, about 50 years later, the first specialized day/partial
hospital program for EDs was developed in Toronto, Canada (Piran et al., 1989). Other
programs soon followed in Australia, Germany, Israel, and the USA.
Fiscal Constraints and Third Party Payers
The costs of day treatment for EDs are substantially lower than those for inpatient care
and are more likely to be covered by insurance companies and HMOs. As patients are living
and sleeping at home, beds/laundry/housekeeping and overnight staff are not needed.
Furthermore, in most programs, at least one meal/snack per day is usually eaten outside the
facility, so food/cafeteria costs are also reduced. This makes this type of approach more
affordable to a wider range and a larger number of individuals and their families (Zipfel et
al.,2002). Also some programs will permit a three day per week attendance, thus allowing
individuals to continue with aspects of work or school, which may be advantageous in the
long-term to them and their families in terms of income or completion of studies.
Clinical Advantages
One clinical advantage of day treatment for some individuals with EDs is that they are
not removed from their usual evening/weekend environment and can continue thereby to
receive support of family and friends. They can also maintain the opportunity to function
normally in at least certain areas of their lives, separate from their illness (e.g., part-time work
or school). For these individuals, regression and dependence on the inpatient unit may be
avoided, as the individual is required to self-regulate and self-monitor whenever not in the
day program. Thus, during evening hours, weekends, and holidays, these patients can remain
involved with their ongoing lives, roles, and relationships. This may contribute to more
independence and also to more ready generalization of newly learned behaviors, attitudes,
skills, and strategies from treatment setting to real life setting. At the same time, the patient
has the support of the group treatments and the program staff to help process, understand, and
manage the difficulties of everyday living in the community. Relationship problems, self-
esteem issues, self-control concerns, social pressures, etc., all can be brought back to the
program and worked through on an ongoing basis (Zipfel et al., 2002).
Pitfalls
For some individuals, the advantages turn into disadvantages if they are unable to keep
themselves from the self-destructive behaviors when outside of the day treatment program.
That is to say, some individuals may continue to engage in disordered eating, starving,
bingeing, and purging on the outside and keep these behaviors hidden and secret from day
program staff. In addition, the families of these patients may not be able to manage their out
of control behaviors in the home environment (Zipfel et al., 2002).
For some adolescents who need transportation to the day program, the requirement of
daily attendance may be a hardship or even an impossibility due to the distance from the
facility or the transportation costs or the tensions that emerge in the time spent driving with a
parent to and from the program.
Inclusion Criteria
Clinically, treaters often turn to day programs for those patients for whom outpatient care
has not been intensive enough or with sufficient structure to provide for improvement or at
least prevent deterioration.
The individual needs to be evaluated by a physician to assess overall medical stability
and to rule out such medical concerns as dehydration, electrolyte disturbances, cardiac
problems, and acute medical complications of malnutrition.
Weight requirements may vary from program to program but generally those who are less
than 75% of ideal body weight for height would be better suited for inpatient care (APA
Practice Guidelines, 2006) and should not be considered for Day Treatment until weight has
been stabilized and restored to at least 75% of IBW and probably higher. In one of the few
studies to examine this, Howard and colleagues (1999) found that, when patients were below
90% of IBW at time of transfer from Inpatient to Day Treatment, they were nine times more
likely to be unsuccessfully treated than were those who were above 90% of IBW at time of
transfer.
Exclusion Criteria
Acute medical conditions, as described above, including severe starvation/ severe

emaciation, that is, weight less than 75%IBW or BMI below 16, can be considered contra-
indications for treatment in a day program. In addition, serious cardiovascular complications,
for example, dysrhythmia or cardiac failure, cannot be managed in a day treatment setting.
Similarly, serious gastrointestinal complications may require fulltime attention. Acute
psychiatric conditions/emergencies, such as acute psychosis, are an indication for inpatient
care. Serious substance abuse, including serious drug/substance use complications, first
requires specialty treatment, as these individuals are not able to make good use of a day
program. Suicidal or parasuicidal crises, which require a safe and contained environment for
the individual, cannot be managed in a day treatment facility in light of the lack of 24/7
monitoring of the patient.
Transition Considerations
Transition from one level of care to another requires consideration of a variety of factors.
The “how, what, where, and when” of the practical decision making process concerning day
program or partial hospital has not been well defined in the literature. For some, it may rest
on the availability of these services in their community. For others, it may be determined by
what the insurance carrier stipulates that the patient’s benefits allow. The admission to a day
program has been most successful in our own experience when it serves as a transition from
inpatient care (Dancyger et al., 2003). Generally, we have observed that, following inpatient
care, anorectic patients tend to be less resistant to the day program than those who were not
hospitalized. Following discharge, individuals are often delighted to be out of the hospital
and able to sleep at home and resume their “normal” lives. When the day program is
integrated with the inpatient program, it can provide a natural progression and be seamless.
When it involves a hospital discharge and transfer to another day treatment setting, it may
require more careful transition planning in order to enhance continuity of care and thereby
increase the likelihood of cooperation and eventual recovery.
In our own experience, it is often difficult to achieve the bulk of the weight restoration
for severely malnourished individuals in a day treatment setting. Generally, achieving the last
10% of weight restoration is more attainable, although there have been individuals who were
able to gain the majority of their weight in a day program setting. However, each person’s
motivational level and family environment needs to be appreciated. Careful monitoring of the
course of treatment allows for the possibility of re-hospitalizing those individuals who fail to
meet their treatment goals in a day program.
Day treatment can also be an intensification of an outpatient plan that failed to
accomplish the goals of care, as outlined in the APA practice guideline. (APA, 2006, Table 8,
pp. 37-39). If outpatient goals are not attained or safety concerns arise, the patient might then
be referred to a day program, provided that there are no acute life-threatening indications for
emergency inpatient admission. In practice, this shift from outpatient to a more intensive
level of care is often met with resistance. Not uncommonly, the clinical situation deteriorates
further, thereby necessitating an inpatient admission. If there is co-operation, outpatients
whose clinical status begins to deteriorate might be able to be adequately served in a day
program. Johnson and colleagues have described their comprehensive program, in which
there is flexibility of care along the continuum of inpatient, day program, and outpatient
settings, including an individual psychotherapist who continues with the patient throughout
her course of treatment (Johnson and Sansone, 1993).
Research Findings
There is good support in the literature for patients with serious mental disorders, who in
the past would have been in inpatient programs, being treated successfully in day
treatment/partial hospitalization programs. This type of treatment seems to be most beneficial
for the more psychologically minded patients (Orgrodniczuk and Piper, 2001). (See Table 1
for a summary of day treatment research for a wide range of subjects but mainly female
adolescents and adults with EDs.) Differences across programs, including age groups, criteria
for admission and discharge, clinical emphases, and international differences in health care
environments, require that further research be conducted to clarify the nature and
effectiveness of this relatively new treatment approach to EDs (Zipfel et al., 2002).
Table 1. Studies of day treatment of eating disorders
Subjects
Authors (Mean age in Diagnosed Findings Follow-up
years)
84% reached IBW,
89% resumed menses,
59% overcame body
Danziger, et al.
32 adolescents AN image distortions,
(1988)
88% stopped
ritualistic exercise
BN displayed
noticeable
Woodside, et al.
91 pts BN improvement in BP
(1995)
and weight gain after
discharge of DTP
Kaplan, Olmsted, 527 pts. AN, ANBN, AN- 88% MPMW 2 years later – 80%
Molleken, (1997) (25 yrs) BN >50% -no B and P remain
asymptomatic
Gerlinghoff, et al. 106 pts.(3 AN, BN, AN-64% weight gain, Mean of 17.2
(1998) males) EDNOS BN-significant months later– 64%
(23.3 yrs) decrease in binges were evaluated,7%
still AN, 4% still
BN
Olmsted and Kaplan, Adult females AN, BN AN-49-58% weight

(1999) restored.BN-44%
abstained from binges
and purges
Howard, et al. 59 females, AN 24% were failures and

(1999) (24.8 yrs) required IP or left
AMA
Olmsted and Kaplan, Adult females AN, BN AN-49-58% weight

(1999) restored.BN-44%
abstained from binges
and purges
Dare and Eisler, 14 adolescents AN, BN Some symptomatic

(2000) improvement
Table 1. (Continued)
Subjects
years)
Tasca, Flynn, 61 females AN, BN, ED DTP proved more
Bissada, (2002) (28.9 yrs) EDNOS engaged and avoiding
than gen. psychiatric
DTP
Dancyger, et al. 82 females. AN, BN, 49% successful, 13%
(2003) (17.9 yrs) EDNOS required IP
Robinson (2003) Female AN There is no conclusive

patients evidence that inpatient
care is more beneficial
than outpatient care.
However, high-quality
outpatient care can
make inpatient care
unnecessary.
Franzen, et al. (2004) 125 pts. AN, BN, 106 completers, 19
(1male) EDNOS non-completers
(22.7 yrs) (15.2%) had more
severe bulimic sxs.
Zeeck, et al. 18 females BN 27.8% complete 1.5 years later -

(2004) (27.1 yrs.) remission at 50% complete
discharge, 50% still remission, 21.4%
BN still BN
Gowers and Bryant- Child and AN, BN, Younger patients can
Waugh (2004) adolescent EDNOS have their ED
patients managed on an
outpatient basis with
inpatient care reserved
for AN patients with
serious complications.
Schmidt and Asen, Adolescents AN Multi-family day
(2005) and Adults treatment therapy is
an effective
alternative compared
to IT for AN
Subjects
years)
Kong (2005) 50 females AN, BN, Day treatment showed
(25.8 yrs.) EDNOS greater improvements
re: frequency of
BandP, BMI,
depression and self-
esteem than the
control group (OP).
Clinical Vignettes
Ms. B
Ms. B was a 19 year-old college student with no history of being overweight, who had
been referred for evaluation of a possible ED.
Ms. B had been notably thinner for three years but, while away at boarding school and
her first year of college, her parents thought that she “looked fabulous, in fact, never better!”
It was only during her summer vacation at home that her parents began to note that she hardly
ate, and they arranged for an evaluation. At the consultation, Ms. B’s dad proclaimed that,
“we are just here for you to tell our daughter what she needs to eat!” Ms. B appeared sad and
annoyed, as she did not think that there was a problem being five-foot eight-inches and
weighing ninety-eight pounds.
Ms. B had little to report other than that she was “fine.” The family had endured
numerous losses and tragedies: a cousin had killed herself at age twenty, the family business
was near bankruptcy, the housekeeper of twelve years had just died, and the family dog had
been run over accidentally by a neighbor. It sounded overwhelming, and yet the parents were
amazed that the therapist thought these circumstances constituted “a big deal.”
Ms. B reluctantly opened up and described her ambivalent relationship with her powerful
father whom she feared and revered and she recounted the sadness she felt for her mother
who lived in a loveless marriage. Ms. B revealed that not only were there things that she was
not prepared to discuss, but that she could not even trust her own memory. The patient then
shared a series of vivid childhood traumatic memories. At the same time, she wondered
whether they could be “a figment of my imagination.” It was clear that this sensitive and
vulnerable young woman had a complex story with traumatic elements. The therapist’s
impression was that Ms. B had had AN for several years, coupled with depression. He
recommended that she be hospitalized to initiate nutritional rehabilitation in a structured
adolescent medicine unit that specialized in EDs. The family was reluctant. As her vital signs
were stable, and the weight loss was not acute, the therapist arranged to see Ms. B several
days later.
The therapist encouraged her to consider a trial of outpatient nutritional rehabilitation
coupled with individual psychotherapy. Although Ms. B stated that she was “confused,” she
reluctantly agreed to accept the proposed plan. Despite her cooperative stance, however,
weight gain was not accomplished during the first four weeks of outpatient treatment, and she
then agreed to inpatient care. Ms. B was hospitalized for six weeks on an inpatient adolescent
medical unit. Weight gain was targeted at approximately 2.5 pounds per week. During the
first month, however, only five pounds were gained, and she was transferred to an EDs unit.
The patient spent three months on the locked EDs unit at a tertiary care, university-based
psychiatric hospital. Weight gain to the goal set was accomplished with a liquid diet. The
patient was then transferred to the EDs day treatment program. This program operated five
days per week from 8:30 am until 5:30 pm. It included three meals and two snacks daily, as
well as therapeutic activities, and individual, group, and family psychotherapy. Ms. B
struggled upon returning home, and her weight quickly plummeted. Day treatment appeared
not to provide sufficient structure to prevent relapse. Following three weeks in the day
program, the patient was re-admitted to the medical unit with dehydration and then
transferred to the general psychiatric unit following disclosure of suicidal intent.
The family struggled with the treatment team and worried that “nothing was helping!”
During the inpatient psychiatric admission, the patient disclosed that she was drinking
alcohol heavily and was treated with an alcohol withdrawal protocol to prevent the
emergence of withdrawal symptoms. The patient was then referred for aftercare to the drug
treatment program. During this period, the patient formed a close working alliance with her
drug treatment counselor, and managed to maintain her weight.
At follow-up, although the patient has struggled with her low weight for many years, she
has managed to remain outside of a hospital for the past ten years. Treatment has focused on
her sobriety and her need to maintain her weight. Despite having a Body Mass Index of only
16, the patient has maintained regular menses.
Ms. M
Ms. M was eleven years old when she first presented to the ED program at a tertiary care
university medical center in suburban New York. Prepubertal, she had failed to make the
expected weight gain necessary for growth. Her parents were reluctant to allow her to be
hospitalized even though she had refused to cooperate with a weight restoration plan on an
outpatient basis. It was a challenge to set limits for her on the adolescent medical unit, as she
would call her parents who would then call the administration of the hospital, requesting a
different approach and undermining the care. Family meetings attempted to engage the family
and educate them about EDs, but were unsuccessful. The patient was discharged home and
outpatient care was initiated, but was unsuccessful. Upon re-admission, the parents were
more cooperative with the treatment team.
Despite this, they continued to undermine the therapeutic plan. The parents demanded a
change of psychiatrists after their daughter complained. Not surprisingly, the patient
continued to fail to make her weight goals and was not satisfied with her new psychiatrist.
The patient was once again discharged home at the parents’ insistence. Several weeks later,
the patient was readmitted. Over the course of the first year of care, the patient was admitted
five times.
It was later learned that the mother had a brother who had been hospitalized
psychiatrically as a teenager and was now a chronic psychiatric patient living in a state
psychiatric hospital. The patient had not known about her uncle. The parents believed that the
uncle would have been “better off dead” than alive in a psychiatric hospital.
The patient was eventually transferred to a psychiatric unit where she reached her goal
weight by age thirteen. Menarche followed, the patient was horrified, and she proceeded to
lose weight until she was readmitted to an ED unit in a private freestanding psychiatric
hospital. The patient was then admitted to a day program where she proceeded to lose the
weight once again. Despite intensive individual psychotherapeutic efforts, family treatment,
and pharmacological approaches, the patient was hospitalized over twenty times in five years.
By the age of eighteen, she had osteopenia and chronic amenorrhea. The family was
exhausted by her frequent crises. They began to make hopeless remarks such as, “If she
doesn’t wish to recover, what can we do?” They stated that not every person can be “saved.”
Despite our efforts to achieve weight restoration, it appeared that the patient, now a young
adult, was headed for chronicity and eventual death. At the time of this writing, the patient is
thirty years old and has severe osteoporosis. Wheel chair bound, the patient remains at a
chronically low weight.
These two cases highlight the severity and complexity of the clinical course of
individuals with AN. Ms. B had co-morbid depression and alcohol dependence, but after
numerous treatment programs has managed to remain at a stable low weight with regular
menses and working fulltime. Ms. M demonstrates chronic relapsing AN with poor outcome,
despite intensive treatment over a long period of time, including all levels of medical and
psychiatric care.
Conclusion
Although there are neither well established evidence based guidelines nor systematic
controlled research studies, clinical decisions about patients and their families regarding the
type and location and duration of treatment are made every day in this country and around the
world. In this chapter, we have attempted to address the place of day treatment as a more
recent therapeutic modality available to some individuals in some cities. The treatment of
EDs is not unlike treatment of many other psychiatric illnesses in that “surveys conducted in
academic centers have found that up to 40% of clinical decisions are unsupported by
evidence from the research literature” (Geddes et al, 1996; Gray, 2004; Greenhalgh, 2001).
Although more research is needed to address the many still unanswered questions, we
have directed our attention to some of the recent clinical and research issues concerning day
treatment of eating disorders. While recognition of the limits of our knowledge is important,
particularly in light of the paucity of scientifically based evidence to inform the decision-
making process, growing clinical experience does suggest that day treatment is a valuable
new modality in the spectrum of care for individuals with AN.
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Chapter VII
Medical and Nutritional Treatment of

Children, Adolescents and Young
Adults with Eating Disorders
Martin Fisher
New York University School of Medicine
Abstract
During the past decade, several consensus statements have been published
describing a team approach to the treatment of children, adolescents and young adults
with EDs. This chapter utilizes these statements, along with the clinical experience of the
author, to summarize four key areas in the state of knowledge of the medical and
nutritional care of patients with EDs: (1) Issues of epidemiology and diagnosis are
discussed, highlighting the difficulties in using strict DSM criteria in the younger age
groups and the high frequency of EDNOS in adolescents. (2) A series of clinical issues
are explored, including optimal goal weights, approaches to nutritional rehabilitation,
criteria for hospital admission and discharge, the refeeding syndrome, and the role of
behavior modification with younger patients. (3) Medical issues are reviewed, focusing
on electrolyte disturbances and cardiovascular abnormalities; endocrine disorders and
osteopenia / osteoporosis; other organ system (including gastroenterologic, neurologic,
hematologic, immunologic and dermatologic) findings; and the medical work-up. And
(4) The outcome literature for patients with EDs is summarized, demonstrating the
improved outcome found in adolescents compared to adults.
While much of the treatment of patients with eating disorders (EDs) is performed by
mental health professionals, the medical and nutritional aspects of care are often provided by
physicians specializing in Pediatrics, Family Practice or Internal Medicine. These physicians
are frequently joined by colleagues in nutrition or nursing to offer a comprehensive team
approach. Many of the practitioners of this team approach are specialists in Adolescent
120 Martin Fisher
Medicine, who run several of the largest programs for the treatment of (EDs) in the United
States and world-wide. These specialists treat children, adolescents and often young adults, in
coordination with psychiatrists, psychologists, and social workers who provide the mental
health care.
In 1995, the Society for Adolescent Medicine published a Position Statement and
Background Paper describing this team approach and summarizing the state of knowledge on
the treatment of EDs in children, adolescents and young adults to that point (Society for
Adolescent Medicine, 1995; Fisher, et al., 1995). The Statement was updated in 2003,
(Society for Adolescent Medicine, 2003) and the team approach it described was also
included in statements by the American Psychiatric Association in 1993 and 2000 and the
American Academy of Pediatrics in 2003 (American Psychiatric Association, 1993;
American Psychiatric Association, 2000; American Academy of Pediatrics, 2003). The
treatment approaches endorsed by these statements are based on expert opinion; there are
very few studies that have been performed to provide specific evidence-based approaches in
the medical and nutritional management of EDs in children and adolescents. This chapter will
provide an update on the medical and nutritional treatment of EDs, beginning with a review
of the epidemiology of EDs in children, adolescents and young adults, and concluding with a
discussion of the outcome literature in these age groups.
Epidemiology
There are several statistics often quoted in the EDs literature regarding epidemiology:
that the prevalence of anorexia nervosa (AN) in adolescent and young adult women is 0.5%;
that 1-5% of young women have bulimia nervosa (BN); and that 5-10% of cases of EDs
occur in males (Society for Adolescent Medicine, 2003; American Psychiatric Association,
2000).. It has also been said that EDs behaviors have been increasing over time, that EDs are
being seen in increasingly younger ages, and that EDs are increasing in minority populations
in the United States and in developing countries internationally (Society for Adolescent
Medicine, 2003; American Psychiatric Association, 2000). What is the evidence to indicate
the accuracy of this information and how do the statistics vary by age group?
There is clear evidence that children at increasingly younger ages are expressing
concerns about their weight and participating in dieting behaviors (American Academy of
Pediatrics, 2003; Krowchuk, Kreiter, Woods, Sinai and DuRant, 1998; Field, Carmago,
Taylor, et al., 1999). However, there is no evidence that the numbers of cases of EDs are
rising in those ages 11 years or below. In fact, the numbers of cases of true EDs in children
remains small, with BN being almost non-existent in this age group and AN being limited to
a relatively small group of children, who tend to be bright (hence, their precocity in having an
adolescent illness) and who generally have an underlying anxiety and/or depressive disorder.
What is found in this age group that is usually not seen in those who are older, are
several specific atypical EDs. These have been classified in an important article by Watkins
and Lask to include several categories (Watkins and Lask, 2002): (1) Food avoidance
emotional disorder (FAE), which is “a term used to describe children who have a primary
emotional disorder in which food avoidance is a prominent feature;” (2) Selective eating,
Medical and Nutritional Treatment of Children, Adolescents and Young Adults... 121
which describes children who “eat very few different foods and sometimes are particular
about the brand of food or where the food was bought” and who have generally been this way
since they were toddlers; (3) Functional dysphagia, which is characterized by “a fear of
swallowing, vomiting or choking, which makes the child anxious about and resistant to
eating normally, and which is often marked by a specific precipitant, such as having choked
on a food or witnessing somebody else choking”; and (4) Pervasive refusal syndrome, which
describes a very small subset of children with a life threatening condition who refuse to “eat,
drink, walk, talk or care for themselves”, “who are unwilling to communicate” and show
“determined resistance to help.” What distinguishes each of these atypical eating disorder
from AN, BN and “eating disorder not otherwise specified” (EDNOS), is that they are not
being driven by a fear of weight gain or a desire to be thin. Accordingly, treatment of these
atypical EDs in children generally requires a behavioral approach, which is different from the
full comprehensive approach required for AN, BN and EDNOS.
One other area of importance in children is that the diagnosis of AN differs in this age
group. In addition to the obvious inability to use amenorrhea as a criterion for diagnosis in
those who are premenarchal, the criterion of requiring weight loss to 15% below ideal body
weight (IBW), as per the DSM IV, will also not apply to those who are not yet fully grown
(American Psychiatric Association, 1994). This criterion is replaced instead by “failure to
make expected weight gain during a period of growth leading to body weight <85% of that
expected.” When making the diagnosis, and evaluating the severity, of AN in children and
early adolescents it is necessary, therefore, to construct a growth chart that plots the weights
and heights throughout childhood in order to evaluate what weight and height an individual
child would have been without the onset of decreased intake.
In the adolescent age group, the striking epidemiologic and diagnostic feature of EDs has
been the finding that a very high percentage of teenagers with EDs have a diagnosis of
EDNOS. In a study of 622 female patients presenting to an Adolescent Medicine eating
disorders program between 1980 and 1995, we found that in 434 patients ages 9-19 years:
36% had a diagnosis of AN, 18% had a diagnosis of BN, 2% had a diagnosis of both AN and
BN, and 41% had a diagnosis of EDNOS (Fisher, Schneider, Burns, Symons and Mandel,
2001). Of note in our study and others, the patients with EDNOS displayed the same
psychiatric attributes and fear of weight gain as those who met full ED criteria and required
the same intensity of treatment (Bunnell, Shenker, Nussbaum, et al., 1990). In most of the
cases of EDNOS, full criteria for AN were not met because the patients had not yet had
amenorrhea for three months or, more commonly, had not lost to 15% below IBW, often
because they had started out significantly overweight. In some cases of EDNOS, full criteria
for BN were not met because there was no binge-eating, despite very frequent vomiting,
which in the author’s clinical experience is a situation that occurs more commonly in
adolescents than in adults.
In our study, we also found that only 2.5% of patients presenting for evaluation were
male. This is different from the 5-10% range generally quoted in the literature (Carlat,
Carmago and Herzog, 1997). We postulated several possible explanations for this
discrepancy. It is possible that adolescent and young adult males are less likely to present for
evaluation and treatment, both for psychological reasons (males being less open to treatment
and more affected by the stigma of an ED diagnosis) and for physical reasons (there is no
122 Martin Fisher
marker of amenorrhea to cause the patient and family to act as quickly). It is also likely that
there are many males who have ED behaviors (such as decreased intake or vomiting) for
sports-related weight control but who do not develop specific ED thinking (fear of weight
gain, distorted body image). This is in contrast to the many females who develop both ED
behaviors and thinking because of activities such as ballet and gymnastics. Also, there have
been some studies of epidemiology that have included the diagnosis of binge eating disorder
(BED), which occurs equally in males and females but is rarely seen in adolescents. Over
time, however, the situation has changed. In recent years, with an increased emphasis on
body shape in males, it appears that the number of adolescent and young adult males with
eating disorders is rising. Unpublished data looking at adolescent patients presenting to our
program between January 2006 and June 2007 revealed that 11.5% are male, more consistent
with what had been previously reported in the general literature.
Our data also demonstrated that 45% of our adolescent patients were “middle class”,
48% “upper class” and 7% “lower class” (Fisher, Schneider, Burns, Symons and Mandel,
2001). Although there have been some articles indicating that the classic finding of higher
socioeconomic status in ED patients is not true, our data does not agree. We also found that
96% of our adolescent patients were white. Although there are indications in the literature
that EDs are rising in Black and Hispanic populations, our studies in urban and suburban high
schools have shown that there are major differences in weight perceptions between White and
Asian adolescents on the one hand and Black and Hispanic adolescents on the other (Fisher,
Pastore, Schneider, Pegler and Napolitano, 1994). It is these differences in perception that
undoubtedly account for what is still a large discrepancy in ED diagnoses in different
populations in the United States. On an international basis, there are both data and anecdotal
evidence demonstrating increases in EDs as Western values are introduced to countries
across the world (Becker, Burwell, Gilman, Herzog and Hanburg, 2002).
Treatment
There are several general treatment principles in the medical and nutritional management
of children, adolescents and young adults with EDs that have received much attention in the
literature and in clinical practice, along with a series of specific medical complications that
also require careful attention. The general principles involve such questions as: (1) What are
optimal goal weights for patients with EDs? (2) What are the most appropriate approaches to
nutritional rehabilitation? (3) What are the criteria for hospital admission and discharge? (4)
What is the refeeding syndrome and how is it prevented and treated? And (5) What is the role
of behavior modification in treatment? The specific medical complications that require
attention include: (A) Electrolyte disturbances and cardiovascular abnormalities; (B)
Endocrine disorders and osteopenia / osteoporosis; and (C) Other organ system (including,
neurologic, hematologic, immunologic and dermatologic) findings. Based on the discussion
of medical complications comes one final question: (D) What should be included in the
medical workup of the individual newly diagnosed with an ED? Each of these topics will be
discussed in the next two sections:
(1) Establishing Optimal Goal Weights
From the time that the initial studies of Frisch in the 1970’s demonstrated that most
female patients with AN resume menses when they return to “90% of IBW,” (Frisch and
McArthur, 1974) it is this number that has been generally used as the treatment goal weight
for most patients with AN, both female and male. While subsequent studies have shown this
90% figure for resumption of menses to be true for most patients, several issues have made
the discussion more complicated over time:
A first issue is one of semantics, as the concept of “IBW” seems to inappropriately imply
that there is a single best weight for each person. In reality, what has been called “IBW” for
many years has really been “average body weight” for each individual’s age, sex and height.
This term, however, also has semantic implications since in this day and age few people want
to be “average”. A second issue involves the actual determination of “average body weight”
since there are many growth charts and tables that have been used and these do not always
agree. As a clinical short-hand, some people use the simple mnemonic of “100 pounds for 5
feet, and 5 pounds for every inch above that” for females and “106 pounds for 5 feet, and 6
pounds for every inch above that” for males to estimate average body weight in adolescents
and young adults. The values calculated by this method end up being very similar to those
determined by the various charts and tables and generally suffice for clinical use.
However, a third issue is the finding that the weight necessary for return of good health,
including resumption of regular periods and a decreased psychological focus on weight and
shape, is not determined solely by age, sex and height, but also by an individual’s previous
weight patterns, which in turn are influenced by eating habits, metabolism and genetics. From
a clinical perspective, therefore, it is now known to be necessary to consider both “average
body weight” for an individual’s age, sex and height along with that person’s previous
maximum weight in establishing an appropriate goal weight for any individual. Finally, a
fourth issue that must be considered is on-going growth in younger patients. Since girls
generally gain approximately 8-10 pounds per year during early adolescence (and boys gain
approximately 10-12 pounds per year during early to mid-adolescence), it is important to not
establish a single goal weight for patients in this age group. Instead focusing on goal weights
that return the patient to his or her growth curve, at which time normal growth and
development can resume, should be the focus in the older child or young adolescent with an
ED (Golden, Lanzkowsky, Schebendach, Palestro, Jacobson and Shenker, 2002).
(2) Nutritional Rehabilitation
Weight restoration is clearly one of the major components of treatment for AN, while
nutritional guidance serves as an adjunctive part of treatment for BN. If one considers
medical stabilization to be the key short-term treatment modality and mental health care to be
the key to long-term outcome, then nutritional rehabilitation is certainly the key component
of intermediate-term care for patients with EDs. In patients with AN, it is weight restoration
that allows both medical stabilization and improvements in mental health to occur. There is
124 Martin Fisher
much evidence that reversal of malnutrition is one of the prerequisites for the reversals in
thinking that need to take place over time.
There are several general principles that are applied in the course of providing nutritional
rehabilitation, but the details of how weight gain is accomplished varies from program to
program, with no studies in the literature demonstrating the superiority of any one approach
(Schebendach and Nussbaum, 1992; Rock and Curran-Celentano, 1996; Golden and Meyer,
2004). In general, hospitalized patients are expected to gain 2-4 pounds per week and out-
patients are expected to gain 1-2 pounds per week, while those in partial hospitalization
programs should gain somewhere in between. In all settings, patients are started on relatively
small amounts of calories (generally around 1400 calories per day) to avoid the refeeding
syndrome in those who are severely malnourished, as described below, and to allow for
physiologic and psychologic adaptation in all patients, as described later in the chapter.
Ultimately, most patients require between 2000 and 3000 calories per day for sustained
weight gain.
How patients are counseled to accomplish these goals is variable. Most hospitalized
patients receive their calorie intake via supervised meals and snacks; some patients require an
all liquid diet, either via a naso-gastric tube or orally, and some programs rely on these
approaches more than others. In the out-patient setting, some nutritionists rely on strict-
calorie counts; some utilize an “exchange system” (i.e., distributing an appropriate amount of
carbohydrates, protein and fat throughout the day); some provide daily or weekly menus; and
some provide only the loose framework of an appropriate diet, with increases or decreases
based on changes in weight over time. These same approaches are applied to patients with
BN, although the main goal for these individuals is usually stabilization of eating patterns,
decreasing binging/purging and maintenance of weight. As noted, there are no studies to
indicate that any one in-patient or out-patient approach is preferable. In our own settings over
the years, we have used all of these approaches based both on patient or family needs and
personnel preference, and have not observed any major differences from a clinical
perspective.
One interesting adjunct utilized in the provision of nutritional rehabilitation is the use of
metabolic rate testing (Golden and Meyer, 2004). Machines are available to measure an
individual’s metabolism at any point in time. Patients with malnutrition generally have a low
metabolism, as a way to preserve energy, and metabolism increases as weight is gained. This
progress can be followed during treatment, with the initial low metabolism serving as a
“proof” of the abnormality to skeptical patients, and continued low values demonstrating that
there is still more to accomplish. In our setting, we find that hospitalized patients generally
start out with metabolic rates that are approximately 70% of expected for age and sex; out-
patients are usually at about 80%; and those patients who have resumed menses are generally
at 90-100% of expected. This information can often help provide guidance for the clinicians,
explanations for the family, and motivation for the patient.
(3) Hospital Admission and Discharge
Criteria for when patients with EDs should be admitted for in-patient hospitalization
have been published in several versions during the past decade (Fisher, Golden, Katzman, et
al., 1995; American Academy of Pediatrics, 2003). The first criterion in all versions is “<75%
of IBW,” indicating that under most circumstances patients are admitted to the hospital at
around the time they have fallen to approximately 25% below the average body weight for
their age, sex and height. Other medical, nutritional and psychological factors included in the
criteria, as outlined in the version published by the Society for Adolescent Medicine, are
listed in Table 1.
These factors include several physiologic abnormalities (hypotension, hypothermia,
orthostatic changes) that tend to occur for most patients at about the time they have lost 75%
of IBW, but whose presence may require hospitalization with lesser amounts of weight loss,
and whose absence may allow out-patient treatment for those who are 25-30% below “ideal
body weight.” Specific definitions have been applied to the criteria of bradycardia (<50
beats/minute daytime, <45 beats per minutes night-time) and orthostatic hypotension (a
decrease of 20mm Hg in systolic blood pressure and 10 mm Hg in diastolic blood pressure
when going from lying to standing), but there is no evidence to indicate that these numbers
must be strictly adhered to. For instance, there are patients with pulse rates in the 40’s who
are athletes and/or have a family history of bradycardia and who are approximately 25%
below IBW who may not require immediate hospitalization.
Also included in the criteria are several that apply more commonly to BN than to AN
(electrolyte disturbances, cardiac dysrhythmia, uncontrollable binging and purging), some
that are related to treatment (failure of out-patient treatment, arrested growth and
development), those that may indicate a more acute situation (dehydration, acute food
refusal), and several specific medical complications (syncope, seizures, cardiac failure,
pancreatitis, etc). Indicators of psychiatric severity, either acute (suicidal ideation, acute
psychosis) or comorbid diagnoses that interfere with treatment (severe depression, obsessive
compulsive disorder, severe family dysfunction) are also included in the criteria. Throughout
the United States, most patients are admitted to psychiatric units, while some are admitted to
medical units. This is sometimes determined by whether it is the medical or psychiatric status
that is causing the need for hospitalization, but is more often determined by unit availability
in the particular geographic region. There are no studies that have determined a difference
between treatment on a medical unit verses a psychiatric unit, with clinical evidence
indicating that both can be equally successful when they contain a dedicated program for
treatment of EDs.
In contrast to admission, there are no published criteria to provide guidelines for hospital
discharge. In reality, while the criteria for admission have remained essentially unchanged
during the past three decades, decisions regarding discharge have changed as pressure from
the insurance industry has increased over time (Kaye, Kaplan and Zucker, 1996). Throughout
the 1980s patients generally remained in the hospital until they reached 90% of IBW, which
was the standard that was felt to give the best chance for full recovery in subsequent out-
patient treatment. Since the early 1990s patients have generally been discharged closer to 15-
20% below IBW, sometimes with a day program providing the next step in care. While there
126 Martin Fisher
is a general feeling that the shorter time of hospitalization has adversely affected outcome for
many patients, and a few studies have demonstrated this effect, it has been difficult to
definitely prove this finding, and it is unlikely that the financial climate will ever allow for a
return to longer hospitalizations (Baran, Weltzin and Kaye, 1995; Silber and Robb, 2002).
Table 1. Indications for Hospitalization in an Adolescent With an Eating Disorder
1) Severe malnutrition (weight ≤75% average body weight for age, sex and height)
2) Dehydration
3) Electrolyte disturbances (hypokalemia, hyponatremia, hypophosphatemia)
4) Cardiac dysrhythmia
5) Physiological instability
a. Severe bradycardia (heart rate <50 beats/minute daytime; <45 beats/minute

at night)
b. Hypotension (<80/50 mm Hg)
c. Hypothermia (body temperature <960 F)
d. Orthostatic changes in pulse (>20 beats per minute) or blood pressure (>10
mm Hg)
6) Arrested growth and development

7) Failure of outpatient treatment
8) Acute food refusal
9) Uncontrollable binging and purging
10) Acute medical complications of malnutrition (e.g., syncope, seizures, cardiac failure,
pancreatitis, etc.)
11) Acute psychiatric emergencies (e.g., suicidal ideation, acute psychosis)
12) Comorbid diagnosis that interferes with the treatment of the eating disorder (e.g.,
severe depression, obsessive compulsive disorder, severe family dysfunction)
(4) The Refeeding Syndrome
The development of medical complications, and even death, from the rapid refeeding of
those who are severely malnourished was prominently discovered toward the end of World
War II, with the liberation of the concentration camps in Europe. The phenomenon received
attention in the EDs field in the early 1990s, with the decrease in length of stay, as discussed
above, and the subsequent re-admission of more severely malnourished patients with
anorexia nervosa.
The medical complications most notable in the refeeding syndrome are neurological
(stupor, coma, death), cardiac (cardiac failure) and hematologic (hemolytic anemia). These
complications occur secondary to the development of hypophoshatemia, which is thought to
develop because of an ability to produce enough adenosine triphosphate (ATP) in depleted
individuals as their previously dormant enzyme systems increase activity with the
introduction of renewed nutrition (Solomon and Kirby, 1990)..
It is rare to encounter the refeeding syndrome in those who are less than 30% below
IBW; it most commonly occurs in those rare patients who are greater than 40% below IBW.
It occurs most often in those who are refed by an intravenous or nasogastric approach, but we
have documented the onset of severe hypophosphatemia even with oral refeeding
(Birmingham, Alothman and Goldner, 1996; Kohn, Golden and Shenker, 1998; Fisher,
Simpser and Schneider, 2002).
Because of the refeeding syndrome, patients with EDs on in-patient units are generally
refed slowly, most programs beginning with 1000-1400 calories per day and increasing 100-
200 calories every 1-2 days. Phosphorus supplementation is given to those who are more
severely malnourished and/or who are exhibiting low or decreasing phosphorus levels on
daily laboratory testing. No specific criteria have been developed for the use of phosphorus
supplementation, but there are no significant dangers to its overuse, so most in-patient
programs have liberalized their use of phosphorus supplementation in recent years.
It is also worth noting that edema develops more rapidly in those who are more severely
malnourished. Therefore, it is important not to provide too much fluids, either intravenously
or orally, in the early stages of in-patient treatment. We have seen cases where it has taken
weeks to months for acute signs of edema to dissipate and months to years for chronic signs
of edema (such as ankle swelling late in the day) to resolve completely.
(5) Behavioral Modification
For the younger patient with AN, behavior modification is often one of the mainstays of
treatment. In the team approach, this aspect of care is usually applied by the medical team,
thus allowing the mental health team to provide psychological care without being placed in
the role of an “enforcer”. There are no studies looking at various behavioral approaches and
their effectiveness, but it is apparent clinically that for many patients with AN, there must be
an “or else” component of care in order to accomplish required changes in eating patterns and
increases in weight. It is understood that a behavioral plan does not substitute for appropriate
mental health care, but serves instead to provide external motivation when internal cues are
absent. It is also understood that behavioral plans are used much less often for BN, since
behaviors such as vomiting or laxative abuse cannot be as readily monitored as can weight
changes in those with AN.
In many cases, discussing a change from one level of care to the next may serve as an
effective behavioral plan. Thus the practitioner in a community setting may discuss making a
referral for specialty care; or the specialist in the out-patient setting may discuss when it will
be necessary for the patient to be placed in a day program or in-patient program; or the team
in a medical program may discuss transfer to a psychiatric setting. When those discussions
take place with adolescent patients it is necessary that parents support the plan; if they do,
then the adolescent understands that it is no longer an issue of whether there will be weight
gain, but only a question of where that weight gain will occur. If the patient complies, then
the discussion serves as a behavioral modification approach; if the patient cannot or does not
128 Martin Fisher
comply, then the move to the next level of care takes place. Either way, the next phase of
required weight gain is accomplished. In our own practice, “weights and dates” are
sometimes used to operationalize the plan (Fisher, 2006). This approach can be utilized for
other behavioral plans (such as restriction of sports or other activities) as necessary in the out-
patient setting. In the in-patient setting, it is more common to have several privileges on the
unit (such as use of telephones and other equipment, mobility on/off the unit, increased meal
choices, increased flexibility of snacks) serve as the incentive for weight increases. Although
not formally studied, it is pretty clear that these behavioral approaches are necessary for
successful treatment of most young patients with EDs.
Medical Complications
(A) Electrolyte Disturbances and Cardiovascular Abnormalities
Although it may seem a surprise, almost all patients with EDs are found to have normal
electrolytes on laboratory testing (Fisher, 1992; Palla and Litt, 1998; Katzman, 2005). In
those with AN, electrolyte disturbances are exceedingly rare; when they occur they are not
due to malnutrition per se, but rather to fluid manipulation on the part of the patient. Some
patients may exhibit hypernatremia as they keep themselves very dry (often so they can
appear drawn and as thin as possible) while others may have hyponatremia because of water
loading (sometimes done out of habit or to suppress appetite, but usually done to add pounds
to the scale for weight checks). It is the latter finding that can be dangerous, as we and others
have seen patients who develop hyponatremic seizures, even resulting in coma. For this
reason it is important to check electrolytes in patients with AN, at the beginning of treatment,
whenever there is a significant weight change, and at selected times throughout the course of
treatment.
It is even more important to check electrolytes in patients with BN. Either vomiting or
laxative use can cause a hypochloremic, hypokalemic metabolic alkalosis, which in turn can
cause cardiac arrhythmia and sudden death. There is no clear relationship between the
amount of vomiting or laxative use and the levels of potassium (K+), chloride (Cl-) or carbon
dioxide (CO2), but it is clear that patients who participate in both vomiting and laxative (or
diuretic) use are at increased risk. On a clinical basis, when following electrolyte levels in
patients with bulimia nervosa, one generally sees a rise in CO2 first, a decrease in Cl- second,
and a decrease in K+ third. It is crucial to respond to changes in electrolyte levels in bulimia
nervosa by very close monitoring of CO2 and Cl- and by immediate hospitalization for the
onset of hypokalemia. There is no definite protocol for when to admit to the hospital, (i.e.
what levels of potassium definitely requires hospitalization – we generally use ≤3.0 or 3.1
mmol / L), how to treat (IV bolus vs IV drip; intensive care unit vs standard medical unit), or
how long to keep patients in the hospital (we recommend allowing enough time for
replenishment beyond just returning to normal electrolytes). It is known, however, that
hypokalemia must be taken very seriously because among the medical causes of mortality in
patients with EDs this has been the most common, and there are anecdotal reports that
treating with oral potassium is not sufficient to prevent sudden death. It is thus crucial that all
practitioners who treat patients with BN be aware of this potential complication and that all
such patients be monitored.
The cardiovascular changes associated with AN and BN also require attention. The
bradycardia and orthostatic hypotension associated with anorexia nervosa are considered
evidence of cardiovascular instability and are utilized as criteria for hospitalization, but
thankfully, neither symptom has been reported to lead to sudden death and both resolve with
renourishment. In contrast, a prolonged QT may at times be found on the electrocardiogram;
this finding, which might possibly be exacerbated by malnutrition in anorexia nervosa or
more likely by hypokalemia in BN, can be a cause of sudden death and requires careful
monitoring. Patients with severe malnutrition can also show evidence of a pericardial
effusion on the echocardiogram, which resolves with refeeding. Ipecac, which is used as a
purgative by some patients with BN, can cause an irreversible cardiomyopathy, which has led
to fatality in some case reports.
(B) Endocrine Disorders and Osteopenia / Osteoporosis
In response to the state of malnutrition that develops in individuals with AN, several
hormonal changes occur in order to preserve energy (Fisher, 1992; Palla and Litt, 1998;
Katzman, 2005). Levels of thyroid hormone are decreased, as a way to lower the metabolism;
this takes place both through a decrease in production at the hypothalamic level (leading to
low levels of T3, T4 and TSH) and through development of the “euthyroid sick syndrome”
(increased conversion of T4 to reverse T3 instead of T3). On laboratory testing, T4 levels are
generally found to be at the lower limits of normal and T3 levels are usually below normal.
Treatment for this condition is simply nutritional restoration; it is important not to mistakenly
give thyroid hormone to patients with AN since that will exacerbate the weight loss. The
distinction between patients with AN and patients with primary thyroid disease is found in
the TSH; patients with AN have low or normal TSH values, while those with primary
hypothyroidism have elevated levels of TSH.
Values of LH, FSH and estradiol are also decreased in patients with AN. The amenorrhea
that results, which is part of the diagnostic criteria of the illness, leads to the major long-term
complication of AN, bone density findings of osteopenia and osteoporosis (Bachrach, Guido,
Katzman, et al., 1990; Katzman and Zipursky, 1997; Castro, Lazaro, Pons, et al., 2000).
These are measured using dual energy x-ray absorptiometry (DEXA), with osteopenia
defined as ≥-1.0 standard deviation (SD) below the mean for age and sex and osteoporosis
defined as ≥-2.5 SD below the mean. Under normal circumstances, bone density increases
throughout the adolescent years before decreasing slowly beginning in the early to mid 20s
and more rapidly after menopause. In those with AN, bone density falls during the time that
the patient has amenorrhea, thus causing problems from both the lack of expected increases
during the adolescent years and the on-going decreases that are similar to those that occur in
menopause.
There is only one treatment, which is to return to normal eating, normal weight and
regular periods; all other treatments that have been studied (including hormonal replacement,
calcium and vitamin D, exercise, and bisphosphanates) have been shown to not protect the
130 Martin Fisher
bones during the time of amenorrhea (Golden et al., 2002; Golden, 2003; Robinson, Bachrach
and Katzman, 2000; Klibanski, Biller, Schoenfeld, et al., 1995; Grinspoon, Thomas, Miller,
et al., 2002; Golden, Iglesias, Jacobson, Carey, Meyer, Schebendach, et al, 2005; Miller,
Greico, Mulder, Grinspoon, Mickley, Yehezkel, et al., 2004). Thus, when individuals with
AN return to having normal periods they will resume increasing their bone density; however,
they will never be able to fully make up what was lost during the previous months or years,
leaving them to enter their later years in life with a lower bone density than would have been
expected based on their genetic predisposition. It is therefore important that treatment of EDs
include a focus on returning to normal periods as quickly as possible. As noted, data show
that this occurs generally around the return to 10% below ideal body weight, and that
resumption of menses may occur immediately for some patients but may take up to 6 months
for others. It is worthwhile to note that patients with bulimia nervosa may also have irregular
menstrual periods, even if they are at normal weight, and that this irregularity may also have
an affect on bone density, though not as severely as for those with AN.
(C) Other Medical Conditions
Almost all patients with EDs have gastrointestinal symptoms at some point during the
course of the illness.29-31In AN there may be gastrointestinal symptoms during starvation, or
more commonly, during refeeding. Symptoms can include abdominal pains, and there is often
constipation, occasionally diarrhea, sometimes nausea, and rarely vomiting. Studies show
prolonged gastric emptying times and decreased peristalsis. The gastrointestinal symptoms in
AN may interfere with weight gain, but are almost never dangerous. Medications to provide
symptomatic relief are sometimes provided but should be used sparingly. In BN,
gastrointestinal symptoms are usually due to esophageal irritation. This symptom is also
usually not dangerous, but the rare case of an esophageal tear can potentially occur. We
carefully evaluate any patient with BN who indicates they see blood when they vomit.
Hematologic complications for patients with malnutrition include: (a) anemia, which is
generally mild because the amenorrhea protects from development of iron deficiency; (b)
neutropenia, which can occur with more significant weight loss; and (c) thrombocytopenia,
which occurs in only the most severe cases of malnutrition. Treatment for the hematologic
changes is refeeding; it is very rare for any other treatment to be required (Fisher, 1995; Pall
and Litt, 1998; Katzman, 2005). Similarly, although multiple immunologic changes have
been discussed in the literature, none have been found to have clinical significance or any
requirement for treatment (Fisher, 1995; Palla and Litt, 1998; Katzman, 2005).
Patients with EDs rarely have pulmonary or renal complications. Neurologic
complications include hyponatremic seizures, as described previously, and occasionally a
peripheral neuropathy that occurs in those who lose a large amount of weight rapidly and that
is responsive very quickly to refeeding. Many studies have shown that there is atrophy of
brain tissue in those with EDs who lose large amounts of weight, especially if done rapidly; it
is thought that these changes are reversible, but few studies have been done to demonstrate
that, and there are some hints that mild neuropsychological effects of malnutrition can be
long-lasting (Kingston, Szmuckler, Andrewes, Tress, Desmond, 1996).
(D) Medical Evaluation
The medical work-up recommended in the literature for patients with EDs follows
directly from the discussion of medical complications (Fisher, 1992; Palla and Litt, 1998;
Katzman, 2005). Laboratory tests that should be performed on all patients at presentation
include a complete blood count (CBC) and metabolic panel (CMP) along with thyroid
hormone studies. Patients with amenorrhea are also tested for levels of LH, FSH, estradiol
and prolactin and those with amenorrhea of 6-12 months or more may undergo bone density
testing. Patients with bradycardia or significant vomiting will generally have an EKG, while
those who are hospitalized with severe malnutrition may also have an echocardiogram. For
patients in whom the diagnosis of an ED is not completely clear, additional tests (such as an
MRI of the brain or studies of the upper or lower intestinal tract) may be performed. On-
going tests are performed at other points in the course of treatment for some patients,
especially those with BN at risk for hypokalemia or those with AN who have not had
resumption of menses despite reaching appropriate goal weight.
Outcome
Those who treat younger patients with EDs have advocated taking an aggressive
approach to the nutritional and behavioral aspects of treatment with the hope that restoring
the patient to normal weight as quickly as possible will result in a better outcome. While no
controlled studies have compared more aggressive treatments, that include behavioral
modification techniques, to slower approaches, that utilize mostly interpersonal therapy, it is
instructive to compare the known outcome data for younger patients with EDs, who tend to
have a more acute illness, to older patients, whose course has generally been more chronic.
The outcome literature for patients with EDs in all age group includes over 100 studies
that have been performed during the past four decades (Fisher, 2003). These studies show
that “approximately half of all patients do well over time with core issues of AN, whereas the
rest are split between those who do reasonably well but continue to have symptoms (30% of
the total) and those who do poorly (20% of the total).” In those studies where it is possible to
distinguish between adolescents and adults, it appears that the younger patients do somewhat
better, but not dramatically so. However, most of the studies are from psychiatric hospitals,
therefore not including adolescents who are treated as either in-patients or out-patients in
Adolescent Medicine settings. The few studies that have evaluated outcome in those setting
have also found a somewhat better prognosis. One long-term study from Strober et al in a
psychiatric setting, showed a good outcome at 6-7 years of follow-up for 50% of adolescent
patients, and 75% (compared to 42% in adults) at 10-12 years (Strober, Freeman and Morrell,
1997). It can thus be concluded that adolescents with AN do have a somewhat better
prognosis than adults and that an aggressive approach to treatment is therefore warranted,
although success is certainly not guaranteed. For BN, the same general outcome statistics
apply (50% excellent, 30% good, 20% poor) but no specific data exists for the adolescent age
group (Fisher, 2002).
132 Martin Fisher
Case Vignette
SR is an 18 year old college freshman who presented to the Division of Adolescent
Medicine because of weight loss of 20 lbs and amenorrhea for 18 months.
SR reported weighing approximately 125 lbs at a height of 66 ¾ inches in 10th and 11th
grades, with normal periods and a slight desire to lose weight. During the summer after 11th
grade she decided to “eat healthier” with no specific weight loss goal in mind, but over time
“became obsessive about it.” She lost weight throughout 12th grade, falling to 119 lbs by
October, 114 lbs by January, 108 lbs by June, and 106 lbs when she entered college locally.
She did not have a period throughout 12th grade and developed abdominal pains; she saw a
gastroenterologist, who performed an upper endoscopy that was negative. SR denied any
vomiting, bingeing or laxative / diuretic use, but did use an exercise tape for 20 minutes daily
and went to a gym for 30 minutes, 3-4 days per week.
SR’s family attempted a “home refeeding program” on their own during the first
semester of college, without the help of a therapist or nutritionist, but when that failed and
she remained at 105-106 lbs for 8 months, they brought her to the Division of Adolescent
Medicine for evaluation and treatment. Her diet on admission consisted of oatmeal and milk
for breakfast, a turkey and cheese sandwich for lunch, a variable amount of the family meal
and desert for dinner, and a granola bar, fruit or pretzels as snacks; this was calculated to add
up to approximately 1300 calories per day by the Adolescent Medicine nutritionist. SR
indicated that she was never very happy in high school socially, that college is only
somewhat better, and that she had a boyfriend for one year in high school, but broke up
during the summer after 11th grade; she acknowledges this may have been the precipitant for
her eating disorder.
At presentation, SR said she did not want to either gain or lose weight from her 105 lbs,
which was calculated to be 22% below her “ideal body weight” of 134 lbs. Vital signs at
evaluation were BP 116/75 and pulse 54 with an otherwise normal physical examination.
Initial laboratory tests showed a normal CBC and electrolytes, normal liver and thyroid
functions, along with a cholesterol of 252 mg/dl, estradiol 22 pg/ml, LH 0.4 IU/L, FSH 6.3
IU/L, and prolactin 5.9 mg/ml. A treatment plan was begun, which consisted of appointments
with the Adolescent Medicine physician and nutritionist every 2-3 weeks and a therapist
weekly.
The nutritionist increased SR’s calories to 1800-2000 per day but she struggled for the
first 6 weeks of treatment. The physician suggested that the family consider a day program
admission for the summer, an idea that was not appealing to SR. In response to that
suggestion, SR increased her calories as an out-patient such that her weight reached 115 lbs
by the 3rd month of treatment and 120 lbs by the 6th month. Menstruation returned in the 9th
month of treatment, but bone density showed osteopenia of the spine and hip.
By one year of treatment, SR has remained at 120 lbs, continues to eat well, her fears of
weight gain are mostly gone, and she has had 3 consecutive normal periods. She continues to
work with the nutritionist on lowering her saturated fat intake (in order to control the
hyperlipidemia, which has a strong family history) while also increasing calories. She is
working on getting back to her original high school weight of 125 lbs, which is a weight at
which she feels comfortable and which also provides a cushion to protect against any future
episodes of weight loss.
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Chapter VIII
Evidence-Informed Care of Children

with Eating Disorders
Sloane Madden
The Children's Hospital at Westmead
Sydney, Australia
Abstract
Eating disorders in children and adolescents are both prevalent and associated with
considerable morbidity; however, the evidence base for the treatment remains weak. This
chapter examines the frequency and types of eating disorder presentations seen in this
age group as well as the evidence to guide their treatment. Particular emphasis is placed
not only on child and adolescent specific evidence but also developmental issues and
their impact on treatment presentations, treatment outcome and the use of adult treatment
studies in guiding care. This chapter aims to provide clinicians with a framework for
identifying and managing children and adolescents with eating disorders including where
to treat, options for in and outpatient therapy and the role of medication.
Introduction
Despite increasing awareness of the occurrence of eating disorders (EDs) in children and
adolescents, coupled with the understanding of high levels of morbidity and mortality
associated with these disorders, the evidence base to guide the treatment and care of this
group remains extremely limited. This lack of research stretches across all aspects of EDs in
this age group including limited information about the prevalence and nature of EDs, the
applicability of current DSM-IV and ICD-10 diagnostic criteria, treatment interventions and
long-term outcomes.
This chapter will look specifically at the classic EDS, namely anorexia nervosa (AN),
bulimia nervosa (BN) and related variants of these. It will not look at feeding disorders and
138 Sloane Madden
eating difficulties seen in infants and younger children. In particular it will focus on in and
out patient therapy for eating disorders in children and adolescence using the current
evidence base available for this group and where necessary drawing on the adult treatment
literature to address gaps in this evidence base.
One of the difficulties in reviewing the treatment literature in this age group has been the
varying definitions of children and adolescents and the interchangeable use of the terms
childhood onset eating disorders and early onset eating disorders. A number of criteria have
been used to define these groups including age, pubertal status and menstrual status. In
general childhood or early onset is defined as an ED commencing at or before 13 years of age
(Peebles et al., 2006), or prior to the onset of puberty in males or menarche in females
(Cooper et al., 2002). Due to the simplicity of age based cut-offs the majority of researchers
are moving to this definition. Similar difficulties exist with defining adolescence with lower
age limits ranging from 12 to 14 years and upper aged based cut offs ranging from 16 to 25
years. Additionally individuals aged 16 and over are frequently treated in adult based units
and have been included in adult based treatment trials (Gowers et al., 2004). In this chapter
children will generally refer to individuals up to the age of 12 years and adolescents as
ranging from 13 to 18 years, a more narrow definition.
How Common are Eating Disorders in Children

and Adolescents?
Community studies have shown lifetime prevalence rates for AN in women to range from
1.4 to 2% and with the inclusion of partial syndrome AN to be as high as 4.3% (Wade et al.,
2006) and lifetime prevalence of BN to affect 4 to 7% of young women (Schmidt et al.,
2007). While eating disorders are most commonly thought to have their onset in adolescence
there are only a handful of epidemiological studies that have focused on adolescents and no
published population based studies that have focused exclusively on children. Not only does
this impact on our ability clearly describe the scale of the problem in this age group, the lack
of findings make it difficult to clearly define the types of eating problems seen, particularly in
children.
Three case register studies have included patients under the age of 18 years with rates of
disorder varying widely between these studies. In the most recent of these studies incidence
rates for AN of between 25.7 and 26.3 per 100 000 girls aged 10 to 14 years and 3.3 and 3.7
per 100 000 boys in the same age group were identified (Lucas et al., 1991 and Lucas et al.,
1999). In the remaining two studies, also using the DSM IIIR diagnostic criteria but stricter
weight loss criteria, incidence rates of between 4.2 and 9.2 per 100 000 girls aged 10 to 14
years (Nielsen 1990 and Joergensen 1992) were found. In all of these studies incidence rates
in the 10 to 14 year old age group were approximately one third of those seen in the 15 to 19
year olds in these same studies
In their community based study of adolescent girls Lewinsohn et al., (2000) found life
time prevalence rates for EDs in adolescent females were similar to those seen in adults with
full syndrome AN or BN affecting 2.3% of individuals and partial syndrome AN or BN
affecting 2.8% with full or partial syndrome BN not seen before 12 years of age. Interestingly
Evidence-Informed Care of Children with Eating Disorders 139
when a sub-sample of adolescents were followed into early adulthood new cases of AN were
extremely rare while BN continued to present at similar rates to those seen in late
adolescence. Rates of EDs occurring in males in this sample were uncommon and accounted
for around 1 in 20 of the total ED presentations.
Based on these findings it appears that AN is a disorder that most commonly has its onset
in late adolescence with up to a quarter of all presentations first occurring in childhood. BN
on the other hand is a disorder primarily presenting in late adolescence and early adulthood
with only rare presentations in younger age groups. For these reasons it is not surprising that
much of the research into EDs in children and adolescents has focused on AN with
adolescent BN lumped in with adult-based research.
Are Eating Disorders in Children the Same as

Those Seen in Adults?
Since the 1970’s, epidemiological studies including clinical case series and case register
studies have included individuals with childhood onset EDs, though with a few exceptions
(Peebles et al., 2006, Irwin 1981 and Atkins et al., 1993) children have made up a small
component of these studies and their results included in overall analyses. In almost all cases,
studies including individuals with early onset EDs have looked exclusively at AN. As a result
while a little is known about the incidence, onset, diagnostic characteristics and severity of
illness outcomes of AN in children and adolescents (Peebles et al., 2006 and Bryant-Waugh
2000), almost nothing is known about the total spectrum of EDs in this age group.
From the small number of case series that have looked specifically at EDs in children it
has been suggested that such individuals are less likely to report fear of weight gain and
fatness (Lask et al., 1992), more likely to deny the severity of their illness (Fisher et al.,
2001), more likely to present with non-specific somatic symptoms (Blitzer et al., 1961), more
likely to be diagnosed with eating disorder not otherwise specified (EDNOS), less likely to be
diagnosed with BN, more likely to be male, less likely to report vomiting or laxative abuse, to
have lost weight more rapidly and to have a lower percentage ideal body weight than older
individuals with EDs (Peebles et al., 2006). It is important to note that the study by Peebles et
al., (2006) was the only study to include more than 100 children and the only study to
compare them with older adolescents from the same cohort on multiple measures.
Developmental Considerations
As with all psychiatric disorders, ED presentations vary according to the developmental
capacity of affected individuals. In EDs it must be remembered that not only are differences
in psychological and social development important but that physical development is also vital
to consider. These considerations have led to an ongoing debate in the literature about the
applicability of current diagnostic criteria for EDs to children and younger adolescents. This
is underlined by rates of EDNOS in studies of early onset EDs of between 50 and 60%
(Peebles et al., 2006).
140 Sloane Madden
Current DSM-IV criteria for AN require patient concerns about body weight, disturbed
body image and fear of weight gain. However, these criteria may not accurately reflect the
clinical features in young children for several reasons. Compared with adults children have
limited expressive language capacity, less ability to think in an abstract fashion and less
awareness of emotions (WCEDCA 2007). Additionally the variable nature of normal growth
in children undermine the utility of weight based cut offs in diagnosis and the use of
amenorrhea as a marker of malnutrition. These differences may manifest in numerous ways
including:
• Children may be unable to express distress in terms of body shape and weight but
may instead describe somatic symptoms such as abdominal pain or discomfort once
re-feeding commences
• Young children may not report fear of weight gain while at a low weight but may do
so only when weight has been restored to a more healthy level
• Young children may be reluctant to confide their symptoms to adults for fear of
censure
• While the presence of amenorrhea is an important diagnostic feature for AN in post-
menarchal girls it may be a developmentally inappropriate criterion in young girls, in
whom a history of delay in onset of puberty may be important
• The DSM-IV criteria specify that weight should be <85% of expected weight for
height, however, this may lead to an underestimate of the severity of low weight in
younger children in whom linear growth has also been affected (Gowers et al., 2004
and WCEDCA 2007).
In order to address these perceived deficiencies a number of groups have not only
suggested modified diagnostic criteria for AN in children and adolescents but also the
addition of a number of child specific diagnoses. Most prominent amongst these groups have
been the Great Ormond Street (GOS) group in the UK who have not only proposed the GOS
criteria for AN but also highlighted the diagnosis of Food Avoidant Emotional Disorder
characterized by food avoidance in the absence of weight and shape concerns (Nicholls et al.,
2000).
As with DSM-IV criteria for AN the GOS criteria focus on weight and eating
abnormalities. However unlike DSM-IV, the GOS criteria allow for diagnosis to be made on
the basis of behavior or psychological distortions rather than expressed psychological
concerns alone. In particular the GOS criteria allows a diagnosis of AN to be made on the
basis of determined food avoidance and weight loss or failure to gain weight in the absence
of any physical or mental illness in addition to any two of the following: preoccupation with
body weight, preoccupation with energy intake, distorted body image, fear of fatness, self-
induced vomiting, extensive exercising or laxative abuse (Nicholls et al., 2000). This focus
on behavior as well as reported concerns allows for diagnosis in younger children unable or
unwilling to express their distress in terms of weight and shape concerns. In a review of 114
consecutive patients admitted for medical resuscitation at The Children’s Hospital at
Westmead, a large paediatric teaching hospital in Australia 87% of children met GOS criteria
for AN while only 67% met DSM-IV criteria (Madden et al., 2005).
Food Avoidant Emotional Disorder

The term Food Avoidant Emotional Disorder (FAED) first coined in the 1980s to
describe children with significant weight loss resulting from food avoidance in the absence of
weight and shape concerns and underlying organic illness (Bryant-Waugh 2000 and Higgs et
al., 1989). In this disorder, children frequently presented with non-specific medical
complaints including abdominal pain, lethargy and nausea that were seen by the family as
responsible for weight loss in addition to emotional problems, such as school avoidance,
obsessional behavior or depression (Nicholls et al., 2002). Such children were reported to
vehemently deny weight and shape concerns and to lack characteristic behaviors seen in AN
including vomiting, exercise, laxative abuse and avoidance of high calorie foods.
Recently presented data on early onset eating disorders in Canada has highlighted the
relative importance of FAED in children. In a prospective study of first presentation eating
disorders in children between 8 and 12 years inclusive, latent class analysis identified 2
common presentations consistent with both AN and FAED. Over 35% of the 159 children
identified fell into the FAED group. These children differed from those in the AN group in
that they were less likely to be concerned about their weight or shape, did not have abnormal
body image, were less likely to exercise and were more likely to have somatic complaints.
Interestingly as a group they were no more likely than the AN group to have comorbid
psychiatric illness or emotional distress (Pinhas et al., 2006).
While many children with FAED come to treatment because of the complications of
malnutrition the lack of weight and shape concerns raises issues of late or missed diagnosis
and appropriateness of current treatment interventions. In the future it will be important to
clarify if this group of children are distinctly different to those with AN or whether they
respond to existing treatments and face similar outcomes. In particular, is this group an early
developmental presentation of AN or a distinct disorder?
In the Absence of a Strong Evidence Base for Child and Adolescent Eating Disorders is
it Reasonable to Rely on Evidence in Adults?
One of the questions facing those treating children and adolescents with eating disorders
is whether it is reasonable and in fact desirable to rely on adult findings in guiding treatment
decisions. This is particularly relevant in the treatment of BN where treatment studies in
children and adolescents are greatly outnumbered by large well run studies in adults.
Similarly in AN, while there is an increasingly solid evidence base for the use of outpatient
family therapy in the treatment of children and adolescents, the lack of studies in children
with regard to inpatient care, individual therapy and medication management raises a similar
dilemma.
Glowers and Bryant-Waugh (2004) have identified four specific issues in support of the
use of adult based evidence in the treatment of children and adolescents including the
similarity of AN and BN symptoms in adults and adolescents, the inclusion of older
adolescents in adult treatment studies particularly for BN, the overlap between the
developmental tasks of early adulthood and adolescence and the successful use of adult based
psychological interventions for the treatment of children and adolescents with depression and
obsessive compulsive disorder (OCD). Even if we accept such arguments it is important to be
aware of the impact of differing cognitive capacity across age groups with developmentally
142 Sloane Madden
limited communication skills, emotional expression and abstraction in children and younger
adolescents when compared to adults. If treatments developed for adults are to be used in
children this necessitates a preparedness to adapt such treatments to match the developmental
capacities of children and adolescents being treated. This may be as simple as altering the
language used to communicate with young people with EDs or involve changing the
emphasis and focus of treatments to accommodate developmental realities.
Further complicating this picture are the differing physiological imperatives of children
and adolescents including growth and puberty and the impact these have on the treatment
priorities and goals. In particular the greater susceptibility of children and adolescents to the
impacts of malnutrition requires a greater focus on intensive refeeding and preparedness for
inpatient treatment earlier in the illness (Gowers et al., 2004). The impact of differing
physiology in children is also relevant to medication management. Children and adolescents
absorb and metabolize medications differently to adults leading to differential responses to
both medication types and medication doses. This has been highlighted in the medication
management of Major Depression in children and adolescents who have failed to respond to
many medications that are effective in adults and been shown to develop serious side-effects
not noted in adult medication trials (Hazell et al., 1995 and Mann et al., 2006)
Finally children and adolescents overwhelming live in families with parents and siblings.
The nature of such relationships needs to be taken into account when planning treatment.
Studies have clearly demonstrated the benefits the involvement of families treatment
particularly in AN for children and adolescents (Rhodes et al., 2005), while legal
requirements mandate the role of parents in consent to treatment as well as the ongoing care
of children and younger adolescents.
Where to Treat
Options for treatment of EDs in children and adolescents range from specialised inpatient
medical and psychiatric settings through to day-hospitals and a variety of outpatient
treatments. There is little evidence to guide us as to which is the most appropriate setting with
current guidelines based on consensus.
In its 2004 guidelines the National Institute of Clinical Excellence (NICE) in one of its
key treatment recommendations for AN recommended specialist outpatient care as the
treatment of choice for adults with AN. Interestingly despite strong evidence for the efficacy
of outpatient family treatment in children and adolescents no similar recommendations were
made for this younger age group.
While there are many potential advantages for managing children and adolescents in an
outpatient setting and thereby allowing them to remain with their families, continue with
education and maintain contact with peers many factors need to be considered in making this
decision. In the case of children and adolescents it is critical to consider the availability of
age appropriate treatment settings including access to educational facilities and placement
with similar aged patients (NICE 2004 and APA 2006).
Admission for children and adolescents with AN is most commonly initiated because of
medical concerns arising from weight loss and malnutrition. Critical indicators for admission
include physiological instability including bradycardia, hypotension, hypothermia,

dehydration, electrolyte abnormalities and cardiac arrhythmias. In children such changes can
occur on the basis of rapid weight loss alone and as such absolute weight can not be relied on
as a proxy for assessing medical risk. It is important to remember that children and
adolescents are also more vulnerable to the ongoing risks of malnutrition due to its impact on
puberty and growth.
Behavioral indicators for admission include severe comorbid psychiatric illness or
substance abuse that prevents the initiation of outpatient care or would require admission in
its own right, failure of outpatient care or a lack of appropriate supports to allow outpatient
care. While motivation and eating behavior are critical in making decisions regarding
admissions in adults, the presence of a motivated family often allows young people to remain
in outpatient family treatment in the absence of motivation to change.
For BN outpatient care is the treatment of choice though indications for inpatient care
may include severe comorbid medical complications including electrolyte abnormalities or
cardiac complications arising from uncontained purging, severe comorbid psychiatric illness
or severe symptoms that have failed to respond to specialised outpatient care. In such cases
inpatient care to achieve containment is appropriate with referral back to outpatient care once
containment has been achieved.
Treatment in the Inpatient Setting

AN is a serious psychiatric illness with severe medical morbidity and mortality and for
this reason its psychological management is necessarily different to other psychiatric
illnesses. In the inpatient management of children and adolescents with AN, significant
malnutrition in association with medical compromise, is the rule rather than the exception.
Such complications can be life threatening and dictate the need for acute medical
resuscitation and monitoring, generating anxiety for both children and parents. Nutritional
rehabilitation and weight restoration remain an important part of treatment for AN and are
associated with decreased anorectic behavior, reduced psychological distress, improved
cognitive performance, reduced morbidity and mortality. They are a prerequisite to benefiting
from psychological and pharmacological interventions (Robb et al., 2002 and Halse et al.,
2005).
It is the containment of this anxiety to allow resuscitation and refeeding that forms the
basis of initial psychological treatment for patients with AN. The further aims of
psychological intervention are; to contain eating disordered behaviors, facilitate the transition
to safe eating, to develop better coping skills, and treat psychological comorbidity associated
with the ED. Finally, an ED has a profound impact not only on the young person but also on
their entire family. For this reason it is vital to consider and involve the patient’s family in
their treatment.
144 Sloane Madden
Managing the Ward Environment

For many decades the mainstay for promoting inpatient weight gain has been ward based
behavioral treatment. Several outcome studies have demonstrated the efficacy of behavioral
treatment in promoting weight gain in the short-term, though only in adult populations
(Peterson et al., 1999). Despite this, behavioral programs are commonly used in child and
adolescent treatment and guided by outcomes in adult treatment studies. While very strict
behavioral programs have been used in the past it has been demonstrated that lenient
programs produce similar gains in terms of weight and eating, lower levels of conflict and
higher levels of patient satisfaction (Touyz et al., 1987).
It has been the author’s experience that lenient behavioral programs with clear
expectations for children and their parents are most effective in building and maintaining
therapeutic alliances and managing eating disordered behaviors. In our own program parents
and patients are provided with a copy of our eating disorder treatment program with
explanations of treatment goals, refeeding, ward activities including school, group and
physiotherapy, dining room rules, visiting hours, ward leave and appropriate interactions with
other patients on the program and ward. The program works on a simple level system with
progress based on medical well-being and safe eating. Progress through the level system
allows more time away from the ward to practice healthy eating with family and friends. Over
the years our own program has moved away from regulating all aspects of behavior to
focusing on the facilitation of medical resuscitation, establishment of safe eating and
containment of eating disordered behaviors.
Individual Psychotherapy in the Inpatient Setting

One of the theoretical benefits of inpatient treatment of AN is the capacity to provide
intensive psychological therapy. This is appealing for several reasons including the obvious
presence of cognitive distortions about eating, weight and shape, the presence of comorbid
anxiety and depression and to address the developmental milestones of adolescence that have
been hypothesized to have an etiological role in AN (Lock et al., 2005). For parents, in
particular, the option of individual therapy is particularly attractive to address the distress and
illogical thinking that have led their child becoming ill and requiring hospital. Despite this
there is limited evidence to support its efficacy both during the initial period of inpatient
hospitalisation and over the longer term.
Two randomized controlled trials (RCTs) have examined individual therapy in
adolescents though both of these trials have involved small numbers of outpatients (Russell et
al., 1987 and Robin et al., 1994). Similarly, while there have been a number of RCTs of
individual therapy in adults with AN, all of these have involved outpatient treatment.
Therapies have included cognitive behavioral therapy (CBT), cognitive analytic therapy
(CAT) interpersonal therapy (ITP), nutritional therapy and psychodynamic psychotherapy. In
all cases benefits from treatment were modest and no data is available to support their use in
children and adolescents in an inpatient treatment setting (LeGrange et al., 2005).
For the reasons listed above it is difficult to recommend any particular type of individual
therapy for children and adolescents whilst inpatients and difficult to recommend its use in
the acutely malnourished where the effects of starvation impair the cognitive capacity for
individuals to benefit from these interventions. In addition, the suggestion in the adult
treatment literature of poorer outcomes from targeted ED treatments over supportive
psychotherapy (McIntosh et al., 2005) indicate the need for caution in the provision of
intensive eating focused psychotherapy in the inpatient setting. It has been the author’s
experience that non-specific supportive psychotherapy focusing on reassurance, explanation,
guidance, encouragement, environmental change and catharsis is more containing and
effective than specific therapies aimed at addressing weight, eating and shape concerns in
severely malnourished individuals.
School and Group Therapy

The ability to keep patients busy with educational, recreational, and group therapy
programs is particularly important in reducing distress, minimizing eating disordered
behavior, and promoting participation in normal activities of daily living. When medically
stable, ongoing school education during hospitalisation is an integral part of treatment. In the
initial stages of treatment malnutrition impairs cognition, in particular attention and
concentration, short term memory, cognitive processing speed, cognitive flexibility and
problem solving. Research has shown that nutritional rehabilitation and weight gain reverse
these cognitive deficits. Anecdotally, experienced school teachers can often flag when
cognition improves providing a useful indicator of improving nutritional recovery during
refeeding. With improved cognition and ability to maintain school work comes a sense of
achievement and self-esteem in these children and adolescents.
Group therapy provides the opportunity to learn new coping skills, ways of relating to
others and improve self-esteem. Groups can be facilitated by any member of the treating team
but are generally run by occupational therapists, nurses, social workers, and psychologists.
Psychological Support of Parents and Families

When parents first present their child for treatment of AN they do so not only with
anxiety about their child’s well being but often with feelings of failure in their role as parents.
Both in the scientific literature and in the popular press AN has been associated with family
dysfunction, parental intrusiveness, over-control, and physical and sexual abuse. For these
reasons early parent-professional interactions may be complex and difficult, with parents
perceived as anxious and needy and professionals as critical and blaming.
In a qualitative study looking at the impact of AN on parents (Honey et al., 2006), the
main priority for families was their child’s physical and psychological well-being. While
these are the same priorities as clinicians working with AN the importance and timing of
these outcomes is often different. For clinicians, AN is a chronic illness where changes,
particularly psychological changes, are a slow and gradual process and distress expected
146 Sloane Madden
(Steinhausen et al., 2002). For many parents, however their child’s psychological distress is
central and its treatment both urgent and necessary. Treatment research in children and
adolescents with AN has emphasized the need to focus on safe eating, even in the face of
escalating distress, rather than underlying eating disordered beliefs (Lock et al., 2005).
Hence, it is essential to meet regularly with parents to establish and build rapport,
provide education about EDs, provide regular information about treatment and treatment
plans and to provide regular feedback about their child’s progress. In the authors’ experience,
regular weekly parental counseling sessions not only serve this process but allow the
containment of parental anxiety and maximize the gains of inpatient treatment. Psycho-
educational groups for parents and families are an efficient way of reducing parental distress
and defensiveness. They also promote an understanding of the biopsychosocial complexity of
the illness, encourage acceptance of change and promote a treatment alliance. Valuable
insight can be gained into any cultural, individual, or family factors that influence the
development and maintenance of the illness.
While strong data exists to support the efficacy of outpatient family therapy in the
management of child and adolescent AN only one RCT has looked at its role in medically
compromised patients in an inpatient setting (Geist et al., 2000). In this study family group
psycho-education was compared with family therapy. Over a four month period both
treatments were associated with weight gain with no difference in outcomes between the two
groups. Interestingly neither treatment demonstrated improvements in ED psychopathology.
While one could take a positive message from this trial about the importance of family
involvement in the inpatient setting the absence of a control arm without family therapy
makes it difficult to isolate the impact of family treatment from overall inpatient care.
Additionally the lack of difference between group psycho-education and family therapy
highlights the difficulty in putting the benefits of family therapy into practice whilst children
and adolescents remain inpatients. A similar result was seen in an outcome trial by Halvorsen
et al., (2004) that highlighted family therapy as one component of a successful multimodal
inpatient treatment program. Again the failure to explore the specific impact of family
therapy and the lack of a comparison treatment make it difficult to draw further conclusions
from this study. The most studied of the models of family therapy, The Maudsley Model,
requires that the patient be out of hospital before treatment begins (Lock et al., 2001). This
makes sense as it is difficult for parents to focus on taking control of their child’s eating when
meals are still provided through inpatient treatment. As a precursor to family therapy
inpatients with AN can be given periods of leave from hospital to practice eating with their
families and successes and difficulties explored as part of routine family counseling.
Outpatient Care in Anorexia Nervosa

For the majority of children and adolescents with an ED, treatment will occur on an
outpatient basis. Even for those individuals who undergo an inpatient admission the majority
of care will occur on an outpatient basis. There are a number of potential advantages for
children and adolescents undergoing outpatient care including ongoing contact with their
families, peers and education. This is particularly relevant given the long-term nature of
eating disorder symptoms with an average length of illness for many individuals of between 5
and 6 years (Steinhausen et al., 2002). Cost factors are also significant with outpatient care
costing around 10% of inpatient care (Katzman et al., 2000). These factors however, need to
be balanced against children and adolescents greater susceptibility to the effects of acute and
chronic malnutrition and the need to carefully medically monitor them whilst in outpatient
care.
The goals of outpatient care include weight restoration, or weight maintenance for those
individuals who have been weight restored in inpatient care, the establishment of healthy
eating, the treatment of eating disordered behaviors and psychological recovery. In order to
achieve these outcomes it is necessary to combine physical treatments in particular refeeding
with psychological therapy. In children and adolescents this should generally include a family
based psychological intervention.
To date there have been four RCTs looking at outpatient family therapy in children and
adolescents (Russell et al., 1987, Robin et al., 1994, Eisler et al., 2000, Eisler et al., 1997 and
Lock et al., 2005). All four of these trials have used a form of family therapy that has focused
on food, eating and weight including three that have used the Maudsley Model of Family
Treatment (Russell et al., 1987, Eisler et al., 2000 and Lock et al., 2005). All four of these
trials have shown positive outcomes from family therapy in terms of weight gain and reduced
eating disorder pathology though only two have compared family therapy to individual
therapy (Russell et al., 1987 and Robin et a., 1994). Both of these trials demonstrated
improved weight outcomes when compared with individual therapy but included only small
numbers of patients. Family therapy has been successful in achieving its outcomes with both
underweight and weight restored patients making it optimally suited to outpatient care.
In the past family treatment has been criticized for its tendency to blame families for their
child’s AN. This concern stems back to Minuchin et al., (1975) description of the
psychosomatic family and the role of abnormal family structure in the genesis of AN. This
view is no longer widely accepted with family therapy seen as a means of utilizing family
resources to treat AN.
While family therapy is successful for many children and adolescents it is not acceptable
or successful for all. For many families the failure of family treatment to “appropriately”
address their child’s ED psychopathology is confusing and distressing. In addition the
presence of comorbid psychopathology including depression or anxiety raises the issue of
individual outpatient psychotherapy.
There are only two RCTs that have examined individual therapy in adolescents. The first
of these trials (Russell et al., 1987) compared individual therapy with family therapy in 20
adolescents following inpatient weight restoration as part of a larger treatment trial. This
study demonstrated a significant advantage for family therapy both at treatment completion
and at five year follow up (Eisler et al., 1997). In the second study (LeGrange et al., 2005)
individual ego-oriented therapy was compared with family therapy. In this treatment family
therapy was associated with more rapid weight gain though no outcome differences were
seen after 12 months.
A review of adult treatment trials has demonstrated efficacy for a number of
interventions though with insufficient evidence to guide us as to an individual therapy of
choice. It is worth noting that outcomes from eating disorder specific therapies such as CBT
148 Sloane Madden
as compared to non-specific supportive clinical management were only superior in weight

restored patients (Bulik et al., 2007).
Given this a number of recommendations can be made. Firstly it is important that all
families be offered family treatment with the clear benefits of this approach explained.
Secondly if individual therapy is to be offered it is worth considering outcomes for individual
therapy seem best in weight restored individuals. Finally it is worth considering whether
individual treatment can be given in a way that can work with family treatment. This is
difficult as individual therapy focuses on enhancing the child’s efforts to beat AN while
family treatment focuses on the parents taking over responsibility for feeding and eating from
their child. One potential compromise is separated family therapy where parents and children
are seen separately by the same family treatment team. This approach has the potential
benefit of reducing family distress and conflict without a reduction in treatment efficacy
(Eisler et al., 2000). A second option is to focus individual treatment on comorbid illnesses
with family therapy remaining the treatment of choice for the ED.
For individual therapy in the absence of family therapy a review of Robin et al., (1994)
provides us with some guide into features that may be helpful including building ego
strength, facilitating adolescent autonomy and addressing emotional blocks to eating. In
cognitive behavioral terms this could include improving coping strategies to address distress
and challenging negative thoughts around shape and eating. In all cases it is important to
consider the important developmental tasks of adolescence including identity and
independence.
Psychological Therapy in Bulimia Nervosa

To date there have been over 60 RCTs comparing behavioral interventions, medication
and a combination of behavioral interventions and medication in the treatment of BN (NICE
2004). Only one of these trials however, has been carried out in an exclusively adolescent
population (Schmidt et al., 2007). A small number of adult based trials have included older
adolescents from 16 of years of age though small numbers have not allowed a separate
analysis of treatment outcomes in this age group.
The predominant therapeutic intervention studied to date has been cognitive behavioral
therapy (CBT) though other interventions have included dialectical behavioral therapy
(DBT), interpersonal therapy (IPT), family therapy, guided self-help (GSH), nutritional and
stress management and behavioral therapy. Psychological interventions have been carried out
on both individual and group basis, and have been implemented on their own or in
combination with medication interventions (Shapiro et al., 2007).
Outcomes of these studies have strongly supported the use of CBT on an individual basis
for the treatment of BN with evidence for a reduction in bingeing, purging, depressive and
anxiety symptoms. Some early support exists for DBT, IPT and guided self-help though CBT
remains the current treatment of choice for management of BN in adults. There is some
preliminary evidence to suggest the addition of medication to CBT may improve treatment
outcomes though this data needs to be replicated. (Shapiro et al., 2007)
While the findings are clear in adults what does this mean for the treatment of BN in
children and adolescents. To date the only study of BN in an exclusively adolescent
population aged between 13 and 20 years, demonstrated that both family therapy and guided
self-help (GSH) were effective in reducing bingeing and purging in adolescents though GSH
produced a more rapid improvement in symptoms, was more acceptable to patients and was
more cost-effective. It is important to note however, in considering the results of this study
that the average age of the participants in the GSH arm was 17.4 years and in the family
therapy arm was 17.9 years. While this reflects the fact that the majority of patients with BN
are older adolescents or young adults it does little to guide treatment decisions in younger
patients. Finally it is important to note that this study used an adult based manual for GSH
rather than modifying the treatment for children and adolescents.
As the majority of children and adolescents presenting for treatment with BN are likely
to be in their late teens it would seem reasonable to recommend CBT as the psychological
treatment of choice. In individuals in whom this treatment is unsuccessful, unavailable or
unacceptable, other options would included GSH, IPT, DBT or medication management with
or without CBT. In younger adolescents or children developmental considerations and the
reality of their living arrangements should raise the option of family therapy as an appropriate
intervention. To date the best evidence for family therapy exists for a BN adapted version of
the Maudsley model of family therapy (Schmidt et al., 2007).
The Role of Medication in Anorexia Nervosa

Current behavioral and psychotherapeutic treatments in AN have a limited evidence base
for their efficacy and recovery rates from the disorder are poor both in the short and long
term. It is therefore no surprise that considerable interest has been shown in the role of
psychotropic medications in the management of anorexia nervosa. This material is
summarized in the chapter on Pharmacological approaches to the treatment of AN.
Conclusion
Eating Disorders are being increasingly recognized in children and adolescents. Up to
one third of individuals with AN will present before the age of 14 while and almost all will
present before 18 years of age. While BN tends to occur in older adolescents this group still
make up a significant number of eating disorder presentations. As children and adolescents
are more prone to the impacts of malnutrition on their growth and development early
recognition and treatment are vital. While many children and adolescents with eating
disorders present with syndromes commonly seen in adults a significant minority present
without body image and food concerns. In these children it is important not only to consider
their expressed concerns but also their observable behavior and the impact of their
malnutrition when making treatment decisions.
There is a growing body of evidence for the efficacy of outpatient treatment
interventions, particularly family-based treatment. While family treatment is not the answer
150 Sloane Madden
for all eating disorders the involvement of families in their child’s care remains central to
positive long-term outcomes. When faced with a child with an eating disorder it is important
to recognize both the seriousness of the illness but also the positive outcomes from early
intervention and close cooperation with families.
Despite the growing evidence base for the efficacy of family therapy there remains
considerable gaps in the evidence base for treating children with eating disorders. Leaving
aside clinical consensus there is little evidence to guide us as to the best setting for eating
disorder care in children; inpatient, outpatient or day hospital and what clinical features may
help guide us in such decisions. For children who are admitted to inpatient or day-hospital
programs there is little evidence to guide as to the essential components and duration of such
treatment and how to transition children between different levels of care. Does the lack of
evidence supporting the efficacy of individual therapy and medication in children with eating
disorders mean that such treatments should not be offered? How should comorbidities be
treated and what happens when family treatment fails?
It is important to remember that in attempting to make such decisions and answer such
questions that the lack of evidence to support the efficacy of treatment interventions in not
evidence of lack of treatment effectiveness but rather a clear indicator for the need for more
child and adolescent specific randomized controlled treatment trials. In the interim clinicians
need to base treatment decisions on a descending hierarchy of existing evidence, expert
consensus and clinical experience. The following clinical vignette highlights many of these
concerns.
Sick, Sad and Grumpy

Charlotte was a nine year old girl living with her parents and two younger sisters aged 6
and 3 years. She presented to the emergency department of a large children’s hospital with a
nine month history of weight loss. Charlotte had lost 22lb over this period, and on admission
had eaten nothing for 48 hours. Charlotte was 68lb (69% IBW) and medically unstable with a
pulse rate of 38 bpm. Charlotte denied concerns about her weight and shape and was
diagnosed with food avoidant emotional disorder rather than anorexia nervosa. Charlotte was
admitted to a specialist eating disorder service for medical resuscitation and behavioral
refeeding.
During the initial part of her admission, Charlotte continued to refuse to eat and was
totally dependent on naso-gastric refeeding. She did not respond to the wards behavioral
program or a modified reward program. Support and focus around eating led Charlotte to
become increasingly distressed somatically focused and socially withdrawn, with associated
fatigue, abdominal pain and a refusal to walk, talk and toilet herself. At this stage
intervention around meal times was terminated and priority was given to maintaining
Charlotte’s overall level of functioning with regular physiotherapy sessions and engagement
in the hospital school.
This vignette highlights some of the difficulties in faced by clinicians treating children
and adolescents with eating disorders. Despite Charlotte’s young age, her malnutrition and
medical compromise necessitated her admission to hospital. Similarly despite her lack of
body image concerns Charlotte was managed in the same way as other eating disorder
patients, with medical resuscitation and behavioral refeeding, with the goal of a rapid
transition to outpatient Maudsley family therapy. While current evidence supports such an
approach there is no evidence to guide clinicians when such treatment not only fails to
generate improvement but leads to a significant deterioration in symptoms. In this case a
decision was made to continue with nutritional rehabilitation with naso-gastric feeding but to
remove the focus from eating and to focus on improving function in other areas of Charlotte’s
life. With this in mind Charlotte was reintegrated to her home school and the family engaged
in therapy during inpatient treatment.
Family therapy commenced at week 6 of Charlotte’s admission. Despite a move away
from the refeeding focus of Maudsley family therapy many features of this approach were
used. Charlotte’s difficulties were externalized, with her physical symptoms framed as a bully
that was bossing her around and preventing her from enjoying her normal life. As in
Maudsley family therapy the aim was to assist Charlotte to join her parents in the struggle
back to health. Charlotte responded well to this approach and while remaining somewhat
suspicious of the intentions of the therapist embraced it in her interactions with her parents.
After three weekly sessions of family therapy Charlotte began to restore her relationship
with her parents. Prior to this she had become particularly close to nursing staff and told her
parents that she never wanted to return home. As a result she began to request weekend leave
and overnight stays from hospital, supported by nasogastric refeeding. Within one week
Charlotte spontaneously began to eat reporting that she didn’t remember food ever “tasting so
good”. A week later she announced that she felt ready to leave hospital and she was
discharged within a few days. She had been admitted to hospital for a total of ten weeks.
While treatment in this case moved away from behavioral refeeding and outpatient
family treatment, evidence based principals were still followed through the focus on
nutritional rehabilitation and the use of many of the core therapeutic principals of successful
family treatment in eating disorders, albeit on an inpatient basis. Though flexibility in our
care of children with eating disorders is important an ongoing focus on the principles of
evidence based care allows us to ensure effective and appropriate treatment.
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Chapter IX
Evidence-Guided Treatment for Males

with Eating Disorders
Fernando Fernández-Aranda and Susana Jiménez-Murcia

University Hospital of Bellvitge and
CIBER Fisiopatología de la Obesidad y Nutrición (CIBEROBN)
Instituto Carlos III, Barcelona, Spain
Abstract
An increasing rate of males with eating disorders (EDs) has been observed during
recent years, specifically bulimia nervosa (BN) and eating disorder not otherwise
specified (EDNOS). Most clinical features and symptoms of men and women with EDs
are similar. In this chapter, we have summarized information on similarities between
male and female ED on clinical, psychopathology and therapy response. Therapy for
males with ED, has received relatively little attention in the literature and most studies on
therapy, have been conducted in anorexic males after undergoing non-specific inpatient-
residential treatment. An extensive and updated overview of studies on therapy in males
with EDs was performed. Data which have not been previously published and a
description of our specific therapy program for males with EDs will be given.
Introduction
Eating disorders (EDs) are less frequent in males than in females (6-12% of cases)
(Kjelsas, Bjornstrom, and Gotestam, 2004). Males make up 5-10% of people with anorexia
nervosa (AN) who seek treatment (Striegel-Moore, Garvin, Dohm, and Rosenheck, 1999) and
10-15% of people with bulimia nervosa [BN] (Carlat, Camargo, and Herzog, 1997).
However, an increasing rate of male ED has been observed during the last years, in Spain
(Rodriguez-Cano, Beato-Fernandez, and Belmonte-Llario, 2005) as well as in other European
countries (Kjelsas et al., 2004).
156 Fernando Fernández-Aranda and Susana Jiménez-Murcia
During the last ten years (between 1997 and 2007), in the ED Centre at the University
Hospital of Bellvitge, in Barcelona (Spain), 104 males with EDs were admitted (7,1 % cases)
from a total whole sample of 1.471 (males and females) ED [22,8% AN, 50,8% BN, 26,4%
EDNOS], consecutively admitted patients in this period of time. If we compare these results
with the male rate obtained in a previous conducted research (Alonso Ortega, Fernandez
Aranda, Turon Gil, Vallejo Ruiloba, and Ramos, 1998), where the percentage of males with
EDs was calculated based on number of treated attended patients between 1975-97 (3,6% of
cases were male), the total number of male has now increased by more than two times.
When considering the ED subtype, during the last years, some specific diagnostic
categories of males have increased more than others, namely BN and EDNOS (see Figure 1),
whereas the percentage of AN has been reduced. This result is similar to recent findings in
female EDs. (Machado, Machado, Goncalves, and Hoek, 2007). In these general data (1.471
ED), there were significant differences (X2. 9,814, p<.007) in ED subtype distribution, when
considering the factor gender (males: 28,6% AN, 35,7 BN v 35,7% EDNOS vs. Females:
22,4%AN, 52% BN, 25,6% EDNOS). Similar diagnostic distribution among males was
described in previous studies (Carlat et al., 1997).
100%
12,5
90%
30 28,6 33,3
80% 38,5 38,9
70% 54,5
60
60%
62,5
% Diagnostic type
15,4
50% 42,9 33,3 EDNOS
50
40% 38,9 BN
18,2
30% AN
46,2
20% 40
28,6 33,3
22,2 27,3 25
10% 20
0% 0
2000 2001 2002 2003 2004 2005 2006 2007
Year
Note: AN: Anorexia nervosa, BN: Bulimia nervosa, EDNOS: Eating disorders non-otherwise specified.
Figure 1. Diagnostic distribution in males with EDs, between 2000 and 2007, at the University Hospital
of Bellvitge.
Evidence-Guided Treatment for Males with Eating Disorders 157
Differences between Male and Female ED

Although most characteristics of men and women with EDs are similar (Andersen, 1999;
Bramon-Bosch, Troop, and Treasure, 2000; DiGioacchino, Sargent, Sharpe, and Miller,
1999), even with regards to pattern of familial aggregation (Strober, Freeman, Lampert,
Diamond, and Kaye, 2001) and in adolescents ED (Geist, Heinmaa, Katzman, and Stephens,
1999), in the literature we can also find gender differences (Andersen and Mickalide, 1985;
Deter, Kopp, Zipfel, and Herzog, 1998; Woodside et al., 2001). Some of the discrepancies
observed in the current literature are partially due to methodological gaps, lack of control
groups or too small sample sizes of the clinical used samples.
Clinical and Symptomatological Differences in

Males with EDs
In general, studies have indicated that the clinical manifestations in males are similar to
the ones of females in terms of age of onset, weight control methods and associated ED
factors (Braun, Sunday, Huang, and Halmi, 1999; Carlat et al., 1997; Keel, Klump, Leon, and
Fulkerson, 1998; Olivardia, Pope, Mangweth, and Hudson, 1995). However, other studies
have revealed gender specific differences on physical activity, more concern with masculine
shape and more laxative use in male as compared to female ED patients (Braun et al., 1999;
Carlat and Camargo, 1991; DiGioacchino et al., 1999; Fichter, Daser, and Postpischil, 1985),
but also later age of onset (Grabhorn, Kopp, Gitzinger, von Wietersheim, and Kaufhold,
2003). For a review, see (Chambry, Corcos, Guilbaud, and Jeammet, 2002; Freeman, 2005;
Lindblad, Lindberg, and Hjern, 2006).
As shown in Table 1, from 1.472 consecutively admitted patients, we compared clinical
and symptomatological features between 104 males with EDs and 1.367 ED females. This
comparison (using 0.01 level of significance, to avoid error type I), revealed significant
differences by gender on higher weekly frequency of laxatives (more frequently in females,
p<.01), but no significant differences were obtained on age of onset or duration of the
disorder.
Regarding weight (see also Table 1), accordingly with previous reports (Andersen and
Holman, 1997), females with ED wished to be thinner (p<.001) and males presented a higher
lifetime maximum reached BMI, than females (p<.001). Concerns about body image is
thought to be one of the key maintaining factors of EDs and is a required criterion for the
diagnosis of Anorexia Nervosa (AN) and Bulimia Nervosa (BN) (Stice, 2002; Stice and
Whitenton, 2002).
Females show more concerns about body dissatisfaction and drive for thinness than
males, both in clinical ED samples (Joiner, Katz, and Heatherton, 2000; Kjelsas, Augestad,
and Flanders, 2003), as in general population samples (Davis and Katzman, 1998; Geist et al.,
1999).
Table 1. Clinical and demographic features of 104 males with EDs and 1.364 ED females
consecutive patients
ED (N= 1.468)
Males (N=104) Females (N= 1.364)
Mean SD Mean SD
Age 24,36 6,60 25,82 7,12
Age of onset 19,08 5,70 19,07 6,12
Duration of disorder 5,27 5,08 6,73 5,64
Number previous
,71 ,96 ,94 1,20
treatments
BMI 22,58 5,72 21,95 6,14
BMI max. 28,30 6,89 25,86 5,97
BMI min. 19,03 4,31 18,29 3,35
BMI ideal 21,95 3,55 19,86 2,67
Weekly frequency of
3,82 7,27 4,83 6,56
binge episodes
Weekly frequency of
5,46 9,79 5,41 7,95
vomiting
Weekly frequency of
,49 2,38 3,97 13,41
laxatives
Weekly frequency of
,02 ,22 1,41 5,68
diuretics
Note: BMI: Body Mass Index (weight/ height2).
Many of our males with EDs were more concerned about their body shape in terms of
muscularity rather than about their weight (Fernandez-Aranda et al., 2004), which is similar
to the findings of many other authors (Andersen and Mickalide, 1983; Andersen et al., 1985;
Benninghoven, Tadic, Kunzendorf, and Jantschek, 2007; Davis et al., 1998; Furnham,
Badmin, and Sneade, 2002).
In a recent study (Nunez-Navarro et al., in press), using a case-control design, we have
compared two groups of ED (60 males and 60 females) with two healthy eating comparison
groups (60 males and 60 females), on several clinical and personality profiles. Regarding
differences due to gender, ED women obtained higher means in two EDI-2 subscales (“drive
for thinness”, p<0.0005 and “body dissatisfaction”, p<0.0005) than males with EDs, but a
similar trend was also observed in healthy eating controls by gender. This result may reflect
just socio-cultural gender differences, as the differential pattern is similar to the one between
males and females in the healthy non ED population.
Regarding motivation to change (assessed by lineal scale, described elsewhere
(Casasnovas et al., 2007), and taking into account the initial 104 males with EDs, when
compared with 1.367 ED females, males were less motivated for therapy than females.
Basically, males were less concerned about their ED (p<.001), and showed low subjective
need for therapy (p<.001) and lower wish to be treated (p<.001). These results are in
concordance with a previous study (Woodside et al., 2004).
Table 2. Eating psychopathology in Eating disorder patients and healthy controls by

gender (adapted from Nunez-Navarro et al., in press)
Mean (SE) ANCOVA

Controls Cases Principal effects:
Males Females Males Females Mean differences (95% C.I.)
(N=60) (N=60) (N=60) (N=60) Sex Diagnose
EDI-2: Drive for
1.9 (0.8) 5.2 (0.8) 9.3 (0.7) 13.5 (0.7) 3.8 (2.2; 5.3)* 7.9 (6.3; 9.4)*
thinness
EDI-2: Body 9.0 (7.2;
2.9 (1.0) 6.8 (1.0) 10.9 (0.9) 16.7 (0.9) 4.9 (3.0; 6.8)*
dissatisfaction 10.8)*
EDI-2:
Interoceptive 1.6 (0.7) 2.3 (0.8) 7.5 (0.7) 11.3 (0.7) 2.2 (0.8; 3.7) 7.5 (6.1; 8.9)*
awareness
EDI-2: Bulimia 0.4 (0.6) 1.0 (0.6) 5.0 (0.6) 6.4 (0.6) 1.0 (-0.2; 2.2) 5.0 (3.9; 6.2)*
EDI-2:
Interpersonal 3.0 (0.5) 1.9 (0.6) 6.1 (0.5) 5.9 (0.5) -0.6 (-1.7; 0.4) 3.6 (2.5; 4.6)*
distrust
EDI-2:
1.7 (0.8) 2.0 (0.8) 8.5 (0.7) 11.8 (0.7) 1.8 (0.2; 3.3) 8.3 (6.9; 9.8)*
Ineffectiveness
EDI-2: Maturity
4.8 (0.7) 4.7 (0.8) 9.4 (0.7) 8.4 (0.7) -0.5 (-1.9; 0.9) 4.2 (2.8; 5.5)*
fears
EDI-2:
4.3 (0.6) 3.3 (0.6) 4.5 (0.5) 6.0 (0.5) 0.2 (-0.9; 1.4) 1.5 (0.4; 2.6)
Perfectionism
EDI-2: Impulse
2.1 (0.8) 1.3 (0.8) 6.4 (0.7) 8.3 (0.7) 0.5 (-0.9; 2.0) 5.6 (4.2; 7.0)*
regulation
EDI-2: Asceticism 2.4 (0.6) 1.9 (0.6) 6.2 (0.5) 7.0 (0.5) 0.2 (-0.9; 1.3) 4.4 (3.4; 5.5)*
EDI-2: Social
2.7 (0.6) 2.3 (0.7) 7.3 (0.6) 8.4 (0.6) 0.4 (-0.9; 1.6) 5.4 (4.2; 6.6)*
insecurity
13.5 (3.0; 62.4 (52.3;
EDI-2: Total score 27.8 (5.4) 32.7 (5.6) 81.6 (4.9) 103.7 (4.9)
24.0) 72.6)*
1
Sex factor: difference obtained for females-males. 1Diagnose factor: difference obtained for cases-
controls.
*The parameter is significant at 0.002 level. EDI: Eating Disorder Inventory.
Psychopathological Differences in Males with EDs

In general terms, ED men have been described to have more general psychopathology
and co-morbidity than ED females (Bean, Maddocks, Timmel, and Weltzin, 2005). In several
comparative studies, males with EDs have shown: higher alcohol dependence (Striegel-
Moore et al., 1999; Woodside et al., 2001) and higher levels of co-morbidity on Axis I
(Weltzin et al., 2007a) or Axis II (Striegel-Moore et al., 1999).
In the previously mentioned study (Nunez-Navarro et al., in press), males with EDs
showed lower general psychopathology (measured by SCL90R) than ED females, and
especially in somatization, depression and anxiety subscales.
Table 3. General psychopathology in Eating disorder patients and healthy controls by

gender (adapted from Nunez-Navarro et al., in press)
Mean (SE) ANCOVA

Controls Cases Principal effects:
Males Females Males Females Mean differences (95% C.I.)
(N=60) (N=60) (N=60) (N=60) Sex Diagnose
SCL-90-R:
0.6 (0.1) 0.7 (0.1) 1.4 (0.1) 1.8 (0.1) 0.3 (0.1; 0.5)* 0.9 (0.8; 1.1)*
GSI score
SCL-90-R:
1.5 (0.1) 1.5 (0.1) 2.1 (0.1) 2.4 (0.1) 0.2 (0.0; 0.3) 0.8 (0.7; 0.9)*
PSDI score
SCL-90-R: 24.9 (19.7;
30.7 (2.7) 39.7 (2.7) 55.3 (2.6) 65.0 (2.6) 9.3 (4.0; 14.6)*
PST score 30.1)*
1Sex factor: difference obtained for females-males. 1Diagnose factor: difference obtained for cases-
controls.
*The parameter is significant at 0.002 level.
Personality and Males with EDs

The few studies assessing personality in men with EDs have shown that male AN
patients exhibited lower scores on harm avoidance, reward dependence, and co-operativeness
and higher scores on novelty seeking than females with AN (Fassino et al., 2001; Woodside
et al., 2004). As regards to BN, another study (Joiner et al., 2000) demonstrated higher levels
of perfectionism and interpersonal distrust in males in comparison to females. In contrast,
other studies (Alvarez-Moya et al., 2007; Fernandez-Aranda et al., 2004; Strober et al., 2006)
were not able to find substantial gender differences in personality traits in ED patients (males
vs. females). When diagnostic ED subgroups were examined, considerably few gender-
specific differences on personality traits were found (Woodside et al., 2004).
Pre-Morbid Obesity and Males with EDs

Compared to females with EDs, a few studies have demonstrated that males tend to have
higher levels of weight problems prior to the onset of their ED (Carlat et al., 1991; Robinson
and Holden, 1986). They report generally being further away from their ideal weight than
female ED patients (Carlat et al., 1997; Fernandez-Aranda et al., 2004). These observations
are interesting because we have previously indicated that men might have certain defenses
from EDs due to their low occurrence of dieting and more positive body image. Nevertheless,
males who are in fact obese may possibly have a negative view of their bodies and might
therefore feel an elevated pressure to lose weight. Therefore their environmental stressors
appear to be similar to the ones of women who are vulnerable to EDs. Accordingly, in a
previous study (Carlat et al., 1991; Fernandez-Aranda et al., 2004), it was found that males
gave a history of pre-morbid overweight or obesity more frequently (45% vs. 15%, p<038),
and basically in those with BN.
Figure 2. Diagnostic variability at 1 year follow-up and drop-out in males with EDs (N=19) and females
(N=19), after following an outpatient CBT group therapy (adapted from Fernández-Aranda, in press).
Therapy and Males with EDs

To date, although most literature connecting gender to EDs has focused on a
symptomatology and psychopathological level, there is a lack of published studies examining
the specific therapy of males with EDs.
Some of the first descriptions of therapy in males appeared in publications at the
beginning of 1970's. Some of the first reports that were published at that time, most of them
single case studies or series of cases, described those atypical ED disorders and the
therapeutic approaches used.
Bruch (Bruch, 1971) described nine registered inpatient treated AN males, at the New
York State Psychiatry Institute, observed between 1944 and 1969. The therapy was evaluated
as successful in some of the cases, after using psychotherapy, nutritional measures and
additional medication.
Roussounis at the Alexandra Hospital (Roussounis and Savage, 1971) described a 11
year old boy with AN. He was treated as an inpatient with a combination of drug therapy
(chlorpromazine -Largactil) and gradually increasing food and weight, with successful results
after 90 days. Furthermore, Crisp and colleagues (Crisp and Toms, 1972) described the
clinical picture and therapy outcome of 13 AN males. They concluded that males with EDs
carried a worse prognosis than the parallel female population.
Later on, additional series on AN males were published using psychotherapeutic and
medical measures (Buvat et al., 1983; Galletly and James, 1979; Goebel, 1976; Larsen and
Skovgard, 1977), however the results were poor.
The therapy for bulimia in males has received relatively little attention in the literature. It
was not until the middle 80’s, when some of the first descriptions of treated male BN cases
were published (Andersen, 1984; Mitchell and Goff, 1984).
The few case-control studies where therapy with males with EDs was specifically
analyzed, obtained heterogeneous results (Andersen et al., 1997; Weltzin et al., 2005). Bean
et al. (Bean et al., 2005), compared the effectiveness of a residential therapy in ED (154
females and 27 males), and obtained that although females present more psychopathology
symptoms at the beginning of treatment, they make better progress than males in reducing
these symptoms over time.
Table 4. Overview of the literature on therapy outcome in males with EDs
Author Year Sample Setting Follow-up Results

(years)
Burns 1985 27 AN males Inpatient 8 Outcome ED males = ED
females
Crisp 1986 36 AN males Inpatient 8 Outcome ED males = ED
100 AN females females
Woodside 1994 15 ED males Hospital - Outcome ED males = ED
334 ED females Day females
Deter 1998 10 AN males Residential 12 ED males better outcome than
84 AN females ED females
Oyebode 1998 13 AN males -- 9,2 ED males poorer outcome than
Grabhorm 2003 20 ED males Residential 2,5 Outcome ED males = ED
764 ED females females
Bean 2005 27 ED males Residential - ED females better outcome than
154 ED females ED males
Strober 2006 14 AN males Inpatient- 1 ED males better outcome than
85 AN males residential ED females
Lindblad 2006 61 AN males Inpatient - ED males better outcome than
general
population
Weltzin 2007 59 AN males Residential 1 Outcome ED males = ED
30 BN males females
16 EDNOS
males
Fernandez- In 19 BN males Outpatient 1 Outcome ED males = ED
Aranda press 19 BN females females
Note: AN: Anorexia nervosa, BN: Bulimia nervosa, EDNOS: Eating disorders non-otherwise specified.
As shown in table 4, to date, several non-specifics therapeutic approaches for males with
EDs have been tested, in comparison with the improvements observed in ED female
counterparts. Their setting ranged from residential or inpatient therapy (Bean et al., 2005;
Crisp, Burns, and Bhat, 1986; Deter et al., 1998; Strober et al., 2006; Weltzin, Weisensel,
Cornelia-Carlson, and Bean, 2007b), to hospital day (Woodside and Kaplan, 1994).
Therefore, most studies dealing with therapy, were conducted in males with AN, after having
successful non-specific inpatient-residential treatment. The therapy for males with BN or
EDNOS is still rather unknown (Weltzin et al., 2007b).
In summary, men with EDs, especially AN, after a non-specific therapy appear to have
similar outcome than females. However, there is some uncertainty about the outcome of the
bulimic disorders. To date, there is also a lack of specific therapy approaches for males with
EDs, and especially outpatient programs.
Recently, we have published a pilot study that compared the short-middle term response
to an specific outpatient cognitive-behavioural therapy (CBT) group intervention in male BN,
and we have compared their results with those obtained in female counterparts after using a
similar approach (Fernandez-Aranda et al., in press). Males appear to have similar outcome
than females, even after one year follow-up.
Regarding randomized trials, as reported in a recent meta-analytical studies, conducted
by the North Carolina Group, to date no controlled trials exists on differential efficacy of
pharmacotherapy or psychotherapy interventions for AN by sex (Bulik, Berkman, Brownley,
Sedway, and Lohr, 2007). Similar lack of studies was obtained, when considered BN
controlled trials (Shapiro et al., 2007). Regarding binge eating disorder (BED), a meta-
analytic review study has shown (Brownley, Berkman, Sedway, Lohr, and Bulik, 2007) that,
although in spite of including also male cases in BED controlled trials (of the 680 individuals
enrolled in the 12 drug or medication plus behavioral intervention trials, less than 10% were
men), no studies explicitly tested differential therapies by sex.
Outcome and Males with EDs

One of the first references (see table 4), came from Burns and colleagues (Burns and
Crisp, 1985), who published data on 27 males with AN, that have been followed up over a
mean of 8 years, and their outcome was also assessed. When compared with outcome in
female patients with similar initial pictures, they found that poor relationship with parents
during childhood, absence of normal adolescent sexual behavior, long duration of illness,
previous treatment and greater weight loss during illness were strongly predictive of a poor
outcome. They have found similarity in outcome pattern between the male and female
patients.
Similar results were obtained in a later study conducted by the same group (Crisp et al.,
1986), where 36 consecutively referred male anorectics were compared with those of a
similar series of 100 female cases. Overall, the same background and presentation factors in
both sexes predict similar outcomes.
Deter et al. (Deter et al., 1998) analyzed possible differences in the disease course of
male and female patients. Total assessment after a mean of 12 years revealed that the male
had a better prognosis than the female patients. Male anorectics were in better physical
condition than their female counterparts at the time of follow-up. Male patients had a more
favorable course regarding psychosocial integration but a similar course as female patients
regarding ED symptoms.
The few case-control studies where the effect of gender on the prognosis has been
analyzed have shown a similar course and outcome in males with EDs when compared with
those results obtained in ED females (Andersen et al., 1997; Deter et al., 1998; Eliot and
Baker, 2001; Muise, Stein, and Arbess, 2003; Saccomani, Savoini, Cirrincione, Vercellino,
and Ravera, 1998), whereas others referred to better outcome (Deter et al., 1998; Lindblad et
al., 2006; Strober et al., 2006) or even poorer outcome in males (Oyebode et al., 1988).
Similarly to ED females, better outcome was found to be associated to less initial severity
of ED symptoms, higher BMI at the admission and lower frequency of obsessive-compulsive
behaviors (Strober et al., 2006; Weltzin et al., 2007a).
Regarding randomized trials , as reported in a recent meta-analytical study (Berkman,
Lohr, and Bulik, 2007), looking across all three disorders (AN, BN , BED), no studies
yielded information on gender and therapy outcome. Very few studies included males and
even if they did, males were underrepresented.
Our Own Experience Treating Males with EDs

At the Eating Disorders Unit (University Hospital of Bellvitge), well-known and
internationally recognized ED center in Spain, several types of therapies are being applied,
from psychological therapy (CBT oriented) to combination with drug therapy. The treatment
is carried out in several optional settings: from outpatient, day hospital and residential
therapy, to internet based self-management. A broad spectrum of ED patients are being
treated, from AN and BN, to EDNOS and BED. Since 2001, we have developed and applied
a specific therapy program, CBT oriented, for males with EDs (both individual and group
therapy). The CBT program for males is based on the cognitive model postulated by Fairburn
and colleagues (Fairburn, Marcus, and Wilson, 1993; Fairburn, 1997). The group intervention
consists of 19 weekly outpatient sessions (90 minutes each) with a total of 8-10 patients per
group. Men and women are treated in separate groups. The group is directed by a
psychologist and a co-therapist (one male and one female).
As in the case of females (Fernandez-Aranda et al., 1998; Fernandez et al., 1998), the
topics to be addressed in the group included: nutritional patterns and monitoring of meal
plans, strategies for decreasing bingeing and purging behaviour, cognitive restructuring,
problem solving strategies and relapse prevention. With males several topics were more
emphasized than with females, such as: difficulties with dealing with stress, interpersonal
relationships and shyness (many times as a consequence of the negative experience of being
criticized for previous obesity or overweight), cognitive style and underlying irrational
believes (e.g. muscularity, fear of gaining weight and becoming obese again), hyperactivity,
autonomy from family and homosexuality in some cases.
In group therapy with males with EDs, two therapeutic factors have a crucial relevance
(even more than in females): universality (other male patients have similar problem) and
overcoming resistance to change. An intensive work about the patients’ own motivational
factors, even during the sessions, to encourage the participation of all group members, will be
conducted. Successful and encouraging results were obtained, even after one-year follow-up,
with this type of specific program (Fernandez-Aranda et al., in press) – see Figure 2-.
Moreover, according to our own experience, we propose eight to nine patients per group
as the ideal number of patients and to consider as exclusion criteria those patients with severe
eating or medical problems, psychiatric instability (e.g. suicidality), and/or severe personality
disorder.
In order to promote group cohesion, variables such as homogeneity (e.g. similar age and
duration of the disorder, closed group), and number of participants will have to be taken into
account.
Conclusion
In summary, an increasing rate of male ED has been observed during the last few years,
mainly in BN and EDNOS. Although males seem to use laxatives with less frequency, have
less preoccupation with thinness, and are less motivated for a therapy, most clinical features
and symptoms of men and women with EDs are similar. Many of males with EDs are more
concerned about their body shape in terms of muscularity rather than about their weight.
Furthermore, males seem to have lower general psychopathology than females and no
substantial gender differences in personality traits were found.
The therapy for males with EDs, especially for BN, has received relatively little attention
in the literature. Most studies dealing with therapy, were conducted in males with AN after
having successful non-specific inpatient-residential treatment, showing similar outcome rates
to the ones of females. However, there is uncertainty about the outcome of the bulimic
disorders, the results of specific therapy approaches for males with EDs, and especially
outpatient programs.
There is a lack of evidence in the literature (particularly controlled trials) that explicitly
tested differential therapies by sex. Future outcome studies should explicitly emphasize the
factor gender. Furthermore, we recommend that specific programs for males with EDs should
be developed.
Case Report
A 26 years old man, technician in telecommunications, developed the complete clinical
picture of bulimia nervosa (purging subtype), according to the DSM-IV criteria (American
Psychiatric Association, 1994), since he was 18 years old. The ED started after extreme diet
behavior to lose weight. The patient described current 3-4 weekly binge-vomiting episodes,
mainly late afternoon, and irregular eating patterns. No abuse of laxatives or diuretics was
described. Weekly consume of drug, when he was 17-18 years old. At the first interview, the
patient had a body weight of 68 Kg (1.74 meters, BMI 22.5) and still presented overconcern
with his body shape in terms of muscularity rather than about their weight. After having
premorbid obesity (maximal body weight of 121 Kg- BMI 36.7, when he was 17 years old),
he has an intense fear of becoming fat again.
The patient was the younger of two children (all boys). He still lived with his family and
reported no relationship problems with them. In partnership, since he was 20 years old. No
other psychiatric illnesses were described by the patient or his relatives. 19 weekly outpatient
cognitive-behavioural group sessions (group therapy for males with ED’s) plus 4 follow-up
sessions (at 1, 3, 6 and 12 months) were conducted. The main goals of the therapy were: to
increase her motivation, to complete a behavioral analysis, to normalize eating habits, to
learn behavioral techniques such as coping with stress and solving problems (in spite of
escaping from them by binging) and to analyze and learn restructuring of irrational beliefs on
weight, shape and food. After the therapy, a reduction of eating symptoms was observed and
maintained after a follow-up.
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Chapter X
Treatment Resistance: Persuasion,

Perceived Coercion and Compulsion
Angela S. Guarda and Janelle W. Coughlin

The Johns Hopkins School of Medicine
Baltimore, Maryland, USA
Abstract
Ambivalence towards treatment and treatment resistance are characteristic of eating
disorders, particularly anorexia nervosa. Because attempts at normalizing weight and
eating patterns threaten the ego-syntonic nature of dieting behavior, patients with
anorexia nervosa rarely enter treatment of their own accord. Instead, some degree of
pressure, or coercion, ranging from gentle persuasion to legal certification, is often
applied to oblige resistant patients into treatment. Coercion is controversial however, and
there is limited research to guide practitioners on the ethics and clinical management of
treatment refusal. This chapter will discuss ambivalence and treatment resistance as core
phenomenological features of eating disorders with emphasis on anorexia nervosa. The
literature on treatment refusal, including competency and capacity to consent to
treatment, perceived coercion about the admission process and compulsory treatment will
be reviewed as well as empirical evidence regarding the therapeutic value and role, if
any, of coercive interventions, ranging from mere persuasion to the extreme of
compulsory inpatient treatment. Finally, the chapter will close with a case study, a
suggested approach for managing treatment resistance and a discussion of directions for
future clinical research.
Introduction
Eating disorders and anorexia nervosa in particular, are behavioral conditions
characterized by denial of illness, ambivalence towards treatment and treatment resistance.
Refusal of treatment raises significant ethical dilemmas for clinicians, family members,
172 Angela S. Guarda and Janelle W. Coughlin
educators and employers given the high mortality of anorexia nervosa (Hoek, 2006; Millar et
al., 2005). In health care practice, conflicts arise between the principle of patient autonomy,
or right to self-govern, and the principles of beneficence (duty to act in the best interest of
patients) and nonmaleficence (duty not to harm patients). Paternalistic acts, which restrict
patients’ freedom to self-govern, are typically justified only when a patient’s capacity to
consent to treatment is impaired and the act ensures good or prevents harm. Eating disorders
present specific challenges in determining: i) whether patients have the capacity to make
treatment decisions, ii) under what instances paternalistic acts are clinically justified and iii)
to what extent and how these acts should be implemented when deemed appropriate.
Ambivalence Towards Treatment Is a Symptom of

Eating Disorders
In anorexia nervosa, “motivated eating restraint” (Schmidt and Treasure, 2006) fuels an
overvalued fear of fatness. Dieting is pursued beyond the bounds of reason and to the
exclusion of other socially and developmentally appropriate activities (McHugh and Slavney,
1998). Since dieting is strongly ego-syntonic in both bulimia and in anorexia nervosa,
attempts at normalizing eating behavior are experienced as uncomfortable. In anorexia
nervosa, treatment avoidance is in essence a symptom of the condition, making it unlike
refusal of medical intervention in other illnesses (Tiller, Schmidt, and Treasure, 1993). When
patients seek treatment they do so to obtain temporary relief from unpleasant physical,
psychological and social consequences of their behavior, however they do not want to give
the behavior up in its entirety. This situation results in a fundamental conflict between the
goals of patient and those of the provider and places clinicians in the position of constantly
attempting to persuade reluctant patients to change their behavior. As a result, the experience
of working with patients with eating disorders can feel exhausting and frustrating to both the
novice therapist and the seasoned clinician.
Because they seek treatment on their own terms, patients with anorexia nervosa act more
like clients than patients. They have been found to favor interventions that allow them to talk
about, rather than to change what they do (Newton, 1993) and may shop around for the
treatment that feels best rather than the one that is best for them (McHugh et al., 1998). In
keeping with these observations, most patients are precontemplative or contemplative rather
than in the action stage in terms of their readiness to change, especially with respect to
altering their restricting behavior (Hasler, Delsignore, Milos, Buddeberg, and Schnyder,
2004).
Although ultimately recovery must be willed and owned by the patient, most patients
initiate treatment following pressure by others. Clinical experience and anecdotal patient
reports suggest that motivation for treatment in eating disorders increases with mastery over
behavior change. Thus, denial of illness and avoidance of treatment are one of the main
obstacles to therapeutic engagement for many patients who might otherwise have a
reasonable prognosis.
Treatment Resistance: Persuasion, Perceived Coercion and Compulsion 173
Eating Disorders are Motivated Behavioral

Disorders
Eating disorders and substance abuse share phenomenological similarities. Both are
driven behavioral disorders characterized by ambivalence towards treatment, increasing
salience of drug/food stimuli, narrowing of the behavioral repertoire, escalation of the
disordered behavior over time despite increasingly negative consequences, and frequent
relapse (Davis and Claridge, 1998). Affected individuals describe loss of voluntary control
over their eating disordered or substance use behaviors, however this loss of control is not
complete and it is state-dependent (Hyman, 2007). Recovery requires consistent, long-term
behavior change by patients’ with waxing and waning rationality and insight. As a result, the
clinician’s role is akin to that of a trainer, repeatedly encouraging the practice of healthy
behaviors and the blocking of conditioned maladaptive behavior patterns.
Trait-related multigenic vulnerability modulated by environmental risk factors
contributes to the etiology of both eating and substance use disorders. Once established
however, these conditions are sustained by both conditioned learning and by state-related
pathophysiological changes (Faris et al., 2006; Kaye, 2007; McHugh et al., 1998). In
anorexia nervosa for example, restrictive eating is sustained by starvation-induced prolonged
gastrointestinal transit times, early satiety and abdominal pain (Waldholtz and Andersen,
1990; Kamal et al., 1991). Starvation also increases preoccupation with food, ritualized
eating behaviors and depressive symptomatology (Keys, Brozek, Henschel, Mickelsen, and
Longstreet Taylor, 1950; Meehan, Loeb, Roberto, and Attia, 2006). In bulimia nervosa, self-
induced vomiting leads to decreased gastric emptying, blunted postprandial cholecystokinin
release (Devlin et al., 1997) and vagal changes that may facilitate the binge-purge cycle
(Faris et al., 2006). Reversing these pathophysiological changes is necessary for recovery
(Hyman, 2007; McHugh et al., 1998).
Common neural pathways have been implicated in both addiction and in feeding (Kelley
and Berridge, 2002) and dopaminergic brain pathways involved in natural rewards (e.g. food
and sex) may be usurped by drugs of abuse and dysregulated in eating disorders (Hyman,
2005; Volkow and Li, 2005; Kaye, 2007). In animals, restricting food intake amplifies the
reward of both food and of drugs of abuse (Levine and Billington, 2004; Carr and
Papadouka, 1994) while chronic exercise decreases mu-opioid sensitivity (Smith and Lyle,
2006), suggesting that opioidergic dysregulation may be involved in the escalating patterns of
exercise observed in anorexia nervosa.
Data on Coercive Treatment for Substance Abuse

The preponderance of data from the substance abuse field suggests that the outcome of
legally coerced addiction treatment provided in lieu of alternative consequences (e.g. jail,
loss of driving license, loss of child custody, loss of job) can motivate reluctant patients to
accept treatment, has outcomes equal to or superior to voluntary treatment, and is more cost-
effective in the long-term (Miller and Flaherty, 2000). Furthermore, no empirical study has
demonstrated the harm or ineffectiveness of using such leverage. Besides legal leverage,
family pressure can play an important role in motivating patients to change substance use
behavior and to engage in treatment (Fernandez, Begley, and Marlatt, 2006; Copello,
Templeton, and Velleman, 2006). Empirical data is limited; however professionally-guided,
family-based interventions for alcohol and substance abuse match or improve on the outcome
of individual interventions. Flexible approaches incorporating motivational techniques have
been gaining popularity and some evidence suggests they are effective in engaging
unmotivated substance abusers into treatment (Meyers, Smith, and Lash, 2003; Meyers,
Miller, Hill, and Tonigan, 1998). Similar approaches may have value for the treatment of
eating disorders given the phenomenological parallels between these behavioral conditions.
Competence to Refuse Treatment in

Anorexia Nervosa
In anorexia nervosa, a central ethical and legal question is whether the disorder impairs
an individual’s capacity to make a rational and free choice regarding acceptance or refusal of
treatment. Legal definitions of informed consent require that patients: (i) are given adequate
information to make informed decisions about risks and benefits of treatment, (ii) make
treatment decisions voluntarily and (iii) are competent to make these decisions (Simon,
1992). Competence (typically a legal term) is task-specific and implies the cognitive capacity
(typically a clinical term) to make an informed rational decision. It does not, however, require
that patients make a rational choice.
Incompetence to refuse treatment in anorexia nervosa has been described as “subtle”
(Gutheil and Bursztajn, 1986) because patients are rarely grossly incompetent. They usually
recognize that their beliefs are not shared by others and demonstrate good reasoning in most
areas. Although usually able to appreciate the need for others with the same disorder to
receive treatment, they demonstrate a subjective defect in self-evaluation, appearing unable to
recognize their own need for weight restoration. They provide seemingly rational and
articulate explanations for their treatment refusal, arguing they are different in some
fundamental way from other patients with the same disorder and need not gain weight or eat
certain foods. Although neither actively psychotic nor suicidal, their behavior (self-
starvation) contradicts their denial of suicidal intent (Appelbaum and Rumpf, 1998).
Although some have argued that select chronic treatment resistant patients may be
competent to refuse treatment even when their life is in danger (Draper, 1998; Gans and
Gunn, Jr., 2003; Draper, 2000), a more convincing argument can be made that in life-
threatening anorexia nervosa, patients are usually incompetent to make treatment decisions
involving their own eating and weight as a result of their starved state and lack the ability to
choose freely and to fully appreciate their risk of death (Appelbaum et al., 1998; Gutheil et
al., 1986; Kluge, 1991). This state-dependent, lack of capacity is supported by clinical
evidence that once weight-restored, many involuntarily treated patients retrospectively view
their treatment as justified (Watson, Bowers, and Andersen, 2000). Consistent with the view
that patients’ reality testing is impaired while acutely ill, a recent study found that 20% of
patients with anorexia nervosa reported a dominant belief related to fear of weight gain that
fell in the delusional category based on the Brown Assessment of Beliefs Scale (Steinglass,
Eisen, Attia, Mayer, and Walsh, 2007).
Evidence suggests that tests of competence may fail to identify individuals with anorexia
nervosa whose capacity is impaired (Gutheil et al., 1986; Tan, Hope, Stewart, and Fitzpatrick,
2003). The most rigorously validated standardized test of competence used in psychiatric
populations, the MacCAT-T, is modeled after the legal criteria for capacity including
understanding, reasoning, and appreciation of illness and treatment options (Grisso et al,
1997). In a small study by Tan and colleagues utilizing the MacCAT-T (Tan, Hope, and
Stewart, 2003a), patients with anorexia nervosa all scored in the normal range, although
qualitative interviews exploring beliefs, attitudes and values surrounding treatment revealed
difficulties in reasoning arising from the ego-syntonic characteristic of the disorder. Beliefs
fell into three general themes: (i) a relative unimportance of the risk of death compared with
anorexia, (ii) an overvalued importance of the anorexia relative to other life roles and (iii)
ambivalence towards treatment and recovery (Tan, Hope, and Stewart, 2003b; Tan et al.,
2003a). The authors conclude that anorexia nervosa challenges current conceptions of legal
capacity and competence to refuse treatment because it affects patient values, values that
arise from the state of having anorexia nervosa and are therefore not independent of the
illness.
Coercive Treatment and the Adolescent Patient

Treatment of the adolescent patient with anorexia nervosa is more paternalistic and
coercive by definition. Minors are usually considered incompetent to make treatment
decisions and consent is typically obtained from a parent or legal guardian. Consistent with
being less free to refuse treatment, hospitalized adolescents with eating disorders report
higher levels of perceived coercion surrounding their admission compared to adult patients
(Guarda et al., 2007). Nonetheless, treatment outcome for adolescent anorexia nervosa is
superior to that for adult patients. Perhaps adolescent anorexia nervosa is a milder self-
limited disorder or the physiological, psychological and social sustaining factors are not yet
established (Fairburn, 2005); however, a third possibility is that family involvement in
treatment helps contain eating disordered behavior by promoting the practice of healthier
eating behavior and blocking habitual conditioned eating disordered response patterns. If so,
then the efficacy of family therapy in the treatment of adolescent anorexia nervosa (Robin,
Siegel, Koepke, Moye, and Tice, 1994; Russell, Szmukler, Dare, and Eisler, 1987) may hinge
more on parental compliance with treatment recommendations than on patient motivation for
treatment. Conversely, when parents are more aligned with their ill children than with care
providers they may reinforce treatment resistance (Fornari, Dancyger, Schneider et al., 2001).
Consistent with this hypothesis, a strong therapeutic alliance between parents and clinical
provider predicted lower drop out and higher total weight gain in an outpatient family therapy
intervention for adolescent anorexia nervosa (Pereira, Lock, and Oggins, 2006).
Formal or informal family education is a component of most outpatient and inpatient
interventions for adolescent anorexia nervosa. Parents model communication with their child
based on the behavior of the treating team. This includes empathically stigmatizing and
enforcing consequences for eating disordered behavior, encouraging and reinforcing healthy
behavior and cognitions and increasing patient autonomy as behavior normalizes. In a small
study of adolescents’ perceptions of treatment decisions, although patients with anorexia
nervosa complained that clinical decisions were made unilaterally by parents or by clinicians
against their will, they denied desiring more freedom to refuse treatment. When asked why
they did not want more autonomy they reported they would want to refuse what was best for
them if they had the choice (Tan and Fegert, 2004). This incongruity between what patients
know is best for them and their desire to avoid treatment illustrates a characteristic dilemma
faced by patients with anorexia nervosa.
Family Therapy and the Adult Patient

Research on family involvement in treatment for adult patients with anorexia nervosa or
bulimia is scant. Many adult patients are functionally impaired and dependent on their
families both financially and emotionally. Although a small study suggests that family
therapy is less effective than individual therapy for adults with anorexia nervosa (Russell et
al., 1987), it is unclear whether the focus of the family intervention included use of
behavioral contingencies and the types of leverage (housing, money, tuition) that have been
found effective in substance abusing adults (Miller et al., 2000).
Voluntary Treatment and Perceived Coercion

Pressure imposed by family, friends, employers, educators or clinicians is a component
of most voluntary psychiatric admissions for anorexia nervosa. Social persuasion can take
various forms including, coaxing, begging, bargaining, selective information or ultimatums.
At the extreme, some patients agree to hospitalization only under threat of involuntary
certification. Whereas coercion is a powerful and evocative term, empathic support and
persuasion are features common to all effective psychotherapeutic interventions (Frank,
1961). The boundary between persuasion and perceived coercion is not always distinct
however and lies to some extent “in the eye of the beholder”.
Amongst 139 eating disorder patients admitted to a behavioral specialty program,
perceived coercion regarding hospital admission was more prominent in patients with
anorexia nervosa than in those with bulimia, consistent with anorexia nervosa’s more ego-
syntonic nature (Guarda et al., 2007). Furthermore, although one-third of the 139 patients
reported that they did not believe they needed to be admitted, within two weeks 40% of these
converted to endorsing a need to be hospitalized. This study was not adequately powered to
examine associations between conversion in belief about need for hospitalization and
behavioral (e.g., weight gain) or cognitive (e.g., change in drive for thinness) outcomes,
however, conversion in belief regarding need for treatment is consistent with the clinical
observation that as patients change their behavior and engage therapeutically with the
treatment team their motivation to change improves. Judicious, thoughtful use of coercive
leverage may help engage those patients who would otherwise avoid clinical intervention.
At least one study suggests that stage of change based on Prochaska’s transtheoretical
model of change (Prochaska, 1995) is predictive of treatment response in eating disorder
outpatients (Geller, 2006), however a second study found that the prognostic value of stage of
change was related to self-referral status (Hasler et al., 2004). This finding suggests that
amongst those patients who avoid treatment altogether, stage of change has less predictive
value with respect to potential treatment outcome. Furthermore, although various markers of
illness severity have been associated with risk of drop-out from inpatient behavioral programs
(Kahn and Pike, 2001; Woodside, Carter, and Blackmore, 2004), unpublished data from our
group suggests that perceived coercion and readiness to change at admission are not
predictive of early dropout amongst underweight eating disorder patients.
Involuntary Treatment
There is uncertainty and confusion on behalf of clinicians and the courts about the
applicability of involuntary treatment to anorexia nervosa (Gutheil et al., 1986; Ramsay,
Ward, Treasure, and Russell, 1999; Appelbaum et al., 1998). Despite the high lethality of this
disorder, involuntary treatment remains controversial and is employed rarely by few
treatment centers, and this is true internationally. In Israel, the Mental Health Act restricts
consideration for compulsory treatment to the category of psychotic disorders, thereby
excluding anorexia nervosa (Melamed, Mester, Margolin, and Kalian, 2003; Mitrany and
Melamed, 2005), while in the United Kingdom the majority of involuntary commitments to a
behavioral specialty unit are instituted only after voluntary inpatients express a desire to
leave the hospital so that patients who avoid treatment altogether are unlikely to be
compulsorily detained (Ramsay et al., 1999).
In the United States, only a handful of eating disorder specialty programs treat civilly-
committed patients (Appelbaum et al., 1998). In the absence of local access to such a unit,
patients with anorexia nervosa are occasionally committed to general psychiatric units or are
treated in medical inpatient settings. Attempts at treatment in these alternate settings are
usually limited to medical stabilization since a specialized treatment team and a critical
patient volume is needed to implement a behavioral protocol capable of weight restoring the
majority of patients.
Research on the outcome of involuntary treatment for anorexia nervosa is limited,
however case-control studies of involuntary vs. voluntary inpatients treated in specialty
programs suggest that discharge BMI is equivalent for both groups (Ramsay et al., 1999;
Griffiths, Beumont, Russell, Touyz, and Moore, 1997; Watson et al., 2000). Higher long-term
mortality for involuntary cases in one study suggests this group may be more treatment
refractory (Ramsay et al, 1999), although their worse long-term prognosis may be explained
by higher case severity. Indeed, longer illness duration, higher number of prior admissions,
and or lower admission BMI have all been elevated in involuntary cases (Ramsay et al, 1999;
Griffiths et al, 1997). History of self-mutilating behavior (Brunner, Parzer, and Resch,
2005,Ramsay, 1999) or of reported abuse (Ramsay et al, 1999), psychiatric comorbidity and
greater likelihood of experiencing the refeeding syndrome during treatment (Carney, Crim,
Wakefield, Tait, and Touyz, 2006; Carney, Tait, Wakefield, Ingvarson, and Touyz, 2005;
Carney, Tait, Richardson, and Touyz, 2007; Carney, Tait, and Touyz, 2007) have also been
more commonly reported amongst involuntary patients.
Empirical data indicating harm from involuntary treatment is absent, and when it is
effective, involuntary treatment is often met with gratitude on behalf of patients and families
(Tiller et al., 1993). In a large U.K. questionnaire survey of patients hospitalized for an eating
disorder, 50% of those who reported being hospitalized against their will retrospectively
described the compulsory order as “a good thing” (Newton et al. 1993). Similarly, in a U.S.
study of 66 involuntarily admitted patients, many endorsed a need for treatment by the time
of discharge and none lodged a formal or informal complaint about the inappropriateness of
their admission, although it appears unlikely the majority would have accessed treatment but
for their involuntary status (Watson et al., 2000). A survey of the perceived acceptability of
compulsory treatment for anorexia nervosa among the general public suggests its
acceptability is more closely linked to the likelihood of a favorable outcome than to a
patient’s emotional reaction to the detention (Newton, Patel, Shah, and Sturmey, 2005). In
sum, a strong argument can be made that when treatment has a reasonable likelihood of
improving prognosis, commitment should be considered in severe cases of anorexia nervosa
(Appelbaum et al., 1998; Watson et al., 2000; Ramsay et al., 1999). Determining which
patients will benefit from imposed treatment and to what extent remains a challenge.
Acutely ill patients with anorexia nervosa have difficulty imagining their lives without
the disorder and describe their anorexia as integral to their identity (Stein and Corte, 2007;
Tan et al., 2003b). The following case report illustrates how involuntary treatment and
pressure for admission by others can result in favorable short-term treatment response,
conversion in patient’s belief regarding perceived need for treatment and formation of a
therapeutic alliance despite the adversarial nature of the admissions process.
Case report: A 41-year-old nursing student was admitted to a behavioral eating disorders
inpatient unit at a BMI of 11.7 with a 27 year history of chronic life-threatening anorexia
nervosa. She reported over 22 prior hospitalizations to at least four different behavioral eating
disorder programs, a psychiatric state hospital and several medical units. During all of these
she had gained little if any weight. Over 15 of these admissions were precipitated by medical
emergencies, including electrolyte imbalances, delirium or seizures attributed to her eating
disorder. Minimum lifetime BMI was 9.0 at age 38. On physical exam she was hypothermic
and bradycardic, had marked lower extremity edema with skin breakdown, cachexia and
osteoporosis. She was edentulous from vomiting. She endorsed marked fear of fatness, had
poor insight and impaired judgment insisting she did not need inpatient treatment. She
maintained she would never recover and repeatedly stated “I am my eating disorder”.
She was brought to the hospital by her father under an ultimatum that she would need to
be evaluated or could no longer live in his house. She agreed to voluntary admission only
after the admitting officer told her he would certify her involuntarily if she refused to sign in.
Once on the unit she immediately requested to leave the hospital and was certified. She
subsequently became agitated requiring seclusion over the first weekend of her stay. She
intermittently exhibited multiple behavioral problems and poor compliance with the treatment
protocol including: hoarding food in her room, vomiting into a newspaper and was often
argumentative with staff. Nonetheless, she participated in group therapy, engaged with peers
and was able to provide positive feedback to other patients regarding their need for treatment.
Her weight gain was slower than average, however she reached a BMI of 17 prior to
transition to partial hospital. She refused to attend the partial program and was subsequently
discharged against medical advice.
In a thank you letter received several months after her discharge she wrote “ … I just
wanted to thank you and the eating disorder team for your kind attention, guidance, patience,
and understanding given to me during my recent stay…Even though as you well know I at
times presented considerable resistance to your treatment, the constant and concerted efforts
of the staff helped me to face and tackle many of the obstacles that have been keeping me
sick for years. When I came to you I was totally hopeless in anyone’s attempt to help me get
better and I was determined to prove to you that I was beyond help. Now that I am home and
am doing relatively well I can see how much progress I have made. I never thought I would
admit you have an excellent program that essentially saved my life. You were able to provide
me with a healthier mind and body while teaching me to be less fearful of food and helping
me to develop more controlled eating behavior patterns. …There is absolutely no question in
my mind that I am much better off now than when I was admitted on the brink of death.
Thank you for not giving up on me, keeping me safe, and allowing me the opportunity to live
a much healthier life where I may follow my dreams to become a nurse. I will never forget
the experience and education I gained from the program and will recommend it to anyone
who may need help and I know you will be there for me if I should ever need you again. I
now understand the “method to your madness”. Once again I would like to express my
sincere gratitude for all you have given back to me”.
Four years later, although still chronically underweight, she has maintained her discharge
BMI, is working as a critical care nurse, and has not been rehospitalized. Her father reports
she is doing the best she has in years.
The Spectrum of Coercion: From Persuasion

to Compulsion
Because the legal process is, by nature, adversarial and can delay and interfere with the
formation of a therapeutic alliance (Geist, Katzman, and Colangelo, 1996), the least
restrictive therapeutic intervention for the individual patient should always be attempted first
in keeping with the principle of autonomy (Melamed et al., 2003). When other attempts fail,
when a patient’s life is at risk and when there is reasonable confidence that the treatment will
be beneficial, involuntary treatment should be considered (Russell, 2001).
Treatment setting is important, with higher likelihood of benefit in specialty programs
experienced in managing treatment resistant patients than on a general psychiatric or medical
unit. Similarly, feeding method may influence outcome. Oral feeding is safer than enteral or
parenteral feeding and may be associated with lower relapse risk. Although preferable, oral
feeding may be ineffective in achieving consistent weight gain outside of a behavioral
specialty unit experienced in implementing behavioral and group therapy techniques with
treatment resistant cases.
When the decision is taken to pursue legal commitment, involvement of family in the
commitment hearing is recommended. Given the adversarial nature of the legal commitment
process, therapeutic progress can be undermined if the family is not aligned with the
treatment team or opposes commitment. At the hearing, parents or the spouse of an adult
patient can supply collateral history to the judge about recent behavior that may be crucial to
the assessment of competence. The family member’s presence also helps convey the message
that both the family and the clinical team are committed to the patient’s recovery and need for
treatment. Civil commitment may be preferable to the appointment of a family member as the
legal guardian since it relieves the family from being the decision maker in compelling
treatment and frees the family to take on a more supportive role in assisting the patient to
follow the clinical team’s recommendations. In this sense commitment may paradoxically
alleviate adversarial tension between patient and family, allowing the formation of a more
collaborative recovery-oriented alliance. Family involvement is likely to remain important
not only during hospitalization and weight restoration but throughout the early stages of
relapse prevention.
Although ethical issues concerning compulsory treatment of anorexia nervosa have
engendered considerable discussion amongst clinicians and academicians (Draper, 2003;
Giordano, 2003; Hebert and Weingarten, 1991; Williams, Pieri, and Sims, 1998), much less
has been written regarding the more ubiquitous issue of treatment resistance. Since treatment
resistance is endemic to anorexia nervosa, ethical decision-making pervades the treatment of
this condition (MacDonald, 2002). Goldner (Goldner, M., Birmingham, and Smye, 1997;
Goldner, 1989) has outlined a series of useful recommendations aimed at preventing or
diminishing treatment resistance. These recommendations include amongst others:
identifying reasons for refusal, carefully explaining treatment recommendations, avoiding
battle and scare tactics and conceptualizing resistance as an evolutionary process.
A Rational Approach to Countering Treatment

Resistance. Patient Role Induction, Family
Involvement, Persuasion and Conversion
Successful treatment must win the cooperation of the patient over time in order to
achieve conversion from seeing dieting as the ideal to stigmatizing it as a negative behavior
(Guarda and Heinberg, 2003). For chronic patients who have been ill for years, recovery must
also address impairment in psychosocial function and assist patients in achieving mastery and
self-confidence in other areas of their life. Role induction, formation of a therapeutic alliance
and empathic persuasion are three important elements of effective treatment.
Role induction includes countering demoralization, instilling hope and covering
expectations for participation in treatment and for clinical progress. Explicit discussion of
target dates for the achievement of measurable treatment goals (e.g. change in frequency of
eating disorder behaviors or expected weight gain per week) and contingency plans should
these targets not be met (e.g. hospitalization or more intensive treatment), are best reviewed
at the outset of treatment. Frankness on behalf of the clinician can help earn a patient’s trust
by conveying commitment to the patients’ recovery and refusal to settle for a view of the
eating disorder as a chronic illness. Treatment should respect patient autonomy and clinicians
should always express empathy and concern, however a caring yet paternalistic stance or
“confrontation with a smile” (McHugh et al., 1998) may help engage patients.
Motivational interviewing strategies (Vitousek, Watson, and Wilson, 1998) are very
useful but may be insufficient to engage those patients with anorexia nervosa whose
judgment is severely impaired. In these cases, judicious and sensitive use of leverage may
help patients progress in treatment. Involving family from the outset is preferable. This can
be done by routinely requesting that patients bring a close family member to the initial
evaluation. Family participation should be presented as an expected and routine part of
treatment. In patients who have life-threatening anorexia there is an argument to be made that
this should be a requirement of treatment since the patient’s competence is at issue.
Interviewing the family member briefly can provide useful collateral information and
including family in a final review of treatment recommendations reinforces treatment goals
and expectations. Relatives may request guidance from clinicians regarding how to support
the patient or in deciding what leverage they might consider applying to help contain the
patient’s eating disordered behavior. Examples of leverage may include financial support for
college for a child who is refusing treatment, involvement of school officials, limiting access
to a gym or use of the car or a cell phone, as well as positive incentives for weight gain and
normalized eating behavior.
The threat of leverage may be sufficient to contain a patient’s behavior. However, if a
decision is taken to leverage treatment it should always be framed by a firm yet empathic
therapeutic stance with the explicit understanding that the plan will be re-evaluated in the
setting of progress towards therapeutic goals. Importantly, continued coercive pressure is not
justified in the absence of clinical progress and consultation should be sought from other
experts regarding treatment alternatives should this occur. Care is needed to assess
countertransference and to avoid the extremes of nihilistic passive care or of heroic yet futile
aggressive intervention. When treatment reaches an extended impasse it may be therapeutic
to discuss termination and referral to another provider if noncompliance and lack of progress
persist. For many patients who have established a therapeutic alliance with their treating
clinician the threat of termination can be a strong motivator for change.
Conclusion
The issue of competency to refuse treatment and coercive treatment of eating disorders
has been understudied and practical guidelines are scarce. Nonetheless, there is a reasonable
argument to be made for the use of coercion in an “honest, transparent and open manner”
(Carney et al., 2007) given that ambivalence towards treatment is “part and parcel” of
anorexia nervosa (Ramsay et al., 1999). Meanwhile, there is an urgent need for clinical
research examining competence, outcome of involuntary treatment and patient views of
treatment. Furthermore, development and empirical assessment of professionally-guided
family interventions aimed at engaging adult treatment resistant patients and preventing
relapse should be encouraged. Future research should also compare the long-term outcome of
patients who report feeling coerced into admission yet who convert to recognizing they
needed intensive treatment to those who fail to convert and to self-referred patients. Data on
the outcome of involuntary treatment of anorexia nervosa on general psychiatric or medical

units or following enteral or parenteral refeeding is altogether lacking with the exception of
anecdotal case reports (Lanceley and Travers, 1993; Geist et al., 1996). There is a need for
comparative studies examining these alternate treatment settings and refeeding interventions
since behavioral specialty units are often inaccessible due to geographic, insurance or other
financial limitations.
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Chapter XI
Cognitive Behavioral Therapy for

Anorexia Nervosa
Kathleen M. Pike and Marisa A. Yamano

Abstract
Cognitive behavioral therapy (CBT) represents one of the most influential theories
and therapies in the treatment of eating disorders. Over the course of the past twenty-five
years, several adaptations of CBT for bulimia nervosa (BN), anorexia nervosa (AN), and
binge eating disorder (BED) have been developed and evaluated. The empirical
foundation for CBT in the treatment of eating disorders is especially strong for BN. In
the case of AN, the emerging data base indicates that CBT has the potential to be an
effective psychotherapy, particularly for individuals with weight-restored AN. This
chapter provides an overview of the empirical research of CBT for AN, core theoretical
principles of CBT for AN, and a discussion of the essential features of CBT for AN in
clinical practice. Further investigations of CBT for AN are necessary to advance an
evidence-based practice in AN treatment.
Introduction
Cognitive behavioral therapy (CBT) is one of the most important and influential theories
of mental health and illness informing clinical practice today. Developed and elaborated by
A.T. Beck and colleagues (e.g., Beck, 1976; Beck, Rush, Shaw, and Emery, 1979; Hawton,
Salkovskis, Kirk, and Clark, 1989; Beck, Freeman, et al., 1990; Young, 1990; Hollon and
Beck, 1993; J.S. Beck 1995, 2005), numerous applications and adaptations of CBT exist to
address a wide range of disorders, including eating disorders. This chapter provides an
overview of the application of CBT to the treatment of Anorexia Nervosa (AN). It includes a
review of the empirical research, a discussion of core conceptual principles and essential
188 Kathleen M. Pike and Marisa A. Yamano
principles of clinical practice of CBT for AN (CBT-AN). It concludes with recommendations

for future directions.
Empirical Support for CBT for Anorexia Nervosa

(CBT-AN)
Within the eating disorders field, CBT for bulimia nervosa (BN) enjoys the most
extensive empirical evidence, with dozens of studies documenting its efficacy. Across a wide
range of treatment settings, and compared to a wide range of alternative psychotherapies and
medications, CBT shows consistent efficacy and is thus widely considered the treatment of
choice for BN (NICE, 2004; Annenberg, 2005). The empirical database for CBT for AN
(CBT-AN) is more limited but initial investigations suggest support for its use in outpatient
treatment, particularly for weight restored individuals.
The first study to provide empirical evidence for CBT-AN was a year-long, post-hospital
study evaluating CBT-AN for weight restored adults (Pike, Walsh, Vitousek, Wilson, and
Bauer, 2003). Results from this clinical trial showed that 77% of the CBT-AN group (N=18)
achieved an intermediate or better outcome. In terms of clinical pathology, as well as dropout
and relapse rates, the CBT-AN group fared significantly better than the comparison group
(N=15) that received supportive nutritional counseling. This study established a foothold in
the field of treatment for adult AN by providing the first empirical evidence of efficacy for
any psychological intervention in the treatment of weight restored AN. However, the sample
size was small and the question remained whether CBT-AN was more effective than other
psychotherapy interventions given that the comparison treatment in this study was supportive
nutritional counseling. Thus, Carter, McFarlane, Bewell and colleagues (2007) conducted a
one-year, non-randomized trial comparing CBT-AN to “Maintenance Treatment as Usual”
(MTAU) to assess whether CBT-AN is more efficacious than standard psychotherapy
interventions offered in the community for adults with weight-restored AN. In most cases,
MTAU consisted of individual psychotherapy with a therapist in the community. Because
these data are based on a non-randomized assignment of treatment condition they must be
viewed as preliminary; however, they offer further support for CBT-AN, suggesting that it is
more effective than MTAU. Specifically, 67.5% of the women in the CBT-AN treatment
condition (N=46) were able to keep their weight above a BMI of 17.5 m/kg2 without
developing bulimic symptoms compared to only 34.4% in the MTAU group (N=42).
In terms of acute treatment, a recent controlled clinical trial examined the efficacy of
CBT-AN for individuals with non-weight restored AN, and the data suggest that CBT-AN
may be as effective as non-specific supportive clinical management (NSCM) but not better
(McIntosh, Jordon, Carter, et al., 2005). In this study, CBT-AN was compared to
Interpersonal Psychotherapy (IPT) and NSCM for non-weight restored adults in a 20-session
outpatient treatment. The intent-to-treat analyses showed that IPT was the least effective
intervention and significantly less effective than NSCM. The efficacy of CBT-AN fell
between IPT and NSCM and was not significantly different from either (McIntosh, Jordon,
Carter, et al., 2005). The drop out rate and the degree of ongoing eating pathology in all
groups was high, suggesting that additional components of intervention and/or longer
Cognitive Behavioral Therapy for Anorexia Nervosa 189
duration of treatment are necessary. The findings from this study challenge us to consider the
different treatment needs of individuals with AN during the weight restoration phase of
treatment as compared to maintenance and follow-up treatment. Clearly replication studies
and studies with larger sample sizes are necessary to further advance an evidence-based
approach to treatment for AN.
Formulation of CBT for Eating Disorders

The application of CBT to eating disorders is well articulated (Fairburn, Marcus, and
Wilson; 1993; Garner, Vitousek and Pike, 1997; Marcus, 1997; Pike, Roberto, and Marcus,
2007). At its core, the CBT model of eating disorders conceptualizes these disorders as the
confluence of cognitive disturbances overvaluing weight, shape and appearance coupled with
behavioral disturbances in weight and dietary regulation. Individuals with low-self esteem are
vulnerable to the ubiquitous and pernicious messages regarding feminine beauty ideals and
the mythology that achieving such ideals will relieve feelings of low self-esteem and self-
loathing. As individuals internalize these beliefs, they develop a set of dysfunctional ideas
that overvalue eating, shape and weight. These cognitive beliefs translate into behavioral
strategies aimed at attaining beauty ideals that are unrealistic or achieved only by engaging in
extreme eating and weight control behaviors. In the case of BN, BED, and bulimic AN, the
extreme efforts to restrict intake backfire, resulting in loss of control and binge eating. In the
case of restrictive AN, severe emaciation sets in.
In addition to the attitudinal and behavioral problems directly linked to eating, weight
and shape, individuals with AN struggle with issues of motivation, affect regulation, extreme
perfectionism, and interpersonal problems, and CBT-AN focuses much care and attention on
these issues. Because at its core CBT is not content-specific (i.e., the fundamental principles
of CBT apply across a wide spectrum of disorders), the broad application of CBT described
in theoretical and clinical writings provide thoughtful, well-articulated discussions of how to
understand and approach these issues from a CBT perspective.
Five Core Conceptual Principles of CBT-AN

1. Self-worth is over-determined by body weight and shape for individuals with AN.
Across all the eating disorders, weight and shape play a disproportionate role in determining
self-worth. Clinical features in the diagnostic criteria for AN include attitudinal and
behavioral disturbances related to body weight, shape and appearance. For individuals with
AN, the excessive importance of body shape and weight reflects not only a beauty ideal but
also an extreme need to rigidly achieve control. If successful, individuals with AN experience
an enhanced sense of self-worth and esteem, albeit resulting in a wide range of other
significant symptoms and co-morbid clinical problems.
For many individuals with AN, the importance of weight and shape in determining self-
worth is so extreme that it typically appears irrational to loved ones and can even appear
almost psychotic. For example Sarah,* a 17 year old high school senior who struggled with
AN for five years, described ambitious academic and professional goals despite the fact that
her body mass index (BMI) was barely 15 m/kg2 and she suffered from primary amenorrhea.
In addition to these core symptoms, she was prone to depressive symptoms at this low weight
and was isolated socially. She was able to identify many reasons to gain weight, including
being able to pursue the university experience that she had always dreamed of; however, she
was not able to stay committed to weight gain during outpatient therapy and co-morbid
medical and psychological symptoms increased during her last year of high school.
Following high school graduation, she was readmitted to an inpatient eating disorders
program for the third time and was not able to enroll in college as planned. During this
hospitalization Sarah decided that she would gain and maintain a low-normal weight despite
her body weight and shape concerns so that she could pursue her education. As is typical for
many individuals with AN, Sarah continued to overvalue weight and shape and decided to
gain weight not because she wanted to but because she no longer wanted to miss out on the
many things that were increasingly difficult or impossible due to her AN.
2. The overvaluation and overcontrol of weight and shape characteristic of individuals
with AN reflects the desire to compensate for low self-esteem. According to the CBT model
of eating disorders, low self-esteem increases the vulnerability of individuals to pursue and
maintain beliefs that attaining thinness will increase self-esteem to compensate for
subjectively experienced deficits. A set of rigid rules that governs behaviors in pursuit of
thinness becomes the central organizing principle for individuals with AN (Pike, Loeb,
Vitousek, 1996). Ironically, empirical data indicate that self-esteem actually increases with
weight gain (Geller et al., 2000), but for individuals with AN, rigid control over weight and
shape and pursuit of extreme thinness prevails.
The issues of control and low self-esteem are often masked at first glance by the apparent
sense of esteem garnered by the eating disorder. However, the centrality of low self-esteem in
the etiology and maintenance of AN becomes readily apparent when individuals enter
treatments that include weight restoration and maintenance as a primary goal. Andrea, a 15
year old girl who had AN for two years, was brought to treatment by her parents upon the
recommendation of the school guidance counselor. She appeared to have positive
relationships with her family and friends and was popular at school. Andrea claimed that
everything was great and she did not appreciate the disruption to her routine and activities
caused by various medical and psychotherapy appointments associated with her AN.
Although Andrea reported feeling content with her life, and although many dimensions of
Andrea’s life actually appeared to be going well, it became evident that Andrea’s AN was
centrally connected to profound issues of low self-esteem and social anxiety. Andrea was
intensely concerned about what others thought of her and she struggled greatly with social
anxiety. School parties and social events were a great strain for her, and the only way that she
managed to function in such situations was to commit to organized participation such as
clean-up or set-up for an event. Andrea excelled at her school work but the awards and public
recognition never seemed to satisfy her anxiety and fears about not being accepted socially.
* All clinical material represents composite cases where details and names have been changed to respect patient
confidentiality.
As she engaged more fully in recovery, she described feeling unworthy of the recognition of
her academic success. She reported that school achievement came easily to her so the real
challenge was restoring her weight and maintaining it, something that she only had brief
periods of success with over the course of several years of treatment. One of the most
significant milestones in her recovery occurred when she opted to limit her studying for a
science test so that she could join some friends for an evening out. She discovered that her
performance was barely affected and she also discovered that her relationships with her
friends and family improved as she loosened her rigid and perfectionistic goals.
3. The overcontrol of weight and food intake characteristic of AN also reflects significant
interpersonal stress and deficits in affect regulation. In CBT-AN, significant focus is placed
on interpersonal issues and self-regulation, with particular emphasis on affect regulation
(Pike et al.,1996; Garner et al., 1997; Marcus, 1997). Empirical evidence suggests that
difficulties in interpersonal functioning and affect regulation are significant in the onset of
AN (Fairburn et al., 1999; Karwauth et al., 2001; Pike et al., 2007). It is also likely that such
problems are further exacerbated as the eating disorder endures. Once an individual develops
AN, all relationships and decisions are made with the preservation of the eating disorder in
mind. Behaviors such as dietary restriction, extreme exercise, binge eating and purging, the
use of laxatives or diuretics, and other compensatory efforts, over time become routine
coping strategies that may serve to create distance in relationships and make difficult
emotional states more tolerable. Although such strategies fail to resolve the underlying
interpersonal or emotional problems, they offer temporary relief for as long as the individuals
can sustain the effort. Thus it is with desperate persistence that individuals with AN redouble
their efforts. CBT-AN strives to identify the relationship between the behavioral patterns of
the eating disorder and their connection to interpersonal difficulties and affect regulation.
CBT-AN explores the ways in which the eating disordered behavior fails to provide deeper
resolution to these interpersonal and emotional issues and works with individuals to foster
healthier, more adaptive strategies of functioning.
Carly was a 22 year old woman with AN who reported an exacerbation of her symptoms
when she ran into difficulties with her roommates as university. Carly went to a large high
school and managed to get by emotionally and socially but reported that at high school
graduation when everyone else was overcome with emotion, she did not feel particularly
connected to any of her high school classmates and had no desire to stay in touch with
anyone when they all departed for university. When she arrived at university, she continued
to be emotionally distant despite efforts by her roommates whose overtures actually created
feelings of anxiety for Carly. She did not know how to manage the emotions she was feeling
and resorted to isolating herself emotionally and binge eating and purging when the social
and interpersonal problems became overwhelming. Carly described retreating from her
relationships with her roommates because she felt too anxious and uncomfortable if they got
too close emotionally, regardless of whether the emotions were positive or negative.
In therapy, Carly often described feeling bored, her affect was flat, and her connection
with her therapist was fragile. It was only with long-term CBT-AN treatment focused on
affect regulation that Carly was able to recognize the pattern of retreat that occured when her
feelings threatened to overwhelm her. Identifying the cognitive and behavioral patterns that
reinforced the social isolation and emotional avoidance were essential in beginning to change
her affect regulation and relatedness. With practice, Carly was able to the challenge cognitive
distortions and learn more adaptive behavioral strategies so that she could more effectively
regulate her affect and build more engaged relationships. As she did so, her eating disorder
symptoms and social relationships improved steadily.
4. AN is a multidetermined eating disorder and the complexity of etiology and
maintenance of the disorder needs to be recognized and addressed in treatment. AN is
multidetermined with genetic, biological, sociocultural, familial, and developmental factors
that render individuals vulnerable (Pike, Devlin, Loeb, 2003; Jacobi et al., 2004; Pike et al.,
2007). Due to the complex etiology of AN, effective therapy must acknowledge the range of
potential contributing factors and have the capacity to provide an integrated understanding. In
addition to recognizing AN as multi-determined, fundamental to all CBT approaches is the
importance of distinguishing factors that maintain eating pathology from the etiological
factors of the disorder. In general, CBT approaches begin with a therapeutic focus on the
dysfunctional attitudes and beliefs associated with maintenance patterns of the disorder and
progress to more distal factors in treatment (Fairburn, Marcus, Wilson, 1993; Pike, Devlin,
Loeb, 2003).
Given that the list of factors associated with increased risk for AN is long, no two
individuals report exactly the same etiological course. Elizabeth reported that she intended to
diet to lose 2 kilograms for a gymnastics competition but that the weight loss got “out of
control.” Prior to this weight loss “everything was fine.” Upon further exploration, Elizabeth
reported that she had been involved with a gymnastics team for many years and that she had
aspirations to compete in the junior Olympics. In the year preceding the onset of her eating
disorder, her parents arranged for her to train with a more competitive team that was coached
by former Olympians. Shortly after joining this more elite team, and upon the
recommendation of her coaches, Elizabeth tried to lose weight to help improve her
performance.
In contrast, Fiona reported a very complicated social and developmental history prior to
the onset of her AN. Her father died when she was eight years old. Prior to her father’s death,
she was very close to him, and they spent a lot of time camping together. Her mother fell into
a major depression and started drinking excessively after Fiona’s father died. Fiona tried
desperately to help lift her mother from depression but to no avail. When Fiona was 12 years
old, her mother married a man who moved into their home and set up a home office across
from Fiona’s bedroom. It was not long after his arrival that he began abusing Fiona sexually.
When Fiona told her mother, her mother did not believe Fiona and told her that if she
continued to make such accusations she would have to go live with her paternal grandparents.
Shortly thereafter, Fiona’s mother became pregnant and Fiona increasingly withdrew from
family life although her performance at school remained stable. With the arrival of the
newborn half-sibling, Fiona’s school performance declined and her weight plummeted.
Although the developmental factors associated with the course for Elizabeth’s and
Fiona’s eating disorders were quite different, from a CBT perspective, the unifying starting
point is determining what the cognitive, behavioral, and emotional factors are that maintain
the pattern of the extreme restriction associated with AN. Through careful inquiry, the goal is
to make explicit the ways in which certain thoughts and behaviors reinforce each other for the
purpose of regulating affect, and achieving control and enhanced self-esteem through AN.
Typically, CBT will begin with a focus on these maintenance factors and over time explore
the ways in which the maintenance and precipitating factors are related. Almost always there
are some continuities and some distinctions to be drawn between how and why the eating
disorder began compared to how and why it is maintained.
5. CBT recognizes the symptoms of AN not simply as symbolic representations of
underlying problems but also as essential problems in their own right that have significant
clinical implications requiring focused attention. It is a fundamental tenet of CBT-AN that
eating disorder symptoms have a direct impact on cognitive, emotional and behavioral
functioning and therefore CBT-AN begins treatment with a focus on resolution of these
attitudes and behaviors. Low weight, restrictive eating, and compensatory behaviors are
therapeutic priorities given that they directly affect the emotional, behavioral, and cognitive
functioning of the individual (Pike, Carter, Olmsted, 2004). Thus, CBT-AN begins with a
focus on overt and specific eating disorders symptoms with the goal of expanding breadth
and depth as necessary and appropriate to promote meaningful and lasting change.
When Michelle began treatment, she reported difficulty concentrating, restless sleep, and
frequent episodes of hypersensitivity and crying. She also described exercising excessively
and compulsively despite increasing pain in one of her knees. In addition to these immediate
symptoms she reported a significant history of trauma and loss from when she was a young
child and two siblings were killed in an automobile accident from which she was the sole
survivor. Although her trauma history had profound psychological significance and impact
on Michelle’s functioning, from a CBT perspective, the strategy is typically to begin with the
more proximal and immediate symptoms and then work back to the more distal factors. In
this case, CBT focused on weight gain and the cognitive, behavioral and emotional factors
maintaining the current pattern of excessive restriction and exercise with the explicit goal of
gaining weight and normalizing eating to reduce the cognitive, mood and physical symptoms
that Michelle found distressing. By focusing on these personally significant and immediately
tangible symptoms, Michelle was able to increase her motivation for recovery because as the
core symptoms of the eating disorder improved so did these other aspects. With time, as the
acute symptoms of her AN resolved and as the cognitive, mood, and physical health
symptoms improved, Michelle was in a much stronger state of mental and physical health to
address the psychological meaning and impact of the earlier trauma.
Ten Essential Principles of Clinical Practice for

CBT-AN
1. CBT-AN requires a sound therapeutic relationship between the client and therapist.
The importance of the therapeutic relationship is perhaps universal to all psychotherapy; but
in the practice of CBT-AN, therapists run the risk of focusing on the content of the CBT
interventions at the expense of the relationship, especially when first learning how to work
from a CBT-AN model. Failing to attend to the relationship will have significant potential
negative effects. Data from psychotherapy studies consistently document that the patient-
therapist alliance mediates treatment outcome (Garner, Rockert, Garner, Davis, Olmsted, and
Eagle, 1993; Orlinsky, Grawe, and Parks, 1994), as do the non-specific qualities such as
warmth, empathy, respect and openness (Truax and Mitchell, 1971; Thompson and Williams,
1987). Although the patient-therapist relationship does not have the same role that it has in
psychoanalytic psychotherapy, a good therapeutic relationship is nonetheless an essential
ingredient to successful CBT-AN.
In addition to these non-specific aspects of the relationship, when working from within a
CBT-AN model, therapists need to feel comfortable being relatively active during
psychotherapy sessions. Especially in the beginning of a course of CBT-AN, therapists play
an important role in providing direction and structure to the session itself. Throughout the
course of therapy, CBT-AN therapists strive to align with individuals and convey the
essential qualities of warmth, genuineness, and acceptance balanced with technical
competence in CBT and knowledge about the phenomenology of eating disorders (Garner
and Bemis,1982; Wilson and Pike, 2001). It is a delicate balance. CBT-AN therapists strive
to suspend judgment, and provide clients with accurate empathy, understanding, and
acceptance. Concomitantly, they challenge faulty thinking and beliefs of clients without
undermining the client’s perception of reality, and at a pace that is therapeutically
appropriate.
Of course, the therapeutic relationship also depends on client characteristics and the
ability of clients to engage in treatment. The success of CBT-AN depends largely on the
active participation and collaboration of the client in therapy (Wilson and Pike, 2001). In
general, individuals with BN and BED seek treatment on their own initiative and are
generally motivated to achieve recovery. In contrast, individuals with AN are often brought
to treatment by other family members, and their investment in building a collaborative
therapeutic relationship may be quite low initially. In addition to motivation, the client’s
capacity to engage in an honest and trusting relationship with a therapist will have a
significant impact on the course of treatment. Even for those individuals who seek treatment
on their own initiative, various interpersonal difficulties, and character pathology,
particularly borderline pathology, can greatly stress the therapeutic relationship (Pike, Loeb,
Vitousek; 1996). In these cases, explicit attention must be paid to the therapeutic relationship
and applications and extensions of CBT described by Marsha Linehan in her work on
Dialectical Behavioral Therapy (DBT) can be extremely helpful (Linehan, 1993).
Sound therapeutic relationships have many variations of personality, and a strong,
healthy therapeutic alliance will be characterized by strong positive connections that can
withstand the tension and conflict that may be part of therapy. The essential issue is that the
range of feelings experienced are acknowledged and understood by therapists. In general,
from a CBT perspective, if the therapeutic relationship is strong and working well, the
therapist and client will not necessarily spend a significant amount of time focused explicitly
on the relationship; however, it is essential that CBT therapists monitor the quality of the
relationship at all times. Betty was a 27 year old woman with a 10 year history of AN who
presented for outpatient CBT following inpatient treatment for acute care and weight
restoration. Betty was extremely friendly and compliant in sessions. She agreed with all the
therapist suggestions and always promised to pursue the behavioral challenges between
sessions. However, upon return to her subsequent session, she would invariably report that
she didn’t get a chance to do as they had planned and had difficulty getting the foods ready
for the challenges they had planned. In another case, Mary openly disagreed with therapist
recommendations and challenged the CBT model. Although at first glance it might have
appeared that the therapeutic relationship was stronger with Betty, in actual practice, the
therapist felt that the therapeutic relationship with Mary was stronger. Mary was able to
engage in more honest and open discussion about profoundly meaningful issues than Betty
who opted to superficially comply with recommendations but did not actually grapple with
the core issues that were associated with the maintenance of her eating disorder. The therapist
addressed these issues with Betty who began to assert herself, timidly at first, to be more
candid and engaged in the therapeutic relationship.
2. The therapeutic relationship in CBT emphasizes collaboration. The centrality of
collaboration in the recovery process is a hallmark feature of CBT-AN. This means that the
therapist and client share responsibility for determining the focus of therapy sessions and
setting the pace for recovery. In the first phase of CBT-AN, therapists may play a more active
role in setting the agenda for a session and focusing the therapy work both in the session and
between sessions. However, by the end of the course of treatment, the goal of CBT-AN is for
the client to learn the skills necessary for her to “become her own therapist.” Thus, even from
the start, it is important that the therapist and client collaboratively build the agenda for a
session and work together to modify aims for each session as needed. Similarly, CBT-AN
frequently entails experimenting with challenges and change outside the therapeutic hour.
The focus and pace of treatment will largely be driven by the client’s motivation, the degree
of distress associated with particular problems, and the practical consideration of how
amenable to change a particular problem is. All these factors are discussed explicitly with
clients as appropriate throughout the course of treatment.
In the example above, one of the fundamental errors that occurred in the work between
the therapist and Betty in the initial sessions was that the therapist was working unilaterally
on what she thought was important without Betty’s full engagement. The therapist took the
lead in formulating an understanding of the maintenance of Betty’s eating disorder, and the
therapist did nearly all the work in focusing sessions, setting agendas, and establishing
treatment goals. Once the therapist recognized this imbalance she attempted to rectify it by
increasing the focus on the relationship and the importance of collaboration in the therapeutic
work of CBT-AN. With time and with the therapist’s assistance in focusing on the quality of
the relationship, Betty gradually grew more comfortable asserting herself and participating
actively in building a more collaborative relationship.
3. CBT-AN begins with a focus on the present. One of the particular defining features of
CBT-AN is that therapy begins in the “here-and-now.” CBT-AN focuses less on how the
eating disorder developed and more on why it continues, especially in the early stages of
treatment. CBT-AN recognizes eating disorders as complex developmental disorders that
often have distant but meaningful origins, and from a CBT-AN perspective, it is important to
conduct a thorough developmental history when beginning treatment. However, whereas
other psychotherapies place greater emphasis on uncovering and exploring antecedent
developmental experiences to achieve recovery, CBT-AN begins with primary focus on
identifying maintenance factors that help account for a client’s unsuccessful struggle,
oftentimes for years, to resolve her eating disorder today.
There are at least two primary and related assumptions that account for this focus. First,
by the time an individual presents for treatment, the eating disorder has often taken on a life
of its own. Therefore, the CBT-AN assumption is that focusing on what maintains the eating
disorder will have greater potential for resolving the eating disordered pathology compared to
focusing on the developmental antecedents. Of course, certain factors (e.g., perfectionism or
depression) may contribute to both the etiology and the maintenance of an eating disorder but
the primary therapeutic focus will be on their relevance to the perpetuation of the eating
disturbance based on the rationale that achieving some resolution of these symptoms
relatively rapidly has the practical implication of relieving stress and increasing self-efficacy.
Thus, the second and related assumption is that this progress will help fuel motivation and
increase momentum for further change.
In the case of Jill, the focus on the present served to relieve Jill of worries about “placing
blame” for her eating disorder. Whereas in past therapies, she had spent much time exploring
developmental experiences associated with her eating pathology with little impact on her
current eating symptoms, CBT – AN gave her a new focus and freed her up to distinguish
between etiological factors and maintenance. This was especially useful since Jill was 12
years old when she developed her AN and 22 years old when she presented for CBT
treatment.
4. CBT-AN begins with a focus on the eating disorder symptoms. When individuals with
AN present for treatment, most often they also are struggling with a number of related
emotional, psychological and interpersonal issues. Depression and anxiety are common co-
morbid conditions, and interpersonal conflicts and complex developmental life experiences
are not unusual (Garner, Vitousek, Pike, 1997; Fairburn, Doll, Welch, 1999; Karwautz et al.,
2001; Pike et al., 2007). With such a complex presentation, it is essential that psychotherapy
focus treatment in an organized way to avoid the risk of superficially covering too many
topics but never reaching the depth necessary to achieve improvement or resolution on any of
the issues.
Because the eating disorder has frequently taken on a life of its own by the time someone
presents for treatment, many of the factors maintaining the eating disorder are entrenched and
automatic, both behaviorally and cognitively. The intensive focus on daily functioning takes
people off “auto-pilot” and catalyzes people to become more cognizant of the thoughts and
behaviors that are integral to perpetuating the self-destructive cycles of the eating disorder.
Once greater awareness is achieved, the goal of CBT-AN is to help individuals challenge
dysfunctional beliefs and thoughts so that they can experiment with changing behavior.
Conversely, CBT-AN also promotes behavioral experimentation and change with the
expectation that modifying behavior will also serve as a catalyst for modifying dysfunctional
thoughts. Many of the initial CBT interventions focus on behavioral assessment,
experimentation, and change because the assumption is that the difficulties encountered in
this realm will inform us of the cognitive and emotional factors at play.
Susan was a 20 year old woman with AN that began when she was approximately 14
years old. She had been in therapy for most of that time and described gaining some
understanding of her very complicated family history which tended to be the focus of
treatment in previous therapies. However, the core eating pathology remained largely
unchanged. In CBT-AN, the focus on the current eating pathology challenged Susan to make
explicit the assumptions she made regarding eating, weight and shape and their relationship
to her sense of self and self-esteem. By keeping the focus at the start of therapy closely tied to
the eating pathology, Susan was able to make significant strides in understanding what the
core thoughts and behaviors were that maintained her eating disorder for so many years. She
was also challenged early on to experiment behaviorally with changes in food choices, social
behaviors related to eating, and exercise activities. Although Susan found this very
challenging, she and her therapist developed a list of behavioral changes that would need to
occur for Susan to feel that she had recovered from her eating disorder. They delineated a list
that identified the many small steps that it would take to attain the larger goal. For example,
Susan acknowledged that in order to recover from her AN she needed to eat foods that had
fat. Having acknowledged this broad goal, she and her therapist went through her daily eating
routines and discussed each food that she is currently eating and explored ways to increase fat
intake (e.g., low-fat or regular fat yogurt instead of no-fat; low-fat or regular fat milk instead
of non-fat, etc.). Together they identified many specific and small steps that would increase
Susan’s fat intake and then they graded them from most approachable to most challenging.
Once the list was established, Susan and her therapist used it to gradually and steadily
support Susan’s experimentation with this aspect of her eating. This behavioral change is an
essential component of CBT, but equally essential is the therapeutic work of discussing,
exploring, and understanding the cognitive and emotional issues that arise in the course of the
behavioral experimentation. By discussing the thoughts and feelings that emerged, Susan and
her therapist were better able to understand the cognitive and emotional components that
were central to maintaining her AN and thus were able to explore the alternative cognitive
beliefs and strategies for regulating emotions in more adaptive ways.
5. CBT-AN attends to client motivation, continuously and explicitly exploring and
clarifying client goals to determine focus and pace of treatment. CBT is a collaborative
psychotherapy both in terms of overall process and in terms of goal setting. In order for
therapists and clients to share a truly collaborative relationship, therapy needs to address
openly and honestly each client’s goals and motivations. Although it might seem self-evident
that a client is motivated to resolve her eating disorder by virtue of the fact that she is in
treatment, this is often not the case. Most notably, many individuals with AN lack motivation
for recovery when they first present for treatment, with a large percentage of individuals with
AN participating in therapy only under duress. In these cases, the lack of motivation for
recovery is readily apparent.
Especially at the start of therapy, cultivating motivation for treatment is core to CBT-AN.
Data suggest that therapy outcome improves when motivation is carefully assessed and
interventions are matched to a person’s stage of motivation (Proschaska and DiClemente,
1983; Miller and Rollnick, 1991; Proschaska, DiClemente, and Norcross, 1992). Within the
field of eating disorders, specific strategies for assessing and enhancing motivation have been
articulated by Vitousek and colleagues (Vitousek, Watson, and Wilson, 1998). In the initial
stages of CBT-AN, a significant focus is placed on articulating the mixed feelings that
individuals are likely to have regarding recovery and addressing the issues that interfere with
the individual’s capacity to commit to recovery. CBT-AN focuses on uncovering a client’s
values and goals and exploring whether she can achieve them without the high costs
associated with the maintenance of the eating disorder. Exploring client goals and values also
entails addressing incompatible goals and fears regarding the meaning and implications of
resolving (losing) the eating disorder (Orimoto and Vitousek, 1992).
As mentioned above, Susan and her therapist worked in a very focused and strategic
manner to develop behavioral challenges to help break down the rigid rules governing
Susan’s restrictive eating and exercise. In the course of developing the behavioral challenges,
Susan’s ambivalence about recovery from her eating disorder became clearly evident as is
typical for virtually all individuals with AN. The goal of CBT-AN is to pursue as thoroughly
and explicitly as possible the client’s thoughts, behaviors, and feelings that work to maintain
the eating pathology. With Susan, it became clear that she was invested in an excessively thin
ideal and despite clear competences in other areas of her life, she struggled greatly with self-
doubt and low self-esteem. Thus, she and her therapist in each session reviewed benefits and
costs associated with maintaining her AN, and her therapist encouraged her to experiment
with challenging the beliefs that the only source of self-esteem for Susan lay in her AN. Over
time, Susan was able to recognize that her eating disorder provided short-term relief from
anxiety but that the cost was that she was also becoming less confident in other areas of her
life. For example, Susan recognized that her social interactions became strained because she
would change plans, isolate herself, or withdraw in situations with family and friends when
meals were involved. She recognized that at one level, she was frequently opting to “indulge”
her eating disorder at the cost of relationships that mattered to her. She became a less reliable
friend and sister, which was painful for her and served to motivate her to challenge the rules
that maintained her eating disorder. These understandings served as sources of motivation for
her as she slowly chipped away at the rigid rules of the eating disorder.
6. The cognitive and behavioral focus of CBT is intimately linked to the emotional world
of the client. One of the most problematic misunderstandings of CBT is the mistaken
assumption that CBT does not address feelings. Distilled down to its simplest principles,
CBT focuses on the link between cognitions, behaviors and feelings. It is unfortunate that its
name fails to acknowledge the emotional or affective component integral to the work of CBT;
however, the omission of affect in the title in no way reflects its omission in the conduct of
the therapy. Good CBT cannot be carried out without regard for the emotional and affective
dimensions of an individual’s experience.
The inclusion of cognitive and behavior in the name CBT reflects the premise that
cognitions and behaviors have a direct impact on one’s emotional world and that in order to
feel better we need to address the problematic thoughts and behaviors that perpetuate
psychological problems. If CBT fails to focus on material that is emotionally significant and
potent, it will fail to achieve significant success. However, from a CBT perspective,
emotional catharsis is not typically sufficient for achieving lasting change. Thus, in CBT,
emotional expression and experience are integral to setting the pace and the targets, and by
focusing on the cognitions and behaviors that are linked to the emotional issues, CBT strives
to improve psychological symptoms and emotional health in general.
Angela was typical of young women with AN in that her emotional world was very
private and protected. When she began CBT-AN, she was compliant with the cognitive and
behavioral work but demonstrated a notable poverty of emotional expressiveness. The
presence of alexithymia is not unusual in AN, and it is essential that CBT-AN therapists work
with clients to develop emotional language and expression of emotion that links cognitions,
behavior and feelings in a meaningful manner. With Angela, this work started at the most
basic level of generating vocabulary for describing a range of emotional experience and
working in session to simulate certain interpersonal situations that would evoke emotional
experiences in a safe environment so that they could be better understood and explored.
As Angela gained weight, she became more expressive emotionally, but it was several
months into therapy when she and her therapist knew that Angela had a break through.
Angela entered the session, and began by saying that she wanted to discuss a problem she
was having with her mom. Previously Angela had been overly compliant and emotionally
withdrawn from her relationship with her mom but the day prior to this session Angela
described taking the risk of talking to her mom about how angry she felt about the way her
mom intruded on her relationships with her friends. Angela reported that her mom was
defensive at first and that it was not until Angela fully expressed her anger that her mom truly
began to listen. The problem was that when Angela’s mom tried to apologize and connect to
Angela emotionally, Angela said that she felt “a freeze come over her” and that she felt “like
a statue.” She realized that she felt “panicked” by the thought of being close to her mom but
did not know why she had such strong feelings of this sort. This served as the starting point
for many subsequent sessions that focused on interpersonal issues, their role in setting the
context in which her eating disorder thrived, and the changes necessary to resolve her eating
disorder fully.
7. CBT-AN adheres to an explicit structure and duration. At the beginning of each CBT-
AN session, clients and therapists set an explicit agenda for that session. Setting the agenda is
a collaborative process: clients bring material from the course of the week that they would
like to address in the session and CBT therapists contribute to the agenda setting based on
information that clients provide and observations of where clients are in the course of
therapy. The CBT therapist’s recommendations will be guided by an understanding of the
CBT model for eating disorders and experience, with possible next steps that could help an
individual move forward in the resolution of the eating disorder.
In the early stages of therapy, CBT therapists need to introduce clients to a number of
concepts, psycho-educational components and cognitive and behavioral interventions. There
is a relatively logical and natural sequence to follow in building a coherent and shared
understanding of the principles and course of CBT with clients. In the manual-based
treatments, a clear, stepwise sequence provides a “standard course” although in actual
practice, the sequence is rarely so clear or straightforward. The essential element is that CBT
therapists collaboratively build a shared understanding of the assumptions, concepts, psycho-
educational components, and change strategies with clients, and that these components of
CBT be introduced in a meaningful and logical sequence for each client. Thus, especially in
the early stages of CBT, it is important that therapists contribute to setting the session agenda
in a way that both connects to the client’s clinical status and expands the client’s
understanding of CBT.
Once the client and therapist agree on the session agenda, the assumption is that they will
work on these issues through the course of the session. If the focus of the therapy sessions
veers significantly from the agreed-upon agenda, therapist and clients will decide whether to
revise the session agenda or redirect the session back to the agreed-upon focus. Of course,
important and interesting issues arise during the course of the session, and it is possible that
the client and therapist will collaboratively agree to revise the agenda for the session.
Alternatively, the issue may become the focus of another session. Either way, the essential
point is that the therapist and client collaboratively agree on the focus of the session and then
see it through. CBT sessions are structured in this way based on the rationale that failure to
focus intensively and intentionally on particular issues will perpetuate cycles of avoidance
and negative reinforcements that serve to maintain the psychological, behavioral and
emotional problems of the eating disorder.
Just as the beginning of the session has an explicit agenda-setting component, time is
allocated at the closure of sessions to summarize the issues covered in the session and to
discuss the work that clients can do between sessions. Therapists typically take responsibility
for the process of summarizing sessions in the early stages of treatment, but as with other
aspects of treatment, over the course of time clients increasingly assume responsibility for
this piece of the work.
In addition to following an explicit session structure, the duration of CBT-AN is often
time-limited, and the course of therapy is structured more explicitly than in open-ended
psychotherapy. CBT-AN treatment programs utilized in clinical research studies represent
time-limited treatments. In the CBT-AN manual by Pike, Carter, and Olmsted (2004),
treatment includes 50 sessions over the course of 1 year. The intervention conducted by
McIntosh and colleagues (McIntosh et al., 2005) included 20 sessions over a minimum of 20
weeks. Of course, these psychotherapy protocols are time-limited in part because it is
necessary to standardize the duration of care when conducting a controlled clinical trial.
However, this is not the only reason why the CBT protocols are time-limited. Increasingly,
psychotherapy research demonstrates that initial gains in treatment strongly predict treatment
outcome (Wilson and Pike, 2001). In addition, much has been written about the clinical
utility of limiting the course of therapy as a means of heightening focus and motivation.
Clearly, in general clinical practice, it is not necessary to set fixed time limits; however, it is
very useful in clinical practice to set assessment and review points to evaluate the efficacy of
treatment. By building these checkpoints into the therapy, both the therapist and client will
share a heightened awareness of the purpose of treatment and its efficacy.
8. CBT-AN relies on active engagement in treatment outside the therapy session. Many
CBT therapists use the term “homework” to describe the between-session work of therapy
but this term has certain negative connotations so may be best avoided. Homework is a term
most commonly associated with school, and as a function of their school experience, many
individuals think of homework as “extra,” “unnecessary,” and “irrelevant.” Moreover, not
only is homework superfluous, but it is often described with negative attributions such as
“useless,” “boring,” and “difficult.”
From a CBT perspective, the between-session work is as important as the work
accomplished in session, and a synergy occurs when both components of treatment are
maximized. Given the intensive focus on the here-and-now in CBT, much can be learned
from carefully monitoring and experimenting with assumptions and routines of daily living.
In the case of AN, the cognitive and behavioral disturbances and the pernicious cycles of the
eating disorders are an integral part of daily life. To the extent that individuals experiment
and extend the work of their CBT sessions to their daily living the potency of treatment is
greatly enhanced.
Just as the psychotherapy session of CBT-AN follows a particular structure, so too, the
work that individuals engage in between sessions reflects a logical and thoughtful sequence
that appropriately challenges individuals to grow and change. Work outside of therapy aims
to bring awareness of cognitive factors that maintain the eating disorder and challenge the
client to experiment with behavior change within a supportive, therapeutic environment.
Between-session work for AN may include self-monitoring of food intake as well as of social
and emotional experiences in the context of the eating disorder, addressing interpersonal
issues, and engaging in exercises that challenge dysfunctional cognitions and behaviors. In
order for clients to invest in this work and perceive it to be valuable, it must be integrally
connected to the focus of the psychotherapy sessions. One of the primary responsibilities of
the CBT therapist is to empower and support clients as they engage in the process of
experimentation and discovery between sessions.
During psychotherapy sessions Michelle appeared to be fully engage in therapy but she
failed to engage in the work between sessions. Although this is not unusual at the beginning
of CBT, it is essential that therapists address lack of engagement between sessions as it
occurs. When Michelle’s therapist explored Michelle’s lack of commitment to the behavioral
challenges and exercises, Michelle’s ambivalence regarding recovery became much more
evident. It also became evident to her therapist that the tasks reflected the therapist’s goals
but not Michelle’s goals. Thus, the focus of CBT shifted back to an exploration of treatment
goals and motivation, and Michelle and her therapist worked extensively on issues of trust
and collaboration in their relationship so that the therapy process had real integrity. Michelle
recognized that her engagement in therapy had been largely to placate her parents and keep
her therapist happy so she had been keeping her “real thoughts to herself.” The issues of
motivation became the central and explicit focus of therapy, and as Michelle shared the
intense conflicts she felt about recovery, she made slow and somewhat fitful but real progress
in recovery from her AN.
9. An important component of CBT-AN is psycho-education. With all the media attention
focused on eating disorders, one might expect that individuals with eating disorders would
have sound and accurate knowledge about their problems. In fact, many individuals with
eating disorders do know a lot about health and nutrition and eating pathology; however, they
typically have many gaps and distortions in their knowledge base as well. Some of the
primary psycho-educational topics addressed in the early stages of CBT for eating disorders
are: the naturalistic course of illness, nutritional education, psychological and physiological
effects of starvation, medical risks associated with eating disorders, and the ineffectiveness of
compensatory behaviors to achieve weight loss. Data from the hallmark study conducted by
Keys and colleagues at the University of Minnesota during World War II (Keys, Brozek,
Henschel, Mickelsen, and Taylor, 1950) are utilized to underscore many of the deleterious
consequences of starvation and distinguish the symptoms of starvation from the symptoms
unique to AN.
10. CBT-AN has certain “non-negotiable” principles. Underlying every relationship is a
social contract of assumptions, rules and agreements related to the interested parties. Most
often, this social contract is implicit and “understood.” In contrast, in the course of initiating
CBT-AN, it is important that certain critical principles be made explicit. In particular, it is
useful to establish either an oral agreement or preferably a written contract that explicitly
stipulates the few but critical situations that have the potential to change the focus and
confidentiality of treatment. The non-negotiable parameters address situations of imminent
danger to self and others consistent with the fundamental ethical obligations of therapists in
general. In the case of CBT-AN, it is useful to articulate explicitly the situations that will
abrogate patient confidentiality and cause the therapist to redirect the focus of treatment or
end treatment. In particular, the contract needs to articulate: 1) procedures for monitoring
weight and managing weight loss; 2) an explicit statement regarding when outpatient
treatment would be considered not viable due to weight loss or deterioration of clinical
condition; and 3) when involuntary inpatient care would be pursued.
Ann is a 26 year old woman who recovered from her eating disorder approximately nine
years ago. She recently contacted her CBT therapist to report that she had graduated from
college and was engaged to be married. One of the primary reasons that Ann wrote to her
therapist and requested to meet for a session was because nine years ago, when Ann ended
treatment with her therapist, she was enraged because her therapist recommended that Ann be
hospitalized due to failure to achieve significant weight restoration in outpatient treatment.
Ann’s parents hospitalized Ann against her will, and Ann’s hospitalization was characterized
by anger and opposition to recovery. After a prolonged hospitalization, Ann did gain weight
and when she was discharged from the hospital she refused to resume treatment with her
outpatient therapist. In her follow-up meeting with her therapist nine years later, Ann
expressed gratitude to her therapist for refusing to negotiate with her about more outpatient
therapy, and in retrospect Ann feels that her hospitalization was an essential part of her
ability to break with her eating disorder. At the time she was furious but with time she
expressed how important it was to her that she knew that she and her therapist had agreed on
certain limits because without such limits she wonders if she would still be alive today.
Conclusion
Clinical research on treatment for AN is limited due to the complexity and relatively low
prevalence of the disorder. Initial studies of CBT-AN suggest that it may be an effective
psychotherapy in the treatment of AN; however, the data are limited and much more research
is necessary. Three specific issues need to be addressed in future investigations.
First, the role of CBT-AN at different stages of treatment of AN needs further
exploration. Each stage of treatment requires the prioritization of different factors. Before
resolution of AN may be possible, issues of motivation need to be addressed. In the acute
phase of care, once treatment begins, weight gain needs to be prioritized. As treatment
progresses, the psychological and emotional issues need to be addressed and explored to
achieve recovery beyond weight gain. Ultimately, issues of maintenance of recovery are
critical given the typically high rates of relapse associated with AN. The particular role and
efficacy of CBT-AN at each of these stages of care should be explored further.
Another extremely important priority for CBT-AN is the question of whether it has a role
in treatment of adolescent AN. Studies of early onset, short duration AN indicate that family
therapy is an effective intervention at this stage of care (Locke and LeGrange, 2001).
However, it may be that CBT-AN also has a role to play in this stage of care, but it has not
yet been scientifically evaluated. In fact, the field lacks empirical evidence to support any
individual treatment approach for adolescents. This gap in our knowledge base has
significant implications because in clinical practice, individual therapy is still commonly

utilized, either as the primary intervention or as part of an overall treatment program. Such
treatment should be informed by an evidence base, and thus, it is appropriate to evaluate
whether CBT-AN may play a role in this stage of care.
Finally, given the complexity and severity of AN, it is clear that no one intervention will
be sufficient or even effective for all stages of care and for all symptoms of AN. Thus, future
investigations that explore combinations of treatment and sequencing of care will be of great
value. This will require significant research funding for multi-site trials that support
collaboration across clinical research centers so that future studies bring together necessary
professional expertise and sufficiently large clinical samples.
Anorexia nervosa is a profoundly debilitating and life-threatening disorder that has
challenged and largely stumped the professional community. Achieving major breakthroughs
in treatment will require persistent and collaborative efforts. This clinical research agenda is
essential so that more fully elaborated, evidence based approaches to AN treatment are
established to guide clinical care and thereby reduce the suffering and loss of life that is
associated with AN.
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Chapter XII
Cognitive Behavioral Therapy for

Bulimia Nervosa
Devra Lynn Braun

Weill Cornell Medical College
New York, New York,USA
Abstract
Cognitive behavioral therapy (CBT) has been widely endorsed as the initial
treatment of choice for bulimia nervosa (BN). According to the cognitive behavioral
model on which the treatment is based, BN develops and is perpetuated as a result of a
vicious cycle of interrelated cognitions and behaviors associated with low self-esteem,
extreme concerns about shape and weight, strict dieting, binge eating and self-induced
vomiting.
While CBT specifically tailored for the treatment of BN (CBT-BN) is generally
considered the single most effective current treatment, fewer than half of subjects
assigned to CBT-BN in most studies are abstinent from binge eating and purging by the
time treatment concludes. Recent advances in our understanding of brain processes and
of the pathogenesis of eating disorders have inspired the modification and expansion of
the original CBT-BN model. This chapter describes the evolution of a more
individualized, broadened CBT-BN treatment protocol and provides practical
information about how to implement it clinically.
Introduction
Cognitive Behavioral Therapy for Bulimia Nervosa: An Evidence-Based
Psychotherapy
Cognitive behavioral therapy (CBT) is widely recognized as the treatment of choice for
bulimia nervosa (BN) (Mitchell, Agras and Wonderlich, 2007; Wilson and Pike, 2001; NICE,
208 Devra Lynn Braun
2004; American Psychiatric Association Practice Guideline, 2006) based on nearly three
decades of outcomes research (Shapiro, Berkman, Brownley, Sedway, Lohr and Bulik, 2007).
CBT specifically tailored for the treatment of BN (Fairburn, 1981) was developed by
Fairburn shortly after BN was introduced in the medical literature in 1979 (Russell, 1979).
According to the model, the development and perpetuation of BN is due to a vicious
feedback cycle of interrelated cognitions and behaviors associated with low self-esteem,
extreme concerns about shape and weight, strict dieting, binge eating and self-induced
vomiting (illustrated in Figure 1, below).
From “Cognitive-behavioral therapy for binge eating and bulimia nervosa: a comprehensive treatment
manual” by Fairburn CG, Marcus MD, Wilson GT. (1993). In Binge Eating: Nature, assessment
and treatment. Fairburn CG, Wilson GT, Eds. New York: Guilford Press, p 369. Reprinted by
permission of CG Fairburn.
Fairburn’s update of the above model (Fairburn, 2008) acknowledges important additional or alternative
triggers including:
Negative affects and mood changes triggered by external events

Interpersonal conflict and loss are important triggering events
Maladaptive cognitive-affective chain reactions resulting from:
perfectionism and dichotomous thinking;
overvaluation of the importance of control of weight and diet
Poor emotion regulation skills
Figure 1. Fairburn’s Cognitive-Behavioral Model for the Development and Maintenance of Bulimia
Nervosa.
Cognitive Behavioral Therapy for Bulimia Nervosa 209
Fairburn and the group at Oxford University used this model as the basis for a
manualized, theory-driven CBT for adult outpatients diagnosed with BN (Fairburn, 1985).
This manual has been widely utilized by both researchers (Fairburn et al., 1991; Fairburn,
Norman, Welsh, O’Connor, Doll and Peveler, 1995) and clinicians (Fairburn, Marcus and
Wilson, 1993; Fairburn, 1985).
In 2004, manualized individual CBT-BN was the first non-pharmacological therapy to be
recommended by the U.K.’s National Institute for Clinical Excellence (NICE) as the initial
treatment of choice for a psychiatric disorder (Wilson, Grilo and Vitousek, 2007; NICE,
2004). NICE recommended offering 16 to 20 sessions of CBT-BN to most adults presenting
with BN (NICE, 2004).
In recent years, eating disorder treatment outcome studies have benefited from
progressive methodological advances. Studies have increased in size and statistical power
(NICE, 2004); and treatments, diagnostic instruments, and outcome measures have been
better standardized. In addition, longer-term follow-up data have accumulated (Agras, Walsh,
Fairburn, Wilson and Kraemer, 2000; Cooper and Steere, 1995; Fairburn et al., 1995; Shapiro
et al., 2007).
General Advantages of CBT-BN

• Effectiveness in treating core bulimia-related symptoms (Agras et al., 2000; Hay,
Bacaltchuk and Stefano, 2004; Shapiro et al., 2007);
• Beneficial influence on a spectrum of associated attitudes including concerns about
shape and weight, dietary restraint, self-directedness and self-esteem (Agras, et al.,
2000; Anderson, Joyce, Carter, McIntosh and Bulik, 2002; Shapiro et al., 2007;
Wilfley and Cohen, 1997);
• Rapid onset of action: significant changes are commonly noted within a few weeks
of beginning treatment (Wilson, Fairburn, Agras, Walsh, Kraemer, 2002; Wilson,
Vitousek and Loeb, 2000);
• Durable effect: improvement is generally maintained at 6 and 12 month follow-up
(Agras et al., 2000; Fairburn et al. 1995);
• Brief duration and cost-effectiveness: Manualized treatment usually involves 18 to
20 sessions over a four to five month period (Fairburn, et al., 1993; Fairburn, 2008);
• Comparable or superior efficacy to medication alone, with better long-term
maintenance of change (Jacobi, Dahme and Dittmann, 2002; Pyle, Mitchell, Eckert,
Hatsukami, Pomeroy and Zimmerman, 1990; Walsh, Hadigan, Devlin, Gladis and
Roose, 1991);
• Potential benefit to individuals who decline medication, cannot tolerate it, or for
whom medication is inadvisable; lower dropout rate for CBT than medication in
some studies (Agras et al., 1992);
• More effective in ameliorating core bulimic symptoms and more likely to result in
abstinence from binge eating than other psychosocial interventions, including
supportive-expressive therapy, behavior therapy, nutritional counseling, group
psychoeducation, and self-help (Fairburn,1986; Fairburn et al., 1991; NICE, 2004;

Shapiro et al., 2007);
• Wide availability of treatment manuals based on prototypes used with documented
effect in clinical trials (Fairburn, 1985; Fairburn, 2008; Fairburn, et al., 1995).
Only interpersonal therapy (IPT) rivaled CBT-BN in outcome at long-term follow-up

(Agras et al., 2000; Fairburn et al., 1995). IPT is an empirically supported focal
psychotherapy that was originally designed to treat major depression (Klerman, Weissman,
Rounsaville and Chevron, 1984). IPT addresses four major areas of interpersonal difficulty:
grief, interpersonal role disputes, role transitions and interpersonal deficits. IPT therapists
take an active, but non-directive role in teaching patients general and problem- specific
strategies for improving interpersonal functioning.
Patients improved more rapidly with CBT-BN than with IPT in two important
comparison studies (Agras et al., 2000; Fairburn et al., 1991). The CBT-BN group showed
greater improvement in bulimic symptoms than the IPT group after the first few weeks of
treatment. The IPT group continued to lag behind the CBT group throughout the formal
treatment period. However, when reassessed after longer-term follow-up of eight months to
five years, the IPT group had continued to improve, and there was no longer any significant
difference in treatment outcome between groups. At the conclusion of successful IPT,
patients often feel fully responsible for their improvement and have a sense of interpersonal
competence and empowerment, which perhaps accounts for their continued improvement
after formal treatment ends.
That IPT can be effective without explicitly focusing on food and weight underscores the
importance of interpersonal conflict in triggering the negative affective states that are
common precipitants for bulimic behaviors. During the past decade, the cognitive-behavioral
model has expanded to more explicitly acknowledge non-weight related factors such as
problems with relationship skills or affect regulation that can lead to a cascade of negative
thoughts, feelings, and actions that may end in a final common bulimic pathway (Figure 2).
The therapist is encouraged to adopt a broad cognitive-behavioral focus that allows for
examination of dysfunctional interpersonal and emotional processes that may contribute to
the bulimic cycle.
Limitations of Standard CBT-BN

• Only 30-50% of intent to treat samples typically achieves abstinence from binge
eating and purging, with substantial variation across studies (Agras et al., 2000;
Fairburn et al., 1995; Wilson et al., 2007).
• Reported measures of statistically significant improvement may not translate into
clinically significant change; for example, statistically significant change in bulimic
attitudes does not necessarily equate with improvement in bulimic behaviors
(Openshaw, Waller and Sperlinger, 2004).
• Dramatic reductions in average binge and purge frequencies following CBT-BN may
convey a deceptively rosy picture as patients who are bingeing and purging multiple
times daily at the outset of a study still remain quite symptomatic even if treatment
reduces binge and purge frequencies by 50%.
A perfectionist who has low self-esteem and overvalued beliefs about the Self
importance of weight and shape begins rigid, restrictive dieting. Social Esteem
reinforcement temporarily boosts self-esteem and sense of control.
DIETING:
Negative moods as well as physiological and psychological responses to

food restriction lead to preoccupation with food, and overwhelming urges
BINGEING: to binge. Inevitable violation of the diet’s restrictive rules leads the all-
or- nothing thinker to conclude that she has “blown everything” so she
“might as well” binge.
Purging can follow, commonly triggered by:
Sensations of physical fullness paired with cognitions equating feeling

full with “feeling fat” or having overeaten;
PURGING: Negative affect, including feelings of guilt and shame;
Distorted belief that purging erases the caloric effects of binge eating can
remove Such cognitions can disinhibit binge eating and encourage larger
binges, which facilitate self-induced vomiting.
Figure 2. Typical Cognitive-Behavioral Cycle Leading to Development and Maintenance of BN.
Incorporating CBT-BN into Eclectic Treatments

In practice, clinicians commonly combine elements of CBT with other psychological
treatments or with medications. There is inconclusive evidence as to whether combining or
sequencing CBT-BN and medications confers an advantage over using CBT-BN alone
(Shapiro et al., 2007), and combined treatments may have higher dropout rates than CBT-BN
alone (Goldbloom et al., 1997).
There is no empirical support for the common practice of combining elements of CBT
with elements of psychodynamic therapy, IPT or addiction-based approaches. Combining
conceptually or procedurally incompatible approaches (Fairburn, 2008; Wilson et al., 2007)

might confuse the patient, dilute the focus of CBT, and undermine its effectiveness (Wilson
et al., 2007). Despite these caveats it is common practice for clinicians to combine
approaches, especially CBT and IPT (Fairburn, 2008; Hendricks and Thompson, 2005).
A preset timeframe for brief treatment may have its advantages; it has been argued that
the brief treatment structure serves to optimally concentrate the minds of patient and
therapist, conveys concrete expectations for rapid improvement, and enables the patient to
take ownership of the improvements that often continue in the weeks and months following
cessation of treatment (Wilson et al., 2007).
What is Cognitive Behavioral Therapy?
CBT draws from the cognitive formulations of Aaron Beck, Albert Ellis, and others
(Beck, 1976; Beck, Rush, Shaw and Emery, 1979) and from the theories of Watson, Skinner,
and other behaviorists (Skinner, 1950). Behaviorist explanations of psychopathology are
based primarily on principles of learning and conditioning. For example a basic tenet of
behaviorism is the prediction that the probability that a behavior will recur in the future
generally increases if it has positive consequences and decreases if it is ignored or penalized .
Behaviorists look for direct or indirect “rewarding” or stress-reducing effects that may be
perpetuating dysfunctional behaviors; they also search for possible adaptive “functions” that
a behavior—even a behavior that is, on the whole, maladaptive or dysfunctional —may have
in a patient’s life. Such “functional analyses” of behavioral logs inform suggestions for
environmental change. The behaviorist model is based on the tenet that environmental change
can shape behavioral changes and that behavioral changes will lead to changed thoughts and
feelings.
If the behaviorist model aims to use behavioral change to foster cognitive and affective
change, then the cognitive model is in some ways the behaviorist model turned on its head.
The cognitive model focuses on cognitive determinants of moods and behavior and the ways
in which cognitive change can foster behavioral and mood change.
The cognitive approach to the treatment of BN is modeled on Aaron Beck’s cognitive
therapy for depression (Beck et al., 1976). Particularly helpful are the examples of ten
common cognitive distortions and interpretive errors synthesized by David Burns (1989).
These include all-or-nothing thinking, overgeneralization, jumping to conclusions,
magnifying negatives, and catastrophization. Cognitive therapy teaches patients to identify
interpretive errors in general and distorted thoughts and attitudes about shape, weight and
eating, in particular. Self-monitoring exercises teach patients to notice the circumstances and
cognitions that precede episodes of restrictive dieting, binge eating or purging. Therapists and
patients then examine the self-monitoring logs together, noting problematic thoughts that
may have preceded episodes of disordered eating.
Clinical Vignette
Directly before an episode of binge eating, Linda, a 19-year-old college student with BN,
wrote the following in her log: “I’m such a loser, I have no self control. I stayed on my 800-
calorie diet perfectly for two days … and then what? I had three Oreos. Here I go
again…Either I am doing great on my diet or I blow it all. I already feel fat.”
To help Linda to recognize her distorted cognitive processes, which include all or
nothing thinking, emotional reasoning (“I feel fat, so I must be fat”), catastrophization,
overgeneralization and labeling, the clinician working with Linda asks her to objectively
evaluate the statement that three cookies constitutes “blowing it all” as if she were providing
evidence in a court of law. She is asked to list arguments or evidence that supports or casts
doubt on the statement’s conclusion and then to arrive at a different reasoned conclusion or
alternative statement. Such restatements are sometimes called “reframes,” a metaphorical
reference to the way in which the same painting may look different in a different frame. A
template for the technique of cognitive challenge is provided in Table 1, below.
Table 1. [Template for a] Cognitive Challenge of a Problematic Thought
Record the problematic thought:
List arguments or evidence that support the List arguments or evidence that
statement: cast doubt on the conclusion:
• ____________________________ • ____________________________
• ____________________________ • ____________________________
• ____________________________ • ____________________________
REFRAME: Arrive at a reasoned conclusion or alternative statement
While “negative self-talk,” and distorted interpretations of reality such as Linda’s

(above) certainly may contribute to anxiety or negative mood states, few clinicians today
would endorse the simplistic perspective that distorted cognitions in themselves actually
cause depression and anxiety.
Our current understanding of brain circuitry, supported by neuroimaging evidence, has
made it apparent that emotional states and behavioral responses are strongly influenced by
forces beneath the level of our conscious awareness (Viamontes and Beitman, 2006).
Among the unconscious determinants of behavior and mood are sensory stimuli that are
registered and responded to by the brain without ever reaching the level of our conscious
awareness, and knowledge and associations held in unconscious pathways such as our
implicit memory system.
Since behaviors and emotional responses may be inaccessible to cognitive notice or
modulation, there are inherent limitations to cognitive therapy. Likewise, general principles
of operant conditioning and behaviorism have limitations in their ability to explain complex
behaviors such as binge eating and purging, which are likely to have genetic and evolutionary
determinants. General laboratory principles of behaviorism do not account for the fact that
humans can develop certain behavior patterns more readily than others. Evolutionary priming
or preparedness makes particular behavioral habits relatively easy to learn and hard to
extinguish (for example, overeating or bingeing on foods high in fat and sugar). Finally, our
individual genetic makeup as it is expressed as a result of our interaction with our particular
environment determines many characteristics that may contribute to the development of BN -
for example, a tendency toward weight gain or particular personality dimensions.
Integrated cognitive-behavioral models provide a framework for attempting to assess and
modulate psychopathological behaviors that result from the dynamic interaction of genes,
environment, and stress-inducing maladaptive patterns of thought and behavior.
CBT Tailored for the Treatment of BN
CBT-BN targets the specific maladaptive cognitive-behavioral patterns that

characteristically contribute to the development and maintenance of BN. CBT-BN also uses
general CBT techniques to defuse nonspecific “negative self-talk” and other dysfunctional
cognitive-behavioral habits that can trigger negative moods and bulimic behaviors.
The BN-specific cognitive behavioral vicious cycle is set in motion in the context of
intersecting environmental stress and genetic vulnerability. Among the most vulnerable to
developing BN are individuals with low self-esteem who are subject to sociocultural
pressures to be thin. Such individuals may develop a belief in the importance of shape and
weight as a principal determinant of their self-worth. As a result, they may come to equate
dieting and weight loss with control and enhanced self-worth. Under certain circumstances,
especially if they have a tendency toward dichotomous thinking and perfectionism, and are
subject to other stressors, some of these vulnerable individuals may make radical attempts to
bolster their self-esteem by implementing severely restrictive, inflexible diets in an attempt to
rapidly lose weight. (Figure 2)
Restrictive diets and rigid dietary rules can cause strong feelings of physical and
emotional deprivation, which may trigger binge eating. Purging may begin as an attempt to
take charge of the out-of-control situation. The myth that purging can effectively prevent the
absorption of calories may have the result of disinhibiting binge eating by uncoupling it from
the deterrent fear of weight gain. Purging may in fact lead to larger binges, because it is
easier to self-induce vomiting after a large binge than a small overindulgence.
In the years since the development of the cognitive-behavioral model for BN, emerging
data have both supported the basic tenets of the model and suggested the need for expansion
and modification. Recent studies in neuroscience and neuroimaging have provided support
for the observation that cognitions are distorted and biased toward the negative in patients
with BN (Legenbauer, Vocks and Ruddel, 2008) as well as in patients with depression and
other psychiatric diagnoses. Neuroimaging studies are beginning to demonstrate that
successful treatment with CBT results in observable changes and even apparent
normalization of pre-treatment abnormalities in neural circuitry that have been observed in
patients with depression and anxiety disorders (Baxter et al., 1992; Goldapple et al., 2004;
Linden, 2006).
The CBT-BN assumption that dieting is a key precipitant for the onset of BN in
susceptible individuals has been generally supported by empirical data (Brewerton, Dansky,
Kilpatrick, and O’Neil, 2000). However, it has become apparent that subsets of individuals
develop BN by purging and then beginning to binge eat, without having previously engaged
in strict dieting (Byrne and McLean, 2002). This is one example of a variant or alternate
pathway to the development and maintenance of BN that was not part of the original model.
Several researchers have experimented with broadening and individualizing basic CBT-
BN, guided by functional analyses and other methods of identifying thoughts, feelings or
behaviors that may play a role in the perpetuation of the eating disorder (Fairburn, Cooper
and Shafran, 2003; Fairburn, 2008; Ghaderi, 2005). The Oxford group and others have
suggested that CBT should be individualized transdiagnostically -- not on the basis of
categorical diagnostic categories, but on the basis of symptom clusters and pathological
cognitive-behavioral patterns that might be addressed in a modular fashion in conjunction
with standard CBT. Examples of individualized areas which might be targeted as potentially
contributing to the maintenance of the disorder include “clinical” perfectionism and
dichotomous thinking, interpersonal difficulties, core low self-esteem, problems with affect
regulation and mood intolerance, and obsessional focus on the control of shape and weight.
Whether the enhanced, more individualized CBT-BN will have greater efficacy than
standardized CBT-BN remains unclear (Ghaderi, 2006).
CBT-BN: 20 Sessions, “from Soup to Nuts”

The following section outlines the structure and content of Fairburn’s CBT-BN (Fairburn
et al, 1993), describes some of the features of the broader approach, or “Enhanced” CBT
(Fairburn, 2008), and includes clinical vignettes. (As the majority of individuals with BN are
female, they are referred to in the female gender for the sake of stylistic simplicity).
Initial Evaluation
Standardized CBT-BN is generally conducted in 16 - 20 sessions over the course of 4 or

5 months. A detailed initial assessment should precede the sessions. The most important
purpose of this assessment is to begin establishing a working alliance with the patient and to
engage her in treatment.
It is recommended that approximately 90 minutes be allotted for the initial evaluation.
A. Topics Should Include:
• Hopes, expectations and fears about treatment;

• Detailed information about current eating patterns;
• Bulimic behaviors, including binge eating, restricting, purging exercising or other
compensatory behaviors;
• Attitude about weight and shape
•
• Feelings about the bulimic behaviors and their ramifications: What aspect most distresses
the patient, her friends and her family? What positive and negative role or “function”
does the bulimia serve in her life? What might motivate her to change or to resist
change?
• Development and evolution of the disorder, and weight history
• Current life circumstances
B. Additional Information to be Obtained

(Screening questionnaires may be used to gain supplemental information if desired):
1) Current and past psychiatric, medical and substance abuse problems;

2) History of psychological or pharmacological treatment
3) Brief social and developmental summary;
4) Family history.
A workbook or text dedicated to CBT for eating disorders (such as those listed at the end
of this chapter before the references) can prove helpful for both clinician and patient. It can
help the clinician structure the assessment and treatment. Such books usually provide
templates for patient self-monitoring records and psychoeducation handouts that can be
distributed to patients in order to reinforce the topics that are covered in session.
The Three Phases Of CBT-BN: Objectives

Phase I: Objectives At A Glance
CBT–BN can be divided into three phases. During Phase I of treatment, the main
emphases are on establishing a treatment alliance, orienting the patient to treatment, and
educating the patient about the cognitive-behavioral mechanisms that maintain eating
disorder behaviors. An additional important objective is to normalize and structure eating
patterns. The first four to eight sessions may be held at a frequency of once or twice weekly.
Principal Objectivesfor the First Few Sessions:
Introduction to Treatment
• Establish a working alliance with the patient

• Establish treatment framework and expectations
• Outline timeframe, structure and goals of the different phases of treatment
• Describe structure and content of individual sessions
• Introduce weekly weighing
• Explain importance and rationale of self-monitoring of food-related behavior and
associated thoughts, feelings and environmental circumstances
Initial Behavior Modification
• Implement self-monitoring
• Implement weekly weighing
• Institute a regular but flexible daily pattern of three discrete meals and one or two
planned snacks
Presenting the Basic Cognitive

Behavioral Model For BN
Using Figure 1 and Figure 2, formulate an individualized cognitive behavioral model of
the forces maintaining the individual patient’s eating disorder pathology.
• Review general principles such as the bi-directional influence between behaviors and
thoughts, feelings and beliefs.
• Explain the rationale for targeting both cognitive and behavioral change.
• Review the bi-directional relationship between binge eating and dieting: Binge
eating motivates patients to diet; dieting also leads to binge eating.
• eview the bi-directional relationship between binge eating and purging: Binge
eatingleads to purging, but purging promotes bingeing and sets the stage for larger
binges.
Additional Objectives of Phase I
• Assess eating disorder patterns

• Discuss treatment expectations and past treatment experiences
• Document specific details about the patient’s binge eating and purging and the
perceived function that they serve (e.g. weight management, self-soothing)
• Harness the expectation effect: Provide information about the effectiveness of
treatment
• Assess patient’s motivation to change and enhance motivation using
psychoeducation;
• Educate patient about health consequences of bulimic behaviors:
• Short and long-term physical and psychological consequences of restrictive dieting,
binge eating, self-induced vomiting, laxative abuse, and compulsive exercise
• Negative psychological and metabolic consequences of starvation, including anxiety,
preoccupation with food, risk of bingeing
Ineffectiveness of purging for weight control
• Assess patient’s resistance to change
Identify, validate and address potential obstacles to treatment, including fear of failure,
fear of change, and fear of giving up the behaviors
Phase 2 Objectives:
In the weekly meetings during the second phase of treatment, further emphasis is placed
on identifying binge triggers, learning cognitive restructuring techniques and establishing
healthy eating patterns. Self-monitoring tasks and cognitive strategies are used to analyze the
thoughts, beliefs and values that trigger and maintain the bulimic behaviors. Patients work on
cognitive restructuring and modifying the environmental factors that contribute to the
perpetuation of the disorder.
Phase 3 Objectives:
During phase three, the focus is on maintenance of change and planning for relapse
prevention. The last few sessions are often conducted at bi-weekly intervals.
Self-Monitoring: A Keystone of Treatment
A keystone of CBT treatment is the self-monitoring of eating behavior. Patients are asked
to record the time and setting of all food intake and associated thoughts and feelings. Since
self-monitoring can be tedious and time-consuming, the therapist must set up conditions
during the first session and reinforce them in later sessions so that the patient will be likely to
follow through with this treatment requirement. Some suggestions for how to do this follow:
1) Explain the importance of self-monitoring to allow the detailed focus on thoughts

and behaviors outside of the session.
2) Educate the patient about the widespread endorsement of self-monitoring as central
to the treatment of BN and the fact that self-monitoring alone may help to reduce
symptoms (Agras, Schneider, Arnow, Raeburn and Telch, 1989).
3) Outline the requirements for self-monitoring, and focus early in each session on the
logs, praising the patient for completing them. If the logs are incomplete, devote
some effort to understanding why they have not been completed, but praise the
patient for any acts approximating working on the logs (e.g. thinking about filling
them out, etc.).
If any episode is perceived as a binge, the patient is asked to record the emotional,
physiological and environmental circumstances that preceded it. After recording these
incidents for a week or so, patterns usually emerge quite clearly. For example, some people
typically binge when they are bored, others when they feel lonely; still others binge on
vacations, or after they drink or use drugs.
In many instances, the patient’s self-monitoring records allow the clinician to present
hypotheses about the factors that may trigger bulimic behaviors. For example, it may become
apparent that a patient not only typically binges at night, but that she binges on nights when
more than six hours have elapsed since her last meal and she is exposed to a sensory
temptation such as a buffet or a nearby bowl of candy.
In CBT-BN, each session has an agenda, and the clinician manages the pace of the
session to adhere to the agenda. To preempt the possibility that the patient might feel that she
is being “pushed around” or might become passive and allow the therapist to take over, the
therapist must establish a therapeutic stance that has been referred to as “collaborative
empiricism.” The therapist and patient must collaborate as an investigative team intent on
taking note of the cognitive and behavioral patterns associated with the bulimic behaviors,
and developing and testing hypotheses about these patterns with the aim of instituting
alternative ways of thinking and behaving.
Clinical Vignettes Modeling the

Essential Elements of CBT-BN
In the following section, essential elements of CBT-BN are modeled in several clinical
vignettes. Table 2 on pages 221-226 describes Pamela, a 33-year old accountant.
Clinical Vignette: Mark, a 25-Year Old Professional Ballet Dancer
Another example of how to fit a patient’s story into the cognitive behavioral model
follows: Mark, a 25-year-old dancer, has a genetic predisposition for weight gain. In a typical
Western social environment, there would not be great social pressure for Mark, as a male, to
attain a weight that was more ideal than average. However, in certain male
microenvironments such as ballet, wrestling, acting, modeling or gymnastics, there is an
extreme emphasis on thinness and ideal shape. In keeping with a stress-diathesis model for
the pathogenesis of psychiatric disorders, the cognitive behavioral model reflects the
importance of the interaction between genes and environment in the pathogenesis of eating
disorders.
Mark is at risk for developing an eating disorder because of his genetic predisposition to
deviate from the exacting weight expectations of his social group, combined with his low
self-esteem and dependence upon the praise of others to sustain a sense of self-worth (which
also may be genetically primed) (Fairburn et al., 1997).
Mark is lonely after breaking up with his girlfriend and has gained a few pounds. After a
ballet rehearsal that did not go well he has been ruminating obsessively about how fat he
looks compared with the other dancers. He goes on a strict 900-calorie diet that drastically
restricts carbohydrates.
He sticks to the diet scrupulously, loses five pounds, and is praised by his instructor.
After the next performance, he has a few drinks at the troupe party, and can’t resist a piece of
chocolate cake. Feeling depressed and angry with himself, he thinks about how he is a real
“loser” who is unable to stick to a diet when everyone else can. He goes back on the low
carbohydrates diet. Over time, the effects of physiological and psychological deprivation
build up. After dancing, he feels irritable and exhausted due to the lack of carbohydrates and
frequently violates the strict diet, leading him to have the repeated experience of feeling like
a failure.
Episodes of simply overeating or violating the diet’s rules alternate with episodes of
binge eating, eroding his already low self-esteem and sense of control. He adopts even more
rigid and restrictive rules, believing that without them he would be completely out of control
and would be binge eating all of the time. As this cycle progresses and he feels more and
more out of control and fearful of weight gain, he begins “compensatory” vomiting and
excessive exercising. The erroneous belief that vomiting removes most calories ingested
during a binge erodes his constraints against both binge eating and purging. His binges
become larger, as that makes it easier for him to self-induce vomiting. His body and brain’s
system of appetite regulation and satiety, which relies on predictable absorption of nutrients
after food ingestion, becomes increasingly dysregulated.
Mark’s therapist explains to him the way in which purging and restricting fuel the fires of
binge eating. The therapist helps Mark to challenge the assumption that a very low
carbohydrate diet is realistic for a dancer and that other people could adhere to it. He
encourages Mark to consider the possibility that his repeated experiences of failure may be a
result of having set such unrealistic standards.
Standard supportive psychotherapy might explore the origins of his low self-esteem and
perfectionism at this point. The CBT-BN therapist however, stays focused on the current
dysfunctional eating. In doing so, the therapist is able to address the way in which bulimic
behaviors are triggered by the negative affective states that indirectly result from rigid
perfectionism, dichotomous thinking, and self-deprecating cognitions.
Mark agrees to institute a regimen of three meals and two planned snacks, each one
containing a balance of carbohydrates (with an emphasis on complex carbohydrates), protein,
and fats. After two weeks of self-monitoring and the balanced food regimen, Mark is relieved
to find that he has ceased binge eating and feels less irritable and more energetic.
CBT-BN helps patients such as the ones described above appreciate that their problem is
not solely binge eating, but a cycle in which dieting, purging and dysfunctional attitudes
about weight and shape all interact to perpetuate the binge eating and the entire eating
disorder. Once patients understand and accept this concept, they may be willing to
experiment with behavioral changes such as instituting a structured pattern of meals and
snacks.
In addition, with the modified and broader model of more individualized CBT-BN,
clinicians can use the powerful tools of CBT to address distorted non-food-related cognitions
that may underlie the negative affective states that commonly trigger dysfunctional eating.
The tools and exercises learned in CBT can help patients to recognize the positive results of
behavioral changes in interpersonal domains as well as in eating behavior, which can further
motivate them to experiment with alternative patterns of thought and behavior.
Table 2. Presenting Essential Elements of CBT-BN
Session 1:
Therapist Vignette and commentary
Objectives
Establish rapport and a The strength of the therapeutic alliance has consistently been correlated with treatment outcome in various types of
therapeutic alliance psychotherapy, including CBT-BN (Loeb et al., 2005). The strength of the alliance has been related to expectation effects,
attunement, and the therapist’s communication of a coherent treatment framework to the patient.
Establish a stance To establish a positive working relationship, it is helpful for the therapist to convey a sense of confidence and positive
of collaborative expectation but to avoid any stance that might be interpreted as controlling or patronizing. Individuals with eating disorders
investigation are often particularly sensitive to control issues. Parents and competitive peers may have scrutinized them and used coercive
force to try to get them to eat differently, to gain weight, or to stop purging. Patients may be in the habit of lying and hiding
bulimic behaviors in order to avoid scrutiny. Therefore, it is vital that the therapist establish a collaborative stance and a tone
of investigative curiosity as opposed to one of accusation or argument. The therapist must convey to the patient the sense
that, for example, a question such as, “Why did you delay dinner until 8 pm?” is meant to communicate neutral curiosity and
interest in the reasoning that led to the delay, not an accusation about, “Why did you do something so stupid as to delay
dinner?”
Validate the During the first session, the therapist explores the patient’s motivation to engage in treatment as well as her concerns about
patient’s concerns, treatment. The therapist validates the patient by acknowledging that the patient has these trepidations and concerns, without
using language that trying to “talk her out of” them at this point.
is as neutral as
possible
Table 2. Presenting Essential Elements of CBT-BN
Session 1:
Objectives
Pamela (P): “I came here because I am fed up with this disgusting out-of-control eating. But I’m worried that if I stop
purging I will gain weight.”
Therapist (T): “I appreciate your letting me know that you are concerned about what might happen to your weight when you
stop bingeing and purging. When I explain our treatment model today, I will specifically address those concerns.”
Avoid reinforcing T is already applying cognitive-behavioral principles in addressing P’s concern. Behavior modification is based upon the
the patient’s premise that behaviors that are rewarded or reinforced will occur more often, and behaviors that are punished or ignored will
negative cognitions occur less frequently. Rewards come in many forms -- including positive thoughts and feelings and positive environmental or
social consequences—such as getting attention from others. Similarly, punishment can involve internal or external
consequences, including negative emotions and being ignored by others.
Communicate positive A premise of cognitive therapy is that negative cognitions play an important role in the chain of events precipitating
expectations about dysfunctional behaviors. In the dialog above, T provides immediate and selective reinforcement of P’s adaptive cognitions
treatment outcome and avoids giving attention (even negative attention) to maladaptive cognitions. T does not ignore or trivialize P’s fear of
weight gain; however, T avoids reinforcing her “worry thoughts” by reiterating them verbatim. Instead, T reframes P’s
Communicate the worries that “I will gain weight” in more neutral language as concern about “what may happen to your weight.” In addition,
importance of fact- T communicates positive expectations about the outcome of the treatment by rephrasing P’s speculation about “if I stop
finding in purging” to a projection about “when you stop bingeing and purging.”
developing a joint
formulation
Table 2. Continued
Session 1:
Objectives
Find out which T: “Since your main concern is ‘out-of-control binge eating’, why don’t we start with your telling me about your last out-of-
bulimic behaviors control binge. I would like you to describe, as if you were an unbiased observer or news reporter, what was going on
most concern the internally and what was going on around you before, during, and after the binge. Then we can use a cognitive behavioral
patient and apply model to figure out what forces are driving you to keep binge eating even though you have been trying so hard to stop.”
the cognitive
behavioral model to P: “I was actually really good all day Monday… I had lost weight two years ago on this lemon cleansing diet, and I have
formulate (together been trying to get back on it again. On Sunday night, I binged and was disgusted with myself. I swore that first thing Monday
with the patient) an morning I would go back to the lemon cleansing diet.”
explanation of the
maintenance of those “On Monday morning, I wasn’t even hungry. I had the lemon drink for lunch and resisted everything else all day, even
behaviors. though I could see my favorite kind of chocolate in my office-mate’s candy jar.”
“At the last minute, though, my boss asked me to stay late. I did not have more of the special lemon drink with me, so I
decided that I should not eat anything at all until I got home. I was perfect until around 8 pm. I don’t know what came over
me then. I grabbed a handful of chocolate and then was really angry with myself for blowing the diet. I had a few more
handfuls of chocolate and then was embarrassed that my co-worker would know what a pig I am.”
Explain to the patient “I made up my mind that I would go back on a strict lemon cleanse regime the first thing in the morning. I decided that I had
the cognitive behavioral to buy another package of chocolates to put in my co-worker’s jar before she got to work, but I was angry at having to buy
model for purging and them. I was also angry that I’d blown the diet when I had been so perfect up until then. I had the thought that it might be a
dieting as driving forces long time before I could eat chocolate again once I got back on board with the diet. So I decided that I might as well finish
that perpetuate binge the chocolate in front of me. I ate everything left in the jar, even though I was stuffed. When I got home I felt so fat and my
eating stomach was so huge that I used a whole package of laxatives.”
Table 2. Continued
Session 1:
Therapist Objectives Vignette and commentary
T now has an opportunity to review with the patient the cognitive behavioral model of the maintenance of bulimia nervosa
(Figure 1) in terms of the patient’s particular issues. While patients commonly consider binge eating to be the problem and
vomiting and strict dieting (“being good” or “perfect”, in P’s words) to be the solution or attempted solution (even though it
may be a dysfunctional one), T explains that laxatives have very little effect on the absorption of the calories taken in during
Relate patient’s dieting, a binge; they mainly affect fluid balance, and that dieting not only does not counteract binge eating but actually perpetuates
bingeing and purging it.
patterns to the
conceptual framework of T gives P a factual handout about the psychological and physiological effects of severe food restriction. It includes a
the treatment model description of the famous Minnesota study of semi-starvation, conducted during World War II (Keys et al., 1950). During
this study, male volunteers were put on a very low calorie diet for six months; by the end of this period, they had lost
approximately 25% of their original body weights. Although the men had no previous history of eating disorders, while on
the diet they became preoccupied with thoughts about food and eating, and many became irritable, apathetic and depressed.
During the refeeding phase of the experiment, many of these normal volunteers were overwhelmed by urges to binge eat.
For months after the restriction ended, many had difficulty stopping themselves once they started eating, even after they felt
very full.
Discuss the T explains to P that an extremely low calorie diet such as the lemon cleanse is interpreted by the body as starvation. The
physiological, body’s response can include a lowering of metabolism and urges to binge eat as well as irritability, obsession with food, and
cognitive, emotional other psychological responses noted in the Minnesota experiment.
and environmental
triggers that may be
involved in
perpetuating P’s BN
Table 2. Continued
Session 1:
Objectives
T points out to P that her episode of binge eating on Monday was preceded by a period of many hours during which P had
eaten very little. T notes that since P has stated during the intake assessment that she always skips breakfast, she is habitually
going for 14-hour periods between nighttime eating and lunch. T discusses how P’s dieting behavior and long periods without
eating are indistinguishable to her body from a famine or starvation. The long periods without food can be reframed to be
viewed as likely precipitants or “set-ups” for a binge eating episode. In addition, she would have been less vulnerable to
having a binge had she been more flexible with her dietary rules, and gotten a healthy meal or snack instead of attempting to
fast.
Formulate an T then returns to P’s concern that she will gain weight during treatment. T explains that the initial focus of treatment is on
individualized cognitive gaining control of the chaotic eating behaviors, not on weight change. T will explain that most patients do not gain weight,
behavioral model for the and in fact may lose weight because they are reducing binge eating. However, T will also educate P about the fact that
maintenance of the habitual laxative abuse can cause dehydration and can cause temporary constipation and water retention after the laxative
patient’s bulimic abuse is discontinued. T can explain that while P may experience fluctuations in water weight and sensations of being
behaviors. bloated, these are usually temporary. P is reminded that by not weighing herself until her weigh-in next week she can avoid
unnecessary distress about temporary water weight fluctuations and focus on the important task of gaining control of her
binge eating and dangerous laxative abuse.
In addition, T explores the emotional and environmental circumstances surrounding the binge, noting that sometimes
negative cognitions and mood states trigger binge eating and purging:
T: “Now that we understand some of the physiological factors that might have made you vulnerable to binge eating on
Monday, it would also be helpful to examine what you were feeling and thinking, as negative moods and thought processes
also commonly trigger binge eating.”
Table 2. Continued
Session 1:
Objectives
P: “Well, Mondays are never great days; I was tired and looking forward to getting home when my boss asked me-- at the
last minute-- to work late. I was angry that he was asking again, but I felt trapped; I felt that I couldn’t refuse. He asks me to
work late more than my co-workers because he knows that I don’t have anything better to do at night. I remember thinking
how pathetic it is that I don’t have a husband or family, and that I only had myself to blame for having to work overtime.”
T comments that P was feeling tired, angry at her boss and at herself, ashamed about eating her co-worker’s chocolates, and
angry at having to buy more. T asks if she ever binged on other occasions when tired or angry. P recalls that she has binged
on previous occasions when she has felt angry with someone but has felt powerless to change the situation.
Now T can review Figure 1 with P and draw up an individualized model illustrating some of the factors that may be
maintaining P’s BN. T can also discuss the negative role of perfectionism, all-or-nothing thinking and other distorted
cognitions. Examples include the notion that a few chocolates constitute the difference between being “good” or “perfect”
and being “a pig” who has “blown it all,” and the idea that since she has gone off the diet, she “might as well” finish the rest
of the chocolate.
Conclusion
CBT-BN remains the first line treatment of choice for BN. Controlled outcome studies
have demonstrated that it is more effective than pharmacotherapy and alternative
psychotherapies, it is brief and cost effective, and it is widely available to clinicians in
manualized form. It is hoped that individualizing this treatment and focusing more on
interpersonal skills and affect regulation may further augment the effects of treatment and
possibly result in higher rates of long-term abstinence.
CBT-Oriented Workbooks
(Cited in The American Psychiatric Association Practice Guideline for the Treatment of
Patients with Eating Disorders, 2006).
Agras WS, Apple RF. (2007).* Overcoming Eating Disorders: A Cognitive-Behavioral
Therapy Approach for Bulimia Nervosa and Binge-Eating Disorder. Patient Manual, 2nd
edition. Oxford University Press).
Agras WS, Apple RF. (2007). Overcoming Eating Disorders: A Cognitive-Behavioral
Therapy Approach for Bulimia Nervosa and Binge-Eating Disorder. Therapist Guide, 2nd
edition. Oxford University Press,
Cash TF. (1997). The Body Image Workbook: An 8-Step Program for Learning to Like Your
Looks. Oakland, CA, New Harbinger.
Fairburn C. (1995). Overcoming Binge Eating. New York, Guilford.
Goodman LJ, Villapiano M. (2001). Eating Disorders: The Journey to Recovery Workbook.
New York, Brunner-Routledge (client workbook).
Goodman LJ, Villapiano M. (2001). Eating Disorders: Time for Change. Plans, Strategies,
and Worksheets. New York, Brunner-Routledge (therapist workbook).
Schmidt U, Treasure J. (1993). Getting Better Bit(e) by Bit(e): A survival kit for Sufferers of
Bulimia Nervosa and Binge eating Disorder. London, Routledge.
*(A.P.A Practice Guidelines cited earlier editions of some of the above books).
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Chapter XIII
Evidence-Informed Strategies for Binge

Eating Disorder and Obesity
Kimberly A. Brownley, Jennifer R. Shapiro and Cynthia M. Bulik

University of North Carolina at Chapel Hill
North Carolina, USA
Abstract
Obesity is a major public health problem in the United States (US), where
approximately two out of every three adults are overweight. Excess food intake is a
driving force behind this problem. Binge eating results in excess food intake, and
approximately 5% to 8% of obese individuals meet criteria for Binge Eating Disorder
(BED). Obesity is associated with increased rates of cardiovascular disease, cancer, and
musculoskeletal pain. Independent of obesity, BED is associated with increased rates of
depression and other psychiatric problems. This chapter reviews current evidence-based
treatments for obesity and BED. Also mentioned are novel therapies that have shown
promise in limited clinical studies. Among the available pharmacological treatments,
sibutramine, orlistat, and buproprion have demonstrated efficacy in short-term (three
months to two years) treatment trials for obesity. Similarly, sibutramine, orlistat, and
various antidepressants have shown promise in the short-term treatment of BED.
Effective behavioral therapies include cognitive behavioral therapy, dialectical
behavioral therapy, and combination diet and exercise therapy. Self-monitoring is an
important component of most behavioral strategies. Surgical techniques are generally
reserved for treating severe obesity and include gastric banding and bypass. The chapter
concludes with a discussion of key challenges and future directions for research and
clinical application in the treatment of obesity and BED. The emergence of technology
(internet, text messaging, etc.) as an important anti-obesity tool along with the clinically
relevant concept of “number needed to treat/harm” (NNT/NNH) are highlighted.
232 Kimberly A. Brownley, Jennifer R. Shapiro and Cynthia M. Bulik
Introduction
The prevalence of overweight [body mass index (BMI) of 25-29.9 kg/m2] and obesity
(BMI ≥30) have increased dramatically in the US population in recent years and have now
reached epidemic proportions, with over 65% of adults currently classified as overweight or
obese (Manson and Bassuk, 2003). Obesity is associated with high costs and considerable
health complications including diabetes, hypertension, cardiovascular disease, sleep apnea,
pain, and certain types of cancer (Daniels et al., 2005; de Sousa, Cercato, Mancini, Halpern,
2008; Eckel et al., 2004; Hjartåker, Langseth, and Weiderpass, 2008; Janke, Collins, and
Kozak, 2006; McMillan, Sattar, and McArdle, 2006; Thompson and Wolf, 2001).
Approximately 5% to 8% of obese individuals meet criteria for binge eating disorder (BED)
(Bruce and Agras, 1992; Bruce and Wilfley, 1996). The prevalence of BED is as high as 30%
to 70% in obese individuals seeking weight-loss treatment (de Zwaan, 2001). BED becomes
more prevalent with increasing severity of obesity and is associated with early onset of
obesity (Yanovski, 1993; Yanovski, 2003). Obese individuals with BED report higher
lifetime prevalence of affective, anxiety, and personality disorders (Mussell et al., 1996;
Specker, de Zwaan, Raymond, and Mitchell, 1994; Yanovski, Nelson, Dubbert, and Spitzer,
1993); greater health dissatisfaction; and higher cumulative rates of major medical disorders
(Bulik, Sullivan, and Kendler, 2002) than obese individuals without binge eating. Also, binge
eating, independent of BMI, is associated with several psychiatric and medical symptoms in
both men and women (Reichborn-Kjennerud, Bulik, Sullivan, Tambs, and Harris, 2004). In
short, BED can have debilitating consequences that affect an individual’s physical,
emotional, and social well-being [see Janice’s Story below]. The purpose of this chapter is to
address evidence-based approaches for the treatment of obesity and BED. Specifically, we
will discuss pharmacological and behavioral approaches for both conditions as well as
surgical approaches for obesity.
Vignette – Janice’s Story

Janice, a 35 year old woman, lives with her golden retriever, Max, and her best friend,
Sarah, in a two bedroom apartment on the east side of town. She has a few close friends but
mainly keeps to herself. Janice has been overweight since she was five years old and she
remembers as a child sneaking food into her room at night, hiding food from her parents, and
always wanting to snack. When she began school, Janice did not like to eat lunch because the
other children would tease her about her weight. As a result, she would come home from
school and eat large amounts of food until she became uncomfortably full. This persisted
throughout high school. Last year, Janice started a new job and began to gain weight. She is
5’3” and weighs about 340 pounds. Her friends never understood why she was very
overweight because Janice barely picked at her food when they all went out to eat. Still, the
weight gain persisted. Then one day while cleaning, Sarah came across an unfamiliar
notebook. Curious, she opened it to find Janice’s handwriting and a page that read “I don’t
know what to do. I feel so out of control. I can go the entire day without having the slightest
urge to binge and then something happens—my boss yells at me, the dog chews another hole
Evidence-Informed Strategies for Binge Eating Disorder and Obesity 233
in the carpet, I lock my keys in my car—anything! It doesn’t even have to be negative. The
other day my sister told me she was getting married. I was so happy for her that I sat down
and ate an entire gallon of chocolate ice cream and two large pizzas, all within two hours. I
can’t explain it. It is as if something triggers this feeling deep within me. I start eating and
lose control. I eat until I can’t possibly swallow another bite. I feel disgusted with myself. I
feel guilty. I am so embarrassed by how much I eat that I hide my binges from my friends and
family. My weight keeps skyrocketing while my health is plummeting. I need help. Every
time I’ve tried to diet, I just fail. I do great all day but then at the end of the night, I blow it. I
have never gone a single week without binge eating. About 5 years ago, I lost 25 pounds but
gained 40 back after I got a blister on my foot and had trouble walking. I have considered
having surgery to take off the excess pounds, but I know that it will only solve half the
problem. Sure, I would no longer be physically able to eat the amounts of food that I do now,
but what about the cravings? My life revolves around food. I’m always thinking of the next
meal. I love eating and once I start, I really can’t stop. Food is always there for me—when I
am happy, sad, angry, stressed—you name it. Without food, I’d be all alone.”
As illustrated by this vignette, Janice’s binge eating was deeply troubling to her—a life-
long battle, her overeating left her feeling out of control, ashamed, and a failure. She relied
on food to cope with strong emotions, perpetuating a vicious cycle of binge eating and self
disgust. Janice’s weight skyrocketed, increasing her risk of other medical problems and
warranting drastic intervention. Janice recognizes that surgery will help with the weight
problem but not necessarily with the craving and lack of control around food. She
understands the importance of addressing the cognitive and emotional triggers for her binge
eating through psychotherapy and possibly medication.
Pharmacological and Surgical Treatment

for Obesity
Medications used for weight loss generally fall into three categories based on their
mechanism of action: a) drugs that reduce food intake and appetite (“appetite suppressants”),
b) drugs that alter metabolism, and c) drugs that increase thermogenesis (heat production or
energy expenditure). To date, the Food and Drug Administration (FDA) has not approved any
“thermogenic” anti-obesity drugs for use in the US. Here, we summarize what is known
regarding the efficacies and limitations of appetite suppressants and lipase inhibitors. Some
discussion is also provided of novel, less well-studied anti-obesity agents that have shown
promise in small clinical studies. Finally, we address surgical approaches for treating severe
obesity. For more in-depth coverage of these topics, the reader is referred to several
previously published reviews (Bray, 2000; DeWald, Khaodhiar, Donahue, and Blackburn,
2006; Douketis, Macie, Thabane, and Williamson, 2005; Dunican, Desilets, and Montalbano,
2007; Leung, Thomas, Chan, and Tomlinson, 2003; Norris et al., 2005; Orzano and Scott,
2004; Padwal, Li, and Lau, 2004; Thompson, Cook, Clark, Bardia, and Levine, 2007) and
meta-analyses (Li et al., 2005; Padwal, Li, and Lau, 2003).
Appetite Suppressants
There are several FDA-approved appetite suppressants; examples include

benzphetamine, diethylpropion, phendimetrazine, and phentermine. These drugs are
centrally-acting stimulants that promote the release of brain chemicals known as
catecholamines (i.e., dopamine, epinephrine, norepinephrine) (Bray, 2000; Li et al., 2005;
Thompson et al., 2007). Early studies suggested that phentermine was superior to placebo in
reducing weight over a period of nine months (Munro, MacCuish, Wilson, and Duncan,
1968). However, in part because drugs in this class have some abuse potential and because
some are associated with significant cardiovascular and central nervous system side effects,
they are approved for short-term (up to 12 weeks) use only. Thus, these medications are not
widely prescribed or used for prolonged weight loss.
In contrast to these short-term options, sibutramine is approved for long-term treatment
and has been widely studied in longer-term trials (Bray, 2000; Bray et al., 1996; DeWald et
al., 2006; Leung et al., 2003; Li et al., 2005; Padwal et al., 2004; Thompson et al., 2007).
Sibutramine is thought to inhibit food intake by blocking synaptic reuptake of both
norepinephrine and serotonin in the brain. Across studies, sibutramine was superior to
placebo in promoting weight loss, with weight loss generally occurring in the initial six
months of treatment and being maintained with continued sibutramine administration for up
to two years (Bray, 1996; Dujovne, Macie, Thabane, Williamson and the Sibutramine Study
Group 2001; James et al., 2000). Sibutramine was also associated with beneficial changes in
blood lipids and other biomarkers of cardiovascular disease risk (Dujovne et al., 2001; James
et al., 2000). A recent study also suggests that sibutramine safely reduces weight and
improves cardiovascular risk profile in adolescents, as well (Daniels et al., 2007).
Overall, this general class of drugs has shown some efficacy in suppressing appetite and
promoting satiety; however, because these drugs produce untoward side effects (such as
nervousness, insomnia, headache, and elevated blood pressure), their clinical utility as agents
of long-term weight loss is quite limited.
Drugs that Alter Metabolism
Limiting dietary intake of fat can be an effective way to reduce caloric consumption and
lose weight. However, compliance with low-fat diets is often poor, limiting the success of
this approach for long-term weight loss. In the past decade, a relatively new approach to
regulating dietary fat has emerged with the development of agents that interfere with fat
metabolism and thereby reduce the amount of ingested fat that is available for absorption.
The most widely used agent in this class is orlistat (Xenical). Orlistat inhibits gastric and
pancreatic lipases, which are enzymes necessary for converting dietary fat (triglycerides) into
forms that can be absorbed by the body and used for energy. In clinical studies, orlistat was
superior to placebo in promoting initial weight loss and in maintaining weight loss after two
years (Drent et al., 1995; Rossner, Sjostrom, Noack, Meinders, and Noseda, 2000; Van Gaal,
Broom, Enzi, and Toplak, 1998). Orlistat also reduced blood cholesterol and other
cardiovascular disease risk factors (Davidson et al., 1999; Tonstad et al., 1994). Orlistat
primarily acts in the stomach and small intestine, with very limited effects elsewhere in the
body. Thus, when side effects occur they generally are gastrointestinal in nature, including
fecal urgency and incontinence. In most cases, these side effects are mild to moderate, and
they often dissipate with continued use (Drent et al., 1995; James, Avenell, Broom, and
Whitehead, 1997; Van Gaal et al., 1998).
“Novel” Anti-Obesity Agents
The atypical antidepressant, buproprion, is approved to treat depression and as adjunct

therapy for smoking cessation. In clinical studies focusing on these outcomes, buproprion
was associated with modest weight loss in a small percentage of participants (Croft et al.,
1999; Weisler et al., 1994). In a more recent study focusing on weight loss as the primary
outcome in obese women, buproprion was superior to placebo in promoting weight loss after
eight weeks of treatment (Gadde et al., 2001). Women who responded well to buproprion
were given the opportunity to continue treatment for up to two years. Average weight loss
after two years was approximately 14% of initial body weight. Buproprion is associated with
mild side effects including dry mouth, nausea, and insomnia but is generally well-tolerated
(Settle, Stahl, Batey, Johnston, and Ascher, 1999). Taken together, these studies suggest that
buproprion warrants further study to understand its potential long-term efficacy as an anti-
obesity agent.
Metformin is an “insulin sensitizing” agent used in the treatment of type 2 diabetes.
Metformin also reduces glucose production in the liver. Together, these effects help
normalize and stabilize blood glucose levels. In several small clinical studies, metformin
consistently was associated with reduced appetite and food intake (Lee and Morley, 1998;
Paolisso et al., 1998; Stumvoll, Nurjhan, Perriello, Dailey, and Gerich, 1995). Nonetheless, in
these studies, the weight loss attributed to metformin was modest, suggesting that metformin
alone is not a good candidate for the treatment of obesity.
Surgical Treatments for Severe Obesity (“Bariatric Therapy”)
Surgical approaches are very effective in the treatment of severe (“morbid”) obesity
(DeWald et al., 2006, for review). Compared to other modalities, surgical treatments usually
result in longer-lasting weight loss and they tend to improve comorbid conditions of obesity,
such as hypertension, respiratory problems, and diabetes (Foley, Benotti, Borlase,
Hollingshead, and Blackburn, 1992; MacDonald et al., 1997; Sugerman et al., 1992).
Surgical therapies fall into two broad categories: a) procedures designed to restrict gastric
volume and b) procedures designed to decrease the functional length of the small intestine.
Thus, certain approaches lead to weight loss by limiting food intake and others lead to weight
loss by limiting nutrient absorption. Some “mixed” approaches apply both techniques
simultaneously. Gastric bypass is generally superior to banding procedures for weight loss
and long-term weight loss maintenance (DeWald et al., 2006), and it now can be performed
using minimally invasive laparoscopy (Wittgrove and Clark, 2000). Thus, bypass is currently
viewed as the gold standard procedure.
Examples of restrictive procedures include gastroplasty, gastric banding, gastric bypass,
and sleeve gastrectomy. In gastroplasty, surgical staples are used to partition the stomach into
two compartments. In gastric banding, an adjustable prosthetic band is placed around the
stomach to reduce its food-holding capacity. Gastric bypass divides the stomach into a small
upper pouch and larger lower pouch, both of which are connected to the small intestine; this
leads to a marked reduction in the functional volume of the stomach, accompanied by an
altered physiological response to food (referred to as “dumping”). Dumping involves the
rapid emptying of hypo-osmolar gut contents from the stomach into the small bowel and
results in nausea, pain, diarrhea, and other symptoms. Dumping signals the patient very
quickly if he/she has overeaten – particularly sweet or high-carbohydrate foods or liquids –
and this signal can serve as a deterrent to further overconsumption. Sleeve gastrectomy
reduces the stomach to about one-third its original size by removing a large portion of the
stomach, itself. Examples of procedures designed to disrupt absorption include jejunoileal
bypass and biliopancreatic diversion. Jejunoileal bypass was the first surgical procedure used
to treat obesity (Payne and DeWind, 1969) but is no longer performed due to a high rate of
serious liver and metabolic complications. As its name suggests, biliopancreatic diversion
shifts biliary and pancreatic secretions to the distal end of the ileum.
Bariatric surgery is the most effective treatment for morbid obesity (Anderson and
Wadden, 1999); however, complications do occur and have increased paralleling the
increasing numbers of procedures performed (Abell and Minocha, 2006). According to a
recent review (Abell and Minocha, 2006), up to 70% of individuals who lose weight quickly
may experience gallstones. In addition, “dumping” occurs in about 14.6% of those who
undergo “mixed” surgery and can be particularly problematic for patients who struggle with
strong food cravings and binge eating. Eleven percent of those who undergo “mixed” surgery
experience vitamin and mineral deficiency (e.g. calcium, iron, vitamins B12 and D) (Abell
and Minocha, 2006). Other complications include vomiting, staple line failure, infection,
bowel obstruction, ulceration, bleeding, and splenic injury. In addition to these
complications, a 0.4% mortality rate of patients who undergo combined surgery has been
reported (Monteforte and Turkelson, 2000). A recent retrospective cohort study (Adams et
al., 2007) compared long-term mortality rate (all-cause and specific cause) in 7925 surgical
patients with 7925 control patients from the general population, matched on sex, BMI, and
age. Results showed that although the all-cause mortality was 40% lower in the surgery group
and mortality from specific diseases (e.g., diabetes, CAD, cancer) was on average 52% lower
in the surgery group, non-disease related deaths (e.g., suicide, accidents, other) were 1.58
times as great in the surgery group than in the control group. This suggests that although
surgery may indeed decrease all-cause and specific-disease mortality, it cannot address
psychological issues and other variables that impact well-being and post-surgical mortality.
For this reason, psychological evaluations are an important adjunct to any surgical treatment
for obesity. In addition, a prospective study (Sjostrom et al., 2007) that compared 2010
patients who underwent bariatric surgery with 2037 patients who received conventional
treatment (lifestyle change, behavior modification, or no treatment) found that after 10.9 year
followup the surgery group had a hazard ratio of 0.76 compared with the control group, with
death occurring in a significantly higher percentage of the control group (6.3%) compared to
the surgery group (5.0%). Although these studies are important, they lack the scientific rigor
of a randomized controlled trial; however, conduct of a randomized controlled trial for
obesity is difficult given potential ethical concerns about assigning patients to either surgical
or behavioral treatment rather than allowing them to select the treatment of their choice.
Pharmacological Treatments for BED
The majority of published randomized clinical trials (RCTs) of pharmacotherapy for

BED have been limited in scope. They have generally been small in size (fewer than 500 total
participants in eight medication RCTs), and the vast majority of participants have been
Caucasian women over age 18 (see Berkman et al., 2006; Brownley, Berkman, Sedway,
Lohr, and Bulik, 2007). Thus far, the medications that have received the most attention in the
treatment of BED are second-generation antidepressants (Arnold et al., 2002; Hudson et al.,
1998; McElroy et al., 2000; McElroy, Hudson et al., 2003; Pearlstein et al., 2003), tricyclic
antidepressants (Laederach-Hofmann et al., 1999), anticonvulsants (McElroy, Arnold et al.,
2003), and sibutramine (Appolinario et al., 2003). Table 1 summarizes the results of these
studies.
Antidepressants (Selective Serotonin Reuptake Inhibitors

and Tricyclic Antidepressants
Fluoxetine, fluvoxamine, sertraline, and citalopram are the selective serotonin reuptake
inhibitors (SSRIs) most widely studied to date. In short-term studies (12 weeks), both
fluoxetine (Arnold et al., 2002) and fluvoxamine (Pearlstein et al., 2003) were effective in
reducing binge frequency and depressed mood. Fluvoxamine was superior to placebo in
reducing binge frequency and improving illness severity after nine weeks (Hudson et al.,
1998). However, remission rates and depression scores did not differ between groups, and
BMI at the end of the study was not reported. Thus, the group receiving fluvoxamine
experienced more rapid reductions in binge eating and weight than the placebo group, but by
the end of the study these changes did not result in clinically meaningful changes (i.e., binge
abstinence and weight loss). After 6 weeks, compared with placebo, both sertraline (McElroy
et al., 2000) and citalopram (McElroy, Hudson et al., 2003) were associated with reduced
binge eating, weight loss, and illness severity ratings in individuals with BED. Citalopram,
but not sertraline, was also associated with reduced depression ratings compared to placebo.
However, neither sertraline nor citalopram was clearly superior to placebo in terms of
remission rate, and the initial rapid response in binge eating observed with citalopram was
not sustained over time.
Table 1. Summary of Pharmacological Treatment Studies for Binge Eating Disorder
Medication Dose Sample Results (Significant Group Differences) Source

Fluoxetine 20 – 80 mg/day 93% female Over six weeks, fluoxetine was superior to placebo in Arnold et al., 2002
Age (range): 18-60 yrs reducing binge frequency, illness severity, and
Age [mean (SD)]: depressed mood, and in controlling weight and BMI
Fluoxetine: 41.9 (9.7) gain.
Placebo: 40.8 (9.0) At study endpoint, fluoxetine was associated with
Enrolled: 60 lower illness severity and depressed mood, and less
Dropout: 40% weight gain, and generally was well-tolerated for
subjects.
Fluvoxamine 50 – 300 mg/day 93% female Over nine weeks, fluvoxamine was superior to Hudson et al., 1998
Age (range):18-60 yrs placebo in reducing binge frequency, BMI, and
Age [mean (SD)]: clinical severity.
Fluvoxamine: 41.2 (9.9) At study endpoint: remission rates and depression
Placebo: 43.0 (9.5) scores were not different and there was no clinically
Enrolled: 85 meaningful change for binge abstinence and weight
Dropout: 12% loss.
Fluvoxamine 150 mg/b.i.d 85% Female No significant improvement for binge frequency, Pearlstein et al., 2003
Age (range): 41.0 yrs depressed mood, or eating psychopathology (eating,
Age [mean (SD)]: NR shape, or weight concerns).
Enrolled: 25 At study endpoint: NR.
Dropout: 20%
Topiramate 50-600 mg/day 87% Female Over 14 weeks, topiramate was superior to placebo in McElroy, Arnold et al., 2003
Age (range): 18-60 yrs reducing binge frequency, illness severity, eating-
Age [mean (SD)]: related obsessions, compulsions, BMI, and weight,
Topiramate: 40.9 (8.2) which decreased in the topiramate group but increased
Placebo: 40.7 (9.1) in the placebo group.
Enrolled: 61 At study endpoint: NR.
Dropout: 15%
Citalopram 20-60 mg/day 95% Female Over six weeks, compared to placebo, citalopram was McElroy, Hudson et al., 2003
Age (range): 18-60 yrs associated with a faster rate of reduction in binge
Age [mean (SD)]: frequency, illness severity, binge eating-related
Citalopram: 42.0 (9.0) obsessions and compulsions, and weight.
Placebo: 39.2 (12.0) At study endpoint: citalopram was associated with
Enrolled: 38 greater reduction in frequency of binge days, BMI,
Dropout: 18% and weight.
Imipramine 25 mg / t.i.d 87% Female Over eight weeks of active treatment and at week 32 Laederach-Hofmann et al.,
(added to Age (range): 20-60 yrs followup, imipramine was superior to placebo in 1999
dietary and Age [mean (SD)]: decreasing binge frequency, depressed mood, and
psychological Imipramine: 40.7 (10.9) body weight.
counseling) Placebo: 35.7 (10.3) At study endpoint: NR.
Enrolled: 31
Dropout: 7%
Sertraline 50-200 mg/day 94% Female Over six weeks, sertraline was superior to placebo in McElroy et al., 2000
Age (range0: 18-60 yrs reducing binge frequency, illness severity, and BMI,
Age [mean (SD)]: and in increasing global improvement.
Sertraline: 43.1 (9.9) At study endpoint: NR.
Placebo: 41.0 (12.2)
Enrolled: 34
Dropout: 24%

Sibutramine 15 mg/day 95% Female Over 12 weeks, sibutramine was superior to placebo Appolinario et al., 2003
hydrochloride Age (range): 18-60 yrs in reducing binge frequency and severity.
Age [mean (SD)]: At study endpoint: sibutramine was associated with
Sibutramine: 35.2 (9.0) less depressed mood. Groups differed in weight:
Placebo: 36.6 (10.2) weight decreased over the treatment period in the
Enrolled: 60 sibutramine group but increased in the placebo group.
Dropout: 20%
Orlistat 120 mg / t.i.d 88% Female Over 12 weeks, CBT plus orlistat was associated with Grilo et al., 2005
Age (range): 35-58 yrs greater total weight loss and % weight loss than CBT
Age [mean (SD)]: plus placebo.
Orlistat: 45.2 (7.4) At study endpoint: greater percentage of CBT+orlistat
Placebo: 47.0 (7.0) group remitted and achieved at least 5% weight loss.
Enrolled: 50 The group difference in weight loss was maintained at
Dropout: 22% 2-month followup.
Abbreviations: BMI (Body Mass Index); CBT (Cognitive Behavioral Therapy); NR (Not reported).
Tricyclic antidepressants have shown some promise in the treatment of BED. When
given as adjunct therapy to standard diet counseling and psychological support, imipramine
significantly reduced binge eating episodes, depressed mood, and body weight after eight and
32 weeks in 31 individuals with BED (Laederach-Hofmann et al., 1999). Unfortunately,
abstinence rates from binge eating were not reported, thus the clinical utility of imipramine in
the treatment of BED remains unknown.
Other Agents
The appetite suppressant, sibutramine (which is marketed for the treatment of obesity),
and the anticonvulsant agent, topiramate, have demonstrated limited efficacy in the treatment
of BED. In a 14-week study of obese individuals with BED, topiramate was superior to
placebo in reducing binge frequency (episodes and binge days per week) and scores on the
Yale-Brown Obsessive Compulsive Scale for Binge Eating (McElroy, Arnold et al., 2003);
however, weight loss, illness severity, and depression scores did not differ between groups
after treatment. In contrast, sibutramine given for 12 weeks significantly reduced binge days
per week, Binge Eating Scale scores, and self-reported depression scores compared to
placebo in individuals with BED (Appolinario et al., 2003). Notably, the sibutramine group
lost on average 7.4 kg whereas the placebo group gained weight.
Orlistat has been studied as augmentation therapy for BED patients undergoing cognitive
behavioral therapy (CBT) (Grilo, Masheb, and Salant, 2005). Compared to CBT plus
placebo, CBT plus orlistat was associated with greater initial weight loss (-1.6 kg vs. -3.5 kg)
and remission rates. However, neither effect was maintained at 2-month followup, and other
eating-related measures and depression did not differ between groups.
Treatment Limitations and Concerns
Virtually all of the medications reviewed here have side effects commonly associated
with second-generation and tricyclic antidepressants (such as sedation, dry mouth, headache,
sexual dysfunction/decreased libido, insomnia, constipation, and gastrointestinal upset).
Inability to tolerate side effects is clearly a major reason for treatment drop (up to 24% in
studies reviewed here). Placebo response rates have also been quite high in medication trials
for BED (6% to 39%). These factors, in addition to a general failure to report abstinence rates
and long-term follow-up data, limit our understanding of treatment options for BED.
Furthermore, there is very little information available about specific factors that contribute to
treatment efficacy in BED. For example, early abstinence from binge eating may be
associated with greater weight loss (Agras et al., 1994). These findings warrant further study,
as do questions regarding treatment efficacy in ethnic, gender, and age subgroups. Initial
findings require replication, and larger more culturally diverse samples need to be studied
before an accurate picture of individual difference factors in BED outcome can emerge.
Overall Summary of Pharmacological Treatments for BED
Taken together, these studies suggest that there are several viable options for
pharmacotherapy in the treatment of BED. Short-term, placebo-controlled trials provide
limited evidence that SSRIs reduce target eating, psychiatric, and weight symptoms in
individuals with BED. However, this evidence must be viewed cautiously because of high
dropout and placebo response rates across studies. Sibutramine, topiramate, and low-dose
imipramine may also benefit individuals with BED by reducing weight, but their impact on
binge abstinence and remission remain uncertain. Additional studies are needed to confirm
the therapeutic potential of these agents in the treatment of BED.
Behavioral Interventions for Weight Control

Prior to the 1960s, psychologists used psychoanalytic theory to treat overweight
individuals by focusing on oral fixations and developmental disturbances, which were
believed to have caused obesity. In the 1960s, learning theory was applied to weight
management. According to learning theory, certain learned behaviors contributed to weight
gain and if these behaviors were unlearned and replaced with healthier alternatives, weight
loss would follow. This idea launched considerable research into the behavioral approach to
weight management.
The behavioral approach for weight control or obesity consists of core techniques
including dietary recommendations, exercise, cognitive techniques, stimulus control, relapse
prevention, and social support. Although weight loss is certainly the goal of treatment, weight
is de-emphasized as it is not a behavior, per se, but a result of the behavior changes. The
treatment requires an active participation of the patient; it is goal oriented, problem focused,
structured, and it uses many techniques to change distorted thinking, mood, and thus
problematic behavior.
Nutrition Education
It is important for patients to understand healthy versus unhealthy eating. Emotional

eating (i.e., eating for any other reason than physiological necessity: including boredom,
anger, frustration, excitement, etc.), eating in response to cravings or urges (which is also
often linked to emotional reasons), and unhealthy dieting (purging, restricting or viewing a
“diet” as a “limited time” rather than a healthy permanent lifestyle change) are examples of
unhealthy eating behaviors that may result in both physical problems (e.g., intense hunger,
low energy, fatigue, headaches, visual problems, weight gain, electrolyte disturbance, dental
problems, gastrointestinal problems), cognitive problems (e.g., focus on food, loss of interest,
poor concentration, memory problems, difficulty with comprehension and decision making),
and emotional problems (e.g., stress, irritability, and anxiety, depression) (Bulik and Taylor,
2005). Incorporating a dietitian into the treatment team is essential so that patients learn
healthy, balanced nutrition and the importanceof remaining within a certain calorie range or
exchange program necessary for weight control/maintenance. A dietitian will help create a
meal plan to consume several small meals per day so that patients do not set themselves up
for overeating due to excessive hunger later in the day. Such healthy eating includes
designating meal times, not allowing greater than 3 to 4 hours between eating times, not
skipping meals, and avoiding eating in between planned meal/snack times.
Self-Monitoring
Self-monitoring of energy intake is a hallmark of weight control interventions and is a

critical element in short and long-term weight management (Wing and Hill, 2001).
Monitoring helps individuals understand their current eating patterns and identify patterns
that need to be changed. For example, some individuals may learn that they go straight to the
refrigerator after a long, stressful day at work (even if they are not physiologically hungry
yet); others may find they are more likely to eat large portions in the evening if they go seven
hours without eating during the day. In addition, monitoring helps individuals learn about the
nutritional value of various foods, and it assists in meal planning/preparation and supports
healthy choices. Monitoring provides a means for holding oneself accountable which, in turn,
aids in helping individuals to avoid overeating or unhealthy eating. Monitoring also helps
individuals notice their behavior changes and new patterns.
Physical Activity
It is recommended that patients gradually increase both lifestyle physical activity (e.g.,
gardening or yard work, climbing stairs, bicycling for transportation) and structured exercise.
Exercise is a key component of any weight loss program and is highly correlated with long-
term weight management. Accumulation of several short bouts of exercise per day (10 to 15
minute bouts for a total of 30 to 45 minutes per day) is as effective in promoting short-term (3
to 6 months) weight loss as exercising once per day for an equivalent length of time (Haskell
et al., 2007; Jakicic, Winters, Lang, and Wing, 1999; Schmidt, Biwer, and Kalscheuer, 2001).
In addition, exercising in short bouts may be superior to exercising once per day in
maintaining weight loss over longer periods of time (12 to 18 months) but only whcn coupled
with access to and use of home-based exercise equipment, possibly because home-based
exercise is more convenient and associated with better adherence (Jakicic et al., 1999).
Cognitive Restructuring
According to cognitive behavioral theory, thoughts and feelings precede actions, and
inaccurate thoughts drive unhealthy behaviors. CBT uses cognitive techniques to challenge
inaccurate/unhealthy thoughts, and it focuses on current thinking, problematic behavior,
precipitating factors, and developmental events. For weight control, patients are asked to
maintain daily monitoring logs in which they record foods eaten, eating disordered behaviors
(e.g., eating in the absence of physical hunger, purging, avoiding food in social settings, food
restriction), thoughts, feelings, and details about the situation in which these behaviors
occurred. In addition to revealing information about food consumed and eating patterns, such
self-monitoring reveals patterns of automatic thoughts (e.g., “I am fat”, “If I eat this, I am
weak”, “I did good today, I deserve this”, “I blew it, now I might as well eat more”) that
reflect broader core beliefs. Over time, individuals become aware of their automatic thoughts;
challenge them; question and evaluate the evidence that supports/opposes the thoughts;
consider alternative views; determine the effect of the automatic thoughts on other thoughts,
feelings, and behaviors; and identify typical thinking errors. Finally, given that negative
mood and stress can result in overeating, cognitive techniques are used to reduce emotional
distress, so that individuals refrain from eating during stressful situations.
Behavioral Chaining
Consistent with learning theory, CBT helps individuals identify the antecedents,
behaviors, and consequences of their diet, exercise, and other behaviors associated with
weight control. Individuals become skilled at understanding both cues/triggers for and
consequences of eating behavior. Cues consist of specific thoughts, feelings, or behaviors and
can be internal or external. Examples of internal cues include thoughts about the past or
future that can generate emotions of sadness or anxiety, and physiological or bodily
sensations such as a growling stomach or fatigue. Examples of external cues include social
situations or events, interpersonal conflict, walking past a favorite restaurant, and food
advertisements. A consequence is the result of behavior and can be either positive or
negative. For example, physiological consequences of eating can include: 1) reduced hunger
(positive) and 2) high cholesterol (negative). Emotional consequences of eating can include:
1) temporary relief of the negative feeling (positive) and 2) depression, guilt, shame after
overeating (negative). Often, when individuals who are attempting weight loss overeat they
do not think of the consequences in advance. Thus, behavioral chaining is a tool that helps
individuals identify connections between cues, thoughts, behaviors, and consequences, and is
used in the therapeutic process to help them resist cues to eating and think about the
consequences in advance.
Behavioral Strategies
Specific behavioral strategies are essential to help individuals avoid unhealthy eating
behavior and reinforce healthier alternatives. Patients are taught to set realistic, specific goals
that are challenging but achievable, and then to gradually modify them to shape their desired
behavior. Patients are often encouraged to identify small material rewards for achieving their
goals. It is important that rewards are: a) not food-based (e.g., a trip to one’s favorite ice
cream parlor or pizza restaurant), b) delivered close in time to the desired behavior, and c)
something the individual would otherwise not obtain. Individuals learn to control stimuli in
their environment by following an eating schedule, food shopping from a list, removing
serving dishes from the table, storing food in cabinets (not on the counter top), and buying
foods that are healthy and require preparation. Individuals also practice avoiding high risk
cues (keeping specific foods out of the house, taking an alternative route so that convenient
stores are avoided), doing one thing at a time (e.g., do not eat and watch TV), and
strengthening cues for desired behavior (plan an afternoon activity instead of going home
alone and eating). Another strategy is to change the response to cues by building in a pause
between having thought about eating and the actual act of eating. During this time,
individuals may practice thought restructuring, focus on the consequences, or find an
alternative behavior. Initially, pause intervals may be short in duration, but with practice they
can gradually increase giving the patient greater opportunity to choose a different course of
action rather than overeating when the urge arises. For example, patients may choose an
alternative behavior to unhealthy eating (e.g., going for a walk, talking on the phone, taking a
bath, knitting) or they may elect to “surf the urge” (i.e., allowing the urge or craving to peak,
experiencing the peak, and then noticing that the urge decreases over time). Individuals also
practice focusing on consequences, including positive consequences from healthy eating and
negative short and long term consequences from unhealthy eating. These strategies can help
patients learn that their cravings do not always lead to a “point of no return” and can build
and reinforce a sense of control in dealing with urges once they arise.
Relapse Prevention
Relapse prevention is essential to long-term weight management. The objective of

relapse prevention is to help patients identify ways in which they will continue to practice the
skills learned during treatment. They also learn to distinguish between an occasional “slip” or
“lapse” versus a “relapse”. A “slip/lapse” happens when a patient engages in unhealthy
eating behavior but regains control; a “relapse” happens when a patient loses control and then
ultimately reverts to his/her original unhealthy eating patterns. Relapse prevention strategies
help individuals identify high risk situations in advance, plan for them (e.g., identify
alternative behaviors), and cope (practice positive thought restructuring: “Just because I
slipped, does not mean that I have fallen off the wagon.”). Patients can develop a personal
“panic card” on which they list positive self-statements, alternative behaviors, and phone
numbers of persons they can call for support. This card can be very useful when patients find
themselves in high risk situations and are having difficulty identifying their newly learned
healthy behaviors.
CBT-based weight control treatments typically consist of 20- to 30-week programs and
are usually offered in group formats. Over the past 30 years, programs have increased from
eight weeks to 30 weeks in recognition of the fact that weight loss accumulates at a rate of
approximately one to two pounds per week and longer programs result in greater total weight
loss (Wadden, Crerand, and Brock, 2005). While some individuals are successful at losing
significant amounts of weight on 30 weeks, the majority of patients lose a modest 10% of
their initial body weight. This amount of weight loss should not be discounted, however, as it
has other important health implications including reductions in hypertension,
hypercholesterolemia, diabetes, and all-cause mortality (Pi-Sunyer, 2002). Long-term
maintenance of weight loss is associated with continued exercise, healthy diet, self-
monitoring, and continued patient-provider contact (Jakicic, et al., 1999; Perri, 1998; Wing
and Hill, 2001).
Cognitive-Behavioral Therapy for BED

Since many individuals with BED are overweight and eat in response to certain cues,
CBT targeting both decreasing binge eating and managing weight may be useful in the
treatment of BED. The primary goal for BED treatment is to achieve abstinence from binge
eating; for overweight individuals with BED, a second treatment goal is sustainable weight
loss. In addition, treatment often focuses on reducing symptoms of anxiety and depression
that are commonly associated with BED and may trigger binge eating episodes (Grilo,
Shiffman, and Carter-Campbell, 1994). Specifically, in therapy, patients learn to identify
depressive or anxious automatic thoughts that lead to binge eating (e.g., “I’m a loser, nobody
wants to be in a relationship with me, I might as well eat and be fat”; “I have to ace this job
interview but I’m so nervous, I’ll just calm myself down with this piece of chocolate cake”).
CBT helps individuals identify and challenge their automatic thoughts, break the connection
between such thoughts and eating, and identify alternative behaviors.
Several clinical studies have shown that CBT can be effective in the treatment of BED
(Gorin, le Grange, and Stone, 2003; Hilbert and Tuschen-Caffier, 2004; Wilfley et al., 2002).
When applied in a group format, patients learn CBT tools while also receiving social support
from other group members. Patients can also benefit from individual therapy designed to
address specific, personally relevant issues in greater depth. Group CBT for BED has been
shown to be effective in reducing the number of binge days and hunger as well as in
improving key psychological features of BED including disinhibition, depression, and self-
esteem (Gorin et al., 2003; Hilbert and Tuschen-Caffier, 2004; Wilfley et al., 2002). CBT
may also increase the likelihood of abstinence from binge eating (Gorin et al., 2003).
However, CBT, as currently delivered, does not appear to lead to significant changes in body
weight. Augmenting CBT with increased spousal involvement in therapy (Gorin et al., 2003)
or body exposure treatment (Hilbert and Tuschen-Caffier, 2004) does not increase the impact
of CBT in patients with BED. In sum, CBT may be effective in helping patients improve their
sense of control over binge eating behavior but may require enhancements to adequately
address weight concerns.
DBT employs both cognitive and behavioral strategies to help patients obtain skills
pertaining to mindfulness, emotion regulation, interpersonal effectiveness, and distress
tolerance. Telch et al. (Telch, Agras, and Linehan, 2001) studied 20 weeks of DBT versus
waiting list control in 44 women with BED and found that DBT resulted in greater reduction
in binge days, binge episodes, and in weight, shape, and eating concerns. However, the two
groups did not differ in weight loss or in change in depression or anxiety. A recent pilot study
found similar benefits of DBT including reductions in binge behavior and eating concerns
without consistent reductions in BMI (Chen et al., 2008).
Our understanding of the potential benefits of CBT for BED is limited for several
reasons. Controversies exist regarding diagnosis, in part, because the diagnostic criteria
continue to undergo revision and there is no universally recognized operational definition of

a “binge episode.” In addition, validated age-appropriate instruments are only now becoming
available for assessing BED in children and adolescents (Bryant-Waugh, Cooper, Tayler, and
Lask, 1996; Johnson, Grieve, Adams, and Sandy, 1999; Shapiro, Woolson et al., 2007).
Finally, most behavioral treatment studies for BED have been plagued by high drop-out rates,
making it difficult to evaluate the true therapeutic impact of CBT in this patient population.
Future research should address questions such as whether calories previously consumed as
binges become distributed over non-binge meals after treatment (thus explaining lack of
weight loss) and whether treatment alters the way in which patients label binges and non-
binge meals (T. Walsh, personal communication, September 8, 2007). A recent evidence-
based review emphasized that research studies should be more standardized and focus on
abstinence from binge eating (not merely reduced binge frequency) as the critical outcome
and target relapse prevention (Berkman et al., 2006; Brownley et al., 2007). Future research
should control for placebo response, which has been shown to be high (yet possibly
transitory) in BED (Carter et al., 2003; Jacobs-Pilipski et al., 2007; Pearlstein et al., 2003).
Finally, given the promising preliminary results, additional studies of DBT (e.g., that can
articulate which aspects of DBT are most applicable to the complex emotional and behavioral
features of BED) are warranted.
Future Directions
In addition to continued research on weight loss and BED, new methods that enhance
motivation and retention in intervention trials need to be developed. This endeavor will likely
includes new information technologies such as e-mail, the Internet, personal digital assistants,
text messaging, and other technological advances. These devices and technologies can be
used to enhance treatment, particularly for those patients experiencing shame, denial, and
interpersonal deficits or for those facing limited availability of specialty care. Our group
(Shapiro, Reba-Harrelson et al., 2007) recently evaluated preliminary feasibility and
acceptability of CD-ROM-delivered cognitive behavioral therapy (CD-ROM CBT) and
compared it to 10 weekly group CBT sessions and to a waiting list control in 66 overweight
individuals with BED. Promising results emerged pertaining to attrition and continued use of
the CD post-treatment. Also, the majority of participants who were in the control waiting list
group chose to receive CD-ROM CBT over group CBT treatment at the end of the waiting
period. Thus, preliminarily, CD-ROM appears to be an acceptable and at least initially
preferred method of CBT delivery for overweight individuals with BED. A more rigorous
study designed to test these ideas directly is on-going.
Similarly, successful computer based programs have been reported for weight loss in
individuals with type 2 diabetes (Tate, Jackvony, and Wing, 2003) and are being piloted for
weight loss interventions in the US and United Kingdom for adults (Harvey-Berino, Pintauro,
and Gold, 2002; Kirk et al., 2003; Kumanyika and Obarzanek, 2003). Tate and colleagues
(Tate et al., 2003) compared an internet-only treatment versus an internet + weekly e-mail
check-ins with a counselor treatment and reported significant weight loss in both groups with
greater loss in the internet +e-mail group. Both groups showed reductions in caloric intake
and increases in energy expenditure indicating that internet-based applications for the
treatment of overweight are efficacious. Thus, the use of technology as a means of treatment
delivery is emerging (Tate et al., 2003); further studies are needed in order to bridge the gap
between clinical research and population-based delivery for the treatment of BED.
When evaluating the overall value of a particular treatment modality, it is useful to
understand the “clinical significance” of a “statistically significant” research finding. Such
understanding comes in the form of an “effect size” that indicates the size or importance of an
observed treatment effect. One approach to determining effect size that is particularly
relevant to the practice of evidence-based medicine is NNT (number needed to treat). Simply
defined, NNT is the number of patients a clinician would need to treat with a particular
modality to prevent one patient from having an adverse outcome over a predefined period of
time. When comparing a particular treatment to placebo or another control condition, NNT is
the number of patients who would need to receive active treatment in order to achieve one
more successful outcome in the treatment group compared to the control group. In a sense,
the NNT also represents the likelihood that a patient who receives treatment will benefit from
it. For example, if five patients must receive treatment in order to prevent one from having an
adverse outcome over the defined treatment period, then the NNT for that treatment is five,
and each patient who received the treatment would have a 20% (one in five) chance of
benefiting from the treatment. Using more traditional epidemiological terms to describe risk,
the NNT is inversely related to absolute risk reduction. Conversely, NNH (number needed to
harm) is defined as the number of patients who would need to receive active treatment in
order for that group to experience one additional adverse event compared to the control
group; NNH is inversely related to the absolute risk increase. The NNT and NNH measures
are most useful when applied to the evaluation of binary outcomes (e.g., treatment success vs.
treatment failures) and when there are reasonably large differences in the success rates of the
treatment vs. the control conditions (Kraemer and Kupfer, 2006). With respect to weight-
related and binge eating outcomes, therefore, it would be meaningful to calculate the NNT
and NNH for outcomes such as obesity status (achieved BMI below 29.9, yes or no) or binge
abstinence (yes/no) that are assessed in treatment trials where the placebo (or control
condition) response rate is low. The NNT and NNH measures would be less applicable for
outcomes such as % ideal body weight, change in binge frequency, time to remission, etc.
With respect to obesity, the NNT varies somewhat as a function of the treatment
modality (medication, surgery, behavioral). In a recent evidence-based review of clinical
trials of effective weight loss treatments, Orzano and Scott (Orzano and Scott, 2004) found
similar results for surgical procedures such as gastric bypass and gastroplasty (NNT range 2
to 8), medications such as sibutramine and orlistat (NNT range 4 to 8), and combination diet
and exercise interventions (NNT = 7). Compared to diet alone, sibutramine was more
effective in helping patients achieve 10% or more weight loss, with the NNT being 50%
lower for those treated with a higher (15 mg, NNT = 4) versus a lower (10 mg, NNT = 8)
dose. While these studies provide some understanding of NNT in the context of obesity, more
data are needed to adequately evaluate treatment modality differences in NNT (as well as
NNH).
The measures of NNT and NNH have received scant attention in the eating disorders
literature thus far. Bacaltchuk and colleagues (Bacaltchuk, Hay, and Trefiglio, 2001)
reviewed randomized controlled trials of antidepressants and psychological treatments for

bulimia nervosa. In five studies comparing an antidepressant alone to psychotherapy alone
over a mean duration of 17.5 weeks, the NNH was four. In seven studies comparing
medication/psychotherapy combinations to psychotherapy alone over a mean duration of 15
weeks, the NNH was seven and the NNT was eight. To date, there have been no published
studies of NNT or NNH in the context of BED. This may, in part, reflect the relatively weak
evidence base for treatment efficacy as it pertains to the benchmark binary outcome of
abstinence. As we move forward in our understanding (and management) of placebo response
and dropout in treatment trials for BED, and we elevate the scientific rigor of future studies to
focus on key outcomes of abstinence and achievement of normal body weight, physicians and
clinicians may be well served by presenting our findings in the clinically-relevant terms of
NNT and NNH.
Conclusion
Treatments for obesity and BED include medications, behavioral interventions, surgery,
and combinations of these approaches. Evidence for long-term success is much stronger for
obesity treatment strategies than for BED strategies, in part, because of a lack of long-term
BED studies overall. Side effects of certain medications and risks associated with surgery
limit the broad application of these interventions; and surgical interventions for obesity are
likely to be more successful when paired with psychological evaluations and therapies.
Assessing for and treating binge eating behavior is an important aspect of supportive therapy
that accompanies surgical interventions. Additional strategies for maintaining initial weight
loss and improvements in eating psychopathology are needed, and observations that certain
anti-depressants and novel techno-therapies may be beneficial for curbing binge eating and
promoting weight loss warrant further investigation. The successful battle against these two
serious public health concerns will depend on our ability to tailor treatments to individual
patients, incorporating evidence-based strategies that are disseminated easily to both the
treating clinician and the patient.
Acknowledgement
The authors wish to thank Xiaofei Mo, M.D. for her valuable editorial contributions.
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Chapter XIV
Interpersonal Psychotherapy (IPT) for

Eating Disorders
Rebecca Murphy, Suzanne Straebler, Zafra Cooper,

and Christopher G. Fairburn
University of Oxford, United Kingdom
Abstract
This chapter is concerned with the use of interpersonal psychotherapy (IPT) to treat
patients with eating disorders. IPT is a short-term focal psychotherapy which was
initially developed as a treatment for clinical depression but has been applied to many
other clinical problems. Its leading indications are as a treatment for depression and
bulimia nervosa. The goal of treatment is to help patients identify and resolve current
interpersonal difficulties, the rationale being that doing so will result in recovery from the
target disorder.
The chapter opens with a detailed consideration of the rationale for using IPT to treat
patients with eating disorders. Then the evidence supporting this use of IPT is presented.
There follows a description of the treatment and a comparison of IPT with cognitive
behavior therapy (CBT). The chapter closes with a discussion of the ways in which IPT
might operate.
Introduction
This chapter focuses on the use of interpersonal psychotherapy (IPT) in the treatment of
eating disorders (IPT-ED). IPT is a short-term focal psychotherapy which was initially
developed as a treatment for clinical depression. The goal of treatment is to help patients
identify and resolve current interpersonal difficulties. The rationale for such a treatment is
that interpersonal problems are known to contribute to the onset and maintenance of clinical
depressions and as such their modification is likely to facilitate recovery. The efficacy of IPT
in the treatment of depression has led to it being applied to other clinical problems, including
258 Rebecca Murphy, Suzanne Straebler, Zafra Cooper et al.
recurrent depressive disorder, bipolar disorder, dysthymia, substance abuse, marital problems,
anxiety disorders and eating disorders (Weissman, Markowitz, and Klerman, 2007). It has
also been adapted for use with adolescents (Mufson, Moreau, Weissman, and Klerman,
1993), older adults (Frank, Frank, Cornes, Imber, Miller, and Morris, 1993), and pregnant
women (Weissman, Markowitz, and Klerman, 2007).
First we consider the rationale for using IPT to treat patients with eating disorders. Then
we review the evidence supporting this use of IPT. This is followed by a concise description
of the treatment and a comparison of IPT with cognitive behavior therapy (CBT). Finally, we
consider how IPT might achieve its effects and suggest avenues for future research.
The Rationale for Using IPT to Treat Patients with

Eating Disorders
There are good reasons for using IPT to treat patients with eating disorders. Most patients
with eating disorders have interpersonal difficulties. These may have been evident before the
eating disorder developed or they may be more recent and possibly a consequence of it. The
majority of adult cases are in their twenties or early thirties and have had an unremitting
eating disorder for on average eight years (Fairburn et al, 2007). Not uncommonly, the eating
disorder has had a profound effect on interpersonal development as late adolescence and
early adulthood are crucial periods for growth in this regard. For example, many patients
have had little experience developing and maintaining intimate relationships, in part because
of the social withdrawal that is a feature of eating disorders and in part because of
accompanying low self-esteem. Some have also had to abandon career plans and are
essentially "at sea" in terms of their life aspirations and goals. As a result, the interpersonal
impact of the eating disorder may be profound. These interpersonal difficulties tend to
contribute to the maintenance of the eating disorder through a variety of mechanisms. First,
patients' psychopathology tends to persist unchallenged as a result of their isolation from the
normalizing influence of their peers. Second, some eating disorder features are maintained by
interpersonal difficulties. For example, both binge eating and dietary restraint tend to occur,
or be intensified, by the occurrence of adverse interpersonal events. Third, interpersonal
difficulties often serve to worsen self-esteem which in turn tends to magnify patients’
attempts to control their eating, shape and weight (Fairburn et al, 2008). IPT is designed to
help patients overcome their interpersonal difficulties, thereby removing a major factor
maintaining their eating disorder.
The Empirical Standing of IPT for Eating

Disorders
Bulimia Nervosa
There have been two main randomized controlled trials of IPT for bulimia nervosa. The
first of these was conducted by Fairburn and colleagues in Oxford (Fairburn et al, 1991,
Interpersonal Psychotherapy (IPT) for Eating Disorders 259
1993). Seventy-five patients were randomized to cognitive behavior therapy for bulimia
nervosa (CBT-BN; Fairburn, Marcus and Wilson, 1993), a behavioral version of CBT-BN
(BT) or IPT, and at the end of treatment were entered into a closed (i.e., treatment-free) 12-
month follow-up period. The treatments were carefully monitored for adherence. Patients in
all three treatment conditions gave equivalent ratings of treatment suitability and expectancy.
CBT was found to be significantly more effective at reducing the key behavioral features of
bulimia nervosa than IPT at post-treatment, but this difference disappeared over the following
eight months due to continuing improvement in the IPT group (see Figure 1). The behavioral
version of CBT was least effective overall due to substantial post-treatment relapse. Thus IPT
was as effective as CBT in the long term, but comparatively slower-acting. In a longer term
follow up of these patients Fairburn et al. (1995) found that on average six years after
treatment the majority of patients who had received IPT and CBT had maintained the changes
seen at 12 months. Indeed, 72% of those who had received IPT no longer met DSM-IV
criteria for an eating disorder (Fairburn, Norman, Welch, O’Connor, Doll and Peveler, 1995).
IPT and CBT also resulted in an equivalent and lasting decrease in general psychiatric
features and an improvement in self-esteem and social functioning. The fact that both CBT
and IPT were superior to BT indicates that the improvements were not simply the result of
non-specific psychotherapeutic processes.
A second, much larger (N=220), two-centre study conducted at Stanford and Columbia
replicated the main Oxford findings (Agras, Walsh, Fairburn, Wilson and Kraemer, 2000).
Again, CBT was found to be superior to IPT at the end of treatment but the two treatments
were equivalent by eight-to-12-month open follow-up. An additional goal of this second
CBT-IPT study was to identify differential predictors of response to IPT and CBT, the hope
being that this would allow the matching of patients to the two treatments. However, no
differential predictors were found (Fairburn, Agras, Walsh, and Wilson, 2004).
Mitchell, Halmi, Wilson, Agras, Kraemer, and Crow (2002) carried out a study to
explore whether women with bulimia nervosa who did not respond to CBT would respond to
IPT or antidepressant medication. Unfortunately, the findings of this study are difficult to
interpret because of a high rate of non-acceptance of the second-line treatment. Overall, there
was no evidence to suggest that IPT was a good treatment for patients who do not make a full
response to CBT.
Anorexia Nervosa
There has been one study of the use of IPT in the treatment of anorexia nervosa
(McIntosh, Jordan, Carter, Luty, McKenzie, Bulik, Frampton and Joyce, 2005). Fifty-six
patients were randomized to IPT, CBT or non-specific supportive clinical management. At
the end of treatment, IPT was found to be the least effective of the three treatments. No data
on follow-up have been presented so it is not yet known whether IPT has the same delayed
effect in anorexia nervosa as seen in bulimia nervosa. It should also be noted that the sample
was an unusual one in that many of the patients were subthreshold cases of anorexia nervosa
with a weight above the widely used diagnostic cut-off point.
Eating Disorder NOS
There has also been one major study of the use of IPT in the treatment of patients with
eating disorder NOS. This focused on a subgroup of these patients, namely those with binge
eating disorder accompanied by obesity (Wilfley, Welch, Stein, Borman Spurrell, Cohen,
Saelens, Zoler Dounchis, Frank, Wiseman and Matt, 2002). In this study, 162 patients were
randomized to group CBT or group IPT and then followed up for 12 months. The patients in
the two treatment conditions showed an almost identical, and substantial, response over
treatment and open follow-up. Overall, the findings are suggestive of a non-specific
psychotherapeutic response.
No studies have addressed the use of IPT with patients with other forms of eating
disorder NOS. This is a serious omission since it is now recognized that eating disorder NOS
is the most common eating disorder diagnosis made in routine clinical practice, and that these
patients have as severe and longstanding an eating disorder as patients with bulimia nervosa
(Fairburn et al, 2007).
Conclusion
Four conclusions may be drawn from this body of research:
1) IPT is an alternative to CBT in the treatment for bulimia nervosa but it takes longer
to achieve its effects. Indeed, systematic review conducted by the UK National
Institute for Health and Clinical Excellence (NICE) concluded that IPT was the
leading empirically supported alternative to CBT (NICE, 2004). There are no
empirical grounds for matching patients to CBT or IPT.
2) IPT cannot be recommended as a treatment for anorexia nervosa, at least not as a
sole form of treatment (as provided in the McIntosh et al, 2005 study).
3) IPT is one of many treatments for binge eating disorder, the other leading treatments
being an adaptation of the CBT for bulimia nervosa (Fairburn et al, 1993) and guided
cognitive-behavioral self-help (Grilo, 2006).
4) There is a pressing need for research on the use of IPT with patients with eating
disorder NOS.
The Practice of IPT for Eating Disorders

IPT for eating disorders (IPT-ED) is based on IPT for depression and closely resembles
it. In essence, it is a slight modification of the empirically-supported adaptation of IPT for
patients with bulimia nervosa (Fairburn, 1997). IPT for bulimia nervosa (IPT-BN) has been
extended for use with patients with any form of form of eating disorder (IPT-ED) so long as
the patient is not significantly underweight (defined in this context as a BMI <17.5) and IPT-
ED addresses a new type of interpersonal problem that we have termed "life goals". This is
described later.
As IPT-ED is an outpatient-based treatment, it is essential that it is safe for patients to be
managed this way. Patients with eating disorders are at risk of suicidal behavior and various
physical complications. Establishing that it is appropriate to provide outpatient treatment is
therefore an essential preliminary to embarking upon IPT. Guidelines for doing so are
provided by Fairburn, Cooper and Waller (2008).
IPT-ED generally involves 16 to 20 50-minute treatment sessions over about four to five
months. Like IPT for depression, the treatment has three phases.
Phase One - This generally occupies three-to-four sessions. The first aim of this phase is
to describe the rationale and nature of IPT-ED. This is part of the process of engaging
patients in treatment. The second aim is to agree jointly upon the current interpersonal
problem, or problems, which will be the focus of the rest of treatment.
Phase Two - This is the main part of treatment and occupies up to ten weekly sessions.
The goal is that the patient first characterizes the identified interpersonal problem(s), and then
addresses it (them). IPT for depression categorizes interpersonal problems into one of four
overarching "problem areas"; grief, interpersonal role disputes, role transitions and
interpersonal deficits. Both problem area-specific and generic IPT strategies and procedures
are used to address these problems.
Phase Three - This generally occupies the final three sessions. There are two goals; the
first being to ensure that the changes made in treatment are maintained, and the second being
to minimize the risk of relapse in the longer-term. .
For details about the practice of IPT, readers should consult the original IPT "manual"
(Klerman, Weissman, Rounsaville and Chevron, 1984) or the more recent version of it
(Weissman, Markowitz and Klerman, 2000).
Phase One
Phase One usually occupies three-to-four sessions. As noted above, there are three goals.
1. Engaging patients in treatment and describing the rationale and nature of IPT-ED - It
is explained that to help people break out of a self-perpetuating problem such as an eating
disorder it is necessary to find out what is keeping it going and then to address the
maintaining processes in treatment. The therapist informs the patient that interpersonal
difficulties are common in patients with eating disorders, although many people have limited
awareness of them due to the distracting influence of their preoccupation with thoughts about
eating, shape and weight. Interpersonal difficulties maintain the eating disorder through a
number of mechanisms. These were summarized earlier. It is often useful to give patient’s
specific examples (related to their individual circumstances) of how interpersonal issues may
maintain their type of eating disorder. It is then explained that treatment will focus on the
patient’s current interpersonal difficulties, rather than on the eating problem, because the goal
is to help patients overcome their eating problem by resolving difficulties in their life and
relationships. Focusing too much on the eating problem would tend to distract the patient and
therapist from this task.
Patients are also forewarned that the treatment will change in style over time. Initially,
during the first three or four sessions, the goal is to identify those interpersonal difficulties on
which the rest of treatment will focus. The therapist may say something along these lines:
"This initial phase of treatment will involve a review of your past and present
relationships, and during this stage I will take the lead in asking you questions. This
phase of treatment will end with us agreeing upon the problem or problems that should
be the focus of the remainder of treatment. Thereafter our sessions will change in style.
You will become largely responsible for the content of the sessions and I will take more
of a back seat role. Gradually we will learn more about your interpersonal difficulties and
ways of changing them. Your role will be not only to explore these difficulties in our
treatment sessions but also to think about what we have discussed between the sessions.
Furthermore, whilst you are having treatment it is important to experiment with making
changes in your life. Doing so will help us better understand the nature of your problems
and may suggest further ways of changing.”
It is important that the patient understands that the treatment is time-limited. The fact that
the treatment has a fixed number of sessions helps the therapist stress the importance of
working hard at treatment.
"This is an opportunity to change - an opportunity to break out of what has been a

longstanding problem. It is essential that you make the most of this opportunity by giving
the treatment priority in your life. Not doing so is likely to limit the progress that we can
make.”
2. Identifying current interpersonal problems - Three sources of information are used to

identify current interpersonal problems:
i) A history is taken of the interpersonal context in which the eating problem developed
and has evolved – As part of this history-taking the therapist asks about how the
eating problem has evolved (e.g. the ages at which the patient first began to diet,
binge and purge, and any significant changes in weight). The therapist also asks
about the patient’s interpersonal functioning prior to and since the development of
the eating problem, including relationships with family and peers. The therapist will
also take a history of co-existing psychiatric disorders if these are present. The
review highlights links between changes in the eating problem and interpersonal
events and circumstances, thereby stressing the importance of interpersonal
processes. This helps the patient see the relevance of IPT and gives clues as to
current interpersonal problems. For most patients the review of the past should be
relatively brief and take only two sessions. It should be noted that the earlier
description of IPT for BN encouraged the construction of a detailed ‘life chart’
(Fairburn, 1997). This has been abandoned as it can become too time-consuming and
adds little to the identification of current interpersonal difficulties.
ii) An assessment is made of the quality of the patient's current interpersonal
functioning and life circumstances - This involves conducting an “interpersonal
inventory” in which the therapist asks about the patient's social network and current
circumstances. Enquiry is made about family members, the patient's partner (if any),
confidants, friends, work contacts and other acquaintances. The topics addressed
include frequency of contact, positive and negative aspects of each relationship,
mutual expectations, intimacy and reciprocity. In addition, the therapist asks about
significant interpersonal changes over the last few years. In particular this
encompasses interpersonal "exits" (i.e. where the patient has lost a relationship,
including bereavements). Patients are also asked about recent significant changes in
their life circumstances (for example, in terms of their home-life, family, social life,
health, and so on) and about their future life goals.
iii) The precipitants of changes to eating are identified - In each of the assessment
sessions, the therapist also asks whether there have been any changes in the patient’s
eating since the last session (i.e., intensification of dieting, binge eating, purging,
etc) and, if so, enquires about the interpersonal circumstances preceding them. Since
it is common for changes in eating to be precipitated by interpersonal events, they
may serve as "markers" of current interpersonal problems. In this way the
relationship between the eating problem and interpersonal events can be carefully
explored. Some secondary accounts of the treatment have implied that this is not
done in IPT for eating disorders (e.g., Weissman, Markowitz and Klerman, 2007).
This is incorrect.
3. Choosing which problems should become the focus of treatment - By the third or
fourth session, the nature of the patient's interpersonal difficulties should be clear. The next
step is to decide which should become the focus of the remainder of treatment. This decision
should be a collective one.
The Problem Areas
Five types of interpersonal problem tend to be present in patients with eating disorders.
These differ somewhat from those identified by Weissman and colleagues in patients with
depression. This is not surprising given the age of these patients and the nature of their
psychiatric difficulties. These patients are quite different from those with depression who
tend to be older and suffering from an episodic disorder rather than an unremitting one.
1. Lack of intimacy and interpersonal deficits - The most common interpersonal problem
encountered is lack of close or satisfactory intimate relationships, romantic or otherwise. We
use a slightly broader definition of ‘deficit’ than Weissman, Markowitz and Klerman (2000),
one which is exclusively present-focused and therefore does not require patients to have
long-standing unfulfilling relationships. Although some patients describe a scarcity in general
of interpersonal relationships and feelings of isolation, many more specifically lack intimate
relationships. Treatment aims to encourage these patients to consider what they want from a
relationship and to take steps to achieve this. It may be helpful to review past significant
relationships and consider any recurrent problems in order to make changes in the present.
2. Interpersonal role disputes - Interpersonal role disputes are also common. Disputes of
this nature may be with any figure of importance in the patients' lives, including partners,
family members, friends and employers. Such disputes are often the result of each party
having differing expectations of each other. The aim of treatment is to help clarify the nature
of the dispute, consider the possibilities for change on both sides (including communicating
expectations), and then to actively explore them. The outcome may be a renegotiation of the
relationship or its dissolution.
3. Role transitions - Problems with role transitions are seen when the patient has
difficulty coping with a life change. Life changes are common in this patient group given
their age. Frequently encountered examples include: moving away from home and
establishing independence from parents, starting a first job or having a partner for the first
time. However, difficulties in this area are not confined to the problems of late adolescence
and early adulthood. They include problems coping with other life changes such as changing
jobs, getting married and becoming a parent. The goal of treatment is to help the patient
abandon the old role and adopt a new one. This involves exploring exactly what the new role
involves and how it can be mastered as well as examining and re-evaluating the old role,
which may have become idealized.
4. Grief - Problems associated with the death of a loved one are not common in patients
with eating disorders given their age. If such difficulties are apparent it is important to help
the patient think in detail about the events surrounding the loss and express their feelings
about it. Reconstructing the lost relationship, both its’ positive and negative aspects, is also of
central importance, as it counters the idealization that commonly occurs. As patients become
less focused on the past, they are helped to think about the future and to create new interests
and relationships.
5. “Life goals” - Problems concerning future life plans are frequently encountered in this
patient group. They are characterized by patients' uncertainty over what course their life
should take in terms of career, lifestyle and relationships. It is broader in nature than
difficulty coping with role transitions because in this instance patients need to develop new
roles in their life and reconsider their goals (rather than to adjust to the current role) and it is
for this reason that we view “life goals” as a new problem area. Treatment is an opportunity
for patients to reconsider their aspirations, to consider taking steps towards meeting them and
to make changes in their life. Typically this is a second problem area and one that is
addressed after the patient has made progress in another area and is feeling more hopeful
about the future.
If more than one problem is identified a decision needs to be made about which problems
will be addressed and in what order. In general it is only possible to tackle one or two
problems in treatment. Our strategy is to address those whose resolution is likely to have the
greatest impact on the patient's eating disorder. Given our view of how IPT is likely to work
(see below) we choose those problems that we think will have the greatest impact on the
patient's overall interpersonal functioning and self-esteem. Clearly, they also have to be
viewed by the patient as a problem. When there are two problems to be tackled they are
generally addressed sequentially, with the simpler and more easily solved being tackled first.
Progress on one front often bolsters the patient's morale and sense of interpersonal
competence thereby facilitating their tackling of other difficulties.
Phase Two
Once the problem area(s) has (have) been agreed by both patient and therapist, the
treatment enters phase two. The second and third phases of the treatment are very similar to
IPT for depression, as described in the IPT manual, although in IPT-ED the patient is placed
under greater general pressure to change. At the end of Phase One the therapist reminds the
patient that the treatment will now alter in character.
"As we discussed at the outset, from this point on the nature of our sessions will change.
Instead of my asking you questions, you will take the lead. Your task will be to focus on
the problems we have identified and consider them in depth and from all possible angles.
In this way we will come to a better understanding of them. A key part of treatment is
thinking about what changes you could make and how to bring them about. While you
are in treatment it is important that you make changes as we will learn much more about
your problems from your attempts to change them”
The sessions from this point on are largely patient-led. The therapist is active but not
directive and throughout the focus remains on the present. Sessions begin by reminding
patients of the session number and how many remain, followed by a general enquiry such as
‘How have things been since we last met?’
The initial task in Phase Two is for the patient to characterize the identified problem(s).
The therapist’s role is to ensure that the patient remains focused on this task. The therapist
asks questions to facilitate this (although this does not extend to making "interpretations"
which depend on a particular theoretical view of the disorder and its treatment). In doing this
the therapist aims to help patients gain a better understanding of their problems.
Generally, after several sessions, the patient has moved on to consider ways of changing.
Using the IPT technique of "decisional analysis" (Weissman, Markowitz and Klerman, 2000),
the therapist helps the patient think through all the options available together with their
implications in order to arrive at a course of action. As the therapist is not directive, possible
solutions are not offered nor are opinions expressed about what the patient should do. The
therapist praises all efforts to identify solutions and change. Patients’ attempts to change
become the focus of subsequent sessions.
As part of the process of understanding interpersonal difficulties and considering ways of
changing, the IPT technique of "communication analysis" may be used to better understand
key interpersonal exchanges. This involves reviewing these exchanges in detail to identify
exactly what was said by both parties, what the patient had intended to communicate, and
how the patient interpreted the communication of the other party. The therapist always
encourages the patient to consider the perspective of the other person. In this way,
ambiguities and misunderstandings may be identified and clarified. This helps patients
consider how effectively they communicate with others. It is often useful to ask patients to
report exchanges verbatim, using the same tone of voice and words as in the original. Role
playing may also be used to prepare patients for key forthcoming exchanges. It is worth
noting that this is in contradiction to some reports which have claimed that IPT-ED does not
include role play (Weismann, Markowitz and Klerman, 2007).
The need for the patient to change is stressed at regular intervals. It is important to note
that this is general pressure to change rather than pressure to take a specific course of action.
Progress in treatment becomes an iterative process. Through making changes patients gain a
greater understanding of their problems and as a result are able to make progressively more
strategic and influential changes. Furthermore, as patients experience successes resulting
from such changes their confidence about making further life changes increases.
At the end of each session the therapist provides a brief summary of what has been
covered in the session using the patient’s own words. This summary is simply an account of
the content of the session and does not involve any additional processing or interpretation
from the therapist. The therapist also encourages the patient to think further about the matters
discussed between this appointment and the next one. In addition, on one or two occasions
during Phase Two, the therapist and patient informally review progress by considering each
of the agreed upon problems and assessing what has been achieved and what remains to be
done.
The therapist's role in Phase Two is to help patients change, to help them appraise the
consequences of these changes and then to make further changes. Reference is rarely made to
the therapist-patient relationship since doing so can complicate and undermine IPT. However,
one exception is patients who have such severe interpersonal deficits that one of the very few
relationships available for examination is that between the therapist and patient. Such patients
may benefit from feedback about how they come across to others.
Interestingly, most patients make few, if any, references to their eating disorder. If they
do, the therapist shifts the topic on to the interpersonal context of the eating problem perhaps
by saying "It is understandable that you are binge eating a lot just now, given what is going
on …." Detailed discussion of the eating disorder is not part of IPT-ED as it distracts patients
and therapists from the interpersonal focus of the treatment. Furthermore, it can trigger
extreme ruminative thinking about shape, weight and eating that can prevent patients from
reflecting on their interpersonal difficulties. However, at times it can be helpful to restate the
rationale of the treatment as this often helps address concerns patients may have about the
absence of a direct focus on the eating disorder.
Phase Three
The third phase of treatment comprises the final three sessions. Ending treatment is an
interpersonal event in its own right and an important part of treatment. The final sessions are
held at two-week intervals, thus allowing patients increased time to continue to make changes
on their own with less input from the therapist. There are two related goals. The first is to
ensure that the changes that have been made continue following termination, and the second
is to minimize the risk of relapse.
Unlike the transition between Phases One and Two, there is no sharp change in style
between Phases Two and Three. Instead, the sessions continue much as before except that
there needs to be a review of what has been achieved in treatment and a consideration of the
future. When progress on a particular problem is being discussed, the therapist should help
the patient project forwards to the future perhaps by saying: "As you know, we only have
three more sessions to go. What do you envisage happening regarding ........... over the
coming months? How can you make sure that you build upon what you have achieved so
far?” By this point, it will be clear what changes are likely to be made during the period of
treatment and what changes may well not take place. The therapist should ensure that the
patient has realistic expectations in this regard. For example, the therapist might say: "Given
what has emerged during treatment, it seems that you think it unlikely that .......... will start to
behave differently in the foreseeable future. If this is the case, what do you think you should
do?"
The therapist should also help the patient predict areas of future interpersonal difficulty.
Both problems in the areas addressed in treatment and broader interpersonal issues should be
discussed. Therapists should ask patients what they plan to do to overcome such difficulties
should they arise.
In Phase Three, as well as at appropriate points earlier in treatment, the interpersonal
competence of the patient should be highlighted so that patients attribute any changes made
to themselves rather than to the therapist. The therapist should explain that, although he or
she acted as a guide during treatment, the patient has actually made the changes that have
taken place.
An assessment of the state of the patient’s eating problem should also be made in Phase
Three. Patients are reminded that it often takes a further four to eight months for the full
effects of IPT-ED to be realized. We advise patients not to seek further treatment in the
meantime. However, patients are also told that their eating problem is likely to remain an
Achilles heel in the sense that they may experience a lapse in the future at times of
interpersonal difficulty. We encourage patients to view any deterioration in their eating
problem (e.g., a return of binge eating or loss of weight) as a potential "early warning sign" of
a developing interpersonal problem and as a cue to review what is happening in their
personal life and, perhaps, to take corrective action.
It is unusual for patients receiving IPT-ED to have difficulty accepting the ending of
treatment. This is because it is made clear at the outset that treatment is time-limited and at
the beginning of each session they are reminded of the number of sessions remaining.
Nevertheless, therapists should always ask patients how they feel about the ending of
treatment, not least because this provides an opportunity to emphasize what has been
achieved and to stress their competence at dealing with future areas of difficulty.
An Illustrative Case History
The patient was a 21-year-old college student, referred by her primary care physician, for
the treatment of bulimia nervosa. This was a longstanding problem, which had begun in
adolescence.
Phase One
Treatment began by taking a history of the interpersonal context in which the eating
problem had developed. The patient began dieting at school and started to binge eat and
vomit about a year later. During this time, she described feeling that she did not have friends
who she could turn to for support. Although she felt unsure as to whether she wanted to
continue her education, she went to college because of pressure from her parents. When she
started college the eating problem became more severe. She reported that her shame and
secrecy over binge eating and vomiting prevented her from making friends. Eventually she
decided to drop-out of school. At the time she requested treatment she was working as a
waitress.
During the first few treatment sessions, the therapist asked her about each occurrence of
binge eating and vomiting and the interpersonal context in which they occurred. This
revealed that they usually occurred in the evenings, when feeling lonely or when bored at
work.
At the end of the third session, the patient and therapist agreed that the patient’s lack of
close relationships should be the problem area on which treatment should focus. The patient
explained that she preferred to keep others at ‘arm’s length’ as she was afraid of becoming
too dependent on them and eventually being let down. She also described being reluctant to
reveal her feelings to her friends especially when she was experiencing any problems in case
they thought that she wasn’t a “fun person” and that she was a burden to them. The patient
found these initial sessions particularly difficult since she had previously been trying to avoid
thinking about problems in her life and relationships. The therapist was able to keep the
patient engaged in treatment by praising her efforts to think about these matters and by
explaining that understanding more about her problems was a necessary first step if she was
to overcome them. At the end of this initial phase of treatment the therapist reminded the
patient of the change in session style that was about to take place.
Phase Two
In the first few sessions of Phase Two, the patient’s past friendships were reviewed. This
revealed that the patient had never felt that they were reciprocal. Although she was able to
listen to her friends’ worries she did not allow herself to talk about her own insecurities. She
also felt uncertain about whether her friends really liked her and so would avoid taking the
initiative in agreeing to meet. The therapist encouraged the patient to consider her options for
developing closer friendships. This involved helping her think about the sorts of friendships
she wished to develop and the expectations she had of them. At this time, the patient was
particularly concerned with a problem at work and decided that she would mention this to a
friend. The therapist helped the patient to role play how she could elicit her friend’s support
without risking the friend feeling burdened. The patient was subsequently pleased that her
friend was supportive so she decided to invite the friend to a family party. The friend did not
come to the party with the result that the patient came to the next session saying that
treatment was not working and she was tired of making efforts to change. The therapist and
patient decided to review what had taken place. It emerged that when she had invited her
friend she had said that she was going to a family party which would most likely be boring
but she was welcome to come. On reflection, the patient realized that from her friend’s
perspective it was not obvious that the patient wanted her to attend the party. It was clear that
the patient needed to learn how to communicate clearly and unambiguously.
During the following weeks the patient continued to make interpersonal changes and
developed new friendships through joining a book group. In one session, the patient asked
what she should do about her eating since she was still struggling in this regard. The therapist
reminded the patient about the rationale underpinning the treatment. The therapist explained
that the patient should be focusing on overcoming difficulties in her life and relationships,
and that over time this would lead to improvements in her eating.
About two-thirds of the way through treatment the therapist asked the patient to review
the progress that she had made. The patient described realizing that she was a likeable person
with whom people wanted to be friends and that her friends accepted that sometimes she
needed support from them. The patient also mentioned that she had recently been feeling
more dissatisfied and bored with her work. Previously, she had welcomed the fact that she
found working as a waitress less demanding than being a student. However, even though she
had been given greater responsibilities at work, she did not find the job challenging enough.
As the addressing of the initial problem area was progressing so well, the therapist and
patient agreed to spend time during the remaining sessions reflecting on the patient’s goals in
life.
The patient was encouraged to think about what she wanted to do in the future. She came
to the conclusion that she wanted to be a teacher. She realized that going back to finish her
college degree would be the best way of working towards this goal and so she negotiated a
return to her studies. She subsequently described looking forward to returning to college
because she felt that she had made the decision to be there rather than being there because of
pressure from her parents.
Phase Three
In the last phase of treatment, the therapist and patient considered what had been
achieved in treatment. The patient felt pleased about the changes that she had made in her life
both regarding her friendships and her plan to return to college. As a result she described
feeling more confident about herself. The patient was encouraged to consider any potential
problems that might occur and how she might use what she had learned in treatment to
address them. She reported that she was more aware of difficulties in her life and that, instead
of avoiding thinking about them; she was able to think about options for resolving them.
In the penultimate session the therapist asked the patient about her eating. The patient
explained that in the initial weeks of treatment she had been concerned that the eating
problem was getting worse but that in the last month or so she had been binge eating and
vomiting much less frequently. She said that she had realized that overcoming the eating
problem did not require her to be more disciplined about eating but rather it involved her
addressing what was happening in her life. The therapist told her that continued improvement
was likely and advised her to regard problems in eating as a marker of other difficulties in her
life and relationships.
Follow-up
The therapist saw the patient for two follow-up sessions, one approximately six months
after treatment and one six months after that. During this time the patient had resumed her
studies and was living with other college students. She described being much happier in her
life and having several close friends. She also reported that she had not been thinking much
about food, eating, shape or weight. More detailed assessment revealed that she had few
residual eating disorder features.
How IPT-ED Differs from CBT

The distinctive feature of IPT is its interpersonal focus and its interpersonal strategies,
rather than its use of particular specific techniques (Weissman, Markowitz and Klerman,
2007). Although IPT employs techniques used in many other therapies, there are certain
procedures that are not utilized. As CBT is considered the leading empirically-supported
treatment for eating disorders (Wilson and Fairburn, 2007), an examination of the differences
and similarities between these two forms of treatment is warranted. It is important to note that
it is a very specific form of CBT that is empirically supported (Fairburn, 2008). It is therefore
this version that is compared with IPT-ED.
IPT-ED and CBT share a range of common features. Both are time limited, short-term
focused psychological treatments which explore current problems; the aim being to change
maintaining mechanisms, rather than to uncover past causes. However, the theory
underpinning each treatment differs. CBT focuses on cognitive and behavioural maintaining
processes and the goal is their direct modification. In contrast, IPT-ED aims to treat the
eating disorder indirectly through the addressing of current interpersonal problems.
Consistent with these differing rationales, the content of CBT and IPT-ED sessions
differs markedly. IPT-ED makes little reference to the eating disorder but focuses on the
identified interpersonal problems, while CBT focuses on the modification of the cognitive
and behavioural processes thought to be maintaining the individual patient’s eating disorder.
Interpersonal difficulties are only addressed in CBT if they appear to be directly maintaining
the disturbances of eating. [A variant of CBT has been developed that also addresses
interpersonal problems – see Fairburn et al, 2002; Fairburn et al, 2008)].
The role of the therapist is similar in the two treatments with respect to being both active
and an advocate for the patient although the sessions differ in form. In IPT, the sessions are
patient-led (except during Phase One) and unstructured, whereas in CBT the sessions are
agenda-led and structured. The IPT therapist is non-directive, whereas the CBT therapist is
more so. The IPT therapist does not encourage patients to change their behaviour in specific
ways: instead IPT relies upon in-session verbal dialogue to produce change, together with
encouragement to continue thinking about the matters discussed between sessions. In CBT,
behaviour change is a major focus of treatment. Indeed, as discussed by Fairburn, Cooper and
Shafran (2008), in CBT the goal is to help patients make personalised and highly strategic
changes to the way that they behave, and then help them analyze their effects and
implications. In IPT, there is only general pressure to make interpersonal change and no
homework. In both treatments, the patient is seen as largely responsible for change with the
therapist guiding them through this process. Both treatments regard much of the therapeutic
progress made during treatment as being the result of work done between the therapy sessions
How IPT Works

There has been little research on how psychological treatments work and IPT is no
exception. This is true of IPT in general and IPT-ED. There has been no research on the
precise relationship between the therapeutic interventions and changes in interpersonal
functioning and eating disorder features. The research findings indicate IPT-BN has a
distinctive course of action with it taking longer than CBT to achieve its full effects (see
Figure 1). This supports the view that it is likely to work through mechanisms that are
specific to it, although another possibility is that it operates through the same mechanisms as
CBT but less efficiently.
Clinical observations can provide insight into the mechanisms of action of treatments. In
conducting IPT-ED we have observed repeated instances of patients making major positive
changes in the identified problem areas and in their life generally. Often these changes set in
progress other positive changes, many of which are still evolving at the end of treatment. In
the absence of research evidence it is possible to suggest several possible processes which
might explain how interpersonal changes might have a beneficial effect on the eating
disorder.
• Improved functioning in the identified problem area(s) might result in there being
fewer interpersonal triggers of dysfunctional eating.
• Patients’ realization that they are capable of bringing about changes in what have
often been entrenched interpersonal problems might lead them to feel more capable
of solving relationship problems in general. Alternatively or additionally, improved
interpersonal functioning might produce an improvement in overall self-esteem.

Either of these changes might result in patients believing that they are capable of
changing other problems in their life, including their eating disorder, with the result
that they start to actively address it.
• Alternatively, an improvement in overall self-esteem might result in a decrease in the
extent to which patients attempt to control their eating, shape or weight, thereby
resulting in the gradual erosion of the eating disorder.
The operation of processes of this type might explain how IPT-ED works (see Murphy,
Cooper, Hollon & Fairburn, in press). It would also explain why the full effects of IPT-ED
take longer to be expressed than those of CBT, since CBT focuses directly on changing the
disturbed eating habits and attitudes whereas with IPT-ED these changes are secondary to
interpersonal change.
Future Directions
There is a clear need for more research on the use of IPT in the treatment of patients with
eating disorders. The body of evidence supporting its use in the treatment of bulimia nervosa
is more modest than it is for CBT. Furthermore, there is a paucity of research on the
effectiveness of IPT for patients with other forms of eating disorder. As well as there being a
need for more data to establish the effectiveness of IPT, research is also required on how IPT
operates. Identification of mediators of change should enhance understanding of eating
disorder psychopathology and its relationship to interpersonal processes, as well as help in
the eventual identification of the active components of IPT. This is the research strategy that
we are pursuing in Oxford (see Murphy, Cooper, Hollon & Fairburn, in press).
Acknowledgements
CGF is supported by a Principal Research Fellowship from the Wellcome Trust
(046386). RM, SS and ZC are supported by a programme grant from the Wellcome Trust
(046386).
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Chapter XV
Using Dialectical Behavioral Therapy

for the Treatment of Eating Disorders:
A Model for DBT Enhanced CBT
Lucene Wisniewski∗, Kelly Bhatnagar and Mark Warren

Case Western Reserve University
Cleveland, Ohio, USA
Abstract
Dialectical Behavior Therapy (DBT) is a behavioral treatment that has become of
interest to clinicians and researchers in the eating disorder field. There is empirical
evidence for the use of DBT with Binge Eating Disorder and Bulimia Nervosa and
interest in its use with patients suffering from Anorexia Nervosa. The treatment focuses
on the effective regulation of emotions via the teaching of a comprehensive set of change
and acceptance-based skills while promoting strategies for treatment compliance and
retention. The current chapter describes DBT, reviews relevant literature, and offers a
novel approach for fusing principles of the current field standard, Cognitive Behavioral
Therapy (CBT), with those of DBT to create a functional model adapted to meet the
specific needs of difficult-to-treat ED patients. Although this model has yet to
empirically establish itself as an evidence-based treatment, it holds great promise as it
attempts to move in this direction.
Manual-based cognitive-behavioral therapy (CBT) is currently considered the treatment

of choice for adults suffering from eating disorders (ED) (National Institute for Clinical
Excellence, 2004). CBT, along with interpersonal psychotherapy (IPT), has solidly
demonstrated its overall effectiveness (Wilfley et al., 1993), however, there continues to be a
∗
Correspondence concerning this manuscript should be sent to Lucene Wisniewski, Clinical Director, Cleveland
Center for Eating Disorders, 25550 Chagrin Boulevard, Suite 200, Beachwood, OH 44122. E-mail may be
sent via Internet to lwisniewski@edcleveland.com.
276 Lucene Wisniewski, Kelly Bhatnagar and Mark Warren
substantial number of individuals that do not successfully recover using these approaches
(Anderson and Maloney, 2001; Lundgren et al., 2004), especially those suffering from
anorexia nervosa (AN) (Ball and Mitchell, 2004; Channon et al., 1989; McIntosh et al.,
2005). These data, along with clinical experiences, have prompted clinicians and researchers
alike to look to other empirically-validated treatments for guidance managing patients with
EDs (e.g. Fairburn et al., 2003; Wonderlich et al., 2001).
DBT as a Potential Alternative Treatment

It is not surprising that Dialectical Behavior Therapy (DBT) was quickly identified as an
alternative treatment for ED patients. DBT is a behavioral therapy, modified to include
techniques of validation, acceptance and mindfulness, while simultaneously utilizing a
manualized approach for skill-building to better manage emotional dysregulation. It was
originally developed by Marsha Linehan, Ph.D. to treat patients with chronic suicidality who
also suffered from Borderline Personality Disorder. Linehan has noted that a central
characteristic of BPD patients was the presence of impaired emotional regulation and the lack
of successful strategies to cope with this impairment (Linehan, 1993a). As a result, self
destructive behaviors become the "solution” to this dysregulation, often creating life
threatening situations. Linehan also discovered that treatment as usual for suicidal
individuals, CBT, was often unsuccessful for this patient population (Linehan, 1993a). DBT
was then derived as an alternative approach for these individuals. In doing so, she modified
not only the content of the therapy, but also its structure, goals, techniques and theory of
change.
While drawing from a wide variety of sources, DBT is based on a unique set of
principles. DBT assumes that the most effective path to health begins by first changing
behaviors. It further assumes that if a patient with emotion regulation problems is faced with
an expectation to change without a concomitant focus on acceptance, then emotional
dysregulation will ensue, resulting in the impairment of the patient's ability to learn new
behaviors. DBT therefore expects that the balance of acceptance and change is more likely to
produce lasting effectiveness than a focus on change alone. To accomplish this goal, DBT
focuses on problem solving and skill-building while embracing validation of the patient’s
experience as a primary task of the therapist. DBT stresses the acceptance of one's current
reality, regardless of the pain this acceptance may cause, as the first step to lasting life
improvement. In DBT terminology, this is referred to as "radical acceptance." Rather than the
traditional therapeutic goal of ending misery or finding happiness, DBT is concerned
primarily with giving patients the opportunity to experience a "life worth living" (Linehan,
1993a).
A central tenet of DBT is that, “patients do not fail therapy, therapy fails patients”
(Linehan, 1993a). This belief, long evident in other aspects of health care, often does not
penetrate the psychotherapeutic setting. A significant number of patients have heard that their
failure to heal is due to their being a non-compliant patient, or being unmotivated or
unwilling to do the difficult work. DBT firmly rejects this conceptualization, instead
asserting that it is the job of the therapy to help the patient, not the job of the patient to
Using Dialectical Behavioral Therapy for the Treatment of Eating Disorders 277
conform to therapy. At the same time, DBT holds that therapy can fail even when the
therapist does not fail. This stance in DBT makes the therapy, not the patient or the therapist,
the central concern in effectiveness.
Why Use DBT for the Treatment of

Eating Disorders?
The rationale for applying DBT to the treatment of EDs, has been described in the
literature by our group and others (McCabe, LaVia and Marcus, 2004; Wiser and Telch,
1999; Wisniewski and Kelly, 2003; Wisniewski, Safer and Chen, 2007). The rationale
proposed suggests that alternative approaches are necessary for EDs because, as previously
discussed, current empirically founded treatments (e.g. CBT and IPT) may only be partially
effective or ineffective for a select number of patients (Anderson and Maloney, 2001;
McIntosh et al., 2005). DBT can be considered a logical alternative because unlike the other
approaches, it is based on an affect regulation model of treating ED symptoms. Eating
pathology (e.g. binge-eating, self-induced vomiting, restriction, etc.) may now be understood
as mechanisms to cope with emotional vulnerability (Telch et al., 2000), as opposed to errors
in cognition or faulty interpersonal relationships alone (Fairburn, 1981; Fairburn et al., 1993).
In its pure form, DBT is specifically designed to teach adaptive regulation skills and to
address target behaviors that result from emotional dysregulation (Linehan, 1993b). Taken
together, this provides a strong theoretical justification for applying DBT to the treatment of
EDs (Telch et al., 2000, 2001; Wisniewski and Kelly, 2003).
In addition to its use of the affect regulation model, other components of DBT may make
it a practical alternative for the treatment of EDs. Its unique synthesis of behavioral
principles, dialectical philosophy, and Zen influences makes it particularly useful to ED
patients, especially in helping those patients who may be struggling with issues of motivation
and commitment. For example EDs, especially AN, differ from other mental illnesses (such
as depression and anxiety) in the considerable degree of ambivalence patients hold about
symptoms and treatment. Treatment of ED symptoms, therefore, requires a sophisticated use
of commitment strategies and must focus not only on helping patients change their behaviors,
but also on coaching patients to accept their present state and condition. This dialectical
tension is a key aspect of DBT and its emphasis on both change-based and acceptance-based
therapeutic strategies. For ED patients, who must accept their current progress in treatment,
their fluctuating weight and shape, and other difficult-to-change aspects of their current
situation, DBT’s acceptance strategies are especially valuable. The focus on acceptance is
equally important for the therapist and family members in that it provides a useful framework
for relinquishing control over the time course for lasting change to occur.
Other crucial elements of DBT, such as the therapist and patient consultation case
management strategies, are similarly suited for work with ED patients. For example, given
the tendency for ED patients and their symptoms to evoke intense feeling and emotion in
their treatment providers, the consultation team for therapists draws upon the expertise of a
diverse group of trained professionals (e.g. psychologists, counselors, social workers, medical
doctors, nutritionists, nurses, etc.) to ensure that primary therapists remain committed to
treating a patient within a DBT framework, even when treatment appears to be slow and
frustrating for all. We believe this support is fundamental in the successful treatment of
chronic EDs. Also, by aiding patients in the management of an often extensive health
provider network, DBT therapists may contribute to the development of their patient’s sense
of mastery, control, and self-efficacy, which reinforces the collegial nature of the therapeutic
alliance. Thus, the DBT strategy of team consultation to the patient promotes respect for the
patient’s capacity to learn new behaviors and meet developmental and interpersonal goals.
Finally, similarities in clinical presentation between BPD and ED also distinguish DBT
as an appropriate treatment for EDs. For example, ED symptoms are often minimized as
insignificant problems despite the high mortality rates found with AN (Steinhausen, 2002)
and the significant impairment of functioning found with other EDs (Hayaki et al., 2003).
Also ED behaviors, similar to symptoms related to BPD, are easily perceived as conniving,
dishonest and superficial by therapists, family and friends. Such negative attributions can
lead to significant difficulties in patient’s treatment, especially if they are held by the
therapist. DBT’s solution to this problem is to place great emphasis upon the importance of
working within a non-judgmental framework. Within this framework, behaviors are viewed
non-critically, and thus usefully defined, as reinforced responses that are within a patient’s
current skill repertoire, but are able to be substituted for more adaptive responses through the
therapeutic process.
Existing Data Demonstrating the Effectiveness of

DBT for Eating Disorders
Because the use of DBT for ED treatment is still considered to be relatively new, the
efficacy literature on the topic is limited. However, preliminary research, spearheaded by a
group at Stanford University, shows great promise for the adaptation of DBT theory and
techniques to the ED population. A case report published by Safer, Telch and Agras (2001a)
applied a DBT approach for the treatment of a previously unresponsive adult female with a
long history of BN symptoms. This approach consisted of an abridged DBT skills training
program to address ED symptoms, as well as consultation team meetings used for the support
of the clinician. This treatment did not include individual therapy per se (sessions were seen
as a proxy for group skills training), the Interpersonal Effectiveness Skill module (see below),
or telephone skills coaching—all of which are typically included in traditional DBT.
Nonetheless, this patient experienced a rapid decline in both binge-eating and purging
behaviors, showing drastic change at both post-treatment and at six-month follow-up (Safer
et al., 2001a).
Other studies have examined the effects of a similar DBT adaptation for the treatment of
binge/purge behaviors (Safer et al., 2001b) or BED (Telch et al., 2001). In both studies,
significant improvements on measures of binge-eating and related eating pathology were
demonstrated. Additionally, a DBT program consisting of weekly consultation team, all four
traditional DBT skills modules, plus the addition of one novel skills-training module
designed specifically to treat individuals with ED and co-morbid BPD appeared to be
effective in treating both eating disorder and self-harm behaviors (Palmer et al., 2003).
The significant results from these studies are encouraging and support further research
for the use of DBT with individuals who suffer from ED. Preliminary findings suggest that
DBT, if adapted correctly, could serve as a powerful treatment for ED patients, especially
those who have traditionally been difficult to treat or who have been previously unresponsive
to the more standard treatment approaches.
Cleveland Center for Eating Disorders Model

The paucity of research notwithstanding, many ED treatment programs around the
country have begun to use DBT with their ED patients. A recent Google search using the key
words DBT and Eating Disorder Treatment resulted in over 107,000 hits! DBT’s popularity
may be moving ahead of the data, however, and guidelines concerning DBT’s use with ED
patients are therefore needed.
The DBT skills group model tested by the Stanford research group shows promise in the
treatment of Binge Eating Disorder (BED) and Bulimia Nervosa (BN) patients but currently
does not have a widely available published treatment manual. In addition, the ED patients
studied in this research had relatively low symptom severity as they were selected to be those
without life threatening behaviors and exhibiting ED symptoms that could be managed in
weekly outpatient treatment, as per the American Psychiatric Association practice guidelines
for eating disorders (APA, 2000). Furthermore, the authors of this chapter were interested in
providing DBT to a more broad patient population, for example, patients who present with all
ED diagnoses, moderate to severe symptoms, significant medical and psychiatric co-
morbidity (that may also include, but does not require self harm/suicidality) and previous
failed treatment attempts.
A treatment model was therefore developed to meet the needs of a broader and more
difficult to treat ED population. The standard DBT model was chosen as its basis, as it has
been the most studied and has a widely available treatment manual (Linehan, 1993a).
However, given the potential symptom severity of the targeted population, with many
patients dangerously underweight, it did not seem prudent to omit the effective CBT for ED
techniques which have been well validated (e.g., meal planning, self-monitoring of intake;
psychoeducation regarding ED). Thus the current model of DBT-enhanced CBT or DBT-
CBT for EDs was developed (see Wisniewski and Kelly, 2003; Wisniewski, Safer, and Chen,
2007).
The assimilation of DBT into traditional CBT treatments for EDs appeared viable to the
authors because first and foremost, the foundation of DBT draws heavily from cognitive-
behavioral theory. There are therefore many areas of overlap between the two treatments, the
most striking of which is the focus on change via self-monitoring and strategies to promote
behavioral self-control. The second rationale for incorporating DBT into standard CBT
treatment for EDs was the assumption that DBT could enhance traditional ED treatments by
integrating these complementary treatment components of acceptance and change.
Therefore, for clinicians who value empirically-researched models such as CBT yet who
also are keenly interested in DBT and its potential application to the treatment of EDs, the
following section on DBT-CBT outlines how appropriately trained clinicians can integrate
DBT into existing cognitive-behavioral approaches for the treatment of EDs.
The Focus of DBT for Eating Disorders

The treatment described below employs techniques from Standard DBT with two
exceptions: the diary card and behavior chain.
Diary Cards. The diary card, which is used in standard DBT treatment (Linehan, 1993a),
focuses on targeted behaviors for individuals experiencing suicidality. The authors felt that to
be used effectively with ED patients, the diary card needed to be adapted on several levels,
the most important of which is to include an opportunity for patients to record food intake, as
many patients present in a malnourished state. The diary card, which has been described
extensively elsewhere (Wisniewski, Safer, and Chen, 2007), may be considered a blend of the
standard DBT diary card and a CBT self monitoring form.
As seen in Figure 1, the DBT for ED diary card includes space to record daily intake,
whether or not the patient has engaged in targeted behaviors and a place to report daily skill
use. To complete a diary card, patients are first asked to write their name and the date at the
top of the page. In the “time” column, the patient is to record the time that each meal or snack
was consumed. This information serves as a helpful time indicator for key behaviors or urges.
In the column labeled "plan," the patient is to write down the number of dietary exchanges
that his or her current meal plan requires as designated by the team dietician. Meal plans tend
to change frequently, thus updates are required on a regular basis. In the "act" column, the
patient should indicate the actual amount of each exchange that was consumed at that meal or
snack. For example, if the patient ate three protein exchanges but the meal plan only required
two, the patient would write that they consumed three exchanges. In the column titled
“hunger scale,” patients are to indicate their subjective sense of hunger immediately before
and immediately after a meal or snack. This scale ranges from "empty" to "stuffed," and can
be helpful to patients as they are relearning physiological signs of hunger. Beneath this scale,
the patient is to describe the approximate quantity and type of foods consumed during the
meal or snack. For example, a patient may record for her morning meal “1 slice of turkey
bacon, 2 fried eggs prepared with butter, 2 slices of wheat bread with grape jelly, etc." The
patient then writes the place the meal or snack was consumed in the “location” column (e.g.
restaurant, home). Patients are asked to be as specific as possible when describing location,
especially when meals are consumed at home (e.g. " home in the living room while watching
television"). In the “fluids” column, the patient records the amount of fluid that was
consumed during the meal or snack in either cups or ounces.
The next several columns are for the patient to record any urges to engage in a "targeted
behavior" (i.e. urges to binge, purge, use dietary pills, restrict, exercise, etc.) as identified by
the patient or treatment team. If the patient actually engages in a targeted behavior, an
asterisk should be drawn under the appropriate column. If the patient had an urge but did not
actually engage in the behavior, a zero to five scale is used to rate the intensity of the urge (0
= no urge; 5 = strongest urge).
Patients should be reminded that if they do not meet all exchanges at any meal or snack,
an asterisk should be placed in the "restriction column." It is important that all columns have
a rating or asterisk in them at all times. The column titled "emotion" is used to indicate any
emotions that the patient may have experienced during the meal or snack. Emotions should
be indicated at every meal. Examples of emotions include calm, anxious, sad, angry, guilty,
overwhelmed, etc. Body image issues that may be occurring may be recorded in this space as
well. The final column, entitled "skills used," should be used to record any DBT skills (e.g,
distraction, act opposite) that the patient used during the meal or snack.
Figure 1. Diary card example.
If the patient is not yet familiar with many of the DBT skills, the patient is to indicate
what he or she did to help get herself through the meal (e.g. watch television, call a friend,
use paging services, etc.).
When used correctly, diary cards can provide a wealth of information to the clinician and
the patient. In order for diary cards to serve as an effective component of treatment, however,
they must be completed on a daily basis. It is often helpful to coach patients to keep the diary
card in plain view to serve as a reminder to fill it out immediately after each meal, thus
providing the greatest amount of accuracy.
Behavior Chain Analysis (BCA). A behavior chain is a detailed analysis of specific
behaviors, automatic thoughts, and emotions experienced by a patient preceding, during and
after a targeted behavior. The BCA used in the DBT-CBT model is similar in spirit to the
BCA used in standard DBT; the authors simply prefer the altered format (see Figure 2).
Patients are asked to complete a BCA for each episode of targeted behavior that occurs
between sessions.
For ED patients who are not concurrently suicidal or engaging in self harm, these
behaviors include typical ED behaviors (e.g., binge eating, purging, restricting, compulsive
exercise, diet pill use). When completing a BCA, the patient is first asked to describe the
targeted behavior. In Figure 2, the patient, “Char”, “purged evening snack.”Detail is
encouraged in the description of the target behavior and Char was coached to avoid using
vague terms [e.g., purged (vague) versus purged evening snack (more specific)]. The next
step in completing a behavior chain is to describe the specific precipitating event(s) that led
up to the targeted behavior. In Char’s case, she identified the precipitant as having followed
her meal plan at lunch and dinner, but having felt as though it was “too much food.”
Figure 2. Behavior chain analysis example.
Char was then asked to detail the sequence of events leading up to the targeted behavior
(e.g., feeling uncomfortable, no one home at snack time, body checking), factors that may
have contributed to feelings of vulnerability (e.g., sleeping and feeling worse after nap), as
well as the emotional and behavioral consequences of the targeted behavior (e.g., feeling
relief and guilt after purging). The final and arguably most important step in the completion
of a BCA is to have the patient brainstorm alternative solutions to the problem behavior. In
other words, the patient will determine what they "will do differently next time." In our
example, Char was able to identify two DBT skills that she would be willing to try the next
time this scenario occurred: 1) calling for Telephone Skills Coaching (described below) and
2) using Radical Acceptance to tolerate the bloating. This in session, non-reinforced,

exposure to and focus on the emotions and thoughts related to symptoms has been posited as
one of DBT’s potential mechanisms of change (Lynch et al., 2006).
DBT-CBT for Eating Disorders: The Model

Individual Therapy. In DBT-CBT for ED, individual therapy includes: a behavioral
review of the preceding week, examination of diary cards and behavior chains, exploration of
thoughts, feelings and behaviors that led to self-destructive acts, and consideration of
alternative strategies going forward. As in standard DBT, the patient meets weekly with an
individual therapist, who functions as the primary therapist for that patient on the treatment
team. The goals of the individual therapy are to promote skill generalization (using skillful
behavior to replace ED behavior outside of treatment) and to aid in the maintenance of
motivation and commitment to treatment. The patient and individual therapist typically meet
once per week for approximately 60 minutes.
Standard DBT provides a structure for managing and prioritizing behaviors to be
addressed in treatment. Standard DBT provides a treatment hierarchy that helps the therapist
to identify which behavior(s) to address first in session, thus providing clear path to
prioritizing the goals of treatment (Linehan, 1993). DBT assumes that by definition, patients
who are difficult to treat have several co-occurring problems making the focus of treatment a
challenge. Take, for example, the dangerously low weight patient who comes late to session,
reports current passive suicidal ideation, as well having had two episodes of self-harm and
multiple purging episodes over the course of the week. However, in the moment she is clearly
upset and wants to talk about having broken up with her boyfriend that morning. Without the
described targeting framework, deciding how to focus the session could be a challenge.
Linehan asserts that the target hierarchy is core to the treatment and goes so far as to assert "a
therapist who ignores the targeting strategies is not doing DBT. That is, in DBT what is
discussed is as important as how it is discussed" (Linehan, 1993a). DBT's target hierarchy
provides a theoretical justification for how to manage these multiple behaviors. As is
discussed below, the use of a Target Hierarch in DBT-CBT for ED is only slightly different
than in standard DBT as there is a need to accommodate ED behaviors.
Target I: Life threatening behaviors (suicide, parasuicide). As in standard DBT, suicidal
ideation and self-injury are the first targets to be addressed in treatment. ED behaviors may
be moved to Target I, however, when they present an imminent threat to the patient’s life as
in a medical emergency (e.g., evidence of bradycardia, orthostatic blood pressure, electrolyte
imbalances, EKG abnormalities, syrup of ipecac use).
Target II: Therapy interfering behaviors. The active attention to behaviors that interfere
with treatment compliance and progress is one of several reasons that DBT has the potential
to contribute to the CBT treatment of EDs. Therapy interfering behaviors that may occur
within the context of ED treatment include: not completing diary cards, an inability to focus
in session due to malnourished state, refusing to be weighed, engaging in behaviors to
surreptitiously alter weight, exercising against medical advice, absence from treatment due to
the need for medical intervention, and engaging in purging that interferes with medication
efficacy.
Target III: Quality of life interfering behaviors. ED behaviors that are not associated with
imminent medical risk are focused on within Target III and are considered behaviors that
interfere with one’s quality of life. These behaviors include, but are not limited to, restricting,
binge eating, vomiting, laxative use, diuretic use, diet pill use, and excessive exercise. The
bulk of treatment for ED patients who are not suicidal or at imminent medical risk will occur
within Targets II and III.
It is important to note here that the same behavior may be considered a different Target
depending on the context. Take, for example, “Cathy,” whose primary ED symptom is
purging. Her purging was considered Target I after having been diagnosed with hypokalemia,
as further purging could result in imminent death. Once the hypokalemia was resolved,
purging then moved to Target III. However, when it became clear that Cathy’s purging was
likely interfering with the effectiveness of her antidepressant (she took the medicine at
breakfast, and purged soon afterward), purging moved to Target II. Focus on purging
behavior in session, therefore changed with the change in Target status..
Skills Training Group. DBT skills are taught in a group format as is described in the
Skills Training Manual (Linehan, 1993b). The focus of skills training is to offer patients
alternative ways to manage their problems. Skills fall into four categories: Mindfulness,
Distress Tolerance, Interpersonal Effectiveness and Emotion Regulation and are taught as
outlined in the Linehan's Skills Training Manual, using examples relevant to patients
suffering from EDs.
Mindfulness Skills
As acceptance-based strategies, Core Mindfulness skills help patients to become
intentionally aware of thoughts, feelings, and behaviors (Linehan, 1993b) with a strong
emphasis on being "present in the moment" and promoting self- awareness without attempts
to alter or suppress the experience. Patients are taught mindfulness techniques through the
basic methods of observation, description, and participation. Mindfulness can be incorporated
into the treatment of ED as it provides a framework for patients to observe and accept
previously avoided emotions thoughts, and sensations, including hunger and fullness.
Mindful eating is a skill that has been suggested to be useful for patients with ED. With
few exceptions (Kristeller et al., 2006), there is little research and writing, on the use of
mindfulness approaches to ED. In the authors’ experience, patients with BN or BED can
benefit from a mindful-approach to eating with a focus on paying attention to hunger and
fullness. This approach is very similar to appetite awareness training (Craighead and Allen,
1995). The authors have also found, however, that for patients with AN, mindful eating can
be extremely anxiety-provoking early in treatment. Distraction techniques, with the intent of
progressive movement towards mindful eating over time, may be more useful in the
beginning stages of treatment with these patients.
Interpersonal Effectiveness Skills

Interpersonal Effectiveness (IE) skills are used to help patients become more assertive
and to teach them to use effective problem-solving to handle difficult interpersonal situations
(Linehan, 1993b). Specifically, patients are trained to say "no" in undesirable situations, to
practice asking for help when necessary, and to resolve interpersonal conflict in a manner that
gets their own needs met without damaging the interpersonal relationship or the person's self-
respect. ED patients can greatly benefit from such skills as they begin to use these IE skills to
manage unsatisfying relationships in their lives as well as to negotiate interpersonal situations
around the ED itself (e.g., managing triggering comments made by others, explaining to a
dinner partner why she needs to eat at a certain restaurant, etc.).
Distress Tolerance Skills

Distress Tolerance (DT) skills aim to teach patients techniques to manage stressful and
upsetting events without engaging in targeted/self-harming behaviors (Linehan, 1993b).
Patients are coached to "bear pain skillfully," (Linehan, 1993) and to view distress as
something with a purpose. In this module, patients are taught to survive personal crises
through the use of distraction, self-soothing, engaging in activities to improve the present
moment, and by radically accepting that one may not be able to change the current
circumstances. For ED patients, these techniques are also useful in the management and
tolerance of urges to engage in disordered eating behaviors.
Emotion Regulation Skills

Similar to patients with BPD, ED patients may frequently experience intense and labile
moods. These emotions may become the “problem to be solved” (Linehan, 1993b) from the
patient’s perspective. Clinically, we often hear “I was upset about what happened at work so
I, binged, purged, or restricted.” Emotion regulation (ER) skills are taught to help the patient
to find more effective ways to experience feelings (Linehan, 1993b). Patients are taught to
identify and label emotions aided by Mindfulness Skills, increase pleasant events to promote
positive emotion, avoid self-defeating moods by acting in a manner opposite to what they feel
(e.g. if while at work, one begins to experience intense anger and has the urge to shout;
"acting opposite" would encourage him or her to listen to upbeat music and attempt to laugh
in order to produce positive emotion), and identify obstacles to changing one's current mood.
In the DBT-CBT for EDs approach, as in standard DBT, all skills training modules are
taught through group discussion and activity. Additionally, patients are asked to complete
outside homework assignments in order to promote skill generalizability.
Consultation Team
The consultation team is the component of DBT that primarily functions to monitor and
enhance the therapist’s motivation and adherence to the treatment model. The weekly
consultation team meeting serves as an opportunity for therapists to practice the skills they
teach to their patients and to receive clinical feedback and support from other members of the
treatment team. This is done in the spirit of providing the most effective care possible while
maintaining therapist motivation and commitment to the work. The consulation team
treatment approach outlined in DBT differs from many other models; especially in its
conceptualization of equality. While some team members may be more experienced or may
hold more or higher-level degrees, all members are considered to be equal. There is no one
expert who makes the decision for the team; similarly, the consultation team is not to be
considered "rounds" as in a medical model, where patients are referred to one-by-one with a
to-do list for each person.
The consultation team is crucial for a therapist working with ED patients. The stress of
working with patients who may be near death and whose illness often denies them sound
judgment and insight into their sickness, are prone to frustration and burnout. The
consultation team provides therapists with a validating environment where they can feel
understood and simultaneously be shaped non-judgmentally to be more effective.
Telephone Skills Coaching. Telephone Skills Coaching (TSC) is a unique and powerful
component of DBT. The goal of TSC coaching in standard DBT is to assist therapists in
balancing the dialectic of providing contact to patients during crises, while simultaneously
extinguishing passive, dependent behaviors while reinforcing active, effective skill use. It is
standard practice for patients enrolled in DBT treatment to be given access to their therapists
between sessions and after hours in order to assist in the generalization of skills learned
during treatment (Linehan, 1993). In CBT-DBT for EDs, unlike other published models of
DBT for EDs (e.g., Stanford), this component is utilized extensively.
The first goal of telephone skills coaching is to decrease suicidal crisis behaviors
(Linehan, 1993a) as well as ED behaviors that could cause imminent death (Wisniewski and
Ben-Porath, 2005). Patients are instructed to call their therapist prior to engaging in
parasuicidal/suicidal behaviors. The hope is that with the therapist’s in vivo coaching, a
patient could learn to manage the urges to self harm without acting on them.
The second goal of telephone skills coaching is to increase generalization of behavioral
skills. This means that telephone coaching may be used to assist patients in generalizing the
skills they are learning in treatment to everyday situations (Linehan, 1993a). For example,
when patients are learning the skill of distraction to manage urges to purge, they may call the
therapist after having tried to use the skill and feel that the attempt has not been wholly
effective. The therapist may work with patients to first ensure that they are using the skill
appropriately and then to offer other skills patients may use so that they will refrain from
purging in that instant. An example of this is “Kerri” who called for coaching because she
was feeling the urge to purge after eating breakfast. She tried unsuccessfully to reach several
friends by telephone and to watch TV as a distraction, but felt her urges to continue to
increase. She called her therapist for help coming up with additional suggestions. After
assessing her current attempts to use skills, the therapist and Kerri were able to
collaboratively develop a plan that included leaving the house and going to the library (Kerri
only purges at home) until her job started two hours later. This plan was effective in having
Kerri avoid purging breakfast, thereby reinforcing skill use and the likelihood that Kerri will
attempt to use skills the next time she feels urges to purge.
The final goal of telephone skills coaching is to decrease the sense of conflict, alienation,
and/or distance from the therapist (Linehan, 1993a). Patients are encouraged to phone their
therapist in between sessions to make a repair in the therapeutic relationship. Therefore, ED
patients are encouraged to call their therapist if they are feeling alienated or angry rather than
waiting for the next session to discuss this. In standard DBT, patients who engage in self
harm do not have telephone access to their therapist for 24 hours (Linehan, 1993a). This rule
was developed to prevent therapist contact from inadvertently reinforcing ineffective
behaviors. It is the authors' experience that the 24-hour rule does not translate well for use
with ED patients. Unlike in episodes of self-harm, ED patients who are in treatment likely
have a scheduled exposure to a potentially triggering stimulus (i.e., a meal or snack) every
four to six hours of the day at a minimum. Therefore each meal or snack will represent a
unique opportunity to engage or not engage in targeted behaviors. Given the potential
frequency of these events, behavioral principles would likely suggest reinforcement of any
attempt to “get back on track” (i.e., engaging in adaptive behavior).
A modification of the 24-hour rule, called the Next Meal/Snack rule (NM/S rule) has
therefore been proposed for use with targeted ED behaviors (see Wisniewski and Ben-Porath,
2005). Like the 24-hour rule, the NM/S rule dictates that if an individual has already engaged
in a targeted behavior prior to calling for telephone skills-coaching, the call is to be
terminated. Take, for example, the patient who calls the therapist after having already purged.
In the short phone call, the therapist explains that the patient should call prior to the behavior
in the future, that they will talk about the purging episode in the next session, and quickly
terminates the call. Unlike the 24-hour rule described above, however, the patient is able to
call back for skill-coaching at the next scheduled meal or snack. For a patient in treatment,
the next scheduled meal or snack is likely to occur within two to four hours. If the patient
does call for coaching later that day however, it is stipulated that the focus of that call be on
the present episode only. The prior episode may be discussed only as a contributing factor to
the current episode (e.g., restricted lunch resulting in heightened feelings of hunger at
dinner). This adaptation reflects a potentially important modification for using the DBT
telephone protocol with ED patients.
For those who read the above section with trepidation related to offering patients
telephone access, it is relevant to note the following. Our research suggests that ED patients
are actually very unlikely to use this service unless required to do so by their therapist
(Lindbrunner, Milstein, Ben-Porath and Wisniewski, 2005). It is often the case that the
therapist needs to require patients to call for coaching as a way to practice and shape this
behavior.
Conclusion
Although still in its introductory stages, DBT is beginning to demonstrate its usefulness
for the treatment of non-responsive and difficult-to-treat ED patients. Its unique blend of
behaviorist principles with mindfulness techniques and skills that emphasize understanding
the delicate balance between change and acceptance make it an appealing intervention for
those individuals that struggle with more traditional treatments such as CBT and IPT. DBT
employs a non-judgmental team working relationship between the clinician and patient which
serves to foster a strong alliance and prevent burnout until therapeutic goals are achieved.
The DBT model presented in this chapter (DBT-CBT for ED) attempts to marry
functional aspects of CBT to the beneficial aspects of DBT to create a useful and practical
intervention that best meets the needs of individuals suffering from ED. The empirical
evidence for using DBT with EDs as described throughout the chapter lends support and
promise to the treatment and programming decisions for which this intervention requires. It is
important to note, however, that the present model should be test empirically before being
widely adopted in order for it to truly establish itself as an evidenced-based treatment.
Author Note
Lucene Wisniewski, Clinical Director, Cleveland Center for Eating Disorders.
Kelly Bhatnagar, Department of Psychology, Case Western Reserve University.
Mark Warren, Medical Director, Cleveland Center for Eating Disorders.
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Chapter XVI
Evidenced-Based Approaches to
Family-Based Treatment for Anorexia
Nervosa and Bulimia Nervosa
James Lock and Kathleen Kara Fitzpatrick

Stanford University School of Medicine
Stanford, California, USA
Abstract
Family-based approaches to the treatment of eating disorders represent important,
empirically supported options for addressing the needs of adolescents with Anorexia
Nervosa and Bulimia Nervosa. Family-based weight restoration treatment for Anorexia
Nervosa, in particular, has mounting empirical evidence to support its use with children
and adolescents. Family-based treatments encourage participation of a wider familial
network to support re-nourishment, establish independence around food and weight
management and encourage appropriate developmental gains. The current chapter
provides an evaluation of existing research on family-based treatments as well as
providing clinicians with information on phases and skills necessary to implement a
family-based model in a clinical setting.
Eating disorders are highly prevalent, devastating illnesses that impact both the
individual sufferer and those closest to him or her. Anorexia Nervosa (AN), Bulimia Nervosa
(BN) and Eating Disorder Not Otherwise Specified (ED NOS) are associated with a great
deal of morbidity and mortality and have a peak age of onset in adolescence, often
circumventing the critical developmental milestones that lead to independence in adulthood.
Given that most adolescents remain imbedded within a family structure and are dependent
upon their parents, it is reasonable to expect that family involvement is viewed by many as a
critical component of successful treatment of adolescent eating disorders. It may seem
somewhat surprising, then, that family-based approaches to the treatment of eating disorders
292 James Lock and Kathleen Kara Fitzpatrick
have been controversial since the earliest documentation of these disorders. As early as 1874,
Gull characterized families as the “worst attendants” for those suffering from AN (Gull,
1874). This sentiment was echoed in early individual treatment paradigms that suggested
families were not a necessary part of treatment, as treatment sought to empower the
individual suffering from AN (Bruch, 1973).
Despite early concerns about the role of family in treatment of AN and a veritable
absence of information on family-based treatments for BN, the nesting of treatment within a
family setting makes ecological sense when one considers that the average age of onset AN
and BN is in adolescence. AN has a prevalence estimated at between 0.48% and 0.70%
among females aged 15 to 19 years (Hoek and Hoeken, 2003; Lucas et al., 1999; Pawluck
and Gorey, 1998). Similarly, BN occurs in approximately 1-2% of the adolescent population
while clinically significant bulimic behaviors (BN-EDNOS) occur in an additional 2-3%. As
with AN, adolescence is a critical time for the development of BN, with a peak age of onset
at eighteen (Mitchell et al., 1987).
The importance of developmental factors coupled with relatively poor treatment
outcomes for the treatment of adults with eating disorders made a focus on family-based
interventions and treatment paradigms natural extensions for the burgeoning family treatment
models beginning in the 1960s. Nearly one hundred years after Gull’s admonishment of
family members in treatment, psychological theory swung back toward the inclusion of
families in eating disorder treatment as we review below.
Theoretical Underpinnings of Family Treatment

for Eating Disorders
Structural, strategic and systemic family therapy models were developed, with a
particular focus on the treatment of AN. Minuchin’s (Minuchin et al., 1978) seminal family
work and characterization of the “psychosomatic family” of AN served to focus on family
work as a critical treatment modality. Family treatment was designed as a means to address
perceived enmeshment and maintenance of these disorders through maladaptive
communication patterns and problem-solving. Minuchin and colleagues focused their work
on modifying intergenerational boundaries with a focus on enmeshment, conflict
management skills and strengthening alliances with the larger social world (Minuchin et al.,
1978).
Salvini Palazzoli at the Milan Center drew upon many of the aspects outlined by
Minuchin, while highlighting the rigid organization of families with AN and the ways in
which this disorder might serve to maintain homeostasis within the family unit(Selvini
Palazzoli, 1974). The therapist’s power in Milan System’s treatment emphasizes the
importance of objective observation and family evaluation of their own processes. By placing
oneself outside of the family dynamic, therapists can both shed light on patterns as well as
expressing empathy for individual family members (Palazzoli, 1974; Palazzoli et al., 1980).
This allows the therapist to remain outside of conflict and supportive of family members in
the face of conflicting needs or desires.
Evidenced-Based Approaches to Family-Based Treatment for Anorexia... 293
Christopher Dare and colleagues at the Maudsley Hospital in London developed an

eating disorder specific set of treatment protocols that drew upon separate elements of
structural, strategic and systemic models with a behavioral re-feeding focus (Russell et al.,
1987). The resulting “Maudsley method” or family-based re-feeding (FBT) model of
treatment views the family as a fundamental resource in the treatment of eating disorder
symptoms, the identified patient as regressed in his/her ability to manage food independently,
and encourages a collaborative approach to systematic re-nourishment of the identified
patient to an ideal body weight. Although clearly drawing upon previous theories of family
therapy, distinguishing it from other approaches is the injunction placing parents in charge of
weight restoration of their child while maintaining an agnostic stance toward the cause of the
disorder (Dare and Eisler, 1997). FBT has the added benefit of existing in manualized form
(Lock et al., 2001).
Interestingly, despite similarities in symptom profiles and age of onset, research
paradigms for the treatment for (BN) have focused largely on the development of individual
approaches. To date, large-scale treatment studies of BN have focused on the use of
cognitive-behavioral therapy and other individual models in adults. Only a handful of studies
have examined BN treatment, whether individual or family based in adolescents. Results
from these studies suggest that both individual and family based treatments are promising for
symptom amelioration (Fairburn, 1988; Fairburn, 1997; Fairburn and Brownell, 2002; Le
Grange and Lock, 2007; Le Grange et al., 2003; Le Grange and Schmidt, 2005).
Existing theoretical models for family treatment of adolescent BN draw upon the same
theoretical models discussed in relation to adolescent AN. As outlined by Le Grange and
Lock (Le Grange and Lock, 2007), parents are urged to assume control over the adolescent’s
eating and binge/purge behaviors; however, in contrast to FBT for AN, the stance is more
collaborative with the adolescent with BN than AN. The primary reason for this is that BN is
generally ego-dystonic and shameful, making a joint effort at changing the behaviors more
likely than in AN where the ego-syntonic nature of the disorder makes collaboration
extremely challenging at the start of FBT. Nonetheless, the core features of FBT remain the
same for both conditions.
Empirical Evaluation of Family Treatment of

Eating Disorders
Given the history of family models for the treatment of eating disorders, one would
assume that a rich empirical literature would exist. Unfortunately, a relative dearth of
empirical evidence for eating disorder treatment exists, particularly in adolescents. Among
existing studies focusing on adolescents, two recent reviews (Le Grange and Lock, 2005;
Tierney and Wyatt, 2005) highlighted the importance and prevalence of family treatments for
the treatment of Anorexia Nervosa. Virtually all randomized clinical studies targeting
adolescents utilized a family approach, with virtually of these focusing on FBT for AN.
Older, general studies included anxiety-based treatments (Goldfarb et al., 1987) and
monitored eating with or without feedback (Touyz et al., 1994).
Controlled studies of family- based treatment for AN have found that family-based
treatment to be superior to individual therapy for adolescents with AN (Russell et al., 1987)
with this maintained at five year follow-up (Eisler et al., 1997). Russell et al. (Russell et al.,
1987) found those with duration of illness less than 3 years, and onset prior to age 18, FBT
was superior (60% vs. 9% good) while Robin et al.’s (Robin et al., 1999) comparison of FBT
to individualized treatment (EOIT) found both groups improved, although weight restoration
was faster for those receiving family-based treatment. In these family studies, “family” was
generally defined as the family of origin, although the constitution of these families has not
been specified. In general, family-based treatments have been utilized with a multitude of
family constellations. Single parent families, grandparents with custody, blended families and
much older siblings have been represented in these and other studies.
In a recently completed RCT for adolescents with BN (BN and partial BN) 80
adolescents aged 12-19 years (M=16.1, SD=1.6) were allocated to either manualized FBT-
BN or manualized Individual Supportive Psychotherapy (SPT). At the end of treatment and 6
month follow-up significantly more patients in FBT-BN were binge/purge abstinent
compared to SPT, suggesting that FBT-BN is superior to SPT. The Chicago study was
sufficiently powered to demonstrate the potential benefits of an active treatment (i.e., FBT)
over a non-specific control treatment (i.e. SPT), and to demonstrate comparable benefits that
were not due to time effects. In addition, there were no differences in remission rates at the
end of treatment or at follow-up for those subjects with BN or partial BN (Le Grange and
Lock, 2007; Le Grange et al., 2003; Le Grange and Schmidt, 2005).
Results from another randomized controlled trial (RCT) for adolescent BN and partial
BN comparing family therapy to CBT-GSC (an individual guided self-help form of CBT),
has also been recently published (Schmidt et al., 2006).
Family therapy as described by these authors resembles FBT; however, these authors
described “family” as any “close other “rather than specifically requiring that a parent be
defined as “family.” This occurred in about one quarter of cases. This definition was likely
utilized, in part, because the mean age of the subjects in this study was 17.6 years (sd = 0.3),
much closer to adulthood, especially in the UK where the age of consent is 16 years. While
defining family as a close other may fit well with this older age group, this might not be the
most effective way to approach FBT with younger adolescents where parental authority is
key to the success of FBT. This point in emphasized further by the take up rates for the UK
study, wherein 28% of eligible participants refused the study because they did not want their
families involved in treatment. In contrast, for the younger adolescents studied at the
University of Chicago, where only 11% dropped out of treatment and none of these reported
involving the family as the reason for discontinuing treatment. Nonetheless, Schmidt and
colleagues found that abstinence rates (41%) achieved by family therapy are comparable to
those achieved using FBT in the Chicago study. However, no statistical differences on
abstinence rates were found between FBT and the comparison treatment. Schmidt and her
colleagues acknowledge that a limitation of their study was the sample size (n = 85), which
was likely too small to detect differences between two active treatments for some of their
outcomes and that the absence of a waiting-list or attention placebo-control group prevented
them from ruling out that improvement was simply due to passage of time or non-specific
effects (Schmidt et al., 2006).
Table 1. Outpatient Psychotherapy Trials of Family Treatment for Adolescent

Anorexia Nervosa
Study Type of N Age Treatment # Drop- End of Tx outcome

therapy Duration sessions out rate Morgan-Russell
(months) good+intermediate
Russell, Whole family Family therapy = 90%*
Szmukler, vs. individual 21 16.6 6-12 13 19% Individual therapy=18%
Dare, and therapy**
Eisler, 1987*
Le Grange, Whole family 68% overall; no differences
Eisler, Dare, vs. Separated 18 15.3 6 9 12% between groups
and Russell, family
1992 therapy***
Robin et al., Family Family therapy = 81%*
1999**** therapy vs. 37 13.9 12-18 47 11% Individual therapy = 66%
individual
therapy
Eisler et al., Whole family 40 15.5 12 16 10% 63% overall; No
2000 vs. separated differences between groups
family therapy
Lock, Agras, Family 86 15.1 6 or 12 10 or 20 12% No differences in outcome
Bryson, and treatment, sessions between groups
Kraemer, 2005 6 vs. 12 96% overall
months
* Denotes statistically significant advantage for this approach.
** Whole family indicates that the family was seen with the identified patient (“Conjoint”).
*** Separated family therapy indicates the parents were seen without the identified patient.
**** Denotes statistically significant disadvantage for this approach.
One concern for those considering family based treatment models has been the burden of
having an entire family present for treatment. A study comparing separated (parents alone) to
conjoint (parents and patient) family based treatment found weight restoration efforts were
successful in both groups. The role of family criticism and hostility has also been suggested
as a reason for focused individual work. Parental criticism is, indeed, a predictor of treatment
drop-out in family-based treatment (Lock, Courturier, Bryson and Agras, 2006), but the role
of criticism and hostility has not been evaluated in individual treatments and thus no
comparison can be drawn between this and other aspects of treatment. Other predictors of
drop-out include co-morbid conditions and length of time to weight gain, with greater early
weight gains predicting treatment retention. Interestingly, however, FBT may, lead to faster
weight gain (Robin et al., 1999) that may retain families in treatment for longer. In general,
treatment is implemented over one year, however, Lock et al (2005) compared short (6
month) to long-term (1 year) FBT and found treatment was equally effective for adolescents
with short duration AN.
Family-Based Weight Restoration for Eating

Disorders
Given the mounting empirical support for FBT, we provide evaluation of the elements of
treatment, utilizing the Treatment Manual for Anorexia Nervosa (Lock et al., 2001). Where
relevant, modifications specific to the treatment of BN are discussed, drawing upon the
manualized version of this treatment protocol (Le Grange and Lock, 2007).
Family-Based Treatment for AN
FBT AN views the adolescent as regressed in terms of her eating disorder, or inability to
maintain an optimal weight for age and height. This regression is viewed as limited in scope,
however, and the adolescent is presumed to be able to assume developmentally appropriate
independence in other domains. As such, treatment addresses the adolescent’s developmental
concerns and the ways in which parental control over eating represent a significant
infringement of typical independence. Expectation that control over eating will be returned to
the adolescent once weight and eating behaviors are stabilized is clearly stated, with a
concurrent shift in focus to negotiating more typical adolescent conflicts or family needs.
Treatment takes place in three phases over six to twelve months, comprised of 10-20
sessions. Sessions in FBT last 1 hour, with the first ten to fifteen minutes being spent with the
patient alone during weigh-in and exploration of patient specific concerns about his or her
response to parental efforts appropriate to the goals of each phase.
Phase 1 (sessions 1-10). In the first phase, the eating disorder comprises almost the full
focus of treatment sessions. The initial session involves history-taking and presentation of the
family’s dilemma in a “grave but sincere manner” that fully communicates both the
significant danger of the patient’s current health crisis as well as a call to action for the family
to directly intervene. At the end of the first session the parents are encouraged to provide a
meal sufficient to “re-nourish their starving (daughter)” to the next session. The family meal
is eaten in the second session to provide the therapist with an opportunity for direct
observation of the familial interaction patterns around eating. This is an excellent opportunity
for observation of dynamics of family meals, to address views about nutrition, to model and
coach parents in ways to approach re-feeding. Paradoxical injunctions, including urging the
identified patient not to eat unless he/she really wants to, encourages families to directly
address the dilemma of their conflicting goals. A primary goal of the family session is to have
the patient eat one bite more than he/she had been planning upon eating at the outset of the
session.
In the remainder of phase one sessions, the therapist exhorts parents to unite and direct
their efforts toward re-feeding, which is the primary focus of treatment. The patient’s weight
is graphed and shared with the family to guide intervention and serve as feedback on the
process of weight restoration. Parents are also urged to take control of binge/purge behaviors
in the subset of patients presenting with a binge/purge subtype. Critical to this is management
of parental feelings of guilt or anxiety – by engaging and collaborating with parents, the
therapist communicates clearly parents have not caused the eating problem and that they can
be empowered to change this pattern in a direct fashion. The therapist builds and reinforces a
strong parental alliance re-feeding efforts while simultaneously aligning the patient with his
or her siblings. The critical goals of this phase are to manage parental guilt and anxiety
sufficiently to spur them to action in taking control of eating. The specific actions of re-
feeding are not defined by the therapist, but rather families are encouraged to work out for
themselves how best to re-feed their anorexic child. The focus is held on food and eating,
with parents being encouraged to review each snack and each meal for what was successful,
how it was eaten, the emotional tenor of the meal and the ultimate outcome in terms of
caloric gain and parental success in managing the AN.
Phase 2 (sessions 11-16). This phase begins with a change in the tenor of the treatment:
the patient submits to parental re-feeding efforts and conflict around regular nutrition
improves, resulting in steady weight gain, as well as a change in the mood of the family (i.e.,
relief after having taken charge of the eating disorder). Often families make subtle transitions
between sessions without realizing that they are taking initial steps toward increasing
independence (e.g., patient begins “plating” their food with parental observation rather than
parent dictated portions). The therapist shifts task demands to emphasize movement toward
independence for the patient. Although symptoms remain a central focus, weight gain with
minimum tension is encouraged. Resumption of developmentally appropriate eating
behaviors are encouraged throughout the sessions; initially with parental monitoring and, in
the face of success, with full independence. Other areas of concern or family functioning
(e.g., trust, defining appropriate independence) might be brought forward, although these are
selectively addressed in terms of their relationship to maintenance of weight and normalized
eating behaviors.
Phase 3 (sessions 17-20). The third phase begins when the patient achieves a stable
weight and is generally able to resume normal eating behaviors without undue parental
monitoring. In our experience, the entry into this final phase can be distinguished by a
distinct lack of concern about or desire to focus on eating symptoms by the family and a
sense that there are either more pressing or enjoyable issues presented for discussion. Rather
than presenting issues of eating conflict, a conversation may focus on dating, curfew or
homework completion and, when eating issues are queried, these are dismissed. At this point,
the central focus is on establishing a healthy adolescent or young adult relationship with the
parents. This is often a challenge, as for many families the illness has constituted the basis of
many interactions. Goals may include working towards increased personal autonomy for the
adolescent, re-establishing a stronger marital relationship that does not include the patient or
siblings, more appropriate family boundaries and improved familial communication.
Modifications Associated with FBT for BN

Although there is a high degree of symptom overlap between AN and BN in adolescents,
several key differences require modifications in the implementation of family-based focus.
There are individual and symptomatic differences in BN that bear discussion. First, although
AN and BN have high rates of co-morbidity with other mental illnesses, BN can be thought
of as having a wider range of co-morbid psychiatric disorders, many of which may be viewed
as compelling enough to shift the focus of treatment (e.g., substance abuse) while in AN the
consequences and physical response to stark emaciation assist both therapists and the family
focused upon the illness. Second, although both AN and BN share a common root in body
image disturbance, the focus for those with BN is on an over-valuation of shape and weight
which leads to maladaptive compensatory behaviors. This contrast is often less striking than
the distortions of AN that clearly highlight the disorder. Thirdly, although it may be
premature to discuss “typical” family presentations of these disorders, clinical perceptions
suggest that AN families tend toward rigidity, perfectionism and compliance while those with
BN may better be characterized as less structured and more disorganized. This may make it
challenging initially to engage families as well as for some of these families to provide the
structure and monitoring necessary for successful implementation of a family-based
approach.
In addition to modifications in the strategic implementation of FBT for BN,
psychological aspects or characteristics represent important areas for assessment and may
require flexibility implementation. Patients with BN are typically perceived as having a
greater level of independence than their counterparts with AN, although this is sometimes
ambivalent independence. Many parents are often reluctant to intervene or may find resuming
control in the area of food or eating more challenging than in patients with AN. Parents may
benefit from adopting a “back on track” approach when facing BN, with a push toward
normal developmental independence and frequent reminders that their adolescent is, with
respect to food, in a regressed state. This is further complicated by the potential for families
to see the identified patient as being “beyond guidance” or having a wider range of
experiences or challenges than average adolescents. Unlike AN, which is characterized by
low levels of insight, levels of insight vary in patients with BN. Symptoms of BN are
generally ego-dystonic and thus many adolescents can accept that they are ill, although they
may not like the nature of parental control. Acknowledgement of illness is an important point
upon which the therapist can establish a therapeutic relationship with the identified patient
and can assist in the development of a collaborative stance including the parents and the
patient. Alternatively, if levels of insight are low, patients with BN may be particularly
resistant to parental control over food and eating behaviors. Level of parental motivation may
be related to the factors above, as well as potential difficulties in recognizing the extent and
seriousness of symptoms in the patient. Although many individuals with AN are secretive in
their illness, the striking emaciation associated with the disorder often prompts parents to
take action. In contrast, patients with BN present at or above normal weight guidelines and
often lack the clear medical fragility of their AN counterparts. Parents may also struggle with
the secretive nature of BN symptoms and may struggle to separate eating disorder symptoms
from more age appropriate adolescent development. This may manifest as more criticism or
family hostility directed at the adolescent and/or difficulty identifying and managing eating
symptoms.
There are many core tenets of family-based treatment that provide a framework for
treatment implementation. First and foremost, the model supports parents as key agents of
change in their child’s recovery and emphasis on parental knowledge and expertise within the
family is reinforced throughout the sessions. In this sense, parents are viewed as experts in
their children, while the therapist is an expert in eating disorders. This changes the nature of
the relationship, with parents expected to play an active role in identifying ways in which
they might modify behavior patterns and the therapist assuming an inquisitive and coaching
role, with less emphasis on behavioral directions and interventions. For a relationship of this
nature to be truly collaborative, parents must not feel they are being pathologized,
stigmatized or responsible for their child’s illness, and thus FBT maintains an agnostic stance
as to the cause of the illness.
The therapist must also bring a set of skills to the practice of family-based treatment for
eating disorders. Critical to success is the therapist’s ability to maintain a fairly single-
minded focus upon the eating disorder, despite often more enticing and seemingly
psychologically fruitful distractions that may arise in family sessions. The focus and
entrainment upon eating disorder symptoms in early sessions serves to keep the family’s
focus on eating pathology and emphasizes the vital importance of parental control over eating
and return to nourishment for the identified patient. This can be quite challenging, as a
patient’s obvious emaciation is replaced by indicators of health, families often wish to shift
focus away from the eating disorder to address other, seemingly more pressing issues. Taking
ones “eyes off the eating disorder” at too early a stage in treatment can lead to decreased
pressure on eating symptoms, failure to make expected weight gains and maintenance at
“partial remission” status. It can be all too tempting to address more compelling family
dynamics and issues raised, and great skill is essential in refocusing the discussion on eating
while validating and tabling these concerns until later in treatment. Preventing complacency
and “burnout” in weight restoration efforts requires a mix of humor, compassion and ability
to manage both the specific eating disorder symptoms with greater familial dynamics.
In addition to a fairly tenacious focus on eating disorder concerns at the outset of
treatment, the therapist must also ground his or her work in a strong developmental
framework. Therapists should be knowledgeable of adolescent development and the ways in
which eating disordered behavior may interfere with or delay normal development. This is
particularly important as self-starvation or highly disorder eating behaviors themselves,
assumes a level of developmental regression in independence skills. The therapist must be
aware of normal developmental patterns to assist parents in encouraging age appropriate
expressions of affect and behaviors, rather than playing out developmental concerns in the
realm of food, weight and shape. This knowledge and support of appropriate adolescent
development forms the core of the connection that the therapist must develop with the
adolescent to sustain rapport and demonstrate respect for the tremendous challenge facing the
family. Namely, the removal of otherwise developmentally appropriate independence skills
(eating) while actively encouraging strides toward independence in other domains (social).
Case Presentation
To assist clinicians in the implementation of treatment, the following case history

outlines implementation of treatment with an adolescent patient with binge-purge subtype
anorexia nervosa. This case was chosen to illustrate the ways in which family therapy tackles
both severe emaciation as well as binge-purge behaviors.
History taking and first session. K.S., a sixteen year-old female, presented with her
family for treatment following several previously unsuccessful therapies to address a three
year history of AN. K.S. presented to the outpatient clinic following an extended stay on an
inpatient unit, where she was admitted directly from residential treatment. She was
accompanied to treatment by her parents, Mrs. C and Mr. S., who had divorced six years
prior. Her older sister, age 17 and her younger brother, age 8, were also present for treatment.
At the time of the intake session, K.S. and her family reported a three-year history of illness,
beginning the summer prior to K.S.’s entry to high school. She began restricting and dropped
in weight, which was not seen as alarming to parents, as K.S. had been overweight for much
of her childhood and was borderline obese at the time of her weight loss. Weight loss was
rapid and significant, falling from 126 pounds at a height of 4 feet, 11 inches to 86 pounds
with a concurrent growth spurt that placed her at five feet, three inches in height. At the time
of admission to residential treatment, K.S. had a one-year history of binge eating and purging
behaviors, which she described as instrumental to keeping her weight low. She had been
binge eating once per day, although her binges had decreased in quantity to reflect subjective,
rather than objective binge eating amounts. She induced vomiting after most meals and had
experimented with laxatives and appetite suppressants. She entered residential treatment after
an inpatient hospital stay and was able to increase her weight to 90 pounds, however, she was
discharged to the inpatient unit for acute food refusal and violent behavior on the unit.
Her mother reported great guilt around her failure to recognize the severity and
significance around this weight loss, while K.S.’s father expressed great hostility toward his
ex-wife for allowing their daughter to become ill, while simultaneously questioning the
significance of the illness, as he felt it was better to be “too thin than too fat.” Parents were
alerted to concerns by K.S.’s pediatrician who monitored her low weight for a year. Mother
noted the family had been reluctant to seek outpatient care during that time, as they felt this
was just a “phase” and a reaction to Mrs. C’s recent remarriage. For his part, Mr. S. reported
that Mrs. C prevented regular contact with the children and that he had “no idea” about the
severity of illness until his daughter was hospitalized. K.S. described her current state as
“borderline fat” and reported great distress at the idea of gaining weight. Despite this, she
was able to note that her illness had prevented her from leading a “normal” life, having
missed a majority of her sophomore and half of her junior year of high school, not being able
to drive, and having “never had a boyfriend.” Her sister noted that K.S. required a great deal
of attention from the family and her frequent hospitalizations or threat of hospitalizations
resulted in great disruption and conflict between Mr. S. and Mrs. C. as well as between Mrs.
C and her husband. K.S.’s sister reported a great deal of love and concern for her sister and
felt AN was a way to “make our parents talk to each other and maybe work together.” K.S.’s
brother remained silent throughout much of intake session, despite questioning, and he
frequently became tearful when asked about his thoughts about his family and his sister’s
illness.
The therapist discussed the medical consequences and concerns associated with
restriction, binge eating and purging. During this conversation, K.S. sat silently and reported
that she had “heard all this before.” When the therapist confronted her fears of weight gain
and concerns that the therapist may try to make her overweight, K.S. stated, “It isn’t your job
to make me fat, it’s your job to make me like it!” Mrs. C wept openly at her concerns
regarding her daughter’s bone density, cardiac functioning and fears that she was “killing
herself.” Mr. S. asked many questions about risk and reversibility of risk. At the end of the
session, the therapist charged the family with the task of bringing a meal that would be
capable of increasing K.S.’s low weight.
The family meal. The family presented with a meal from a local restaurant. As the family
unpacked the meal and began eating, the therapist observed, then began asking questions.
The family all had similar meals: burritos, tortilla chips and salad, served “family style” apart
from the burritos, which were served individually. Mr. S and Mrs. C appeared tense,
watching K.S. closely as her siblings divided up the food and served themselves. K.S.’s sister
took the lead in serving the family, passing out burritos and placing chips and salad on a plate
for each family member. She provided her sister the same portions to each member of her
family, serving K.S. last. All other family members ate readily, while watching K.S.
surreptitiously. The family ate quietly, although they were able to laugh about the unnatural
situation (eating in front of a therapist) and admitted their regular meals were less quiet at
home. The therapist discussed who had chosen the food and the parents admitted that Mrs. C.
had chosen a meal she felt K.S. was likely to eat and something she had requested, rather
than “risk upsetting her.” The therapist discussed how this played out at home, with the
family allowing K.S. to select meals and what happened when she did not eat the foods
offered by the family. Mrs. C. expressed great frustration around this and noted that she felt
she was “bending over backwards.” K.S.’s siblings reported that this was very unfair, as they
were not able to get their parents to purchase their favorite foods on a regular basis. Mr. S.
reported that his ex-wife had long “given in” and did not like conflict with K.S. or anyone
else. The therapist noted that the family re-feeding approach was one in which conflict and
struggles were brought out into the open and faced directly. With that, the therapist provided
a paradoxical injunction to K.S. – to eat only as much as she wanted to and not to give in
without a challenge.
During the discussion of conflict avoidance, K.S. began crying. The therapist wondered
if she was feeling criticized or attacked by her family and she nodded quietly, stating that she
didn’t “ask” to have her parents treat her in a certain way or “give in” to her. The therapist
guided a discussion of the ways in which parent choices for meals and taking the “power of
choice away from anorexia” can be challenging in the moment but provide relief from eating
disordered choices and ruminations. The therapist also encouraged the family to move away
from resentment of K.S. for being ill and to make a separation between K.S. and the illness.
During this discussion, K.S. ate very little and took very prominent bites of food only
when watched closely by her family. The therapist noted this and modeled separation of the
patient and her illness by suggesting that it was easier for the AN to allow her to eat when
observed. She resisted this suggestion, but her parents both eagerly responded that they had
noticed exactly this pattern – K.S. would cut her food into “micro-portions” that were then
moved about the plate, but eaten only when “fixated with a death stare.” The therapist
encouraged the parents to move in closer to K.S. to provide support and help her fight her
eating disordered thoughts, since her eating improved when she was monitored. At this
suggestion she immediately picked up her food and began eating, as though to show she did
not need this assistance. Her parents, however, moved to the seats on either side of her and
took turns talking to the therapist while the other provided gentle verbal encouragement.
Although she resisted, crying, pushing away her food, the therapist encouraged the parents to
remain steadfast in their alliance. Both Mr. S. and Mrs. C. joked that this was the most they
had agreed and worked together since their divorce and this statement led to K.S. tearfully
crying that she did not want her AN to be the only thing that made them work together. Her
siblings agreed vocally and the parents began to discuss this as a family, with the therapist
encouraging their return and focus to AN as the most important issue facing the family in the
moment. The therapist highlighted for the family the ways in which AN can distract from the
task at hand and divert focus and controversy as a means to maintain a grip on the patient.
The parents agreed that this occurred frequently in both households: diversions, arguments
and provocations all occurred more frequently at mealtimes. The therapist encouraged the
parents to maintain a steadfast focus on eating disordered behaviors and to take control,
which would strengthen their resolve as well as allow K.S. some relief from her eating
disordered symptoms. This also helped the parents in making a separation between their
daughter and her illness.
Remainder of Phase 1. At the subsequent sessions, the family explored many issues that
prevented the parents from confronting the eating disorder, although they quickly gained
skills as evidenced by K.S.’s steady weight gain. Mrs. C. struggled when K.S. would escalate
in her upset around food and eating and reported it was a challenge to keep her “eye on the
AN.” However, she did an excellent job in distinguishing her daughter from “the beast” and
took active steps to keep K.S. active between meals. This was particularly useful to prevent
purging behaviors, which required monitoring for an hour or more after meals and
significantly curtailed K.S.’s independence. Mrs. C. was creative in her distracting techniques
and also provided many age-appropriate activities, such as hosting “movie madness” nights
with peers, “bake-a-thons” that allowed K.S. to cook and eat a snack with her peers or sister
and kept boredom to a minimum. She required repeated reassurance that her confrontation of
the eating symptoms would actually relieve anxiety for K.S. and would not be “overly
stressful.” In session six she proudly stated that she had set a goal for herself to require K.S.
to finish all of her portions and realized that this not only did not engender as much conflict
as she feared, it resulted in a tremendous feeling of power and satisfaction in her ability
handle AN. At that point she was able to provide and monitor sufficient caloric intake at each
meal. She also felt empowered to search K.S.’s room to remove all laxatives and created a
contract in which K.S. agreed to toxicology screens in exchange for greater privacy.
For his part, Mr. S. struggled to make the distinction between his daughter and AN, often
unwittingly making statements about K.S.’s behavior that assumed she was in complete
control and directed her symptoms to provoke or express upset. This was more delicate, as
K.S. was able to admit that this was sometimes the case when she was alone with the
therapist. The therapist worked with the family to distinguish normal adolescent strivings for
independence and control and the ways in which the eating disorder had modified this
expression. At times Mr. S. was overtly critical of K.S., and the therapist worked directly
with this to modify these interactions. As Mr. S. was better able to make a distinction
between his daughter and her illness, the entire family began to speak of the illness as “the
beast” and K.S. began to be more vocal in expressing other demands, particularly related to
independence. Mr. S. often compared K.S. to her sister, much to the chagrin of both girls,
who encouraged him to view them as separate and quite unique. This had the effect of
unifying the girls against their father and supporting one another.
At the end of phase 1, K.S. had reached approximately 90% of her ideal body weight,
had ceased using laxatives and had decreasing self-induced vomiting episodes greatly, with
only six purging episodes during the first phase. The family demonstrated many of the skills
that are key to success in family re-feeding – they were able to acknowledge that K.S.’s goals
were concerning to them, but expressed a belief that she could, in fact, handle independence
and set up parameters for maintenance of this. For her part, K.S. had enlisted her sister to
support this independence and had been able to find a voice to more easily discuss her desire
for the ways in which she wanted her parents to help her. Rather than arguing against the AN,
K.S. began to externalize the illness herself and was able to discuss her more shameful and
conflict-ridden behaviors more openly. This had a cyclical effect of helping parents find ways
to assist her in managing these behaviors. Parental openness and flexibility, as well as a
decrease in hostility in communication set the stage for K.S. to assume greater independence.
Phase 2. K.S. had returned to school during phase 1 and had meals monitored by school
staff. This was perceived as embarrassing and socially awkward by K.S., who suggested that
she move to independent meals at lunch. As noted above, her parents were initially quite
concerned but were able to recount her significant progress and identified this as an important
area in which K.S. could resume a “normal” life. They agreed on a “partial monitoring”
program in which K.S. ate with her friends, then brought her lunch to a school staff member
who observed the remainder. K.S. was aware that she could be observed by school staff at
any point and that staff would report to her parents if they had concerns. As expected, this
transition was difficult for K.S., who was able to note that she had appreciated the structure
that observation gave her to remove eating disordered choices. She worked with her family to
discuss options that made it less likely that she would limit portions or hide food, including
calling her sister or her mother if stressed during lunch, asking for help with friends or going
to her guidance counselor. K.S. took the step of recruiting a peer to support her, and this
system worked well. However, both parents and K.S. noted on-going concerns related to
purging behaviors, with K.S. noting an increasing desire to binge eat. One two occasions the
family felt K.S. had hidden or hoarded food and perceived her eating as “out of control”
although K.S. denied binge eating. This led to negotiation around trust, independence and
ways in which parents could monitor behaviors appropriately.
At home, meals were less structured over time and K.S. was able to serve her own meals.
However, the family struggled eating out of the house, as K.S. often expressed great anxiety
about portion sizes and calorie counts in restaurants. With parental encouragement, K.S.
agreed to take steps toward eating out of the home, with the family agreeing to eat out once
per week. This initially caused sibling conflict, as K.S. requested that she choose the
restaurant. However, the family compromised, by allowing K.S. to choose two separate
restaurants in two weeks (until the next session). At the following session the family
negotiated that K.S. would choose one week, but one of her siblings would choose the
following week. This worked well and K.S.’s siblings showed great compassion in discussion
whether it was better to surprise her with the choice or allow her the opportunity to plan
around this “uncontrolled” meal.
K.S. struggled with independence in other domains, however, and as independent eating
improved, K.S.’s family expressed concern that she appeared to continue to be “overly
dependent” on them and unwilling to go out with peers. Mrs. C. acknowledged her own
feeling that this helped K.S.’s recovery – “she won’t get into trouble with us watching her” –
but also created a significant limitation, as K.S. “needed a life.” The therapist worked with
the family to notice areas of gains and to continue to modify family criticism toward K.S. The
family shifted focus to both encouraging independence, by scheduling previously enjoyable
activities, while also managing their anxiety about the way this independence would impact
weight and eating.
Phase 3. In this final phase of treatment, K.S. and her family set a goal of encouraging
attainment of important milestones of independence – getting a driver’s license, visiting
colleges for applications and spending the night at a friend’s house. She established these
goals for herself and recruited her parents in managing her anxiety about engaging in these
behaviors. This phase of treatment highlighted the ways in which K.S. responded with great
sensitivity to any perceived criticism. She worked with her parents to “check in” with the
meaning of their statements and improved her ability to confront and discuss concerns. The
family also made a specific behavior plan with “rewards” for K.S. to engage in independence
seeking behaviors. As a marker of her new independence, K.S. drove to the final family
session.
Conclusion
Although the evidence base for treatment of adolescent eating disorders is remarkably
limited, family treatment appears to be a reasonable approach for many. What studies have
been conducted, despite their limitations and flaws, suggest is that Gull was mistaken in his
observation about parents in most cases. Overall, treatment models of adolescent AN and BN
both deserve further study and evaluation. Larger studies that compare family treatment to
individual treatment may identify not only if one approach is superior to the other, but may
identify for whom which treatment is best suited. In addition, studies that compare types of
family treatment are also needed. FBT, with its strong behavioral focus, is the approach that
has been systematically examined; however, other family therapy approaches may also be
effective for AN. There is also a definite need for more definite studies of family based
treatments for BN. A study comparing individual approaches such as cognitive-behavioral
therapy to family based treatment would be particularly important to build upon the
extremely limited data base for these two approaches in adolescent BN.
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Chapter XVII
Emotion, Eating Disorders, and

Integrative Cognitive-Affective Therapy
Scott G. Engel1, Andrea Wadeson2, Chad M. Lystad3,

Heather K. Simonich,3 and Steve A. Wonderlich1
1University of North Dakota, Grand Forks, North Dakota
2North Dakota State University, Fargo, North Dakota
3Neuropsychiatric Research Institute
Fargo, North Dakota, USA
Abstract
Recent clinical reports and empirical findings suggest that emotion is an important
factor in the etiology and maintenance of eating disorders. As a result of this, emotion
may have an important role in the treatment of eating disorders. In this chapter we briefly
review a selected sample of empirical research on emotion and eating disorders. We
briefly discuss the role of neurobiology and emotion, emotional processing, and
ecologically valid findings in eating disorder research. We then discuss how this research
has shaped new treatments of eating disorders. Finally, we describe the key features of a
new treatment for bulimia nervosa, called Integrative Cognitive-Affective Therapy
(ICAT). ICAT is an emotion-focused treatment that highlights modifying emotion
regulation skills in bulimic patients. We discuss core features of the four phases of ICAT
and provide prototypical examples of clinical interventions in each phase.
In the past three decades, research on emotion has increased exponentially.

Accompanying this dramatic increase in research are new theories of emotion, new research
methodologies for studying emotion, and a variety of therapies that incorporate emotion as a
core component of treatment (Rottenberg and Johnson, 2007). Emotional processes are often
thought to be key constructs in a number of forms of psychopathology, for example, bipolar
disorder, alcoholism, anxiety disorders (Johnson, Gruber, and Eisner, 2007; Curtin and Lang,
2007; Farach and Mennin, 2007). In eating disorder (ED) research, scientists have begun to
308 Scott G. Engel, Andrea Wadeson, Chad M. Lystadet al.
investigate emotion and the role it may play in the etiology and/or maintenance of ED
behaviors (e.g., Engel et al., 2007).
The field of emotion is often considered to be “messy”, with few areas agreed upon. For
example, even the fundamental structure of emotion is debated today (Feldman-Barrett,
2006), with scientists questioning whether we have discrete emotions for example, fear,
sadness, anger (Watson and Vaidya, 2003) or whether emotion is best described as a
dimensional construct (Russell, 1980). Regardless of the many debates in the area of emotion,
we will attempt to provide some definitional information regarding the basics of the affective
science field (which, of course, are highly debated!)
In this chapter we use emotion-related terms that are generally consistent with Russell
(2003). Emotion is a general term meant to refer to both affect and mood. Mood is thought to
be enduring, trait-like experience of core affect. The use of the term affect is meant to convey
the momentary experience of state-like emotional experiences. We will most frequently make
use of the terms emotion (the more general term) and affect (the more specific term that
implies momentary experience), but, admittedly, use them somewhat interchangeably.
Emotion and Models of Eating Disorder Behavior

An increasing amount of research attention has been devoted to studying etiological and
maintaining variables in EDs. Much of this research, particularly the initial studies, has
focused on dietary restriction as a causal and maintaining factor in EDs. More recently, the
research has focused on alternative predictive variables, such as negative affect.
Dietary Restraint Model
According to the dietary restraint model, before individuals engage in bulimic behaviors
they experience low self-esteem and appearance concerns. These concerns are defined mainly
by an excessive focus on one’s weight and shape. In an attempt to improve their self-esteem
and reduce these concerns, the individual begins a period of extreme dieting. This severe
food restriction leads the individual to be both physiologically and psychologically
vulnerable, which then leads to binge eating. In order to compensate for the binge eating, the
individual then engages in purging behavior which may take the form of vomiting, excessive
exercise or abuse of laxatives. Following this behavior, the original shape and weight
concerns often reappear and the individual will return to the original dieting behavior, which
begins the cycle again (Fairburn and Cooper, 1989).
While the dietary restraint model has a great deal of empirical support (Steiger, Lehoux,
and Gauvin, 1999; Stice, Nemeroff, and Shaw, 1996; Stice, 2001), not all available data are
consistent with the model. Stice, Presnell, Groesz and Shaw (2005) recruited 188 adolescent
females to test the dietary restraint model. Each participant was randomly assigned to a
healthy weight management program or a control group. Stice and colleagues found that
those in the experimental condition showed a significant decrease in bulimic symptoms and
negative affect, less risk of obesity and weight gain, and better weight management. These
Emotion, Eating Disorders, and Integrative Cognitive-Affective Therapy 309
findings are contradictory to the dietary restraint model, which would argue that a weight
management program, which involves dietary restriction, would increase one’s bulimic
symptoms. Further, research has shown that not all individuals with bulimia nervosa (BN)
engage in dieting prior to engaging in bulimic symptoms; with as many as 9-17 percent of
individuals with BN reporting no dieting preceding bulimic symptoms (Mussell et al., 1997;
Bulik, Sullivan, Carter, and Joyce, 1997).
Negative Affect Model
Contrary to the focus on dieting in dietary restriction models, negative affect models
argue that negative affect is an important predictor in the etiology and maintenance of EDs,
particularly BN. Much of the data concerning the negative affect model come from
Heatherton and Baumeister’s (1991) escape theory. This theory contends that binge eating
serves as a way to escape from negative affective states, often related to an awareness that the
person is not living up to a standard or expectation. The theory posits that in the face of such
negative self awareness, individuals will “cognitively narrow” their thinking style which
produces a more concrete and potentially irrational thought process, which is associated with
a decreased inhibition of behavior. While the individual is in the “cognitively narrowed”
state, binge eating is thought to be more likely because inhibitory restraints are diminished
and also such behavior may reduce negative affect.
Stice, Nemeroff, and Shaw (1996) proposed a dual pathway model that states it is both
dietary restraint and negative affect that lead to body dissatisfaction, which in turn leads to
BN. Extreme dieting is, in part, caused by body dissatisfaction given the belief that it is a
valuable method of weight control. Further, dietary restraint has also been shown to lead to
negative affect, due to the failures associated with such extreme dieting (Stice, 2001).
Furthermore, body dissatisfaction has also been shown to produce negative affect (Stice and
Shaw, 1994). The binge-purge behavior characteristic of BN becomes a way to regulate such
negative affect, at least temporarily (Heatherton and Baumeister, 1991). It is important to
note that it is not necessary for both pathways to be present for BN to develop; rather each of
the pathways is considered sufficient to cause the onset of BN (Stice, 2001). In support of
this model, it has been found that body dissatisfaction, negative affect, dietary restraint, along
with the thin-ideal internalization, are all risk factors for the development of BN (Stice,
Nemeroff, and Shaw 1996; Stice, 1998, 2001).
To summarize the negative affect model, those who binge eat tend to have high demands
of themselves and a high level of self awareness. Since their expectancies are so high, they
become aware of their inadequacies, which results in negative affect. Binge eating allows
these individuals to escape from these negative affect states, at least temporarily, and is
therefore negatively reinforcing (Heatherton and Baumeister, 1991). Below, we will examine,
in a selective and limited review, empirical evidence indicating that emotional variables may
have significance in terms of both onset and maintenance of ED behavior.
Research on Emotion and Eating Disorders

While currently, there is little research that specifically investigates emotional processes
in patients with EDs, there are a number of studies that are relevant to those interested in
emotions and the role they may play in EDs. In an attempt to briefly review some of this
literature, we pose three interesting and clinically relevant questions below about emotion
and EDs and offer a brief review of the literature that addresses each question.
1) Is there a neurobiological explanation for the emotional problems of ED

patients?
A number of studies have examined neurobiological causes and/or correlates of EDs. The
work of Kaye and colleagues has suggested that disturbances in serotonin regulation are
associated with negative emotions in BN patients (Kaye, Weltzin, and Hsu, 1993). Providing
support for their hypothesis, Kaye et al. (2000) showed that BN participants were particularly
likely to display negative affect, mood lability and binge urges following tryptophan
depletion. Further, research implementing PET scans suggests that such abnormalities persist
after patients have recovered from BN (Kaye et al., 2001).
Studies of the neurobiological correlates of emotion function have also been conducted
with anorexia nervosa (AN) patients. Similar to BN, AN patients have also been found to
have abnormal serotonin functioning (Bailer et al., 2007) and also, several studies have
shown that AN patients display serotonin irregularities after they are weight restored and no
longer meet diagnostic status for an ED (Bailer et al., 2004; Frank et al., 2002; Kaye et al.,
2003; Bailer et al., 2005, 2006). These findings are consistent with the idea that emotion
regulation difficulties may represent a predisposing trait for AN. The findings also strongly
implicate a neurobiological explanation for the emotion dysregulation seen in ED patients.
2) Is there evidence that ED individuals display Deficits in emotional

processes?
As previously mentioned, Stice, Nemeroff and Shaw (1996) found that in addition to
dietary restraint, negative affect mediated the relationship between sociocultural pressure for
thinness and BN symptoms. Stice (1998) has also found that both dieting and negative affect
predict an increase in BN symptoms in a nonclinical sample of girls. Finally, a number of
studies have shown that ED patients report a number of emotional abnormalities (compared
to controls): difficulty recognizing and verbally expressing emotions (Zonneyvylle-Bender et
al., 2004), difficulty recognizing and describing their emotional states (Zonneyvylle-Bender
et al., 2005), decreased emotional awareness and deficient emotional control (Gilboa-
Schechtman, Avnon, Zubery, and Jaczmein, 2006), and increased suppression of both
positive and negative affect (Nandrino et al., 2006). All of these studies suggest that patients
with EDs may have difficulty identifying and regulating emotional experiences. These
emotional experiences appear to increase their risk of ED behavior, which in turn, may assist
these individuals in regulating or controlling negative emotional states.
3) All that research is great, but it is often done in artificial laboratories

and I’m not sure how well it generalizes to patients. Has any research
been conducted on emotion and eating disorders that is specifically
designed to generalize to the lives of patients?
Research employing experience sampling methodology (ESM; Csikszentmihalyi, 1994)

or ecological momentary assessment (EMA; Stone and Shiffman, 1994) is specifically
designed to maximize the extent to which the research environment parallels the participants’
natural environment. Therefore, findings from ESM or EMA research theoretically generalize
to the participants’ every day lives to the greatest extent possible. Besides conducting
research in the participants’ natural setting, ESM and EMA research use real-time assessment
techniques to reduce memory biases that are problematic with many other forms of
assessment (Engel, Wonderlich, and Crosby, 2005). EMA technology has recently been used
to clarify the relationship between emotion and ED behavior (Smyth et al., 2001). While
EMA and ESM research are technically not the same, they are conceptually very similar and
will be referred to as EMA research in the rest of this chapter.
EMA research has been conducted to better understand the role of environmental factors,
emotion states and behaviors in AN, BN, and binge eating disorder (BED). Early research
suggested that AN participants experience more negative affect than controls (Larson and
Johnson, 1991). Two other small EMA studies have suggested that: 1) negative affect is
related to AN behaviors (Pieters et al., 2006), but 2) AN patients report considerable
variability in mood functioning (Engel et al., 2005). It is worth noting that these findings are
somewhat preliminary given that all three of these studies had very small sample size.
Two EMA studies of particular relevance to BED are worth noting. Wegner et al. (2002)
found that BED participants reported worse mood on binge days compared to non-binge
days. Similarly, Stein et al. (2007) found that negative mood was higher before a binge, but
contrary to their expectations, they also found that participants’ post-binge negative mood
was even higher than pre-binge mood.
The first EMA study of BN patients was conducted in 1982, by Johnson and Larson.
They found that BN participants reported significantly more negative affect than control
participants. Steiger et al. (1999) expanded on this finding and reported that BN patients and
recovered BN patients reported greater levels of negative affect and self-criticism than non-
ED participants following a negative social interaction, thus implying that BN subjects may
be particularly sensitive to social cues. Several recent studies further clarify the relationship
of emotion and bulimic behavior in the natural environment. Smyth et al. (2007) found that
significant increases in negative affect precede BN behaviors and, importantly, negative
affect markedly drops following a BN behavior. Engel et al. (2007) reported that the
relationship between negative emotion and binge eating does not appear to be the same
across all individuals with BN: those high in impulsivity displayed a much stronger emotion-
behavior relationship than less impulsive subjects. These findings imply that while emotions
may predict the likelihood of binge eating in some BN patients, they do not do so for all
subgroups of people with BN. In total, the findings from this area of research demonstrate
that emotions may be a particularly relevant antecedent to eating disorder behavior, not only
in the research laboratory, but also in the natural environments of ED patients.
Summary
Although the evidence presented in this chapter is selective and brief, there is increasing
data suggesting that emotional variables have a significant, and potentially clinically
important, relationship to ED behaviors. This opens up potential opportunities for new
treatments which target emotional correlates of ED behavior. Below, we will provide a brief
overview of recent psychological treatments which target emotion related variables and also a
small, but developing, literature on emotion focused treatments in the EDs.
Rationale for Focusing on Emotion in the

Treatment of Bulimia Nervosa
Currently, cognitive-behavioral therapy (CBT; e.g., Agras et al., 1992; Fairburn et al.,
1993; Mitchell et al., 1990) is the most widely tested and effective form of treatment for BN
and represents a variation of standard cognitive therapy as defined by Aaron Beck (1967,
1976, 1987). In spite of continued demonstrations of at least moderate effectiveness,
cognitive therapy has come under criticism (e.g., Beidel and Turner, 1986; Safran, 1990a,
1990b; Stoppard, 1989; Westen, 2000; Zinbarg, 2000) regarding several issues. Clark (1995)
has summarized the criticisms of cognitive therapy and suggested they fall into four
categories. These include: 1) a limited view of emotional responding; 2) an inadequate
consideration of interpersonal factors; 3) insufficient attention to the therapist-client
relationship and 4) overemphasis on conscious controlled cognitive processing. Samoilov and
Goldfried (2000) suggest that CBT may be enhanced by eliciting, rather than managing or
suppressing emotion in CBT. Zinbarg (2000) suggests that CBT may also be criticized for
failing to address issues of resistance, or ambivalence, which may influence compliance with
CBT techniques and consequent magnitude of change. Associated with these criticisms of
cognitive therapy, there have been numerous efforts to extend or modify traditional cognitive
theory and therapy. For example, it has been argued that cognitive therapy should maintain a
stronger focus on interpersonal and affective issues (Safran and Segal, 1996; Samoilov and
Goldfried, 2000); consider borrowing from constructivist theories to enhance treatment
technique (Neimeyer, 1993); include narrative and metaphorical strategies (Meichenbaum,
1993); utilize the therapeutic relationship more thoroughly as a clinical technique (Robbins
and Hayes, 1993; Safran and Segal, 1996; Westen, 2000; Zinbarg, 2000); and place greater
emphasis on developmental and systemic issues (Guidano, 1986).
At the same time, there have been recent developments in the broader behavior therapy
community in which emotion focused models of psychopathology and associated treatments
have emerged (Farach and Mennin, 2007). For example, Allen, McHugh, and Barlow, (2007)
outline a unified protocol for emotional disorders which highlights identification of typically
avoided emotional responses and exposure to such disavowed emotions as a core of
treatment. Similarly, Hayes and colleagues (Hayes, Strosahl, and Wilson, 1999) argue that
behavioral analysts should carefully consider the functional relationships between emotional
states and efforts to manage or cope with such states when deriving their clinical
interventions. Their Acceptance and Commitment Therapy (ACT) is another example which
attempts to minimize the avoidance of negative emotions and experience as core

interventions. Furthermore, the work of Greenberg (2002) depicts an emotion focused
treatment which emphasizes identification, experience, expression, and modification of
emotional states and structures in the treatment of a variety of forms of psychopathology,
including depression and marital dysfunction. All of these approaches highlight an increased
emphasis on emotional experience and a new range of interventions which not only modify
such emotional responding, but also have been shown to reduce various forms of
psychopathology.
Clinical research in EDs has also supported the idea of expanding or extending the range
of interventions in CBT for BN. Recently, the original CBT model of BN was tested and
found to have more power in predicting bulimic symptomatology when factors such as
interpersonal variables and emotional variability were included (von Ranson and Schnitzler,
2007) , thus providing some empirical support for a broader conceptual model. Additionally,
Fairburn and colleagues have adapted their original CBT and created a new treatment (i.e.,
Cognitive Behavior Therapy-Enhanced or CBT-E; Fairburn, Cooper and Safran, 2003) which
includes interventions that target perfectionism, low self-esteem, interpersonal factors, and
emotional lability. Such adaptations were included because these variables were thought to
serve as significant maintenance factors which limited the efficacy of original CBT for BN.
Also, recent developments in the application of dialectical behavior therapy (DBT; e.g., Safer
et al., 2001) reflect the research community’s interest in the potential relevance of this
emotionally focused treatment for severe personality disturbances in bulimic individuals.
Although modified from its original form, the current DBT treatment for BN retains an
emphasis on emotion regulation, distress tolerance, and interpersonal factors and has been
shown to be at least somewhat effective in a randomized control trial with CBT as the
comparison condition (Safer et al., 2001). These extensions and modifications of the original
CBT for BN seem to reflect a growing consensus that a broader model with associated
interventions for previously untargeted maintenance factors could provide incremental
treatment efficacy.
Thus, CBT-E and DBT are examples of ED treatments which have more fully targeted
emotion related variables and processes. Another emotion-focused treatment that not only
targets emotion, but other important maintaining variables is integrative cognitive-affective
therapy (ICAT) for BN, which is a new emotion focused treatment. We are in the process of
finalizing pilot testing with ICAT and have received a federal grant to ultimately conduct a
randomized control trial comparing it to the original CBT for BN. Hopefully, this will further
clarify the relevance of emotion focused treatments for the treatment of EDs.
Integrative Cognitive – Affective Therapy for BN:

A New Emotion-Focused Treatment
The model of etiology and maintenance of BN which underlies ICAT is multifactorial
and attempts to integrate a broad array of emotional, interpersonal, cognitive, and biological
factors thought to increase the risk of developing, and maintaining behaviors associated with
BN. The conceptual model underlying ICAT has been more completely described in several
publications (e.g., Wonderlich et al., 2001; Peterson et al., 2004). The model is graphically
depicted in Figure 1 and can be summarized in the following manner. Bulimic individuals are
thought to display high levels of a harm avoidance trait (e.g., Bulik et al., 1995) and to have
experienced significant interpersonal problems and conflicts (Fairburn et al., 1997), which
together, result in high levels of self-discrepancy (Higgins, 1987). That is, their actual self
does not correspond to standards regarding how they wish they could be ideally or feel they
must, or ought to be. Such discrepancy is thought to provoke high levels of negative emotion,
which influence the bulimic individual’s behavior in a momentary fashion. Furthermore,
individuals with such high levels of self-discrepancy who internalize an ideal of thinness
(Stice et al., 1994) are likely to display appearance discrepancy which manifests itself as
body dissatisfaction.
The right half of Figure 1 depicts the posited behavioral reaction to negative emotions in
BN associated with high levels of self discrepancy. Specifically, bulimic individuals are
thought to attempt to regulate negative emotion with coping strategies which are defined as
self-directed styles and interpersonal patterns. (Wonderlich et al., 2001). Bulimic individuals
may also perceive a discrepancy between who they believe they are and who they feel they
would like to or must be (self-discrepancy; Higgins, 1987). Further, they may deal with their
discrepancy-oriented negative emotion with high levels of self-control (e.g., dietary
restriction) or self-attack (e.g., self- disparagement, self-harm behaviors) in an effort to
reduce negative affect and underlying self-discrepancies. Alternatively, some bulimic
individuals may use a neglect oriented self-directed style (e.g., excessive drinking, numbing
out), again in an effort to manage underlying emotional states. Furthermore, bulimic
individuals may attempt to regulate emotions through a variety of interpersonal patterns
including extreme submissiveness, social withdrawal, or a hostile attack oriented pattern.
Each of these interpersonal styles is thought to be a means of trying to regulate emotional
states and relationships in a fashion that minimizes the experience of discrepancy.
Finally, in the face of high levels of discrepancy, associated negative emotions, and self-
damaging coping styles, bingeing and purging are likely to emerge (Smyth et al., 2007). Such
behaviors may serve to block negative emotions or provide a sense of escape from the
awareness of such negative feelings. In this regard, bulimic behaviors are considered emotion
driven behaviors which are likely to be elicited when emotion states reach exceedingly high
levels.
Structure and Format of ICAT

Presently, ICAT is a structured, short term therapy developed explicitly for individuals
with normal weight bulimia or subclinical variations of this disorder. It consists of 20
psychotherapeutic sessions distributed over 16 weeks. Patients are seen twice a week during
the first four weeks of treatment. Treatment is guided by a clinician manual, patient
workbook, and a series of computerized treatment modules on a hand held personal digital
assistant.
Figure 1. ICAT Model of Bulimia Nervosa.
The treatment is typically administered in a series of four phases which sequentially

address motivation and psychoeducation (Phase I), the development of a meal plan and
exposure to emotions related to eating (Phase II), modification of self-directed styles and
interpersonal patterns associated with emotion regulation (Phase III), and relapse prevention
(Phase IV). Furthermore, over the course of treatment five core skills are used to organize the
various phases of treatment and focus the clinician and patient on essential processes thought
to promote recovery in ICAT. These core skills are outlined in Table 1 and are identified in
the treatment by their acronym (second column of Table 1). The FEEL skill is an essential
emotion identification skill which is introduced early in Phase I and maintained throughout
treatment. The CARE skill is introduced in Phase II and focuses on meal planning and food
logging. The SAID and SPA skills refer explicitly to interpersonal patterns and self directed
styles, respectively. Finally, the WAIT skill is a generic skill which targets reduction of
impulsive or urgent decision making which can result in eating disorder symptomatology.
The Patient Workbook complements and extends these skills and they are also included as a
series of PDA based modules. Below, we will provide a more detailed description of each of
the central phases of ICAT.
Table 1. Core Skills in ICAT
Coping Skill Acronym for Skill Elements in Acronym

Emotion Identification FEEL Focus, Experience, Examine and Label
Meal Planning CARE Carefully Arrange Regular Eating
Assertiveness SAID Sensitively Assert Ideas and Desires
Self Regulation SPA Self Protect and Accept
Impulse Control WAIT Watch All Impulses Today
Phase I: Enhancing Motivation and Psychoeducation - Sessions 1-2
Early sessions of treatment emphasize educating the patient about BN, largely through
the patient workbook, and also conducting a collaborative interview with the patient to
identify general discrepancies between their current behavior and broader life goals (Miller
and Rollnick, 1991). This process is typically done by conducting a brief review of the
history of their bulimic symptoms and the social and interpersonal context in which they
developed. Relying on techniques from Motivational Interviewing (Miller and Rollnick,
1991), these early sessions are utilized to explore and enhance the patient’s motivation for
treatment. Clearly, the first step in treatment is to attempt to establish a collaborative
therapeutic relationship that provides a safe context in which the patient may examine her
behavior and consider the implications of change.
In addition, the therapy must remain focused on the patient’s emotional reaction within
each session. This emotion-focused aspect of the treatment is thought to be essential in
assisting the patient to cope effectively with fear associated with behavioral change and
recovery. The therapist is encouraged to acknowledge and explore patients’ feelings as they
occur in the session. Therapist interventions may appropriately consist of questions such as
“Can you describe what the feeling is like for you as you consider change?” This may then be
followed by a series of questions or statements that deepen or clarify the emotional response
(e.g., “Is it frightening?” or “It seems hard to even think about it”). By exploring the
emotional significance, the therapist clarifies motivational forces that may maintain the ED
symptoms.
Another important consideration in Phase I is the introduction of the first core skill,
which is the FEEL skill. This skill is essentially an emotion-focused skill designed to assist
the patient in the identification and experiencing of emotions. The skill is introduced in the
first and second session and the therapist is encouraged to underscore the importance of this
skill throughout the treatment. It will be particularly important during Phase II, when meal
planning will be introduced and identification and exposure to feelings associated with food,
shape, and weight will be emphasized.
In an effort to complement learning of the FEEL skill, patients are asked to carry a
Palmtop computer for two days and complete the Positive and Negative Affects Scale
(PANAS) on several occasions. Completion of this scale allows the patient to begin to
develop a language for identifying feelings in the moment. It is easy to collect the
information on Palmtop computers, but this scale could also be delivered through a paper and
pencil means if a Palmtop was not available.
Below, we present the case of Ms. S as a demonstration of the importance of emotion
avoidance. Ms. S is a 28 year old, divorced, female who had a long standing history of BN
and significant abuse of alcohol. Ms. S displayed a significant difficultly tolerating and
managing negative emotional states. Although many interpersonal and work related situations
posed significant difficulties for her, she had a fundamental inability to identify her emotional
experience and, in ICAT terminology, demonstrated an emotional avoidance through eating
disorder behavior and alcohol use which became a target in treatment. The transcript clarifies
such emotional avoidance.
Therapist: Now, what are we doing here? What I’m noticing is I’m hammering away at
this with you and you are holding firm and steady with a hint of curiosity.
Patient: Well right, I mean how have I done it up until this time in my life…with alcohol
and throwing up. That’s where my serenity, if I’m going to have any comes from. Just numb
me up which means I’m not actually having any serenity in the first place. I’m just numbing
the rest of my world out.
Therapist: Right, and if you begin to tune into instead of numbing out, so if you use the
Palm Pilot to begin to tune into what’s going on inside of you…
Patient: That’s going to suck.
Therapist: Because?
Patient: Because it’s going to be work and who knows what I’m going to see.
Therapist: What are you going to see?
Patient: I mean, I don’t know.
Therapist: I think you have a clue otherwise you wouldn’t be so afraid.
Patient: Well probably a lot of things I don’t like.
Therapist: Like?
Patient: I don’t know.
Therapist: Take a minute.
Patient: I really - I don’t know, I mean probably—
Therapist: Slow down,
Patient: I thought I was going too slow.
Therapist: Slow down and think about it. What are you so afraid of?
Patient: I guess probably seeing what’s in there and we’re both pretty certain there is pain
in there and probably seeing that. Not only seeing it but having it come out and deal with it.
No, no, not only deal with it, but having it come out.
Therapist: And what will happen if it comes out?
Patient: It will be painful. Pain is uncomfortable and there is no room.
Therapist: It would swamp what you do. There would be no room for it.
Patient: Nope. Well there is no room because I’ve not ever allowed there to be room
because the feeling of pain is not something like the feeling of wanting to cry or crying, or if
like I’m going to be angry. I just don’t like that feeling. I don’t like the feeling of being hurt. I
just don’t and so…and if you are hurt and allow yourself to be hurt that infects the rest of your
world.
Patient: A perfect example is the phone call that I had where I hung up the phone and I
was almost immediately in tears because I had felt like such a failure I took everything told to
me by the other teacher so personally that it just overwhelmed me to the point I lost all of my
business-like composure and I became emotional - like creeped in without me realizing it was
going to. I don’t like that feeling because it a) hurts and b) there is no control.
Therapist: So it’s just better to just block it out than try to figure out what it is, try and
respond to it?
Patient: That’s all I’ve ever known
Much of the early phase of treatment with Ms. S was focused on trying to identify her
emotional experiences and states. This was a difficult procedure for Ms. S and she frequently
denied the importance of her feelings and attempted to engage the therapist in a process
which identified her as hopeless and untreatable. Although it took considerable time, Ms. S
ultimately did benefit from continued psychotherapy and an intensive inpatient stay which
gave her some control over her eating and drinking behavior and appeared to substantially
improve her ability to process her emotional responding.
Phase II: Normalization of Eating and Associated Coping Skills – Sessions

3-8
Phase II, which generally runs from Session 3 through Session 8, relies on the direct
encouragement of behavioral change in the area of eating and meal planning. Similar to other
treatments for BN (e.g., CBT), patients are encouraged to eat three meals a day along with
several snacks by prescribing a formal meal plan. Eating a variety of foods is encouraged and
introducing feared foods is also part of this intervention. The treatment assumes that much of
the reluctance that patients exhibit when asked to increase food intake is based on fear and
Goals of Phase I
1) Establish a treatment relationship which clearly includes the patient as a

significant collaborator in her treatment.
2) Enhance motivation by noting discrepancies between the effects of the eating
disorder symptoms and broader life goals.
3) “Side with the disorder” in terms of acknowledging possible benefits of the
symptoms.
4) Remain sensitive to patients’ emotional state and make efforts to identify
emotional reactions. This will serve as a basic strategy that will be employed
throughout the therapy.
5) Introduce FEEL skill and PDA methods.
6) Begin self-monitoring of food intake.
anxiety rather than oppositional defiance or characterologic resistance. Consistent with this
perspective, the introduction of the meal plan is considered not only a nutritionally oriented
exercise, but an emotion specific exercise. That is, while the therapist will assist the patient in
incorporating food related issues, there will be a thorough and committed effort to understand
emotions with the patient as they approach the meal plan, change their eating patterns, and
particularly when they continue to have difficulty with eating regular meals and engage in
binge eating.
An important element of Phase II is to emphasize continuation of the FEEL skill while
the new core skill entitled CARE is introduced. The CARE skill is considered a very
significant companion to the FEEL skill during this early phase of treatment. Using a variety
of formats (e.g., PDA’s, index cards, and their workbook), the therapist and patient together
will attempt to increase the direct practicing of these skills in therapy sessions and outside of
sessions. The acronyms for the core skills will be used to facilitate a language which
emphasizes these skills. For example, the therapist may say to the patient “While you are
working on your CARE skill tonight, it might be important to leave yourself time to practice
FEEL again as well.” This combination of identifying emotions while in the process of
arranging meals and eating is a critical component of the therapy at this point in time.
Goals of Phase II
1) Continue self-monitoring food intake.

2) Implement formal meal planning with an emphasis on nutritionally adequate
meals and snacks.
3) Introduce the CARE skill while continuing to practice the FEEL skill in and
outside of sessions.
Phase III: Interpersonal Patterns, Self-Directed Styles, and Cognitive
Processes Sessions 9-18

In Phase III of treatment, there is a clear shift in therapeutic focus from nutritional
rehabilitation to the interpersonal patterns, self-directed styles, and cognitive processes that
are considered coping strategies in ICAT. Of particular interest is how these factors may
serve to manage negative emotions, potentially related to self discrepancy, and may
ultimately lead to emotion driven bulimic behaviors. These concepts are outlined in Figure 2,
which is included in the Patient Workbook.
Figure 2. Phase III Treatment Components.
A major task in Phase III of treatment is for the therapist to work with the patient to
clarify the patient’s interpersonal patterns and self-directed styles developed to cope with
negative moods. Also, the negative emotions should be elicited and experienced thoroughly
by the patient. Through careful listening to the patient’s descriptions of their interpersonal
transactions, the therapist hypothesizes about the interpersonal rules, or “scripts” (Leahy,
1991), which seem to guide the patient’s interpersonal patterns and self-directed styles
(Benjamin, 1996, 2003). Thus, the patient gains an understanding of their interpersonal and
self-directed behavior in “if-then” terms (e.g., “if others do x, I do y”). For example, a patient
may have an interpersonal pattern which incorporates the if-then statement “If I submit to
others, then others will love me.” Alternatively, a patient may have developed a self directed
style which relies on the “if-then” statement “If I can control myself perfectly, I will be O.K.”
The therapist’s focusing on the elements of the interpersonal patterns and self-directed
styles must continue to be emotion-focused. That is, if the patient is only able to describe
such interpersonal patterns or self-directed styles in a sterile and intellectualized manner, it is
unlikely to be optimally effective in terms of behavioral change. Thus, the therapist must
remain attentive to the emotional quality of the patient’s descriptions of their interpersonal
encounters and their self-views.
Below, we provide a transcript from Ms. M., a patient with AN-binge purge type. This
section of a therapy session highlights the efforts to identify the interpersonal patterns and
self directed styles that this patient frequently experienced and figured prominently in her ED
behaviors.
Therapist: O.K., so something happened last night when you were talking to your
boyfriend on the phone.
Patient: Yeah.
Therapist: Can you tell me about what took place last night, all of what happened with
him?
Patient: Well, it was a bad night. I got home from work and called him and I just got the
feeling he was preoccupied. Some of the guys from his softball team wanted him to go out
later and I had thought we were going to do something. (She sees him as SEPARATE)
Therapist: Can you say what it was like, that is what you were feeling, when he was
talking about going out with his friends on the phone.
Patient: I was mad! He always does this. He has got softball games all summer and every
time he has a softball game, he has to be with his friends. But then when he has got time free,
he expects me to be available. (“mad” is obviously an emotion word and explored further
below)
Therapist: So you saw him as sort of doing his own thing and not being very available to
you and you noticed that you were angry? Can you describe more completely what that was
like for you when you were angry? (Further effort to clarify feelings)
Patient: I don’t know, I just get mad.
Therapist: Yes, I understand that, but what happens when you get mad? What does it feel
like internally and what do you do? (continued emotion exploration)
Patient: I just get crazy. I feel like I want to cry and scream. I pace and I don’t seem to be
able to sit still. That’s when I do my (bulimic) behaviors. (beginning to see the action
tendency)
Therapist: Did you in this case?
Patient: Yeah.
Therapist: Did those behaviors help you?
Patient: For a little while, but I was still freaking out.
Therapist: Can you tell me what you wound up doing then, after your behaviors, when
you were feeling so upset and your boyfriend was not going to be available to you?
Patient: Well, I talked to him later and screamed at him and told him what a jerk I thought
he was. I told him that he was insensitive and spoiled and that I was sick of being treated like
dirt. (therapist is beginning to identify a possible ATTACK pattern)
Therapist: So you really sort of let him have it?
Patient: Yeah, I did and he really deserved it.
Therapist: And what happened then? (looking for consequences of behavior)
Patient: Well, then he got really quiet. He wouldn’t talk to me and I got sort of nervous. I
kept asking him to talk to me and he told me that he thought that maybe we needed a break
from each other and that he was sick of dealing with my tantrums. (Boyfriend appears to be
WALLING-OFF)
Therapist: So he was sort of pulled back. Sounds like he was threatening to leave.
Patient: Yeah, that freaked me out. (“freaked-out” is an emotion word)
Therapist: Freaked you out? What did you do? (identifying the action tendency)
Patient: Well, I did what I always do. I told him I was sorry and I would never do it
again. That I was out of line. That I was acting like a bitch and I would try and do better next
time. (possible evidence of reaction of SUBMIT and self-directed behavior of SELF-BLAME)
Therapist: Do you remember what you were feeling once you started to take the blame?
Patient: I am not sure. I know I get really nervous when he threatens to leave me. I think
that I just keep telling him I’ll be better and kind of begging him to stay. I don’t know what I
feel. Probably something like scared.
Therapist: There is one more thing I want to clarify. Earlier you told me that when you
were angry at your boyfriend because he was not going to be able to see you, you were pretty
mad. As I understood it, you called him some names and kind of put him down (ATTACK). I
was wondering what you were hoping he might do when you got down on him. Any thoughts?
Patient: I don’t know. I wanted him to know that he was a jerk and he was hurting me and
I didn’t like it.
Therapist: What did you hope he would do?
Patient: Well, I suppose I wanted him to say that he wouldn’t go with his friends and that
he would be with me. I wanted him to change his mind. (Wants CONTROL and wishes for
boyfriend to SUBMIT)
Therapist: I see. You wanted to have some influence on him. I never did understand if it
worked. Did he spend the night with you or did he go with his friends?
Patient: He went with his friends. (He WALLED-OFF)
Finally, during Phase III three additional core skills are introduced. Each of these focuses
on a particular aspect of interpersonal or self directed behavior or action tendencies. For
example, the SAID skill focuses on expression of feelings, desires, and ideas to other people
assertively. The SPA skill emphasizes the development of self protecting and self accepting
self directed styles. Finally, the WAIT skill targets impulsive behaviors and encourages a
careful reflection on feelings and needs before acting (see Table 1). Each of these skills is
again included in the PDA, on index cards, and in the workbook.
Phase IV: Relapse Prevention and Lifestyle Management - Sessions 19-20
The final phase of treatment focuses on consolidating improvements and preventing

relapse. This process requires the therapist and patient to review progress in treatment,
especially identifying interventions that were particularly helpful and effective. Final sessions
should also include discussions of the patient’s feelings and thoughts about ending treatment.
Goals of Phase III
1) Identify and modify maladaptive self-directed styles.

2) Identify and modify maladaptive interpersonal patterns.
3) Identify the connection between emotion and interpersonal patterns and self-
directed styles and how these relate to bulimic symptoms.
4) Continue to modify extreme discrepancies between actual self and evaluative
standards for the patient.
5) Implement SPA, SAID, and WAIT core skills.
An essential component of Phase IV is to educate the patient about the nature of relapse
in order to prevent its occurrence. Specifically, the therapist should emphasize the distinction
between a “lapse” compared to a “relapse” in order to prevent the patient from
overgeneralizing the importance of a minor slip, a process that can lead to symptomatic
deterioration. In addition, the patient is asked to consider various relapse scenarios, and to
formulate coping strategies using skills developed in treatment. The patient also identifies her
own potential cognitive, interpersonal, and behavioral triggers of lapses and relapses, and
develops plans to get back on track should these occur.
Finally, the patient and therapist review the changes made in treatment and develop a
maintenance plan to facilitate continued improvement. As part of the maintenance plan,
components of a healthy life style are identified and implemented. In addition, the therapist
should focus on emotions related to ending the treatment.
Goals of Phase IV
1) Review coping strategies that can be used to prevent relapse from occurring and
learn about the nature of relapse. Include an emphasis on 3-D coping.
2) Identify risk factors of relapse and plan specific strategies for getting back on
track if symptoms worsen.
3) Review progress in treatment.
4) Develop a maintenance plan for continued improvement and healthy lifestyle.
5) Focus on emotions related to termination.
An increasing amount of research suggests that emotion may be particularly relevant to a

number of forms of psychopathology (Rottenberg and Johnson, 2007). In particular, research
shows that emotional processes may be particularly important to eating disorders.
Accordingly, new therapies for eating disorders have attempted to better incorporate
emotional processes into treatment. In particular, the present chapter provides a brief
overview of integrative affective therapy, which is a new emotion- focused therapy for BN.
This treatment integrates the direct modification of meal planning and eating behavior with
emotion-oriented interventions which address identification of feelings states and also
adaptive emotion regulation strategies. Given the apparent strong association between
emotional experience and eating disorder behaviors, new treatments which attempt to modify
the experience of emotions and eating disordered individuals strategies for managing such
emotions may provide an important step in the next generation of ED treatments.
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Zinbarg, R. E. (2000). Comment on "Role of emotion in cognitive behavior therapy": Some

quibbles, a call for greater attention to patient motivation for change, and implications of
adopting a hierarchical model of emotion. Clinical Psychology: Science and Practice, 7,
394-399.
Zonnevylle-Bender, M. J. S., van Goozen, S. H. M., Cohen-Kettenis, P. T., van Elburg, A.,
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Chapter XVIII
Pharmacological Therapies for

Anorexia Nervosa
James L. Roerig1,2, Kristine J. Steffen2, James E. Mitchell1,2,

and Scott J. Crow3
1.University of North Dakota School of Medicine and Health Sciences
Fargo, North Dakota, USA
2.Neuropsychiatric Research Institute, Fargo, North Dakota, USA
3.University of Minnesota Medical School
Minneapolis, Minnesota, USA
Abstract
This chapter will review the evidence surrounding the use of pharmacotherapy in the
treatment of anorexia nervosa [AN]. Medications are divided into three classes;
antidepressants, atypical antipsychotics and miscellaneous agents. Randomized, double
blind, placebo controlled trials will be emphasized. In the absence of controlled trials
uncontrolled data is presented. Lastly, suggestions for future studies will be presented.
Introduction
In recent years, substantial advances in pharmacological treatment approaches have been
realized in many psychiatric conditions, including schizophrenia, bipolar disorder, and major
depressive disorder. This progress has not been paralleled in AN, and definitive data to
support the routine use of any pharmacotherapy in this disorder remains lacking. Historically,
pharmacological agents have been chosen based on their ability to cause weight gain or to
improve mood rather than their efficacy on other core AN symptoms. This may have
contributed to the current state of affairs, in which the number of controlled pharmacological
trials in the field has been modest and the few studies that have been completed have
generally yielded negative or inconclusive results.
332 James L. Roerig, Kristine J. Steffen, James E. Mitchell and Scott J. Crow
This chapter will review the state of the art, as it is somewhat shy of science, in terms of
pharmacotherapy approaches. Discussion of the use of antidepressants, second generation
antipsychotics and miscellaneous agents will serve to inform the current practice of
pharmacotherapy. Lastly, a discussion of future treatment approaches and areas of inquiry
will be presented.
The treatment course of AN is generally regarded as being biphasic; the initial focus of
treatment is on promoting medical stability and encouraging weight restoration whereas the
goal later shifts toward facilitating weight maintenance which requires a focus on the
psychopathological symptoms of the illness. Currently, this treatment includes
psychotherapy, education and nutritional rehabilitation, with pharmacotherapy in an
adjunctive role.
As will be discussed below, there is little data on which to base treatment decisions.
However, that may not reflect current clinical practice. As with any difficult to treat illness,
clinicians will attempt to treat symptoms that the patient presents even in the absence of clear
data supporting efficacy. In some cases the patient will benefit from this practice. However,
many patients also experience complex therapies and are at times
exposed to the risk of medication side effects, drug interactions and finally, high costs.
In exploring the “core” AN symptoms, a possibility exists to discover clues to aid in the
development of more effective drug treatment. Some of the AN symptoms are illustrated in
the following case:
Denise was a 20-year old female with a diagnosis of AN binge/purge subtype. She had
developed AN about one year previously and had been quite resistant to outpatient
treatment when she presented at 92 pounds and 5’5” tall. She was admitted to the partial
hospital program and managed to gain weight to 98 pounds; but in general she continued
to be quite resistant to weight gain. She was then placed in twice a week in outpatient
psychotherapy and was seen by a family physician every other week to monitor her
weight and laboratory work. However, she continued to do poorly and lost to 90 pounds
at which time she was hospitalized as an outpatient treatment failure.
In the hospital she was quite depressed, and in general, not cooperative with treatment.
She was quite obsessed with body image concerns and spent much of the day attempting
to measure body parts with her hands or by checking in the mirror. She was very moody,
but generally down, and she was also very obsessional and perfectionistic. She attempted
to do all her assignments “perfectly”, and repeatedly complained about having to eat all
her meals. She had slept poorly and had a great deal of difficulty relating to staff or other
patients. Because of this the decision was made to try her on the atypical antipsychotic
olanzapine in addition to the therapeutic milieu on the inpatient unit and the behavioral
contingencies for weight gain. She was started at a dose of 2.5 mg. which was increased
five days later to 5 mg., and five days subsequent to that to 7.5 mg. The effect was
dramatic. She reported, and the staff observed, decreased symptoms of anxiety and
depression, and in particular less obsessionality about weight and shape issues. She
reported that she was finding it somewhat easier to eat and began a steady pattern of
weight gain. Her mood continued to improve and she became much more amenable to
psychotherapy, and developed a good working relationship with her inpatient therapist.
She was discharged several weeks later at a target weight of 110 pounds and was
transferred back to fairly intensive outpatient treatment. The medication was continued
Pharmacological Therapies for Anorexia Nervosa 333
for the next two months while her weight gain continued and then stabilized, as she
progressed in psychotherapy.
Treatment
Antidepressants
The antidepressant class of medications has received the most extensive study among
psychotropic agents in the treatment of AN. Although this research is arguably not yet
exhaustive, the majority of antidepressant trials conducted to date have yielded negative
findings. As reflected in the preceding case, patients with AN frequently have comorbid
psychopathology which in itself might be an indication for the use of an antidepressant
medication, including major depressive disorder, anxiety symptoms, and obsessive-
compulsive disorder symptoms
Early controlled trials failed to demonstrate the superiority of tricyclic antidepressants
[TCAs] over placebo [Lacey and Crisp, 1980; Biederman et al., 1985; Halmi et al., 1986].
Tricyclic antidepressants work by inhibiting reuptake of norepinephrine and/or serotonin, and
also act as antagonists at a variety of receptors including alpha-1 adrenergic, muscarinic
acetylcholine [M1], and histamine-1 [H1] receptors [Feighner, 1999]. It is the H1 antagonism
of these drugs that is thought to lead to sedation as well as weight gain [Richelson, 2003].
Depression treatment research has shown that TCA use leads to a continuous, dose-dependent
weight gain of 0.57-1.37 kg/month [Garland, Remick and Zis, 1988]. Although the H1
antagonism of the TCAs may therefore be of theoretical benefit in AN, their antagonism of
alpha-1 and M1 receptors can lead to adverse effects such as orthostatic hypotension and
anticholinergic effects, respectively.
Lacey [1980] compared clomipramine, 50 mg/day, to placebo in 16 hospitalized patients
with AN. In this study, there were no significant differences in weight gain or the time that
elapsed prior to achieving target weight between groups. Clomipramine appeared to increase
hunger ratings during the first two months of treatment, but was equal to placebo during the
final three weeks of the study. Participants in this trial received concomitant psychotherapy
and a 2600 kcal/day nutritional rehabilitation program. In addition to the potential
confounding effects of these multiple interventions, the clomipramine dose used in this study
was likely subtherapeutic. Currently, therapeutic antidepressant clomipramine doses are
generally regarded to be above 100 mg/day.
Similarly, Biederman [1985] studied a mixture of 38 inpatients and outpatients with AN.
In a five week trial, amitriptyline [mean dose 115 + 31 mg/day, maximum dose 175 mg/day]
was compared to a placebo group and a control group. The control group was comprised of
drug-refusers who received psychosocial treatment only. Across the three groups, weight gain
was similar and no greater decrease in depressive symptoms occurred in the amitriptyline
group. The amitriptyline group did, however, experience side effects that included
diaphoresis, drowsiness, dry mouth and hypotension.
Finally, Halmi [1986] studied 72 inpatients for four weeks, comparing amitriptyline
[maximum of 160 mg/day], cyproheptadine [maximum of 32 mg/day], and placebo.
Cyproheptadine is a histamine, acetylcholine, and serotonin antagonist. This study was
conducted in two locations, with differing findings in each. There were 15/46 treatment
failures in one location versus 4/26 at the other location. Patient’s pretreatment weight status
appeared to influence outcome. Cyproheptadine increased what was termed treatment
efficiency in the non-bulimic subgroup and decreased efficiency in the bulimic subgroup.
There was an antidepressant effect in the bulimic subgroup with cyproheptadine.
By virtue of their improved adverse effect profile, the SSRIs have largely supplanted
TCA use in the field of psychiatry. In patients with AN, there are additional issues related to
TCA use that should be considered. First, it has been reported that underweight patients are at
higher risk of developing an arrhythmia with TCA use [Kotler and Walsh, 2000]. Secondly,
many patients with AN are adolescent and TCA’s have been associated with sudden death in
children. A series of eight cases of sudden death are described in a 2001 review in which
child or adolescent patients were treated with either imipramine or desipramine [Varley,
2001]. This author postulates that this risk extends to all TCA’s, not just imipramine and
desipramine. Finally, all antidepressant medications now contain a Black Box warning
regarding an increased risk of suicidal thinking and behavior in children, adolescents, and
most recently also in young adults between the ages of 18 and 24. This warning has been
instituted in response to a request from the U.S. Food and Drug Administration [FDA]. This
risk appears to be highest within the first two months after initiating treatment with an
antidepressant (FDA U.S. Food and Drug Administration, 2007). The FDA does make it clear
that patients under age 24 can still receive antidepressants and treatment should be based on
an assessment of the risk-benefit ratio in each patient. These warnings, however, do
necessitate educating patients and caregivers about this risk.
SSRI’s have been studied in the treatment of AN. There are essentially two types of trials
with SSRIs; acute treatment trials and maintenance trials. Acute treatment typically occurs in
patients who are often severely underweight and are hospitalized, and the primary treatment
goal is weight gain. Maintenance treatment occurs after weight restoration has occurred, and
the primary goal of treatment becomes relapse prevention. There are currently controlled data
with fluoxetine both in acute treatment and as maintenance treatment. There are also
uncontrolled data with a variety of other SSRIs.
Controlled data includes a study by Attia [1990], who showed that in low-weight AN
inpatients, seven weeks of fluoxetine at a maximum daily dose of 60 mg failed to improve
weight gain or mood over placebo. Several explanations may exist to account for this finding.
Tryptophan, the amino acid precursor required for serotonin synthesis, decreases following
acute dieting [Anderson et al., 1990; Wolfe, Metzger and Stollar, 1997]. Therefore,
underweight patients may be unable to synthesize sufficient serotonin for the SSRIs to be
effective. However, findings regarding plasma tryptophan levels have been inconsistent in
AN. Some data have suggested lower concentrations of tryptophan in AN versus matched
control subjects [Askenazy et al., 1998] and other data showed no difference between
underweight AN patients and controls [Goodwin et al., 1989]. A “ceiling effect” may also be
operative, in which the unique contribution of a drug would be statistically indiscernible over
and above the array of simultaneous andgenerally to some degree effective, interventions
these patients already receive.
Controlled relapse-prevention trials have also been performed with SSRIs in weight-
restored patients. While an earlier controlled trial demonstrated improved weight
maintenance and decreased core symptoms with fluoxetine over placebo at one year [Kay et
al., 2001], a subsequent, more rigorously controlled, larger trial failed to substantiate these
findings [Walsh et al., 2006]. The latter trial enrolled 93 AN outpatients and demonstrated
that similar percentages of patients remained in the trial at 52 weeks and maintained a BMI of
at least 18.5 [fluoxetine, 26.5%; placebo, 31.5%; p=0.57].
Table 1. Controlled Antidepressant Trials in Anorexia Nervosa
Reference Drug and Dose Duration N Inpatient or Outcome

(mg/day) Outpatient
Lacey and Crisp, Clomipramine Variable 16 Inpatient Trial continued until patients met
1980 50mg Length females target weight. Concomitant
Versus Placebo Study psychotherapy and nutritional
program. No significant difference
in amount or rate of weight gain
between groups.
Biederman et al., Amitriptyline 5 Weeks 38 Inpatient Control group comprised of
1985 Max 175mg (sex not and patients who refused drug and were
Mean 115mg (+ reported) Outpatient given psychosocial treatment. No
31) mg Versus difference on weight gain or
Placebo Versus depression measures between
Control groups. There were adverse effects
in the amitriptyline group,
including diaphoresis, dry mouth,
and hypotension.
Halmi et al., 1986 Amitriptyline 4 Weeks 72 Inpatient Cyproheptadine increased
Max 160mg females treatment efficiency in the non-
Versus bulimic subgroup. Cyproheptadine
Cyproheptadine group also had an antidepressant
Max 32mg effect.
versus Placebo
Attia et al., 1998 Fluoxetine Max 7 weeks 33 Inpatient Participants also involved in
60mg females nutritional and cognitive behavioral
Mean therapy program. Groups did not
56mg differ on weight gain or mood
symptoms. Fluoxetine was tolerated
well.
Kaye et al., 2001 Fluoxetine 52 39 Outpatients Higher number of fluoxetine
range of doses; weeks females treated patients remained on drug at
20mg every one year (10/16) versus placebo
other day to (3/19). Fluoxetine group increased
60mg/day weight and decreased core eating
disorder symptoms at 52 weeks.
Participation in psychotherapy was
optional in this study.
Walsh, et al., 2006 Fluoxetine 52 93 Outpatients No difference between groups in
mean: 63.5 (+ weeks females time to relapse. 26.5% of the
15.8) mg/day fluoxetine group and 31.5% of the
versus Placebo placebo group maintained a BMI of
18.5 and remained in the study for
52 weeks.
Abbreviations: BMI=body mass index
Atypical Antipsychotics
The second class of compounds that are clinically used in AN treatment are antipsychotic
agents. While traditional [1st generation] antipsychotics have not been shown to be of benefit
relative to placebo [Vandereycken and Pierloot, 1982; Vandereycken, 1984], atypical [2nd
generation] antipsychotics have recently demonstrated some promise in uncontrolled reports
and modest trials. As with antidepressants, the weight gain liability of some of the 2nd
generation agents contributed to interest in these agents. Also, it has been suggested that
patients with AN have distorted perceptions of body shape and/or weight, which have a
delusion-like quality [Jones and Watson, 1997]. Symptoms of anxiety surrounding meals,
obsessive features and sleep disruption have been reported to improve with atypical
antipsychotic use. While they are not devoid of side effects, the atypical agents are generally
less likely to cause extrapyramidal side effects [EPSE] including pseudoparkinsonism,
dystonias, and akathisia as well as being less likely to cause tardive dyskinesia [TD], a
condition for which adequate treatment does not exist [Umbricht and Kane, 1996].
Unfortunately, only three small controlled trials have been presented as posters/oral
presentation at several meetings [Bissada et al., 2007; Kafantaris et al., 2007, Attia et al.
2008]. The Bissada trial has now been published [Bissada et al. 2008]. However, several
uncontrolled studies and case series have suggested benefit of using these drugs in AN [See
Table 2].
In reviewing these data, an effect on core AN symptoms has been described. Areas such
as anxiety, depression and obsessive compulsive symptoms as well as thought disturbance are
frequently improved with the atypical agents [Powers et al., 2007; Mondraty et al., 2005;
Malina et al., 2003; Mehler, et al., 2001]. In addition, rating scales have demonstrated
significant improvement including the Positive and Negative Symptom Scale [PANSS] total
score and subscales of general psychopathology, anxiety and depression, the Brief Psychiatric
Rating Scale [BPRS] total score, the Eating Disorder Inventory- 2 [EDI-2] total score and the
subscales drive for thinness, perfectionism, impulse regulation, social insecurity, bulimia
subscale, body dissatisfaction, ineffectiveness, interoceptive awareness and maturity fears
[Powers et al., 2007; Powers, Santana and Bannon, 2002]; and the Yale Brown Cornell Scale
for Eating Disorders [YBC-EDs] [Barbarich et al., 2004].
One consideration is that weight gain, rather than the drug therapy, may be responsible
for these improvements. However, a difference in the comparison group’s weight gain was
not consistently shown. Thus, while weight gain is associated with improvement of
symptoms, it may be that the drug’s effect in reducing the core symptoms of the illness allow
the patient to return to healthful eating and a better quality of life. These speculations must be
demonstrated however, in larger, randomized, double blind, placebo controlled trials. These
studies will have to address relevant questions including choice of agent, dosage and side
effect liability.
Table 2. Antipsychotic Trials in Anorexia Nervosa
Reference Drug and Study N Inpt/ Outcome

Dose Design Outpt
[mg/day]
Gaskill et al., Olanzapine Open-label 46 (sex Inpt Study enrolled inpatients. Weight gain was not
2001 Range: 1.25- [non- not different between olanzapine and non-treated
15 mg randomized] reporte group.
d)
Mehler et al., Olanzapine Case Report 5 --- Age range of 12-17. Olanzapine failed to
2001 Range: 5- 6 – 8 weeks females increase weekly average weight gain.
12.5 mg Decreased delusional thinking and improved
social interaction observed in 5 patients.
Ruggiero et Fluoxetine Single-blind 35 Inpt Patients were treated during the beginning of
al., 2001 28 [+10.32] 3 months females refeeding phase. Exclusion of subjects with
clear depression, anxiety, obsessive
Clomipramin compulsive disorder, and delusional body
e image thinking. Weight increase was not
57.69 significantly different between groups.
[+25.79]
Amisulpride
50 [+0]
Carver et al., Risperidone Retro- 30 ---- Study enrolled refractory inpatients with AN.
2002 Range: 0.5- spective females Risperidone treated patients demonstrated
1.5 mg Chart slightly higher weight gain [3.6 vs. 3.4 kg] and
Review caloric intake [1017 vs 943 kcal].
Powers Olanzapine Open-label 18 (16 Outpt 10 of 14 completers gained average of 8.75 lb.
et al., 2002 10 mg 10 weeks female, 4 drop-outs gained an average of
2 male) 3.25 lbs.
4 completers lost an average of 2.25
lb but 3 of the 4 had low OLZ plasma levels.
Patients who gained weight had
significant improvement on psychiatric rating
scales by week 10
Barbarich, et Olanzapine Open-label 17 Inpt Depression, anxiety, and core eating disorder
al., 2004 Mean: 4.7 6 weeks (sex symptoms improved. Weight increased
[+1.6 mg] not significantly, from entrance weight of 69 [+
Range: 2.5- reporte 10] % IBW to final weight of 81 [+9] % IBW
7.5 mg d) [p=0.000]. Some subjects were also taking
SSRIs.
Mondraty, et Olanzapine Randomized 15 (sex Inpt Duration of the trial was 46 + 31 days for
al., 2005 Range: 5-15 open-label. not olanzapine and 53 + 26 days for
mg [mean: Up to 79 reporte chlorpromazine. Patients were hospitalized.
10 mg]. days d) The reduction in ruminative thinking on the
Padua Inventory was significantly greater in
the olanzapine group [54% decrease] vs. the
Chlorpromaz chlorpromazine group [9% decrease]
ine [p=<0.01]. Average weight gain was 5.5 kg,
Range: 25- with no significant differences between
100 mg groups. Participants also received standard
[mean: 50 inpatient care, consisting of psychiatric,
mg] nutritional, and medications.
Reference Drug and Study N Inpt/ Outcome

Dose Design Outpt
[mg/day]
Powers, et al., Quetiapine Open-label 19 (18 Outpt Study enrolled outpatients. 10-wk study.
2007 150-300 mg 10 week females LOCF analysis performed. 14 participants
,1 completed the study. Total scores on the
male) PANSS as well as on the psychopathology
and depression scales decreased significantly
[p=0.024, 0.10, 0.0005, respectively].
Improvements were seen in anxiety,
depression, and obsessive-compulsive
symptoms. Mean weight gain was 0.73 kg.
No participants withdrew due to adverse
effects.
Bosanac et Quetiapine Open-label 8 Inpt 7 completed 4 weeks
al., 2007 50 – 800 8 week females 5 completed 8 weeks
mg/d 4 weeks significant difference in the EDE-12
8 wk =mean restraint score
dose 520mg, 8 weeks significant differences on
SD 277.49 BMI and EDE-12 restraint subscale scores SE
of initial mild sedation
Bissada et al., Olanzapine Double 14 each Outpt. Olan. + DH gained weight at a faster rate than
2007 2,5 – 10mg/d blind, group 4 plac. + DH. [p=.04 intent to treat]. Of
placebo (sex day/w completers 100% of Olan group was weight
controlled not k DH restored [BMI > 18.5] vs. 71.4% of the
13 week reporte placebo group [p=.03]. No evidence of
d) adverse side effects among any patients.
Depression, anxiety, OC symptoms
significantly improved in both groups.
Kafantaris et Olanzapine Double 20 9 No difference in weight gain.
al., 2007 (dose blind, subject hospit Significant improvement in total BPRS
unknown) placebo s total al- (p<.004) and Ham-D (p<.014) scores and
controlled (sex ized, significantly less depressed affect [p<.003],
10 week not 11 in insomnia [p<.005] and increase in appetite
reporte day [p<.039] in Olan group.
d) progr
am
Attia et a l., Olanzapine Double 23 Outpt. Olan. associated with statistically significant
2008 blind, subject higher rate of weekly weight gain (0.9 + 0.94
placebo s vs. -0.15 + 1.07, p = 0.043).
controlled, No significant difference between groups on
8 week multiple psychological symptoms
Abbreviations: BMI =Body Mass Index; BPRS =Brief Psychiatric Rating Scale; DH = Day Hospital;
EDE-12=Eating Disorder Examination-12th Edition; Ham-D =Hamilton Depression rating scale;
IBW=Ideal Body Weight; Inpt=Inpatient; OC=Obsessive Compulsive; Olan.=Olanzapine;
Outpt.=Outpatient; PANSS=Positive and Negative Syndrome Scale; SE=Side Effects; wk=week
As can be seen in Table 2, olanzapine, quetiapine and risperidone are frequently used
agents. All of these agents can cause weight gain with olanzapine having the greatest effect,
quetiapine somewhat less [Allison et al., 1999] and risperidone’s effect being approximately
half of olanzapine [Roerig et al., 2005]. Is the weight gain liability of the atypicals necessary
for a positive effect? No data currently address this question. The weight liability may cause
non-compliance with the drug treatment in AN patients due to their fear of gaining weight.
Also the weight liability may not have any role to play in response to the agent. Studies with
weight neutral agents are needed to explore this question. Currently there are two weight
neutral atypical agents marketed in the U.S., aripiprazole and ziprasidone. As discussed
below, ziprasidone has the liability of affecting cardiac conduction and would not be
recommended in this population.
Dosages of these agents have run from low to moderate levels [see Table 2]. Usually the
dosage of the selected agents is initiated at a low level and gradually titrated to effect or mid
dosing range. However, controlled data will have to guide these selections in the future, as it
is always best to utilize the minimum effective dose to avoid side effect burden.
In general, these agents are well tolerated and the various reports listed above confirm
this. However, the agents do differ somewhat in adverse reaction liability. As mentioned,
olanzapine has the greatest effect on weight and in the population of patients with
schizophrenia also has the greatest effect on serum lipids and glucose control [Lieberman et
al., 2005]. Both olanzapine and quetiapine are sedating, although this effect usually decreases
in the first week of treatment. Lastly, risperidone represents the agent with the greatest
dopamine-2 receptor blocking affinity which results in elevated prolactin and dose related
EPSE particularly as the dose approaches and exceeds 4 mg/day [Lieberman et al., 2005;
Hamner, 2002]. Another concern in underweight AN patients is cardiac conduction. Many
agents can lengthen the QTc interval and result in a higher risk for cardiac arrhythmias such
as Torsade De Pointes. Of the atypicals, olanzapine has the least effect on the QTc interval
and ziprasidone the greatest [Harrigan et al., 2004]. For this reason we would recommend
against using ziprasidone in this population.
Finally, if data support the efficacy and effectiveness of selected atypical agents in the
acute treatment of AN, the question of maintenance treatment becomes important. Currently
there are no data addressing the duration of treatment. Various case reports and series have
patients continuing on the atypical for weeks to months. As with the data reported by Walsh
et al [2006] concerning fluoxetine maintenance therapy, it will be important to design
rigorous trials to determine if there is any benefit to continuing atypical agents and if so, how
long.
Miscellaneous Agents
Medications other than antidepressants and antipsychotics have also been tried in a
handful of controlled trials in AN. Owing either to unfavorable adverse effect profiles or to a
lack of demonstrated efficacy, these medications have not earned a place in the clinical
management of AN. Medications in this category include tetrahydrocanabinol [Gross et al.,
1983], naltrexone [Marrazzi et al., 1995], clonidine [Casper, Schlemmer and Javaid, 1987],
recombinant human growth hormone [Hill, Bucuvalas and McClain, 2000], and the
prokinetic agents metoclopramide, domperidone, and cisapride [Stacher et al., 1986; Saleh
and Lebwohl, 1980; Szmukler, Yound and Miller, 1995]. Trials are summarized in Table 3.
In contrast to the preceding list of medications, zinc supplementation has also been studied
[summarized in Table 3. and may have some role in the management of AN [Birmingham,
Goldner and Bakan, 1994; Katz and Keen, 1987]. Although the results of the studies with
zinc showed benefits on some outcome measures and not on others, the risk of side effects
with zinc is low, potentially creating a favorable risk-benefit ratio and warranting
consideration of its use.
Table 3. Miscellaneous Agents in Anorexia Nervosa
Author Intervention Proposed N Study Outcome Comments

Year Mechanism Inpt/Outpt Duration,
Design
Gross et al., Lithium Weight 16 female Four-week, Significant group x All patients
1981 carbonate gain, Inpt Double- time interaction received a
(dosed to Improveme Blind, occurred for weight behavior
achieve nt in Parallel gain. No difference modification
serum affective Group between groups at treatment
concentratio state weeks 1 and 2. At program and
n between weeks 3 (p=0.04) tube feedings as
0.9-1.4 and 4 (p=0.03), needed. Three
mEq/liter) lithium group of eight lithium
versus gained significantly treated patients
Placebo more weight. had minor
Overall, weight gain tremor and
in lithium group dizziness. No
was 6.8 + 0.4 kg electrolyte
(baseline weight abnormalities in
35.7 + 1.1 kg) either group.
versus 5.2 + 0.1 kg Thyroid
(baseline weight assessments did
32.7 + 1.9 kg) in the not differ
placebo group. between groups.
Gross et al., Delta-9- Appetite 11 female 4week 3 patients had Concomitant
1983 tetrahydroca Stimulation Inpt Crossover, dysphoric reactions behavior
nnabinol 30 Improveme Double- (paranoid ideation modification,
mg/day nt in Blind, and feeling of loss occasional tube
versus affective Randomized of control) on THC feedings. After
diazepam 15 state and withdrew (ITT two weeks,
mg/day analysis performed). participants
No difference in crossed over to
weight gain or opposite
caloric intake treatment. No
between treatments. washout period
between
treatments.
Author Interventio Proposed N Study Outcome Comments

Year n Mechanism Inpt/Outpt Duration,
Design
Casper Clonidine Stimulation 4 female 8 week, Significant Patients were
et al., 1987 500-700 of eating. Inpt Randomized, reductions in blood selected due to
mcg/day Clonidine is Placebo- pressure on failure to
versus an alpha-2 Controlled clonidine vs. improve during
Placebo adrenergic Crossover. placebo. No hospitalization.
agonist. Multiple trials significant No washout
per differences in period.
participant. weight change, Concomitant
hunger, or satiety psychotherapy,
during clonidine nutritional
versus placebo program. All
administration. patients
considered
clonidine an
“unpleasant
drug.” Side
effects
included
sedation,
lightheadednes
s, one patient
had severe
bradycardia
with a Wolf-
Parkinson-
White
syndrome.
Katz et al., Elemental Correct zinc 14 females 6 months, Decreased Patients also
1987 zinc 50 depletion double-blind, depression (p<0.05) received
mg/day (patients placebo- and anxiety psychotherapy
versus found to controlled (p<0.05) in the zinc and nutritional
Placebo have low group. Weight gain treatment
zinc intake not statistically
and urinary different between
zinc groups.
excretion)
Stacher Cisapride Acceleratio 12 6 week Acceleration of During the
et al., 1993 10 mg tid n of gastric Outpt (sex double-blind, gastric emptying of open –label
versus emptying not then 6-week a semisolid meal phase, 4/6 of
placebo reported) open label occurred in all 6 the patients
patients on originally
cisapride. Weight treated with
gain in 5/6 cisapride placebo had
patients versus 4/6 gastric
on placebo. emptying
acceleration
when switched
to cisapride

Year Mechanis Inpt/Outpt Duration,
m Design
Birmingham Elemental Weight 35 females Randomized, Rate of increase in Patients
et al., 1994 zinc 14 gain double-blind, BMI in zinc group received
mg/day placebo- was 0.079 standard
versus controlled (+0.07)/day, versus inpatient
Placebo 0.039 (+ 0.06)/day treatment,
in the placebo group including
(p=0.03). Number nutritional,
of days in the study psychological,
did not differ and
between groups. concomitant
medication
therapy
Marrazzi et Naltrexone Narcotic 19 female 6 weeks per Significant Population was
al., 1995 100 mg bid antagonis Outpt treatment differences between both AN and
versus m to block Sample period. groups on binges, BN patients.
placebo the included Crossover, purges, urges to Patients drug-
endogenou both AN Randomized, binge, urges to free except for
s opioids (N=6)and Double-Blind purge, daily food hormone
and BN intake, and binge preparations
interrupt food ratio (p<0.05). and prn use of
the Some patients with antihistamines
addictive AN gained weight and antibiotics.
cycle of while others did not 1 month
dieting achieve weight antidepressant
restoration. washout before
trial. Weekly
psychotherapy.
No washout
between
treatment
periods.
Szmukler Cisapride 10 Promote 29 Inpt (sex 8 week No difference on Patients also
etal., 1980 mg tid before gastric not Randomized, gastric emptying undergoing
meals versus emptying reported) Double-Blind, time between refeeding
Placebo Placebo- groups or on weight program with
Controlled gain. Cisapride psychological
group showed support. No
greater side effects
improvement on that warranted
ratings of hunger participant
versus placebo withdrawal
(p<0.02), although from the trial.
prior to trial
commencement
they were
significantly less
hungry than placebo
patients. Cisapride
treated patients also

Year Mechanism Inpt/Outpt Duration,
Design
rated themselves
better on the global
rating of
improvement in
symptoms
associated with
eating (p<0.03).
Hill et al., Recombinant Promotion of 15 Inpt (14 28-day, rhGH treated All patients
2000 Human nitrogen females, 1 Randomized, patients reached received a
Growth retention, male) Double-Blind medical/CV standard
Hormone increase in stability sooner refeeding
0.05 serum IGF-1 than the placebo protocol.
mg/kg/day levels, patients (median 17
SQ versus enhancement vs. 37 days,
Placebo of fluid p=0.02). Median
retention, length of
improve hospitalization
dehydration, decreased for rhGH
improve CV group vs. placebo
instability (32 days vs. 39
days, NS).
Difference in rate
of weight gain NS
between groups.
Abbreviations: AN=Anorexia Nervosa; BN=Bulimia Nervosa; bid=twice daily; BMI=body mass index;
CV=cardiovascular; Inpt=inpatient; NS=nonsignificant; Oupt=outpatient; SQ=subcutaneous; tid=three times daily
Pathophysiology
The current state of pharmacotherapy for AN leaves much to be desired. The matching of
drugs to symptoms thus far has not produced strong therapeutic effects. SSRIs appear
ineffective for mood and OC symptoms. Traditional antipsychotics appear to add nothing to
treatment. The use of atypical antipsychotic agents is providing some hint of potential utility.
Rather than matching traditional symptoms to drug entities a better approach may be to
explore what is known about the pathophysiology of AN and seek out agents that can modify
the pathology. Dopamine, serotonin and norepinephrine have been associated with novelty
seeking, harm avoidance and reward dependence respectively [Gerra et al., 2000; Hennig et
al., 2000]. In addition, these transmitters have effects on eating. Thus, these neurotransmitters
provide a starting point to explore possible drug targets. In exploring the function of these
systems the binding affinity at receptor sites can be determined as well as binding affinity at
the 5-HT transporter [5-HTT]. Also, regional blood flow can be explored through the use of
functional Magnetic Resonance Imaging [fMRI].. Selected studies exploring these questions
are listed in Table 4.
Table 4. Neurotransmitter and Receptor Studies in Anorexia Nervosa
Parameter Method Subjects Result Effect Reference

5HIAA CSF analysis AN-R Ill Significantly Reduced 5-HT in Kaye et al.2005Kaye
reduced brain et al. 1991
5HIAA CSF analysis AN-R Significantly Increased 5-HT in Kaye et al. 1991
Recovered elevated brain
HVA CSF analysis AN-R Decreased Decreased Kaye et al. 1999
Recovered compared to dopamine in brain
recovered AN-BP
or BN women
5-HT1A PET AN-R Ill 30%–70% Reduced firing of 5- Bailer et al. 2007
increase in binding HT neurons
potential
5-HT1A PET AN-R 30 to 60% increase Correlated with trait Bailer et al. 2005
Recovered anxiety and harm
avoidance
5-HT2A PET AN-ill Normal binding Positive correlation Bailer et al. 2007
potential to harm avoidance
5-HT2A PET AN-R Activity reduced Bailer et al. 2004;
Recovered Frank et al. 2002;
Kaye et al. 2001
5-HT2A SPECT AN-BP Reduced in the Positive correlation Goethals et al. 2007
parietal cortex in between reward
AN-BP in dependence and
comparison parietal 5-HT2A
with AN-R binding
index
5-HTT PET Bulimic ED Reduced binding Kuikka et al. 2001;
Binding Tauscher et al. 2001
5-HTT PET AN-R Increased Increased 5-HTT Bailer et al. 2007
Binding Recovered compared to activity may
REC AN-BP respond to
higher SSRI doses
rCBF fMRI AN-R Significantly Insular neural Wagner et al. 2007
Studies of the Recovered reduced fMRI activity did not
insula signal response correlate with
pleasantness ratings
for sucrose in AN
women but did for
the control women
Dopamine PET AN-R Significantly Binding potential Frank et al. 2005
D2/D3 Recovered higher was positively
[11C]raclopride related to harm
binding potential avoidance.
in the antero-
ventral
striatum than CW.
5HIAA= 5-hydroxyindolacetic acid; 5-HT Transporter=5-HTT; AN-R Ill =Anorexia nervosa-restrictor ill; AN-
BP=Anorexia nervosa-binge/purge; Control Women= CW; HVA=Homovanillic acid; Positron emission
tomography=PET; rCBF=regional cerebral blood flow; Single photon emission
computed tomography=SPECT
Future Directions
As listed above, in acutely ill AN patients, the 5-HT1A receptor has been shown to be
up-regulated. This activity may give rise to anxiety, dysphoria and rigid behavior. The 5-
HT2A activity is normal to down-regulated. Recovered AN patients also have an increase in
activity of the 5-HT transporter. It also appears that the insula activity is reduced which could
give rise to the distorted body image, diminished motivation to change, lack of recognition of
the symptoms of malnutrition, and failure to appropriately respond to hunger. This recent
literature provides interesting findings regarding the pathophysiology of AN. However,
further work will be needed before this data can guide our drug selection.
At this point an immediate need in the pharmacotherapy of AN is to conduct placebo
controlled, randomized, double blind trials utilizing selected atypical antipsychotics.
Repeatedly, drugs that have looked beneficial in case reports or uncontrolled studies have
been proven to have no effect when subjected to the more rigorous study design. The large
number of reports of possible benefit in selected patients is very interesting. However,
atypical antipsychotics have significant side effects that could be detrimental to the therapy of
AN patients. Thus, it is necessary to definitively answer the question of their efficacy.
In light of the data that indicates heightened 5-HT1A receptor activity, a treatment that
affects this system may prove to be beneficial. Also, recent evidence that glutamate
antagonists possess antidepressant effects would indicate another avenue of exploration
[Zarate et al., 2006].
Multiple problems present themselves in this type of research. AN is a very difficult
disorder in which to study treatment interventions, given that many of these patients are not
motivated for treatment, that many of them require a multiplicity of interventions
simultaneously, and that AN is a relatively rare condition compared to many psychiatric
disorders. In addition, randomized, controlled trials investigating new treatments are
methodologically very complex and expensive to conduct. The development of a short-term
method of screening pharmacological agents for possible efficacy in treating core symptoms
associated with AN would aid in identifying potentially efficacious agents. Such paradigms
could be utilized in searching for and evaluating the potential of new drug moieties for
further study. The identified agents could then be tested in full, placebo controlled,
randomized clinical trials; allowing these more complicated and expensive assessments to be
carried out on the most likely agents to show a benefit in the treatment of AN.
Conclusion
In summary, much work has to be done to determine the role, if any, of pharmacotherapy
in AN. It seems reasonable to search for compounds to target the core symptoms of the illness
rather than just agents that cause weight gain as a side effect. With lessening or elimination of
at least some of the core symptoms, individuals with AN may be able to return to healthful
eating and a better quality of life. In the absence of such agents, aggressive nutritional
rehabilitation remains critical, however, difficult in the face of the core symptomatology of
AN.
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Chapter XIX
Pharmacological Therapies for

Bulimia Nervosa
Amanda Joelle Brown1, Lisa A. Kotler2 and B. Timothy Walsh2

1. The New York State Psychiatric Institute
2. Columbia University College of Physicians and Surgeons
Abstract
There are a number of established pharmacologic therapies for the treatment of
bulimia nervosa (BN). In response to clinical observations suggesting a link between BN
and mood disorders, the majority of double-blind, placebo-controlled trials have tested
the safety and efficacy of antidepressant medications for the treatment of BN. Positive
outcomes in early trials using tricyclic antidepressants (TCAs) and monoamine oxidase
inhibitors (MAOIs) suggested that antidepressants were indeed effective treatments for
BN, although they were often associated with various side effects. Newer antidepressant
agents, particularly selective serotonin reuptake inhibitors (SSRIs) such as fluoxetine,
proved to be as effective as earlier classes of medications while causing fewer side
effects, and this combination of safety and efficacy prompted the FDA’s approval of
fluoxetine for the treatment of BN in 1994. This chapter summarizes the evidence-based
literature on medication trials in BN and concludes with a case example illustrating the
application of evidence-based pharmacological treatments for BN.
Introduction
Since bulimia nervosa (BN) was first described in print (Russell, 1979), more than 20
clinical trials have been conducted to assess the safety and efficacy of various
pharmacological agents for reducing the behavioral and psychological symptoms of BN (see
Shapiro et al., 2007; Zhu and Walsh, 2002 for reviews). Early trials were brief (i.e. six to
352 Amanda Joelle Brown, Lisa A. Kotler and B. Timothy Walsh
eight weeks) and mainly focused on testing the efficacy of antidepressant agents such as
tricyclic antidepressants (TCAs), monoamine oxidase inhibitors (MAOIs), and atypical
antidepressants, as it was commonly noted that many patients with BN presented for
treatment with co-morbid depressive symptoms that had historically responded well to
treatment with these medications. The majority of these early studies showed that almost all
of the then-available classes of antidepressant medication were significantly more effective
than placebo in reducing the symptoms of BN, including the frequency of binge eating and
purging. As new classes of antidepressants have become available, particularly selective
serotonin reuptake inhibitors (SSRIs), research groups have conducted double-blind, placebo-
controlled trials in BN using these agents. More recent clinical trials have focused on novel
pharmacological interventions such as the anticonvulsant topiramate and serotonin receptor
agonist ondansetron, and many of these trials have produced promising data, opening up new
avenues for future research.
Many clinical trials of pharmacological therapies in BN have focused exclusively on the
effectiveness of a single medication, while others have compared more than one
pharmacological agent, and still others have looked at the effectiveness of medication in
conjunction with psychological treatments such as self-help, cognitive-behavioral therapy
(CBT), and interpersonal therapy (IPT). Overall, clinical trials of pharmacological
interventions for BN have had varying degrees of success in treating the symptoms of the
disorder, and many of the pharmacological interventions have both costs and benefits that
must be considered before making a recommendation for any individual patient. This chapter
summarizes the available evidence-based literature on randomized, double-blind, placebo-
controlled trials of pharmacological therapies for children, adolescents, and adults with BN. It
will then apply the relevant data to a clinical case example provided at the end of the chapter.
Early Clinical Trials of Pharmacological Therapies

for BN
In response to a growing awareness of the frequent co-morbidity of BN and affective
disorders, particularly major depression (Pope and Hudson, 1982; Stewart et al., 1984), the
first placebo-controlled medication trials in patients with BN examined the efficacy of both
short-term and longer-term treatment with antidepressant medications. The most commonly
studied classes of antidepressants were the TCAs and MAOIs, but other atypical
antidepressants also received some attention in early clinical trials.
TCAs
Six clinical trials have investigated the safety and efficacy of TCAs for the treatment of
BN. Pope and colleagues (1983) found that six weeks of treatment with imipramine (200
mg/day) was associated with a mean 70% decrease in binge frequency and 50% reduction in
Hamilton Depression Scale (HAM-D) scores, while placebo treatment had no effect on eating
or mood symptoms. Agras et al. (1987) reported comparable decreases in the behavioral and
Pharmacological Therapies for Bulimia Nervosa 353
psychological symptoms of BN following a 16-week course of treatment with imipramine

(average dose: 167 mg/day), suggesting that this medication may be efficacious for the
treatment of BN over various lengths of time. Hughes et al. (1986) reported that desipramine
(200 mg/day) was not only superior to placebo in reducing binge frequency, but also effective
in completely eliminating behavioral symptoms in nearly 50% of participants by the end of
the six-week trial. Walsh et al. (1991) replicated Hughes’ findings in an eight-week,
randomized, double-blind trial of desipramine (200-300 mg/day) versus placebo, and then
openly treated those who had achieved at least a 50% reduction in binge frequency with
desipramine for 16 more weeks. Participants who sustained their initial improvement during
the open trial then entered a 24-week double-blind “discontinuation trial.” While desipramine
was superior to placebo in the short-term treatment of BN, longer-term treatment was neither
well-tolerated nor effective; in fact, only five of the original 78 participants completed all 48
weeks of the study, as many discontinued treatment due to lack of efficacy or on account of
side effects associated with desipramine use such as sedation, dizziness, and tremulousness.
Two trials investigated the efficacy of TCAs in combination with a behavioral
intervention for the treatment of adults with BN. Mitchell and Groat (1984) studied the
effects of amitriptyline (150 mg/day) in the context of a treatment program that incorporated
elements of CBT and found that both active drug and placebo groups improved significantly
from baseline but did not differ from each other on any behavioral measures. This negative
finding may be due to a “ceiling effect” resulting from the overall benefit of the behavioral
intervention. In another study investigating the efficacy of a combined treatment approach,
Agras and colleagues (1992, 1994) randomly assigned women with BN to receive either 16
weeks of desipramine alone (average dosage: 168 mg/day), 16 weeks of desipramine
combined with CBT, CBT alone for 16 weeks, desipramine alone for 24 weeks, or 24 weeks
of desipramine combined with CBT. The 24-week combined treatment proved superior to 16
weeks of medication alone in terms of reducing binge eating and vomiting frequency, both at
the end of the trial and at a one-year follow-up assessment point. The results of these studies
indicate that combining TCAs with behavioral interventions may be an effective method for
treating adults with BN.
MAOIs
As trials of TCAs were underway, another class of antidepressants, MAOIs, also began
to receive attention from clinicians and researchers working in the field of eating disorders.
MAOIs were thought to be potentially effective in patients with BN because these patients
frequently presented for treatment with atypical depressive symptoms such as mood reactivity
and anxiety, symptoms that generally responded well to MAOIs in patients with mood and
anxiety disorders. Walsh and colleagues (1988) found that eight weeks of treatment with
phenelzine (60-90 mg/day) reduced binge frequency and scores on several measures of
psychological functioning to a significantly greater degree than did placebo treatment.
Kennedy et al. (1988) found that iscarboxazid (60 mg/day) was associated with greater
improvement in the frequency of vomiting, but not binge eating, episodes compared with
placebo. After the isocarboxazid trial, Kennedy’s group (Kennedy et al., 1993) found similar
results in a trial of brofaromine (average dose 175 mg/day). Brofaromine-treated patients

reported significantly fewer vomiting, but not binge eating episodes compared with the
placebo group at the end of the trial. More recently, Carruba and colleagues (2001) found no
difference in outcome between adult female outpatients treated with moclobemide (600
mg/day), a selective and reversible MAOI, and those treated with placebo over the course of
a six-week trial. Overall, the results of clinical trials using MAOIs indicated that this class of
medications may be helpful for treating symptoms of BN, but a number of side effects
including orthostatic hypotension, sleep disturbance, dizziness, constipation, and sedation
have been associated with members of this class of medications, and the emergence of newer
agents limit the use of MAOIs in this population.
Other Early Clinical Trials

While TCAs and MAOIs received the most attention in early clinical trials of treatments
for BN, other medications known to affect the psychological and behavioral symptoms of BN
were also being tested. The atypical antidepressant mianserin (Sabine et al., 1983) and mood
stabilizer lithium (Hsu et al., 1987) were not found to be more effective than placebo in
reducing binge eating and vomiting frequency in adults with BN. Pope et al. (1989) found
that the antidepressant trazodone (400 mg/day) was superior to placebo in reducing binge
eating and vomiting frequencies over the course of their six-week trial. Horne and colleagues
(1988) found that eight weeks of treatment with bupropion (300-450 mg/day) resulted in
significantly greater improvement in patients with BN compared with placebo treatment.
Unfortunately, four patients assigned to treatment with bupropion reported grand mal seizures
during the trial, and this 5.8% prevalence of seizures could not be accounted for by
commonalities in the medical history, laboratory findings, concurrent medication use, or
other clinical characteristics of the four affected patients. The study was prematurely
terminated, and the investigators concluded that bupropion should not be prescribed as a first-
line treatment for BN. Based on the above findings, bupropion is now contraindicated by the
FDA for the treatment of patients with a prior or current diagnosis of BN. The extended
release version of the medication also carries this contraindication, although studies assessing
the safety and efficacy of this newer agent have not been conducted.
Based on an earlier open trial (Jonas and Gold, 1988) in which naltrexone (200-300
mg/day) was found to be associated with significant reductions in binge eating and purging,
Mitchell et al. (1989) conducted a randomized double-blind trial of naltrexone (50 mg/day)
versus placebo and found that this low dose of the opioid antagonist was not superior to
placebo in reducing bingeing and purging frequency or HAM-D scores. Likewise, Alger et al.
(1991) found that treatment with naltrexone (100 mg/day) did not reduce binge frequency
significantly more than did treatment with placebo. However, the lower doses of naltrexone
used in these studies may not have been sufficient to cause a significant decrease in BN
symptom severity, and future research with naltrexone may benefit from an investigation of
the safety and efficacy of higher doses. In light of research demonstrating the efficacy of
naltrexone in the treatment of alcohol dependence (see Assanangkornchai and Srisurapanont,
2007 for review), future clinical trials in BN may be warranted both to investigate the benefit
conferred by naltrexone and to better understand links between the neurobiological

underpinnings of eating and substance use disorder.
Summary
The early years of clinical research assessing the safety and efficacy of various
pharmacological therapies were rich with evidence to suggest that many patients respond
well to treatment with medications such as TCAs, MAOIs, and atypical antidepressants.
However, the introduction of newer agents, particularly SSRIs, has relegated these older
agents to second or third-line treatment status.
More Recent Clinical Trials: The Advent of SSRIs

and Beyond
SSRIs
In 1987, the antidepressant medication fluoxetine was approved by the FDA for the
treatment of mood disorders. Fluoxetine specifically targets the intercellular transmission of
serotonin, a neurotransmitter implicated in the etiology of mood disorders and in the control
of eating behavior. As the efficacy of antidepressant medications for the treatment of BN had
been supported by much of the early clinical trials, fluoxetine soon received the attention of
clinicians and researchers in the field of eating disorders because of its improved safety and
tolerability compared to TCAs and MAOIs. After open-label trials produced encouraging
results (Freeman and Hampson, 1987; Mitchell et al., 1989), double-blind, placebo-controlled
clinical trials of fluoxetine for the treatment of BN were initiated. Two large multisite trials
have investigated the efficacy of fluoxetine in reducing the symptoms of BN in nearly 400
outpatients, and the significant benefit conferred by fluoxetine treatment in these trials led the
FDA to approve a specific indication for BN in 1994. To date, fluoxetine is the only
medication approved by the FDA for the treatment of BN, although newer SSRIs such as
fluvoxamine and sertraline have also received research support in small controlled trials.
Many studies have focused exclusively on medication management with fluoxetine while
others have investigated the synergistic and comparative effects of fluoxetine and behavioral
interventions such as CBT or supportive psychotherapy. The promising results from these
trials have led to the widespread use of fluoxetine in the treatment of BN.
Fluoxetine without Behavioral Intervention

Freeman and colleagues (1988) reported significant improvements in binge eating and
vomiting frequency, Eating Disorder Inventory (EDI), and Eating Attitudes Test (EAT)
scores among those subjects assigned to fluoxetine (60-80 mg/day) but not those assigned to
placebo in their six-week double-blind trial. They also noted that six of the 20 fluoxetine-
treated patients achieved abstinence from binge eating and vomiting by the end of the trial,
whereas no patients assigned to placebo experienced complete symptom remission. Shortly
thereafter, the Fluoxetine BN Collaborative Study Group (1992) conducted a randomized,
eight-week, double-blind, multisite trial comparing the efficacy of fluoxetine (20 mg/day or
60 mg/day) versus placebo in 382 female outpatients. The results of this Eli Lilly-sponsored
trial indicated that fluoxetine (both 20 mg/day and 60 mg/day) was associated with greater
reductions in binge eating, vomiting, weight, body dissatisfaction, and food/diet
preoccupation compared with placebo. Furthermore, a fluoxetine dose of 60 mg/day was
superior to 20 mg/day in reducing binge eating and vomiting frequency. Side effects were
relatively rare and the dropout rate due to adverse events was not significantly different
between the fluoxetine and placebo groups (8.5% and 6.2%, respectively).
As a follow-up to these encouraging findings, Goldstein et al. (1995) conducted a second
large Lilly-sponsored multisite trial aiming to assess the safety and effectiveness of treatment
with fluoxetine (60 mg/day) over a 16-week period in 398 male and female late adolescent
and adult outpatients. On the primary efficacy measure, change in the number of vomiting
episodes per week over the course of the treatment period, fluoxetine-treated patients
experienced significantly greater improvement than the placebo-treated group. Fluoxetine
was also associated with greater improvement on the EDI, Clinical Global Impression (CGI)
scale, and Patient’s Global Impression (PGI) scale over the course of the trial. The rate of
discontinuation due to an adverse event did not significantly differ between the two treatment
groups. The results of this trial supported the longer-term use of fluoxetine in the treatment of
BN.
In an even longer-term trial, sponsored by Lilly after fluoxetine had received FDA
approval for BN, Romano and colleagues (2002), randomized 150 adult patients with BN to
receive fluoxetine (60 mg/day) or placebo in a double-blind fashion for up to 52 weeks
following response to an eight-week single-blind trial of fluoxetine (response was defined as
reporting at least a 50% decrease from baseline in vomiting frequency for at least one of the
final two weeks of the single-blind phase). Although the dropout rate was substantial in both
groups in the double-blind treatment phase (83% for the fluoxetine group and 92% for the
placebo group), fluoxetine treatment significantly prolonged the time to relapse and was
correlated with a significantly lower rate of relapse (33% versus 51%) compared to treatment
with placebo. Fluoxetine was also associated with smaller mean increases in vomiting, binge
eating, and symptom severity as assessed by the CGI Improvement and Severity scales during
the relapse prevention phase. Side effects and adverse events were similar in the two
treatment groups, with rhinitis being the only side effect that was reported with significantly
higher frequency in the fluoxetine group. The results of this trial offer support for the use of
fluoxetine for relapse prevention following acute pharmacological treatment for BN, although
the significant benefit conferred by fluoxetine must be interpreted in the context of an
extremely high rate of dropout from both arms of the study. In summary, the evidence from
the four studies described above demonstrates the efficacy of fluoxetine as a treatment for
adults with BN, both in the short term and over longer periods of time.
Fluoxetine in Younger Populations

While nearly all clinical trials of fluoxetine have enrolled adult patients with BN, recent
evidence from a small, eight-week open trial of fluoxetine (60 mg/day) for the treatment of
BN in adolescent females (Kotler et al., 2003) suggests that fluoxetine may also be
efficacious in younger populations. All ten subjects showed improvement on the CGI
Improvement scale at the end of the trial. Overall, patients experienced significant decreases
in the average number of weekly binge eating and purging episodes over the course of the
treatment. Scores on the EAT, EDI, and Self-Report for Childhood Anxiety Related
Disorders (SCARED) scales also declined significantly from baseline to week eight of the
trial. Furthermore, no patient discontinued fluoxetine because of side effects from the
medication. These results indicate that fluoxetine may be useful for treating the symptoms of
BN in adolescent populations, although future placebo-controlled trials must be conducted
before the safety and efficacy of fluoxetine for a younger population can be considered
clearly established.
Additionally, in response to recent concerns about a potential link between increased risk
of suicidal thoughts and behaviors and antidepressant medication treatment in adolescents
and young adults, the FDA has recommended that antidepressant medications such as
fluoxetine carry a black box warning against their use in patients under the age of 25.
Certainly, adolescents and young adults undergoing treatment with an antidepressant for BN
should be carefully monitored for clinical worsening. Families should also be advised to
closely observe younger patients and to communicate frequently and openly with their child
or adolescent’s treatment provider to ensure the continued monitoring of these at-risk
patients.
Fluoxetine Following Inadequate Response to

Psychotherapy
Walsh and colleagues (2000) conducted an eight-week double-blind trial of fluoxetine
(60 mg/day) versus placebo for patients who had not responded during or had relapsed
following a 20-week course of either CBT or IPT (patients were randomly assigned to either
treatment condition). Lack of response and relapse were defined as binge eating and vomiting
at least once weekly over a one-month period. This research team found that treatment with
fluoxetine was associated with decreased frequency of binge eating and purging episodes
compared with placebo treatment; in fact, patients on placebo tended to increase the
frequency of these behaviors. Furthermore, five of the 13 fluoxetine-treated participants
reported abstinence from binge eating and purging during the last 28 days of the study, while
no participants receiving placebo reported complete symptom remission at the end of the
trial. The results of this study suggest that pharmacotherapy with fluoxetine may benefit
patients with BN who do not respond to a course of a psychological treatment such as CBT
and IPT.
In another study of fluoxetine treatment after failure to respond to a psychotherapeutic
intervention, Mitchell et al. (2002) randomized 62 adult patients with BN who remained
symptomatic after completing 20 sessions of CBT (defined more strictly than in Walsh et
al.’s study as exhibiting any remaining purging behavior) to receive either 20 sessions of IPT
or medication management beginning with fluoxetine (60 mg/day) and switching to
desipramine (maximum 300 mg/day) if abstinence from bingeing and purging was not
achieved within eight weeks of treatment with fluoxetine. Symptoms were reassessed at the
end of the trial (week 33) and again at a week 60 follow-up point. Only 37 of the 62
randomized patients completed the full course of treatment, and no differences were found
between the IPT and medication-only groups on measures of eating behavior, rates of
abstinence from bingeing and purging, or any psychological measures. Data from the week
60 follow-up assessment indicated that those patients who were abstinent at the end of the
trial remained so at week 60, and none of the 26 subjects who failed to achieve abstinence in
the trial became abstinent in the post-treatment period. The lack of a placebo control group
and the high dropout rate makes the value of a sequential treatment approach in BN difficult
to interpret from this study.
Fluoxetine in the Context of Inpatient Treatment

In one of the earliest double-blind, placebo-controlled trials of fluoxetine, Fichter et al.
(1991) randomized 40 patients with BN who were participating in an intensive inpatient
program to five weeks of treatment with fluoxetine (60 mg/day) or matched placebo. Both
groups significantly improved on the Symptom Checklist-90-Revised (SCL-90R), EDI,
HAM-D, and CGI over the course of the study, but there were no significant differences on
any outcome measure in those treated with fluoxetine compared to those treated with placebo.
However, the clear therapeutic benefit of the intensive inpatient program may have
overshadowed any additional effects of the medication, and therefore no firm conclusions can
be reached about the relative efficacy of fluoxetine and placebo during inpatient treatment for
BN based on this study.
Fluoxetine with Nutritional Counseling

Beaumont and colleagues (1997) enrolled 67 adult outpatients with BN in an eight-week,
double-blind trial of fluoxetine (60 mg/day) versus placebo accompanied by individual
nutritional counseling with a dietitian. As in Fichter et al. (1991), Beaumont et al. (1997)
reported that both groups showed similar decreases in the frequency of binge eating and
vomiting episodes over the course of the trial. Furthermore, while the fluoxetine-treated
patients showed greater improvement on some subscales of the Eating Disorder Examination
(EDE) during the active phase of the treatment compared with those taking placebo, the
group assigned to active medication experienced a higher rate of relapse during the three-
month follow-up period. Again, these results must be interpreted cautiously, as no waitlist
control group was used, and the lack of significant difference between the groups may be
indicative of a “ceiling effect” whereby the benefits of nutritional counseling limit the
measurement of further clinical improvement with either fluoxetine or placebo.
Fluoxetine with CBT

In response to clinical trials supporting the efficacy of CBT for the treatment of BN (see
Wilson, 2005 for review), Goldbloom et al. (1997) compared the efficacy of fluoxetine (60
mg/day) alone, CBT alone, and combined treatment over the course of 16 weeks. Seventy-six
adult women with BN were enrolled into the study, but only 43 (57%) completed the
minimum number of weeks of treatment to be considered “treatment completers” (14 weeks).
This high dropout rate was mainly due to side effects from fluoxetine and noncompliance
with session attendance. A completer analysis found that treatment with fluoxetine alone was
significantly inferior to both CBT alone and combined treatment in decreasing frequency of
binge eating and vomiting. There was no difference between CBT alone and combined
treatment on these measures, and no differences were found between any of the three
conditions in terms of EDE and BDI scores. Again, limitations with the study’s design
including a high dropout rate, lack of placebo and waitlist control groups, and variable
amounts of time participants in each group spent with a treatment provider (fluoxetine alone:
10 sessions each lasting approximately 10 minutes, CBT alone: 16 weekly sessions each
lasting one hour, combined: 10 10-minute medication sessions plus 16 one-hour CBT
sessions) limit the interpretation of these results. The authors’ main conclusion from the
results of this trial was that fluoxetine alone appears to be less effective than a treatment
combining fluoxetine and CBT for reducing the behavioral symptoms of BN.
In another study looking at the relative efficacy of medication, psychotherapy, and
combined treatment, Walsh and colleagues (1997) randomly assigned patients with BN to
one of five treatment groups: CBT plus medication, CBT plus placebo, supportive
psychotherapy (SP) plus medication, SP plus placebo, or medication alone. Patients first
received desipramine (200 mg/day) or matched placebo, and after eight weeks had passed,
non-responders (those whose binge frequency remained above 25% of their baseline
frequency) and those experiencing intolerable side effects on desipramine were tapered off
and started on fluoxetine (60 mg/day) or matched placebo for the remainder of the trial.
Overall, patients receiving the combined treatment showed more significant reductions in
binge eating frequency, EAT scores, BDI scores, and SCL-90 depression scores compared
with those who received placebo with psychological treatment. CBT proved to be superior to
SP in reducing behavioral symptoms of BN, and no significant differences were found
between the outcomes of patients who received SP plus medication and those who received
medication alone. Taken in sum, the results of Walsh et al.’s (1997) study suggest that CBT
is more effective than SP in adults with BN, whether used in combination with active drug
treatment or with placebo; antidepressant medication is superior to placebo in reducing binge
eating and purging frequency and improving mood; and the combination of antidepressant
medication and psychological treatment is modestly more effective than either CBT or SP
combined with placebo. Since this study did not include a psychotherapy-only group, no
conclusions can be drawn about the relative efficacy of psychological treatment without
medication management and a treatment combining psychotherapy and medication.
Fluoxetine with Self-Help

Increased demand for more affordable treatment options for patients with eating
disorders and concerns about the accessibility of specialized eating disorder treatments have
led researchers to examine the effectiveness of self-help manuals for treating patients with
BN. In 2001, Mitchell and colleagues conducted a trial comparing the effects of fluoxetine
(60 mg/day) alone, placebo alone, combined fluoxetine and self-help, and combined placebo
and self-help in 91 adult outpatients with BN. At the end of the 16-week trial, those patients
who had received fluoxetine reported reduced vomiting frequency compared with placebo.
Access to the self-help manual magnified this differential reduction in vomiting frequency.
CGI and PGI scores differed significantly from baseline for the groups receiving fluoxetine
but not placebo, with no evidence of additional benefit from the self-help manual. There were
no significant differences in outcome on any secondary measures, and remission rates did not
differ between the three treatment cells. These results suggest that self-help manuals only
modestly augment the benefits of fluoxetine in the treatment of adults with BN.
In another self-help trial, Walsh et al. (2004) randomized participants to either fluoxetine
(60 mg/day) alone, placebo alone, guided self-help and fluoxetine, or guided self-help and
placebo. Treatment took place in a primary care setting. All patients met with an internist
once a month for medication management, and those who received the self-help manual also
met with a nurse six to eight times throughout the duration of the study. 91 women entered
the study, but nearly 70% dropped out of the trial before the scheduled point of termination.
Compared with placebo treatment alone, treatment with fluoxetine alone was associated with
decreased frequency of binge eating and vomiting, depressed mood as indicated by the BDI,
and lower general symptom index as assessed by the SCL-53. The self-help manual had no
independent effect on treatment outcome, and there were no significant interactions between
the medication and self-help conditions. At the end of the trial, only eight of the 91
randomized patients had achieved abstinence from binge eating and purging. Although
limited by the low rate of treatment completion, which decreased the statistical power to
detect differences between combined treatment and medication-only conditions, the available
data suggest that a guided self-help manual does not significantly enhance treatment of BN
with fluoxetine in a primary care setting.
Other SSRIs
Although fluoxetine is currently the only medication approved by the FDA with an
indication for the treatment of BN, other SSRIs have been studied and found useful for
reducing symptoms of BN and for preventing relapse following inpatient hospitalization.
Milano et al. (2004) conducted a 12-week trial of sertraline (100 mg/day) and found that it
reduced binge eating and purging frequency to a significantly greater degree than did placebo
treatment. Furthermore, patients reported no serious side effects from the medication. Fichter
et al. (1996, 1997) conducted a placebo-controlled trial of fluvoxamine (average dose 182
mg/day) for relapse prevention following intensive inpatient treatment and found that the
fluvoxamine group showed significantly less deterioration on behavioral measures compared
with the placebo group during the 12 weeks following hospitalization. However, more recent
evidence from a double-blind trial (Schmidt et al., 2004) suggests that fluvoxamine (50-300
mg/day), combined with a “stepped care” psychotherapy intervention, may not be more
effective than placebo in the short-term or long-term treatment of BN. Fluvoxamine treatment
was also associated with severe side effects such as seizures and impaired liver function in
this study.
New Research and Future Directions

With the support of the data described above and an FDA approval for the treatment of
indication of BN, fluoxetine (60 mg/day) is currently considered the “gold standard” of
pharmacological therapies for the disorder, especially when combined with a psychotherapy
like CBT. However, while fluoxetine is typically the pharmacological treatment of choice for
BN, other medications may be equally or more safe or effective for any given patient, and
further research is required to investigate the efficacy of new pharmacological agents. Recent
clinical trials have highlighted the potential efficacy of topiramate (100-250 mg/day), an
anticonvulsant and mood stabilizer, in the treatment of BN. In two 10-week, randomized,
double-blind, placebo-controled trials (Hoopes et al., 2003, Hedges et al., 2003, Nickel et al.,
2005), topiramate was associated with significant reductions in binge eating and vomiting
frequency, and no patients in either study reported serious side effects resulting from
topiramate treatment. These encouraging results point to topiramate as a pharmacological
therapy for BN that warrants further investigation in larger randomized clinical trials.
Other medications that may hold promise for the future are ondansetron, a 5-HT3
antagonist typically prescribed to alleviate nausea associated with chemotherapy (Faris et al.,
2002); flutamide, an androgen receptor antagonist (Sundblad et al., 2005); and baclofen, a
GABA-B agonist used to treat alcohol and drug dependence (Broft et al., 2007). Each of
these pharmacological agents has shown at least some evidence of utility in reducing
symptoms of BN in double-blind or open trials. Faris et al. (2002) found that patients who
took four milligrams of ondansetron when feeling an urge to binge eat or vomit significantly
reduced the frequency of binge eating and purging and increased consumption of normal
meals compared with those assigned to placebo treatment. Sundblad et al. (2005) conducted a
randomized 12-week trial comparing treatment with flutamide (500 mg/day) to treatment
with citalopram, an SSRI (40 mg/day) and found that patients treated with flutamide reported
significantly greater global improvement than those taking citalopram. Most recently, Broft
and colleagues (2007) reported that, in an open trial, baclofen (60 mg/day) was associated
with a greater than 50% decrease in binge eating frequency in two of three patients with BN,
and one of these achieved complete symptom remission by the end of the trial. These results
suggest that GABA-B receptors may be implicated in controlling aspects of binge eating, and
the utility of future clinical trials of baclofen for the treatment of BN lies not only in
examining its efficacy in reducing symptoms, but also in learning more about the underlying
neurobiology of the disorder.
One innovative trial has investigated the effectiveness of a non-medication biological
intervention; evidence suggesting that patients with BN may have neurochemical
disturbances similar to those of patients with seasonal affective disorder led Braun et al.
(1999) to conduct a randomized, double-blind, controlled trial of bright light therapy for the
treatment of BN. Patients who received the active treatment (10,000 lux bright white light)
showed significantly greater improvement in binge frequency during the treatment phase
compared with those participants who were given the “placebo” treatment (50 lux dim red
light). However, there were no significant differences between the groups during the two-
week post-treatment phase, nor were changes in BDI, HAM-D, or HAM-SAD significantly
different between the groups at any time point. No subjects withdrew from the study due to
side effects. A strong placebo response was observed in this study, which is possibly
explained by the fact that every patient guessed at the end of the trial that she had been
randomized to receive the active treatment. The findings from this small and short-term study
suggest that bright light therapy may be a treatment option for BN, but further study is
needed.
The majority of studies that have investigated sequencing pharmacological and
psychological interventions have studied the efficacy of medication after insufficient
response to psychotherapy (Walsh et al., 2000; Mitchell et al., 2002). Two psychotherapy
treatment studies have produced data on outcome predictors in BN, and both have found that
early behavioral change in psychotherapy predicts overall outcome (Fairburn et al., 2004;
Agras et al., 2000). More specifically, a greater than 70% reduction in purging frequency by
the sixth session of CBT is the best predictor of treatment response. Thus, an interesting area
of future clinical research might be to examine the benefit of adding a medication at the sixth
psychotherapy session if purging frequency has not yet been reduced by 70% or more. In a
similar vein, Walsh and colleagues (2006) recently reported evidence that patients with BN
who ultimately fail to respond to treatment with an antidepressant medication can be reliably
identified by their response during the first two weeks of treatment with that medication.
Future research aimed at determining the most appropriate length of time to allow before
trying a different medication or recommending a supplemental psychotherapy intervention
would be of significant clinical relevance.
Conclusion
BN is a psychiatric disorder that is often characterized by distressing physical and
psychological sequelae and affects approximately 1% of women and 0.1% of men (Hoek and
van Hoeken, 2003). On average, patients seeking treatment for BN have been ill for 5-9 years
(Reas et al., 2001), and as many as 50% may relapse within the first six months after attaining
full symptom remission in treatment (Fairburn et al., 1993; Halmi et al., 2002). Fortunately,
there are data demonstrating that several pharmacological treatments benefit adults with BN.
There is solid evidence indicating that the FDA-approved antidepressant fluoxetine,
especially when combined with CBT, aids in the reduction of the behavioral and
psychological symptoms of BN. In the case of inadequate response to fluoxetine, a variety of
second- and third-line treatment options are available that have received at least some support
from clinical studies. Additional controlled trials are needed to refine existing treatment
methods to assist an even greater number of patients with BN to achieve complete symptom
remission and to protect against relapse.
Clinical Case Example

Melissa is a 26 year-old graduate student with a three-year history of BN who lives alone
in an apartment in a large U.S. city. She started dieting three and a half years ago after
gaining five pounds while on vacation in the Caribbean. She began cutting out carbohydrates
from her meals and was soon skipping breakfast and sometimes lunch. She found it
increasingly difficult to sustain this level of restriction and began to have binge eating
episodes once or twice a week. She felt excessively guilty after these episodes and began to
self-induce vomiting in hopes of counteracting the effects of these binges. The frequency of
these binge eating and vomiting episodes has increased steadily over the past three years, and
she is currently experiencing daily episodes. She severely restricts her food intake during the
day in an attempt to control her body weight and shape, but then typically loses control over
her eating during dinner, the one meal she allows herself each day. She is often preoccupied
with thoughts about food, and is therefore having a difficult time concentrating in class and
completing her assignments on time. She feels sad and down on herself, has little energy, and
is experiencing insomnia despite feeling a constant profound tiredness. Formerly a stellar
student and devoted friend, Melissa is finding that her academic performance and
interpersonal relationships are slowly deteriorating as a result of her impaired concentration,
dwindling motivation, and increased social isolation.
After years of avoiding treatment out of feelings of shame and guilt, Melissa finally
contacts Dr. X hoping that the psychiatrist will be able to help her break the cycle that is
“controlling her life.” She is relieved to find Dr. X reassuring and knowledgeable about
treatment approaches for BN. Dr. X initiates CBT, as she knows that this type of
psychotherapy has received significant research support as a treatment for BN. After six
treatment sessions, the frequency of Melissa’s binge eating and purging episodes has dropped
to four times per week, but she continues to eat restrictively and erratically, and remains
preoccupied with thoughts of food, eating, body shape, and weight.
Encouraged by the reduction in Melissa’s disordered eating behaviors but concerned
about the persistence of her symptoms, Dr. X decides that Melissa, not having been
prescribed pharmacological agents in the past, may be a good candidate for treatment with
fluoxetine. She chooses this SSRI based on its success in randomized clinical trials and the
relatively low rate of side effects associated with its use compared with older agents such as
MAOIs and TCAs. Dr. X recommends that Melissa begin with a dose of 20 mg/day and
titrates the dose up to 60 mg over the course of a week, as she knows that patients with BN
are more likely to respond to this higher dose. She chooses to continue seeing her for weekly
CBT sessions, as a number of studies she reads suggest that a combination of psychotherapy
and medication is superior to medication treatment alone for BN. After three weeks on 60
mg/day of fluoxetine, the frequency of Melissa’s binge eating and purging episodes has
decreased to two to three times per week, but she reports experiencing increased anxiety and
difficulty sleeping, so Dr. X lowers the dose to 20 mg/day. At this dose, Melissa’s binge
eating and purging behaviors increase in frequency and her side effects do not abate. She and
Dr. X together decide to discontinue the fluoxetine treatment.
Dr. X is encouraged by the improvement in Melissa’s eating disorder symptoms while on
fluoxetine and suggests that she try a different SSRI. She prescribes sertraline and titrates up
to a dose of 100 mg/day. Unfortunately, Melissa’s anxiety and insomnia persist on sertraline,
although she also does note a slight decrease in her urges to binge and purge. Melissa decides
that her side effects are too uncomfortable and requests a change in medication. Dr. X and
Melissa decide to try topiramate, a mood stabilizer that she knows has received recent
research support for treating BN, and slowly titrates the dose to 250 mg/day. Melissa adjusts
well to this medication without experiencing significant side effects. Her positive response to
topiramate allows her to better utilize the tools of CBT, and through continued therapy and
medication treatment, the frequency of her bingeing and purging episodes continues to
decrease. By the end of her second month of combined psychological and pharmacological
therapy with Dr. X, Melissa achieves full symptom remission and reports improvements in
her mood, physical health, concentration, and overall quality of life. She remains concerned
that she may fall back into her old habits of binge eating and purging, but she feels confident
that she has gained essential tools to control these symptoms.
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Index
adolescence, ix, 10, 22, 45, 46, 123, 138, 139, 141,
5
144, 148, 153, 258, 264, 268, 291, 292
adolescent boys, 169
5-hydroxytryptophan, 44
adolescent female, 14, 15, 18, 138, 154, 168, 185,
308, 357
A adolescent patients, 91, 92, 93, 98, 112, 122, 127,
131, 334
abdomen, 95 adolescents,, x, xiii, 3, 8, 9, 16, 40, 43, 49, 88, 90,
abdominal, 94, 130, 132, 140, 141, 150, 173 96, 102, 108, 110, 111, 116, 119, 120, 121, 122,
aberrant, 9 123, 131, 133, 134, 135, 137, 138, 139, 140, 141,
abnormalities, 3, 34, 63, 89, 94, 97, 119, 122, 125, 142, 143, 144, 145, 146, 147, 148, 149, 150, 152,
140, 143, 215, 283, 310, 340 153, 154, 157, 168, 169, 175, 183, 202, 204, 234,
absorption, 214, 220, 223, 234, 235, 236 247, 251, 253, 258, 291, 293, 294, 295, 297, 298,
abstinence, 37, 209, 210, 226, 237, 238, 241, 242, 305, 306, 334, 348, 349, 352, 357, 366
246, 247, 248, 249, 294, 356, 357, 358, 360, 365 adult, 4, 9, 11, 30, 36, 42, 46, 47, 50, 63, 87, 89, 90,
academic, xiii, 75, 76, 115, 190, 191, 363 95, 96, 97, 104, 107, 115, 120, 121, 137, 138,
academic performance, 363 139, 141, 142, 144, 145, 147, 148, 149, 154, 169,
academic success, 191 175, 176, 180, 181, 188, 209, 250, 258, 278, 297,
access, 62, 80, 90, 95, 104, 142, 177, 181, 243, 286, 354, 356, 357, 358, 359, 360
287 adult population, 144
accessibility, 360 adulthood, ix, 22, 42, 46, 52, 88, 139, 141, 153, 258,
accidents, 236 264, 291, 294
acculturation, 29, 43 adults, x, xiii, 56, 57, 67, 69, 88, 89, 90, 102, 104,
accuracy, 120, 281 107, 110, 119, 120, 121, 131, 134, 138, 140, 141,
acetylcholine, 333 142, 143, 144, 148, 149, 176, 183, 188, 209, 231,
achievement, 38, 145, 180, 249 232, 247, 251, 254, 255, 275, 292, 293, 352, 353,
Achilles heel, 268 354, 356, 357, 359, 360, 362
acid, 21, 344, 348 adverse event, 248, 356
activity level, 92 advertisements, 244
acute, 4, 46, 48, 49, 50, 62, 103, 106, 109, 110, 113, affective dimension, 198
125, 126, 127, 131, 143, 147, 188, 193, 194, 202, affective disorder, 352
300, 326, 334, 339, 347, 356, 367 affective states, 6, 210, 220, 226, 309
adaptation, 124, 261, 278, 287 African-American, 49
addiction, 173, 182, 184, 186, 212 afternoon, 165, 245
adenosine, 126 age, 1, 4, 21, 22, 27, 32, 33, 63, 73, 90, 93, 104, 107,
adenosine triphosphate, 126 110, 111, 112, 113, 115, 119, 120, 121, 123, 124,
administration, 114, 134, 234, 341, 348 125, 126, 129, 131, 137, 138, 139, 141, 142, 148,
administrative, xiii 149, 150, 157, 165, 178, 205, 236, 237, 241, 247,
370 Index
264, 291, 292, 293, 294, 296, 298, 299, 300, 302, anemia, 91, 130
334, 357 anger, 18, 95, 199, 202, 242, 285, 308, 325
agenda-setting, 200 anhedonia, 26
agent, 234, 235, 241, 336, 339, 352, 354 animals, 173
agents, 57, 96, 184, 233, 234, 242, 298, 331, 332, antagonism, 333, 342
333, 336, 338, 339, 343, 345, 348, 351, 354, 355, antagonist, 333, 350, 354, 361, 364, 367
361, 363 antagonists, 333, 345
aggressive behavior, 34 antecedents, 196, 244, 252, 327
agonist, 341, 361 anterior cingulate cortex, 15
aid, 283, 332, 345 antibiotics, 342
aiding, 278 anticholinergic, 333
akathisia, 336 anticholinergic effect, 333
alcohol, 27, 41, 42, 43, 97, 114, 115, 159, 174, 182, anticonvulsant, 241, 352, 361
317, 354, 361, 364 anticonvulsants, 237
alcohol abuse, 42 antidepressant, 96, 229, 235, 249, 251, 260, 284,
alcohol consumption, 27 333, 334, 335, 342, 345, 347, 351, 352, 354, 355,
alcohol dependence, 41, 115, 159, 354, 364 357, 359, 362, 367
alcohol use, 43, 317 antidepressant medication, 96, 260, 333, 334, 347,
alcohol withdrawal, 114 351, 352, 355, 357, 359, 362
alcoholism, 24, 307 antidepressants, 96, 231, 237, 241, 249, 326, 331,
alexithymia, 6, 16, 28, 198 332, 333, 334, 336, 339, 347, 349, 351, 352, 353,
alienation, 287 355, 366, 367
alkalosis, 94 antihistamines, 342
alpha, 333, 341 antipsychotic, 332, 336, 348, 349
alternative, 6, 101, 107, 112, 173, 184, 188, 197, antipsychotic drugs, 349
208, 213, 219, 226, 244, 245, 246, 261, 276, 277, antipsychotics, 331, 332, 336, 339, 343, 345, 348
282, 283, 284, 308, 366 antisocial, 39, 96
alternative behaviors, 245, 246 antisocial behavior, 39, 96
alternatives, 181, 242, 244 anxiety, 3, 4, 7, 12, 19, 21, 23, 25, 26, 27, 28, 34, 35,
alters, 247, 346 36, 38, 40, 41, 44, 57, 93, 97, 116, 120, 143, 144,
ambivalence, x, 171, 173, 175, 181, 198, 201, 277, 145, 146, 147, 148, 160, 190, 191, 196, 198, 213,
312 215, 217, 232, 242, 244, 246, 258, 277, 284, 293,
ambivalent, 7, 113, 298 296, 302, 303, 304, 307, 319, 325, 332, 333, 336,
amelioration, 293 337, 338, 341, 345, 353, 357, 363, 364, 365
amenorrhea, 2, 91, 115, 121, 122, 129, 130, 131, anxiety disorder, 4, 23, 25, 35, 41, 44, 57, 93, 215,
132, 140, 190 258, 307, 325, 353
American Academy of Pediatrics, 120, 125, 133 appetite, vii, 97, 128, 220, 233, 234, 235, 241, 284,
American Heart Association, 84, 252 300, 338
American Psychiatric Association (APA), 2, 11, 20, application, 45, 89, 187, 189, 204, 231, 249, 279,
39, 53, 54, 55, 65, 85, 87, 90, 98, 103, 109, 110, 290, 313, 351
116, 120, 121, 133, 142, 151, 165, 208, 226, 227, argument, 174, 178, 181, 221
279, 288 aripiprazole, 339
American Psychological Association, 80, 82, 205, arrest, 134
290, 325, 326, 327, 328 arrhythmia, 334
amino, 52, 334 arrhythmias, 91
amino acid, 52, 334 artificial, 311
amino acids, 52 Asian, 122
amylase, 94, 95 assault, 27, 74
analysts, 312 assessment, 16, 24, 25, 36, 44, 54, 56, 64, 65, 66, 68,
androgen, 361, 367 93, 95, 163, 180, 181, 185, 200, 203, 204, 208,
Index 371
215, 216, 224, 228, 263, 267, 270, 273, 289, 298, behavioral aspects, 102, 131
311, 325, 327, 328, 334, 353, 358 behavioral assessment, 196
assessment techniques, 311 behavioral change, 31, 197, 212, 217, 220, 226, 317,
assignment, 188 318, 321, 362
assimilation, 279 behavioral disorders, 173
associations, x, 11, 176, 213 behavioral medicine, 328
assumptions, 7, 195, 196, 199, 200, 201 behavioral models, 214
asymptomatic, 24, 25, 26, 27, 111 behavioral modification, 127, 131
athletes, 29, 51, 125 behavioral problems, 178, 189
Atlantic, 84 behavioral theory, 243, 279
atmosphere, 105 behaviorism, 212, 214
atrophy, 130 behaviorists, 212
attachment, 10, 29, 30 behaviours, 2, 5, 6, 7, 8, 9, 10, 11
attacks, 54 Belgium, 84
attention, vii, ix, x, 8, 54, 92, 105, 109, 115, 122, beliefs, 7, 13, 33, 35, 36, 52, 146, 166, 174, 175,
126, 129, 145, 155, 162, 165, 179, 189, 193, 194, 185, 189, 190, 192, 194, 196, 197, 198, 211, 217,
201, 222, 237, 248, 283, 284, 294, 300, 308, 312, 218, 244
329, 352, 353, 354, 355 benchmark, 249
attentional bias, 7, 13, 16 bending, 301
attitudes, 8, 10, 11, 36, 39, 47, 49, 108, 133, 168, beneficial effect, 271
175, 192, 193, 209, 211, 213, 220, 272, 365 benefits, 89, 109, 142, 144, 146, 148, 174, 185, 198,
atypical, 120, 161, 235, 331, 332, 336, 339, 343, 246, 294, 340, 352, 358, 360
345, 348, 352, 353, 354, 355 Best Practice, 170
atypical antipsychotic agents, 343 beta, 34, 41, 349
Australia, 74, 107, 137, 140 bias, 65, 228
autonomic, 89 bicarbonate, 90, 95
autonomy, 5, 148, 164, 172, 176, 179, 180 biliopancreatic, 236
availability, 102, 103, 104, 106, 109, 125, 142, 210, biliopancreatic diversion, 236
247, 349 binding, 13, 21, 39, 41, 50, 324, 325, 343, 344, 346,
avoidance, vii, 5, 15, 19, 26, 27, 39, 41, 105, 120, 347, 348
140, 141, 152, 160, 172, 191, 200, 313, 314, 317, binge drinking, 97
324, 343, 344, 346 binge eating disorder (BED), ix, x, 6, 17, 20, 27, 41,
avoidant, 5, 10, 96, 150 45, 47, 53, 54, 55, 56, 57, 58, 59, 60, 61, 62, 63,
awareness, 6, 78, 137, 140, 159, 196, 200, 201, 228, 64, 65, 66, 67, 68, 69, 122, 163, 164, 167, 187,
262, 284, 288, 309, 310, 314, 336, 352 189, 194, 205, 229, 231, 232, 237, 241, 242, 246,
247, 248, 249 250, 252, 253, 254, 255, 256, 260,
261, 278, 284, 290, 311, 328
B
bingeing, 20, 26, 31, 35, 37, 40, 49, 57, 108, 132,
148, 149, 164, 211, 214, 217, 222, 223, 227, 314,
backfire, 189
354, 358, 364
Badia, 168
biologic, 97
bankruptcy, 113
biological, ix, 1, 2, 11, 12, 19, 21, 33, 102, 192, 313,
bargaining, 176
361
bariatric surgery, 236, 249, 255
biologically, 9
barriers, 72, 83
biology, 46, 204
base rate, 9
biomarkers, 234
behavior modification, 116, 119, 122, 127, 205, 236,
biopsychosocial model, 38
326, 340
bipolar, 258, 307, 326, 331
vehavior modification, 222
bipolar disorder, 258, 307, 326, 331
behavior therapy, 92, 95, 99, 104, 203, 209, 227,
birth, 13, 22, 23, 29, 38, 40
229, 251, 255, 289, 290, 312, 313, 325, 327, 350
372 Index
birth weight, 22 brain structure, 2

births, 23 breakdown, 178
black, 56, 68, 357 breakfast, 95, 132, 224, 284, 286, 363
black women, 56, 68 Brief Psychiatric Rating Scale, 336, 338
blame, 64, 147, 196, 224, 322 British, 11, 12, 13, 14, 15, 16, 39, 42, 45, 47, 48, 49,
blaming, 145 50, 51, 54, 91, 98, 116, 133, 152, 167, 184, 185,
bleeding, 236 186, 229, 254, 290, 306, 348, 349, 350, 365, 367
blocks, 148 broad spectrum, 164
blood, 2, 3, 90, 126, 130, 234, 235, 283, 341, 343, Brussels, 84
346 bupropion, 251, 255, 256, 354, 366
blood flow, 2, 3, 343 bupropion, 252
blood glucose, 90, 235 burnout, 105, 286, 288, 299
blood pressure, 126, 234, 283, 341 business, 113, 318
body dissatisfaction, 8, 9, 10, 63, 157, 158, 169, 309, butter, 280
314, 336, 356 bypass, 231, 235, 236, 248, 249, 253, 256
body fat, 23
body image, 9, 11, 17, 29, 62, 63, 65, 92, 93, 111,
C
122, 140, 141, 149, 151, 157, 160, 298, 327, 332,
337, 345
cabinets, 245
body mass index (BMI), 23, 30, 31, 34, 35, 38, 56,
cachexia, 178
57, 63, 64, 88, 89, 90, 97, 109, 113, 157, 158,
CAD, 236
164, 165, 177, 178, 179, 188, 190, 232, 235, 236,
calcium, 90, 91, 129, 236
237, 238, 239, 240, 246, 248, 261, 335, 338, 342,
California, 291
343
caloric intake, 247, 302, 337, 340
body shape, 7, 8, 16, 28, 30, 33, 63, 122, 140, 158,
calorie, 8, 91, 124, 141, 213, 219, 223, 242, 303
165, 189, 336, 363
Canada, 1, 85, 107, 141, 183, 289, 346
body size, 7, 59
cancer, 64, 231, 232, 236, 252, 254
body temperature, 126
candidates, 90
body weight, 1, 7, 8, 14, 33, 54, 89, 90, 106, 121,
cannabis, 42
123, 125, 126, 140, 165, 189, 190, 223, 235, 239,
capacity, x, 79, 89, 139, 140, 144, 171, 172, 174,
241, 245, 246, 249, 251, 346, 349, 363
175, 185, 192, 194, 197, 236, 278
bolus, 128
carbohydrate, 220, 236
bone, 92, 129, 130, 131, 132, 133, 134, 301
carbohydrates, 124, 219, 220, 363
bone density, 129, 130, 131, 132, 133, 134, 301
carbon, 128
bone loss, 92
carbon dioxide, 128
borderline, 37, 96, 99, 194, 204, 251, 289, 290, 300
cardiac arrhythmia, 94, 128, 143, 339
borderline personality disorder, 37, 204, 251, 289,
cardiac dysrhythmia, 125
290
cardiac function, 301
Borderline Personality Disorder, 276
cardiologist, 92
boredom, 242, 302
cardiomyopathy, 129
borrowing, 312
cardiovascular, 64, 109, 119, 122, 129, 231, 232,
Boston, 68, 347, 348
234, 254, 343
bounds, 172
cardiovascular disease, 64, 231, 232, 234
bowel, 92, 94, 236
cardiovascular risk, 234, 254
bowel obstruction, 236
caregivers, 334
boys, 48, 49, 123, 133, 138, 166
Caribbean, 363
bradycardia, 91, 125, 126, 129, 131, 143, 283, 341
carrier, 109
brain, x, 2, 18, 91, 130, 131, 134, 173, 207, 213, 228,
case study, 171, 228
234, 324, 344, 346, 349
cast, 213
brain functioning, x
catalyst, 196
Index 373
catechol, 42 clinical depression, 257

catecholamines, 234 clinical judgment, 80
category a, 53 clinical presentation, 76, 278
category b, 175 clinical psychology, 64
catharsis, 145, 198 clinical trial, 37, 188, 200, 210, 237, 248, 255, 274,
Caucasian, 8, 22, 47, 60, 88, 237 345, 351, 352, 354, 355, 357, 359, 361, 363
Caucasians, 22 clinical trials, 210, 237, 248, 255, 274, 345, 351,
ceiling effect, 334, 353, 358 352, 354, 355, 357, 359, 361, 363
cell, 181 clinically significant, 211, 292
central nervous system, 234 clinician, vii, viii, xi, 73, 74, 75, 76, 79, 82, 83, 94,
cephalohematoma, 4 172, 180, 181, 213, 216, 219, 248, 249, 278, 281,
cerebral blood flow, 344 288, 314, 316
cerebrospinal fluid, 21, 348 clinicians, vii, viii, ix, x, xi, xiii, 6, 54, 64, 72, 73,
certification, 171, 176 74, 75, 76, 77, 79, 80, 82, 83, 84, 87, 90, 92, 93,
Chad, 307 97, 124, 137, 145, 150, 171, 172, 176, 177, 180,
channels, 77 181, 182, 185, 209, 212, 213, 226, 249, 275, 276,
chaotic, 37, 61, 90, 224 279, 291, 299, 332, 353, 355
chemicals, 234 clonidine, 339, 341, 347
chemotherapy, 361 close relationships, 268
Chevron, 210, 228, 262, 274 closure, 200
Chicago, 294 clustering, 60
childhood, ix, 4, 10, 17, 18, 23, 25, 27, 28, 36, 39, clusters, 215
47, 48, 50, 52, 113, 121, 138, 139, 153, 163, 300 CNS, 33, 34, 38
childhood sexual abuse, 18, 28, 52 coaches, 192
children, x, xiii, 10, 16, 17, 23, 40, 42, 52, 56, 67, cocaine, 42
68, 90, 107, 119, 120, 121, 122, 134, 135, 137, cocaine abuse, 42
138, 139, 140, 141, 142, 143, 144, 145, 146, 147, Cochrane, 28, 29, 42, 45, 81, 85, 228, 250, 254
148, 149, 150, 151, 153, 154, 166, 169, 175, 232, Cochrane Database of Systematic Reviews, 85, 228,
247, 250, 251, 255, 291, 298, 300, 334, 348, 349, 250, 254
350, 352 coercion, x, 171, 175, 176, 177, 181, 182, 183, 185
Chinese, 15, 43, 167 coffee, 97
chloride, 90, 94, 95, 128 cognition, 145, 277
chlorpromazine, 161, 337 cognitive behavior therapy, 72, 154, 228, 257, 258,
chocolate, 220, 223, 225, 233, 246 259, 273, 288, 289, 325, 329
cholecystokinin, 34, 40, 173, 182 cognitive behavioral therapy, x, 35, 95, 144, 148,
cholesterol, 91, 132, 234, 244 228, 231, 241, 247, 252, 274, 335, 365
chromosome, 3, 14, 21, 41 cognitive biases, 8
chromosomes, 3 cognitive capacity, 141, 145, 174
chronic, viii, 8, 9, 10, 61, 115, 127, 131, 145, 147, cognitive deficit, 145
168, 173, 174, 178, 180, 276, 278, 349 cognitive deficits, 145
chronic illness, 145, 180 cognitive flexibility, 4, 145
citalopram, 237, 239, 361, 367 cognitive function, 3, 193
classes, 60, 331, 351, 352 cognitive impairment, 92
classification, 54, 59, 60, 64, 65, 66, 153 cognitive performance, 143
classified, 31, 64, 120, 232 cognitive process, 145, 213, 312, 320
cleaning, 232 cognitive processing, 145, 312
clean-up, 190 cognitive style, 164
clients, 6, 172, 183, 194, 195, 197, 198, 199, 200, cognitive therapy, 92, 205, 212, 214, 222, 290, 312,
201, 251, 289, 326 325, 326, 327, 328
clinical approach, 77 cognitive-behavioral therapies, 204
374 Index
cohesion, 30, 36, 165 computer, 247, 317

cohort, 1, 3, 12, 15, 44, 49, 58, 60, 139, 154, 169, computers, 317
236 concentration, 40, 126, 145, 242, 340, 350, 363, 364
collaboration, 74, 75, 76, 81, 82, 83, 84, 194, 195, conceptual model, 153, 313
201, 203, 293 conceptualization, 5, 6, 9, 78, 276, 286
collateral, 180, 181 conceptualizations, 1
college students, 47, 270 concordance, 158
colleges, 304 concrete, 6, 212, 309
colon, 94 conditioning, 212
colostomy, 94 conduction, 339
Columbia, 260, 351 conductor, 305
Columbia University, 351 confidence, 32, 179, 221, 266
coma, 126, 128 confidence interval, 32
communication, 30, 40, 71, 72, 78, 142, 175, 221, confidentiality, 190, 201
266, 292, 297, 303 conflict, 10, 30, 33, 40, 144, 148, 172, 194, 208, 287,
communication skills, 142 292, 297, 300, 301, 302, 303
communities, 71, 78, 81 conflict avoidance, 301
community, ix, 14, 22, 28, 29, 31, 43, 47, 55, 56, 57, conflict resolution, 30
58, 60, 67, 84, 94, 95, 101, 108, 109, 127, 138, confrontation, 181, 302
170, 188, 203, 312, 325 confusion, 28, 177
community-based, 28, 29, 31, 43, 55, 56, 58, 325 conscious awareness, 213
co-morbidities, 98 consensus, x, 59, 94, 97, 106, 119, 142, 150, 313
comorbidity, 3, 16, 19, 27, 39, 41, 47, 98, 143, 169, consent, x, 89, 107, 142, 171, 172, 175, 182, 294
177, 256, 365 constipation, 94, 95, 130, 224, 241, 354
compassion, 185, 299, 303 constraints, 75, 97, 101, 102, 220
competence, 78, 96, 175, 180, 181, 183, 185, 194, construction, 263, 327
210, 265, 267, 268 constructivist, 312, 327
competency, x, 171, 181 consumption, 14, 234, 253, 361
competition, 38, 105, 192 contingency, 180
complement, 317 continuing, 259, 339
complementary, 279 continuity, 110
complete blood count, 90, 131 control condition, 248
complete remission, 112 control group, 4, 6, 7, 113, 236, 248, 294, 308, 333,
complex behaviors, 214 358, 359
complex carbohydrates, 220 controlled research, 115
complexity, viii, 82, 115, 146, 192, 202, 203 controlled studies, 106, 131
compliance, 5, 102, 175, 178, 234, 275, 283, 298, controlled trials, xi, 75, 76, 87, 106, 116, 144, 152,
312, 339 154, 163, 165, 167, 169, 229, 242, 249, 250, 254,
complications, 22, 44, 64, 88, 89, 92, 94, 95, 97, 258, 331, 333, 336, 339, 345, 351, 352, 355, 357,
102, 106, 109, 112, 122, 125, 126, 130, 131, 133, 358, 362, 367
134, 135, 141, 143, 232, 236, 249, 254, 261, 305, conversion, 129, 176, 178, 180
349 coordination, 120
components, 30, 123, 150, 188, 197, 199, 200, 272, coping strategies, 148, 191, 314, 320, 323
277, 279, 323 correlation, 9, 185, 344
composite, 190 correlations, 22
compounds, 336, 345 cortical, 3, 228, 347
comprehension, 242 cortisol, 35, 50
compulsion, 182 cost-effective, 149, 173, 209
compulsive behavior, 169 costs, 108, 197, 198, 232, 332, 352
computed tomography, 3, 344, 349
Index 375
counseling, 87, 93, 102, 104, 146, 188, 209, 239, delirium, 134, 178
241, 253, 255, 358, 364 delivery, 247, 248
courts, 177 delta, 3, 12, 340
coverage, 103, 233 delusion, 336
covering, 180, 196 delusional thinking, 337
craving, 233, 245 demand, 360
creativity, viii demographic, 60, 158
credit, 20 demoralization, 180
crime, 27, 43 denial, 88, 171, 172, 174, 247
criticism, 6, 30, 295, 298, 304, 311, 312 Denmark, 49, 152, 153
cross-cultural, 9 density, 50, 129, 130, 133, 134
cross-sectional, 25, 29, 31, 56, 67 depressants, 249
cross-talk, 71 depressed, 9, 26, 30, 220, 223, 237, 238, 239, 240,
crying, 193, 301, 302, 318 241, 332, 338, 360
cues, 7, 127, 244, 245, 246, 311 depression, 7, 12, 24, 30, 34, 36, 40, 42, 44, 48, 57,
cultural, ix, 8, 9, 28, 29, 146, 158 63, 90, 92, 94, 96, 97, 113, 115, 125, 126, 141,
cultural factors, 29 144, 147, 152, 160, 192, 196, 203, 212, 213, 214,
cultural influence, 8, 9 227, 231, 235, 237, 238, 241, 242, 244, 246, 255,
cultural norms, 9 257, 261, 264, 265, 273, 277, 313, 324, 326, 328,
culture, vii, 10, 14, 37, 72, 78 332, 335, 336, 337, 338, 341, 359, 365
curiosity, 221, 317 depressive disorder, 25, 34, 120, 258, 326
cycles, 196, 200 depressive symptomatology, 173
depressive symptoms, 36, 37, 182, 190, 333, 352,
353
D
deprivation, 214, 220
dermatologic, 119, 122
daily living, 145, 200
desensitization, 305
dairy, 61
desert, 132
dairy products, 61
desipramine, 250, 334, 353, 358, 359, 366
danger, 89, 174, 202, 296
desire, 8, 76, 121, 132, 176, 177, 190, 191, 297, 303
data base, x, 187, 304
desires, 292, 322
data collection, 65
detection, 7, 16, 169
database, 188
detention, 178, 185
dating, 297
developing countries, 120
death, 9, 64, 102, 115, 126, 128, 129, 174, 175, 179,
developmental disorder, 195
192, 237, 264, 284, 286, 301, 334, 350
developmental factors, 192, 292
deaths, 236
developmental milestones, 144, 291
decision making, 78, 109, 184, 242, 316
diabetes, 57, 66, 67, 90, 232, 235, 236, 245, 252,
decision-making process, 115
253, 255
decisions, viii, 77, 101, 107, 115, 125, 141, 143, 149,
Diabetes, 57, 66
150, 172, 174, 175, 176, 191, 288, 332
diabetes mellitus, 67, 253, 255
defense, 36, 50
diagnostic, vii, x, 2, 9, 24, 53, 54, 55, 58, 59, 60, 62,
defenses, 36, 48, 160
63, 64, 66, 68, 69, 87, 121, 129, 137, 138, 139,
defensiveness, 146
140, 154, 156, 160, 189, 209, 215, 246, 260, 310
deficiency, 236, 348
Diagnostic and Statistical Manual of Mental
deficit, 6, 327
Disorders, 11, 20, 39, 53, 65, 133
deficits, 18, 190, 191, 210, 247, 261, 264, 266
diagnostic criteria, 2, 9, 53, 54, 55, 63, 64, 66, 68,
definition, 40, 58, 80, 138, 175, 247, 264, 283, 294
129, 137, 138, 139, 140, 189, 246
degree, 8, 21, 22, 23, 29, 30, 50, 59, 60, 61, 64, 102,
diaphoresis, 333, 335
169, 171, 188, 195, 269, 277, 297, 334, 353, 360
diarrhea, 130, 236
dehydration, 91, 94, 109, 114, 125, 143, 224, 343
376 Index
diastolic blood pressure, 125 double-blind trial, 252, 347, 353, 354, 355, 357, 358,
diet, vii, 31, 48, 57, 94, 97, 103, 114, 124, 132, 165, 361, 364, 365, 366, 367
192, 208, 213, 217, 219, 220, 222, 223, 225, 231, dream, xiii
233, 241, 242, 244, 246, 248, 253, 263, 282, 284, drinking, 97, 114, 192, 314, 318
328, 356 driver’s license, 304
diet pill, 94, 282, 284 drowsiness, 333
dietary, 51, 61, 66, 102, 104, 189, 191, 209, 214, drug abuse, 24
219, 224, 234, 239, 242, 258, 280, 308, 309, 310, drug dependence, 361
314, 327, 328 drug interaction, 332
dietary fat, 234 drug targets, 343
dietary intake, 234 drug therapy, 161, 164, 336
dieting, vii, 8, 9, 10, 20, 26, 30, 31, 33, 40, 41, 44, drug treatment, 114, 332, 339, 359
45, 49, 57, 65, 68, 104, 120, 134, 160, 167, 171, drug use, 184
172, 180, 207, 208, 211, 213, 214, 215, 217, 220, drugs, 152, 173, 184, 218, 233, 234, 333, 336, 343,
223, 224, 227, 242, 263, 268, 308, 309, 310, 328, 345
334, 342, 350, 363 dry, 128, 235, 241, 333, 335
dieting status, 26 DSM, viii, 2, 11, 17, 20, 27, 29, 48, 53, 54, 56, 58,
diets, 214, 234 59, 60, 61, 62, 63, 64, 65, 66, 68, 69, 119, 121,
differentiation, 62 137, 138, 140, 152, 153, 154, 165, 205, 259, 273
diffusion, 73, 77, 80, 81, 83 DSM-II, 17, 20, 27, 29, 48, 152
dilation, 94 DSM-III, 17, 20, 27, 29, 48, 152
direct observation, 296 DSM-IV, 11, 29, 53, 54, 56, 58, 59, 60, 61, 63, 65,
directives, 80 66, 68, 69, 137, 140, 165, 205, 259
discipline, viii dumping, 236
disclosure, 114 duration, 61, 62, 106, 115, 150, 157, 163, 165, 177,
discomfort, 10, 96, 105, 140 189, 199, 200, 202, 209, 245, 249, 294, 295, 327,
discrete emotions, 308 339, 360, 367
diseases, 236 dysfunctional, 7, 10, 29, 33, 37, 94, 95, 189, 192,
disinhibition, 246 196, 201, 210, 212, 214, 220, 222, 223, 226, 271
disputes, 210, 261, 264 dyslipidemia, 251
dissatisfaction, 9, 63, 96, 159, 168, 232, 309 dysphagia, 121
disseminate, 73, 75 dysphoria, 345
dissociative disorders, 28 dysregulated, 173, 220
distal, 192, 193, 236 dysregulation, 5, 36, 40, 41, 96, 173, 276, 277, 310
distortions, 35, 38, 92, 111, 140, 144, 192, 201, 212, dysthymia, 258
298
distraction, 281, 285, 286
E
distress, 26, 58, 62, 63, 96, 140, 144, 145, 146, 148,
195, 224, 246, 285, 300, 313
early warning, 268
distribution, 22, 57, 156
eating disturbances, 17, 26, 50, 56
diuretic, 22, 88, 91, 128, 132, 284
echocardiogram, 129, 131
diuretics, 94, 103, 165, 191
ecological, 292, 311, 325, 327, 328
diversity, viii
economic, vii, 72, 101, 106
divorce, 302
edema, 91, 105, 127, 178
dizziness, 97, 340, 353, 354
education, 71, 72, 73, 77, 80, 82, 83, 84, 85, 93, 142,
doctors, 277
145, 146, 175, 179, 190, 201, 242, 268, 332
dopamine, 2, 14, 34, 45, 234, 339, 344, 347, 348
educators, 172, 176
dopaminergic, 3, 173
efficacy, 82, 88, 106, 142, 144, 146, 147, 148, 149,
dosage, 336, 339, 353
150, 163, 175, 188, 200, 202, 209, 215, 231, 234,
dosing, 339
235, 241, 249, 251, 252, 257, 278, 284, 288, 313,
Index 377
331, 332, 339, 345, 347, 351, 352, 353, 354, 355, England, 15, 17, 18
356, 357, 358, 359, 361, 362, 366 enthusiasm, xiii, 83
eggs, 280 environment, 7, 9, 16, 20, 36, 37, 39, 40, 42, 47, 102,
ego, 88, 147, 148, 171, 172, 175, 176, 293, 298 108, 109, 134, 199, 201, 214, 219, 227, 244, 286,
ego strength, 148 311
electrocardiogram, 89, 90, 91, 92, 93, 96, 129 environmental, 9, 10, 32, 39, 97, 145, 160, 173, 212,
electrolyte, 88, 89, 90, 94, 95, 97, 105, 109, 119, 214, 217, 218, 222, 224, 311
125, 128, 143, 178, 242, 283, 340 environmental change, 145, 212
electrolyte imbalance, 88, 90, 94, 178, 283 environmental factors, 39, 97, 218, 311
electrolytes, 91, 96, 128, 132 environmental influences, 32
emission, 3, 21, 344, 349 enzyme, 127
emotion, xi, 5, 6, 16, 191, 198, 208, 246, 276, 277, enzymes, 234
281, 285, 307, 308, 310, 311, 312, 313, 314, 316, epidemic, 69, 232, 251, 256
317, 319, 320, 321, 322, 323, 327, 329 epidemics, 252
emotion regulation, 6, 208, 246, 276, 307, 310, 313, epidemiological, 5, 20, 82, 138, 139, 248
316, 324 epidemiology, x, 12, 18, 46, 49, 53, 66, 119, 120,
emotional, 5, 6, 10, 13, 18, 31, 33, 62, 89, 90, 92, 122, 350
120, 141, 142, 148, 150, 152, 178, 191, 192, 193, epinephrine, 234
196, 197, 198, 200, 201, 202, 203, 210, 213, 214, episodic, 264
218, 224, 227, 228, 232, 233, 242, 244, 247, 276, equality, 286
277, 282, 297, 307, 308, 309, 310, 312, 313, 314, equating, 211
316, 317, 318, 321, 323, 324, 326, 328 equipment, 128, 243, 252
emotional abuse, 90 erosion, 272
emotional disorder, 120, 150, 152, 203, 227, 312, esophageal, 94, 130
324, 326 estradiol, 129, 131, 132
emotional distress, 10, 141, 244 estrogen, 91, 134
emotional experience, 6, 198, 201, 308, 310, 313, ethical, 87, 171, 174, 180, 182, 202, 237
317, 318, 324 ethical concerns, 237
emotional health, 198 ethical issues, 180
emotional processes, 210, 310, 323, 328 ethics, 171, 183, 184
emotional responses, 214, 312 ethnicity, 17
emotional state, 5, 62, 191, 213, 310, 312, 314, 317 etiology, ix, 3, 8, 14, 19, 38, 90, 97, 173, 190, 192,
emotionality, 5, 26 196, 307, 308, 309, 313, 355
emotions, xi, 6, 13, 28, 140, 191, 197, 233, 244, 275, Europe, 74, 126
281, 283, 284, 285, 310, 311, 312, 314, 316, 317, European, 12, 13, 14, 15, 16, 18, 51, 84, 116, 117,
319, 323, 324, 325 118, 152, 155, 166, 167, 168, 169, 182, 185, 228,
empathy, vii, 181, 194, 292 254, 255, 329, 347, 348, 349
employers, 172, 176, 264 European Commission, 84
empowered, 297, 302 euthyroid sick syndrome, 129
empowerment, 210 evening, 108, 191, 243, 282
encouragement, xiii, 145, 271, 301, 303, 318 evolution, 207, 216
endocrine, 119 evolutionary, 180, 214
endocrine disorders, 119 evolutionary process, 180
endogenous, 342 excitement, 242
endophenotypes, 24, 50 exclusion, 101, 165, 172
endoscopy, 132 excretion, 341
energy, 61, 68, 124, 129, 140, 233, 234, 242, 243, exercise, 20, 31, 33, 93, 102, 103, 104, 111, 129,
248, 363 132, 141, 167, 168, 173, 185, 191, 193, 197, 198,
engagement, 36, 150, 172, 195, 200, 201 217, 231, 242, 243, 244, 246, 248, 252, 280, 282,
engineering, 72, 77 284, 308, 319
378 Index
experimental condition, 308 February, 17

expert, 80, 94, 97, 120, 150, 154, 286, 298 fecal, 235
expertise, xi, 72, 79, 80, 103, 203, 277, 298 feedback, 15, 92, 146, 208, 266, 286, 293, 296, 306
experts, viii, ix, xi, 181, 298 feeding, 10, 23, 105, 137, 140, 148, 151, 152, 173,
explicit knowledge, 79 179, 183, 184, 293, 296, 297, 301, 303, 326
explicit memory, 7, 14 feelings, vii, 5, 6, 7, 35, 63, 74, 93, 95, 97, 145, 189,
exposure, 4, 8, 11, 15, 18, 29, 37, 39, 133, 246, 283, 191, 194, 197, 198, 199, 210, 211, 212, 214, 215,
287, 312, 316, 317, 328 217, 218, 222, 243, 244, 264, 268, 282, 283, 284,
Exposure, 43, 83, 98 285, 287, 296, 314, 317, 318, 321, 322, 323, 326,
external locus of control, 26 363
eye, 176, 302 feet, 89, 123, 300
eyes, 299 females, 2, 4, 8, 20, 33, 44, 56, 63, 90, 91, 111, 112,
113, 122, 123, 138, 155, 156, 157, 158, 159, 160,
161, 162, 163, 164, 165, 170, 250, 252, 254, 292,
F
335, 337, 338, 341, 342, 343
feminist, 40, 50
factor analysis, 60
fiber, 92, 95
failure, 35, 73, 77, 88, 109, 117, 121, 125, 126, 140,
Fiji, 8, 11
143, 145, 146, 147, 200, 202, 218, 220, 233, 236,
financial resources, 77
241, 276, 299, 300, 318, 332, 341, 345, 357
financial support, 181
faith, 74
financing, 94
false, 64, 68, 69, 169
fires, 220
false negative, 169
first degree relative, 21, 22
familial, ix, 1, 2, 28, 157, 192, 291, 296, 297, 299
fitness, 252
familial aggregation, 157
flexibility, 110, 128, 151, 298, 303
family conflict, 44
flow, 3
family environment, 10, 33, 36, 37, 43, 90, 110
fluctuations, 91, 224
family factors, 47, 146
fluid, 91, 92, 105, 128, 223, 280, 343
family functioning, 15, 37, 43, 116, 297
fluid balance, 223
family history, 21, 125, 132, 196
fluoxetine, 228, 237, 238, 250, 334, 335, 339, 346,
family life, 192
348, 349, 351, 355, 356, 357, 358, 359, 360, 361,
family meals, 296
362, 363, 364, 365, 366, 367
family members, 24, 30, 90, 93, 107, 171, 194, 263,
fluvoxamine, 237, 238, 254, 355, 360, 365
264, 277, 292, 301
fMRI, 343, 344
family physician, 332
focusing, 119, 123, 144, 145, 193, 195, 196, 198,
family structure, 107, 147, 291
210, 226, 235, 242, 245, 269, 293, 321
family studies, 21, 51, 294
follicle, 91
family therapy, 87, 92, 93, 98, 102, 104, 141, 146,
follicle-stimulating hormone, 91
147, 148, 149, 150, 151, 152, 153, 154, 175, 176,
food, vii, 6, 7, 8, 9, 12, 14, 16, 29, 30, 39, 52, 57, 58,
185, 202, 288, 292, 293, 294, 295, 299, 304, 306
61, 67, 68, 89, 91, 92, 96, 104, 108, 120, 125,
famine, 224
126, 140, 141, 147, 149, 150, 151, 152, 161, 166,
fasting, 8, 16, 48, 51
173, 178, 179, 182, 191, 197, 201, 210, 211, 217,
fat, 2, 7, 15, 17, 35, 50, 61, 105, 124, 166, 197, 211,
218, 220, 223, 224, 226, 231, 232, 233, 234, 235,
213, 214, 219, 223, 234, 244, 246, 300
236, 242, 244, 250, 253, 254, 270, 280, 282, 291,
fatigue, 150, 242, 244
293, 297, 298, 299, 300, 301, 302, 303, 308, 316,
fats, 220
317, 318, 319, 342, 348, 350, 356, 363
FDA approval, 356, 361
Food and Drug Administration (FDA), 233, 234,
fear, 26, 31, 37, 54, 59, 60, 121, 122, 139, 140, 164,
334, 347, 354, 355, 356, 357, 360, 361, 362
166, 172, 174, 178, 214, 218, 222, 308, 317, 318,
339
fears, 2, 5, 6, 132, 159, 190, 197, 216, 300, 336
Index 379
food intake, 52, 57, 58, 61, 67, 173, 191, 201, 218, gifted, xiii
231, 233, 234, 235, 254, 280, 318, 342, 348, 350, girls, 11, 13, 16, 24, 26, 27, 31, 33, 39, 43, 44, 45,
363 47, 48, 49, 123, 133, 135, 138, 140, 152, 154,
forecasting, 28 169, 302, 310, 328
fractures, 92 glucose, 90, 227, 235, 339
fragility, 298 glutamate, 345
France, 56 goal setting, 197
fraternal twins, 22 goals, 53, 73, 110, 114, 124, 142, 144, 147, 166,
free choice, 174 172, 180, 181, 190, 191, 195, 197, 201, 217, 244,
freedom, 95, 172, 176 258, 261, 262, 263, 265, 267, 269, 276, 278, 283,
frustration, vii, 72, 73, 75, 242, 286, 301 296, 297, 303, 304, 316
FSH, 129, 131, 132 gold, viii, 236, 361
fuel, 196, 220 gold standard, viii, 236, 361
functional aspects, 288 grades, 31, 132
funding, 75, 76 grandparents, 192, 294
fusion, 7, 16, 76 granola, 132
gray matter, 3
grief, 210, 261
G
group climate, 118
group therapy, 40, 93, 104, 145, 161, 164, 166, 168,
GABA, 361
178, 179, 326
gallstones, 64, 236
groups, 23, 25, 28, 34, 36, 56, 59, 62, 63, 64, 73, 75,
games, 321
81, 82, 93, 96, 110, 119, 120, 138, 139, 140, 141,
gastrectomy, 236
146, 157, 158, 164, 177, 188, 210, 237, 241, 246,
gastric, 10, 94, 97, 124, 130, 150, 151, 173, 182,
247, 294, 295, 333, 335, 337, 338, 340, 341, 342,
183, 231, 234, 235, 236, 248, 249, 252, 253, 255,
343, 352, 353, 356, 358, 359, 360, 362
256, 341, 342, 349
growth, 91, 98, 114, 121, 123, 125, 126, 140, 142,
gastroenterologist, 132
143, 149, 258, 300, 339, 348
gastrointestinal, 109, 130, 173, 184, 235, 241, 242,
growth hormone, 339, 348
255
growth spurt, 300
gender, 20, 43, 46, 63, 93, 156, 157, 158, 159, 160,
guardian, 175, 180
161, 164, 165, 168, 169, 215, 241
guessing, 15
gender differences, 43, 63, 157, 158, 160, 165, 168,
guidance, xi, 79, 83, 95, 123, 124, 145, 179, 181,
169
190, 276, 298, 303
gender role, 20
guidelines, viii, 55, 61, 64, 67, 69, 75, 78, 79, 80, 81,
gene, 2, 9, 14, 36, 39, 42, 227
82, 83, 87, 91, 97, 115, 125, 133, 142, 181, 183,
gene expression, 36
279, 298, 305
generalizability, 71, 75, 77, 285
guilt, 7, 26, 36, 96, 211, 244, 282, 296, 300, 363
generalization, 108, 283, 286
guilty, 233, 281, 363
generation, 237, 241, 336
gut, 236
genes, 2, 12, 21, 214, 219
gymnastics, 122, 192, 219
genetic, 2, 9, 15, 19, 21, 24, 38, 45, 46, 47, 130, 192,
gymnasts, 29
214, 219
genetic factors, 2, 9, 21, 24
genetics, 14, 20, 123 H
Geneva, 69
genotype, 2, 42 hands, 332
genotypes, 50 handwriting, 232
geography, 72 happiness, 276
Germany, 107
gestational age, 4, 23
380 Index
harm, 5, 6, 16, 19, 39, 41, 160, 172, 173, 178, 231, hospital, 89, 92, 95, 96, 97, 98, 101, 102, 106, 107,
248, 278, 279, 282, 283, 286, 287, 314, 324, 343, 109, 114, 115, 116, 117, 118, 119, 122, 125, 128,
344, 346 140, 144, 146, 150, 151, 163, 164, 170, 176, 177,
Harvard, 12, 15, 117, 305 178, 183, 188, 202, 205, 300, 332, 338
head, 212 hospital stays, 106
headache, 234, 241 hospitalization, 88, 90, 93, 94, 95, 96, 102, 104, 107,
healing, 183 110, 117, 118, 124, 125, 126, 128, 129, 176, 180,
health, vii, viii, 87, 94, 102, 107, 110, 120, 123, 127, 190, 202, 341, 343, 360
135, 151, 172, 193, 201, 217, 232, 233, 245, 263, hospitalizations, 88, 97, 126, 178, 300
276, 278, 296, 299 hospitalized, 36, 88, 89, 91, 93, 109, 113, 114, 115,
health care, vii, viii, 107, 110, 120, 127, 172, 276 124, 131, 154, 169, 175, 176, 178, 183, 202, 300,
health care costs, viii 332, 333, 334, 337
health care professionals, vii hospitals, 88, 106, 142
health care system, viii, 107 host, 19
health insurance, 135 hostility, 8, 295, 298, 300, 303
healthcare, 81 household, 56
hearing, viii, 179 households, 302
heart, 55, 64, 67, 90, 126, 251 housing, 176
heart disease, 251 human, 14, 46, 83, 134, 204, 251, 339
heart rate, 126 human nature, 83
heat, 233 humans, 214, 347
height, 1, 64, 89, 90, 109, 121, 123, 125, 126, 132, husband, xiii, 89, 224, 300
134, 140, 200, 296, 300 hybrid, viii
hematologic, 119, 122, 126, 130 hybrids, 73
hemolytic anemia, 126 hydration, 89
heritability, 21 hyperactivity, 164
heterogeneity, 44 hypercholesterolemia, 245
heterogeneous, 87, 162 hyperlipidemia, 64, 132
Higgs, 141, 152 hypernatremia, 128
high risk, 245 hypersensitivity, 193
high school, 10, 43, 48, 122, 132, 190, 191, 232, 300 hypertension, 64, 232, 235, 245, 252
Hilbert, 205, 246, 252 hypochloremia, 94
hip, 132, 285 hypokalemia, 126, 128, 129, 131, 284
Hispanic, 50, 67, 122 hyponatremia, 126, 128
Hispanic population, 122 hypophosphatemia, 94, 126, 127, 133
Hispanics, 22 hypopnea, 251
histamine, 333 hypotension, 125, 143, 333, 335
HMOs, 108 hypothalamic, 129
Holland, 21, 45, 51, 365 hypothermia, 125, 143
homeostasis, 103, 292 hypothesis, 25, 30, 175, 310
homework, 200, 271, 285, 297 hypothyroidism, 129
homogeneity, vii, 165
homosexuality, 164
I
homovanillic acid, 34
Hong Kong, 9, 15, 42, 167
ICD, 53, 54, 58, 69, 137
hopelessness, 74, 104
ice, 233, 244
hormone, 129, 131, 135, 342
ideal body weight, 91, 103, 105, 109, 121, 125, 130,
hormones, 4, 167
132, 139, 248, 293, 303
horse, 72
idealization, 264
Index 381
identification, 1, 8, 23, 61, 67, 263, 272, 312, 316, injunction, 293, 301
317, 323 injury, 26, 236, 283
identity, viii, 5, 11, 148, 178 innovation, 73, 77, 78, 80, 81
idiosyncratic, 7 Innovation, 71, 77, 86
ileum, 236 insecurity, 159
illicit substances, 95 insight, 89, 104, 146, 173, 178, 271, 286, 298
illusion, 152 insomnia, 234, 235, 241, 338, 363, 364
images, 8, 15, 18 instability, 89, 94, 126, 129, 143, 165, 343
imagination, 113 institutions, 75, 76
imaging, 91 instruments, 209, 247
implementation, 81, 82, 83, 297, 298, 299 insulin, 57, 235, 253, 255
implicit memory, 213 insulin resistance, 57
impulsive, 5, 15, 27, 34, 47, 50, 311, 316, 322 insurance, 95, 97, 102, 103, 108, 109, 125, 182
impulsivity, 5, 21, 26, 34, 36, 41, 96, 311, 325, 328, insurance companies, 95, 108
346 integration, 71, 75, 77, 78, 79, 80, 82, 83, 164, 228
in situ, 198 integrity, 201
in vivo, 286 intelligence, xiii
incentive, 128 intensity, 117, 121, 280
incentives, 181 intensive care unit, 128
incidence, x, 9, 22, 44, 48, 138, 139, 153, 305, 366 intentions, 151
inclusion, 59, 76, 138, 141, 198, 292 interaction, 29, 32, 42, 71, 76, 77, 214, 219, 296,
income, 94, 108 311, 337, 340
incongruity, 176 interactions, 10, 11, 39, 42, 49, 118, 144, 145, 151,
independence, 108, 148, 264, 291, 296, 297, 298, 198, 297, 302, 327, 360
299, 302, 303, 304 interdisciplinary, 77
India, 9 interest groups, 78
indication, 103, 109, 333, 355, 360, 361 interface, 73, 83
indicators, 37, 40, 90, 106, 142, 143, 299 interference, 7, 10
indices, 50 intergenerational, 292
individualization, 228 internalization, 8, 18, 309, 328
induction, 180 international, viii, ix, xi, xiii, 1, 73, 76, 83, 110, 122
industrialized countries, 8 International Classification of Diseases, 53, 54
industrialized societies, 8, 9 internet, 164, 231, 247, 253
industry, 125 Internet, 247, 252, 255, 275
ineffectiveness, 6, 10, 25, 93, 173, 201, 336 internist, 89, 92, 93, 360
infants, 17, 138 interpersonal conflict, 196, 210, 244, 285
infection, 236 interpersonal conflicts, 196
influenza, 23 interpersonal events, 258, 263
influenza a, 23 interpersonal factors, 312, 313
information processing, 3, 13 interpersonal processes, 263, 272
informed consent, 174 interpersonal relations, 95, 96, 164, 264, 277, 285,
infrastructure, 82 363
infringement, 296 interpersonal relationships, 95, 96, 164, 264, 277,
ingestion, 220 363
inherited, 21 interpersonal skills, 205, 226
inhibition, 3, 5, 21, 309, 348 interpretation, 266, 359
inhibitor, 46, 251, 255, 366, 367 interrelationships, 36
inhibitors, 96, 233, 367 interval, 32, 339
inhibitory, 309 intervention, viii, 90, 102, 143, 147, 148, 149, 150,
initiation, 89, 143 163, 164, 172, 175, 176, 179, 181, 188, 200, 202,
382 Index
203, 233, 247, 284, 288, 296, 318, 353, 357, 361, laundry, 108
362, 367 law, 89, 97, 184, 185, 213
interview, 56, 60, 61, 165, 246, 316 laxatives, 92, 95, 103, 157, 165, 191, 223, 300, 302,
interviews, 55, 59, 60, 175 303, 308
intestinal tract, 131 lead, xi, 30, 35, 103, 129, 140, 195, 210, 211, 212,
intimacy, 263, 264 214, 235, 245, 246, 262, 265, 269, 271, 278, 291,
intoxication, 94 295, 299, 301, 309, 320, 323, 333
intravenous, 44, 48, 89, 127 learning, viii, 71, 78, 81, 83, 95, 173, 183, 193, 212,
intravenously, 127 218, 229, 242, 244, 286, 317, 361
invasive, 236 learning process, 78
Investigations, 8 legal issues, 88
investigative, 219, 221 legislation, 183
investment, 194 leptin, 3, 34, 39, 40, 45, 48
Ipecac, 129 lethargy, 94, 141
iron, 90, 105, 130, 236 Levant, 80, 82, 85
iron deficiency, 130 liberation, 126
irritability, 26, 52, 92, 223, 242 libido, 241
irritation, 130 life aspirations, 258
isolation, 258, 264 life changes, 264, 266
Israel, 21, 34, 50, 107, 177, 182, 184, 327 life cycle, ix
Italy, 53 life experiences, 196
life style, 323
lifestyle, 53, 64, 236, 242, 243, 265
J
lifestyle changes, 53
life-threatening, 2, 107, 110, 174, 178, 181, 203
JAMA, 350
lifetime, 4, 25, 27, 28, 30, 56, 57, 61, 63, 138, 154,
January, 17, 55, 67, 122, 132
157, 178, 232
Japan, 187
likelihood, 7, 9, 36, 106, 110, 177, 178, 179, 246,
Japanese, 49
248, 287, 311
jobs, 264
limitation, 294, 304
Jordan, 153, 204, 260, 274, 289
limitations, 55, 97, 182, 214, 233, 304, 325, 359
judge, 180
linear, 140
judgment, 80, 82, 89, 178, 181, 194, 286
linkage, 2, 12, 41
justification, 182, 277, 283
links, 62, 198, 263, 355
lipase, 233, 251, 255
K lipases, 234
lipids, 234, 251, 255, 339
K+, 128 lipoproteins, 255
killing, 301 liquids, 236
knees, 193 listening, 320
knowledge transfer, 72, 73, 78, 79, 80, 81, 83 literature, x, xi, 1, 7, 8, 9, 21, 22, 24, 59, 69, 74, 77,
80, 82, 87, 88, 92, 96, 101, 107, 109, 110, 115,
L 117, 118, 119, 120, 121, 122, 124, 130, 131, 134,
138, 139, 145, 155, 157, 161, 162, 165, 166, 169,
labeling, 213 171, 208, 248, 275, 277, 278, 293, 310, 312, 345,
lack of control, 106, 157, 233 351, 352, 367
language, 72, 81, 82, 140, 142, 198, 221, 222, 317, lithium, 340, 347, 354, 366
319 liver, 90, 91, 132, 235, 236, 361
laparoscopy, 236 liver function tests, 91
large-scale, 293 living arrangements, 149
Index 383
lobby, 76 mass media, 43

location, 7, 106, 115, 280, 334 mastery, 172, 180, 278
locus, 107 maternal, 10, 28, 30, 37, 44
Locus of Control, 107 maturation, 31
logging, 316 meals, 95, 104, 105, 114, 124, 146, 198, 217, 220,
London, 85, 117, 153, 183, 226, 230, 274, 290, 293, 243, 247, 280, 300, 301, 302, 303, 318, 319, 332,
305, 306 336, 342, 361, 363
long period, 115, 224 meanings, 152
longitudinal studies, 1, 23, 24, 25, 26, 31 measurement, 358
longitudinal study, 23, 28, 39, 42 measures, 5, 24, 28, 34, 62, 63, 139, 161, 162, 209,
long-term, viii, 2, 13, 17, 18, 21, 34, 75, 80, 83, 87, 211, 241, 248, 278, 328, 335, 340, 353, 358, 359,
96, 97, 108, 123, 129, 131, 135, 137, 146, 150, 360, 365, 366
152, 153, 154, 167, 173, 177, 181, 185, 191, 209, media, 8, 9, 14, 15, 18, 29, 43, 201, 328
210, 217, 226, 228, 234, 235, 236, 241, 243, 245, median, 343
249, 251, 254, 273, 295, 348, 361 mediators, 272, 274
loss of control, 62, 173, 189, 340 medical care, 93
losses, 96, 113 medication, 93, 137, 141, 142, 148, 149, 150, 161,
love, xiii, 233, 300, 320 163, 209, 233, 237, 241, 248, 249, 284, 332, 342,
lying, 96, 125, 221 351, 352, 353, 354, 355, 357, 358, 359, 360, 361,
362, 363, 364
medications, 93, 142, 188, 212, 234, 237, 241, 248,
M
249, 333, 337, 339, 351, 352, 354, 355, 357, 361
medicine, vii, viii, 64, 72, 77, 79, 80, 104, 113, 117,
magazines, 33
248, 284
magnesium, 90, 91
membership, 73, 82
Magnetic Resonance Imaging, 343
memory, viii, xiii, 3, 7, 65, 113, 183, 242, 311, 327
maintenance, 2, 4, 5, 34, 35, 87, 94, 95, 124, 134,
memory biases, 311
146, 147, 169, 185, 189, 190, 192, 193, 195, 196,
men, 29, 54, 56, 57, 63, 66, 68, 155, 157, 159, 160,
197, 202, 209, 214, 215, 218, 223, 224, 227, 235,
163, 165, 167, 169, 170, 223, 232, 362
243, 246, 252, 254, 256, 257, 258, 283, 292, 297,
menarche, 138
299, 303, 307, 308, 309, 313, 323, 328, 332, 334,
Mendel, xiii, 251
335, 339
menopause, 129
Maintenance, 188, 203, 208, 211, 229, 334
menstrual, 90, 91, 130, 138
major depression, 29, 35, 36, 39, 52, 103, 192, 210,
Menstrual cycle, 134
228, 256, 350, 352
menstruation, 105
major depressive disorder, 25, 27, 331, 333
mental disorder, 19, 20, 54, 61, 110, 288
maladaptive, 5, 7, 173, 212, 214, 222, 292, 298
mental health, 42, 64, 67, 101, 119, 123, 127, 187,
Malaysia, 9
203
males, ix, x, 20, 56, 63, 111, 120, 121, 123, 133,
mental health professionals, 67, 119
138, 139, 155, 156, 157, 158, 159, 160, 161, 162,
mental illness, 19, 107, 140, 277, 297
163, 164, 165, 166, 167, 168, 169, 170
mentoring, 81
malnutrition, 109, 124, 126, 128, 129, 130, 131, 140,
messages, 8, 30, 38, 44, 189
141, 142, 143, 145, 147, 149, 150, 345
meta-analysis, 2, 6, 12, 152, 254
management, viii, 16, 67, 78, 87, 88, 89, 93, 98, 102,
metabolic, 34, 63, 89, 90, 91, 124, 128, 131, 217,
120, 122, 135, 141, 142, 143, 146, 148, 149, 153,
227, 236, 348
154, 171, 188, 227, 229, 242, 249, 252, 253, 254,
metabolic alkalosis, 128
260, 273, 274, 277, 285, 290, 292, 296, 305, 308,
metabolic rate, 34, 124, 227
339, 355, 358, 359, 360
metabolism, 123, 124, 129, 223, 233, 234
manipulation, 128
metabolite, 21, 34, 45
marriage, 113
metformin, 235, 254, 255
Maryland, 171
384 Index
microenvironments, 219 motor behavior, 3

middle class, 122 mouth, 235, 241, 333, 335
milk, 132, 197 movement, 58, 71, 73, 78, 79, 284, 297
milligrams, 361 multidimensional, 2, 14, 54
Minnesota, 46, 184, 201, 204, 223, 228, 331 multidisciplinary, x, 73, 87, 91, 98
minorities, 29 multiple factors, 91
minority, 20, 42, 120, 149 multiplicity, 345
minority groups, 42 multivariate, 24, 25, 72
minors, 107 musculoskeletal, 231
mirror, 332 musculoskeletal pain, 231
mobility, 128 music, 285
moclobemide, 354, 365 myopathies, 94
modalities, 75, 102, 106, 235
modality, 106, 115, 123, 248, 292
N
modeling, 30, 219
models, 6, 8, 17, 29, 48, 58, 59, 60, 64, 69, 71, 77,
naming, 7, 54
79, 146, 227, 279, 286, 292, 293, 295, 304, 309,
nasogastric tube, 152
312, 324, 328
National Institutes of Health, 64, 67, 253
moderators, 274
National Research Council, 84
modern society, 8
Native American, 22, 50
modernization, 29
Native Americans, 22
modulation, 214
natural, 60, 66, 110, 153, 173, 184, 199, 292, 311,
modules, 278, 285, 314, 316
325, 327, 328
moieties, 345
natural environment, 311, 327, 328
momentum, 196
nausea, 130, 141, 235, 236, 361
money, 176
negative affectivity, 26
monoamine, 46, 351, 352, 366
negative body image, 31, 64
monoamine oxidase, 351, 352, 366
negative consequences, 173
monoamine oxidase inhibitors, 351, 352
negative emotions, 5, 14, 222, 310, 313, 314, 320
mood, 6, 8, 21, 23, 25, 26, 27, 28, 38, 46, 93, 94, 96,
negative mood, 210, 213, 214, 224, 244, 311, 320
116, 193, 208, 212, 213, 215, 224, 237, 238, 239,
negative reinforcement, 200
240, 241, 242, 285, 297, 308, 310, 311, 326, 327,
neglect, 28, 32, 38, 88, 90, 107, 116, 183, 314
328, 331, 332, 334, 335, 343, 351, 352, 353, 354,
negotiating, 296
355, 359, 360, 361, 364
negotiation, 303
mood change, 208, 212
nervousness, 234
mood disorder, 21, 23, 25, 93, 94, 351, 355
nesting, 292
mood states, 6, 224
network, 278, 291
morale, 105, 265
neurobiological, 2, 64, 310, 355
morbidity, 26, 60, 64, 75, 77, 97, 102, 137, 143, 159,
neurobiology, xi, 184, 307, 361
279, 291, 297, 352
neurochemistry, 20
morning, 92, 222, 223, 280, 283
neuroendocrine, 347
mortality, 2, 12, 58, 97, 128, 137, 143, 172, 177,
neuroimaging, 3, 15, 213, 214, 228
183, 184, 185, 236, 245, 249, 253, 255, 278, 291
neuronal systems, 14, 348
mortality rate, 2, 12, 236, 278
neurons, 344
mothers, 4, 15, 17, 22, 28, 30, 37, 56
neuropeptide, 2, 39
motion, 214, 326, 327
neuropeptides, 2, 3
motivation, 64, 75, 89, 103, 105, 124, 127, 143, 158,
neuropsychological tests, 4
166, 172, 175, 176, 186, 189, 193, 194, 195, 196,
neuroscience, 42, 184, 186, 214
197, 198, 200, 201, 202, 205, 217, 221, 247, 277,
neurotic, 5
283, 286, 298, 316, 329, 345, 363
neuroticism, 5, 26
Index 385
neurotransmitter, 2, 34, 349, 355

O
neurotransmitters, 3, 33, 343
neutropenia, 130
obese, 54, 56, 58, 61, 62, 63, 64, 65, 66, 67, 68, 69,
New England, 249, 255, 349
160, 164, 231, 232, 235, 241, 250, 251, 252, 253,
New Jersey, 12, 289
254, 255, 256, 300, 364
New Mexico, 41
obese patients, 58, 67, 251
New York, 11, 12, 13, 14, 16, 17, 40, 41, 47, 51, 65,
obesity, ix, x, 12, 17, 23, 31, 49, 53, 54, 56, 57, 58,
66, 67, 68, 69, 85, 87, 98, 101, 114, 116, 117,
60, 63, 64, 65, 66, 67, 69, 116, 161, 164, 166,
119, 134, 153, 161, 183, 203, 204, 205, 207, 208,
205, 231, 232, 233, 235, 236, 241, 242, 248, 249,
226, 227, 228, 230, 254, 273, 274, 289, 290, 304,
250, 251, 252, 253, 254, 255, 256, 260, 289, 308
305, 324, 325, 326, 328, 351, 365
obesity prevention, 253
New Zealand, 67, 154, 168, 182, 183, 364
obligations, 103, 202
newsletters, 76
observable behavior, 149
Newton, 172, 178, 184, 185
observations, vii, 54, 72, 160, 172, 199, 249, 271,
next generation, 324
289, 351
Nielsen, 49, 138, 153
obsessive-compulsive, 11, 14, 16, 19, 21, 24, 38, 41,
Nigeria, 9
44, 164, 227, 333, 338
nitrogen, 343
obsessive-compulsive, 16
N-methyl-D-aspartate, 350
obsessive-compulsive disorder, 14, 24, 44, 227, 333
non-clinical, 4, 8, 31
obstruction, 92
non-clinical population, 8, 31
obstructive sleep apnea, 251
non-pharmacological, 209
occupational, 62, 145
non-profit, 81
occupational therapists, 145
non-random, 188, 337
octapeptide, 40, 48
norepinephrine, 234, 326, 333, 343
odds ratio, 22, 28, 31
normal, 1, 3, 20, 23, 24, 29, 32, 34, 46, 48, 54, 63,
Ohio, 275
93, 94, 95, 96, 104, 110, 123, 128, 129, 131, 132,
olanzapine, 332, 337, 338, 339, 346, 347, 348, 349
140, 145, 151, 163, 175, 190, 223, 249, 252, 297,
old age, 138
298, 299, 300, 302, 303, 314, 324, 345, 346, 361,
older adults, 258
366
omission, 57, 198, 260
normal development, 298, 299
online, 66
normalization, 215
openness, 194, 303
norms, 8, 118
operant conditioning, 214
North America, 15, 40, 45, 47, 55, 64, 65, 67, 74, 98,
opioid, 2, 12, 173, 182, 354
99, 117, 134, 135, 185, 256
opioidergic, 173
North Carolina, 163, 231, 250
opioids, 185, 342
Northeast, 184
opposition, 202
novel stimuli, 4
oral, 57, 127, 128, 134, 179, 201, 242, 336, 347
novelty, 21, 26, 160, 343
organ, 119, 122
novelty seeking, 21, 26, 160, 343
organic, 90, 141
Novelty Seeking, 26
organization, xiii, 73, 78, 81, 153, 185, 292
nurse, 179, 360
organizational development, 77
nurses, 145, 277
organizations, 87, 94
nursing, 92, 119, 151, 178
orientation, 6, 14
nurturance, 92
Orlistat, 234, 240, 241, 251, 253, 254, 255
nutrient, 235
orthostatic hypotension, 125, 129, 333, 354
nutrients, 220
osmotic, 95
nutrition, 93, 99, 119, 127, 201, 242, 296, 297, 326
osteoarthritis, 64
nutritional deficiencies, 4
osteopenia, 115, 119, 122, 129, 132, 134, 135
nutritional supplements, 104, 105
osteoporosis, 92, 97, 115, 119, 122, 129, 134, 178
386 Index
outpatient, 37, 45, 57, 73, 89, 90, 91, 92, 94, 95, 97, pathology, 4, 5, 45, 60, 104, 147, 169, 188, 192, 194,
102, 103, 106, 109, 110, 112, 113, 114, 117, 126, 196, 198, 201, 217, 277, 278, 299, 328, 343
137, 141, 142, 143, 144, 146, 147, 149, 150, 151, pathophysiological, 173
161, 163, 164, 165, 166, 175, 188, 190, 194, 202, pathophysiology, 182, 251, 343, 345
261, 279, 300, 332, 343, 349 pathways, 173, 213, 228, 309
outpatients, 6, 110, 144, 177, 209, 333, 335, 338, patient care, xi, 76
346, 354, 355, 356, 358, 360, 366 pediatric, 101, 116
overeating, vii, 54, 57, 61, 62, 64, 214, 220, 233, pediatrician, 92, 93, 300
243, 244, 245 peer, 9, 43, 78, 93, 183, 303
oversight, 82 peer group, 9
overtime, 224 peer support, 93
overweight, 8, 54, 56, 57, 61, 63, 64, 67, 68, 113, peers, 9, 31, 33, 104, 142, 146, 178, 221, 258, 263,
121, 161, 164, 231, 232, 242, 246, 247, 248, 250, 302, 304
251, 252, 254, 256, 274, 300 Pennsylvania, 84
ovulation, 97 peptide, 38
ownership, 212 peptides, 33
perceived control, 36
perception, viii, 7, 37, 43, 75, 116, 122, 194
P
perceptions, 37, 40, 91, 122, 176, 298, 336
perfectionism, 4, 14, 17, 21, 24, 44, 93, 160, 189,
pain, 94, 140, 141, 150, 173, 193, 232, 236, 253,
196, 208, 214, 215, 220, 225, 273, 298, 313, 336
276, 285, 318
performance, 26, 191, 192, 220
Pakistan, 9
pericardial, 129
palliative, 186
pericardial effusion, 129
palliative care, 186
perinatal, 2, 4, 22, 38, 44
palpitations, 97
periodic, 105
pancreatic, 94, 234, 236
peripheral neuropathy, 130
pancreatitis, 125, 126
peristalsis, 130
paradox, 8
permit, 108
paradoxical, 301
personal, 59, 60, 94, 95, 96, 185, 245, 247, 268, 285,
parameter, 159, 160
297, 314
parental authority, 294
personal autonomy, 297
parental control, 36, 296, 298, 299
personal communication, 247
parenteral, 179, 182
personal identity, 185
parenting, 10, 28
personal life, 268
parents, xiii, 28, 30, 37, 43, 56, 67, 88, 91, 113, 114,
personality, 1, 4, 5, 11, 13, 14, 15, 16, 17, 21, 24, 26,
115, 127, 142, 143, 144, 145, 146, 148, 150, 151,
27, 36, 40, 43, 44, 47, 48, 60, 96, 158, 160, 165,
154, 163, 175, 176, 180, 185, 190, 192, 201, 202,
166, 194, 203, 205, 214, 232, 313, 324, 347, 348
232, 264, 268, 269, 291, 293, 295, 296, 297, 298,
personality dimensions, 214
299, 300, 301, 302, 303, 304
personality disorder, 5, 13, 14, 15, 16, 17, 24, 27, 44,
parietal cortex, 344
47, 48, 96, 165, 203, 205, 232, 324
Paris, 50, 65, 67, 167
personality factors, 4
Parkinson, 341
personality traits, 5, 11, 21, 26, 40, 47, 96, 160, 165,
paroxetine, 21, 50
347
partition, 236
persuasion, x, 171, 176, 180
partnership, 83, 166
pessimism, 26
partnerships, 71, 82
PET, 21, 310, 344
passive, 181, 219, 283, 286
PET scan, 310
paternal, 30, 37, 192
pathogenesis, 10, 207, 219, 227
pathological gambling, 166
Index 387
pharmacological, x, xi, 53, 88, 96, 115, 143, 154, population, 2, 5, 9, 22, 32, 44, 46, 49, 52, 56, 57, 59,
216, 231, 232, 331, 345, 351, 352, 355, 356, 361, 60, 95, 118, 138, 148, 149, 153, 157, 158, 162,
362, 363, 364 170, 232, 236, 247, 248, 250, 276, 278, 279, 292,
pharmacological treatment, x, 96, 154, 216, 231, 305, 339, 348, 354, 357
331, 351, 356, 361, 362 positive correlation, 63
pharmacotherapy, 87, 98, 104, 163, 226, 237, 242, positive feedback, 178
253, 254, 331, 332, 343, 345, 357 positive reinforcement, 37
phenomenology, 194 positive relation, 190
phenotype, 11 positive relationship, 190
Philadelphia, 66, 84 positron, 21, 324, 346, 347
philosophy, 277 positron emission tomography, 324, 346, 347
phobia, 25, 167 posttraumatic stress, 26, 40
phone, 181, 245, 287, 318, 321 posttraumatic stress disorder, 26, 40
phosphorous, 105 potassium, 90, 91, 94, 95, 97, 105, 128
phosphorus, 90, 91, 127 poverty, 198
photon, 3, 344, 349 power, 74, 76, 92, 104, 209, 292, 301, 302, 313, 360
physical abuse, 28, 36 pragmatic, 101
physical activity, 157, 243 prediction, 42, 48, 98, 212
physical health, 193, 364 predictors, 11, 25, 33, 42, 135, 184, 260, 295, 362,
physical treatments, 147 365
physicians, 119, 249, 351 predisposing factors, 10, 19, 38
physiological, 51, 89, 102, 103, 106, 142, 143, 175, preference, 124
201, 211, 218, 220, 223, 224, 236, 242, 244, 280 pregnancy, 4, 22, 90
physiological factors, 224 pregnancy test, 90
physiology, 142 pregnant, 192, 258
physiotherapy, 144, 150 pregnant women, 258
pica, 23 prematurity, 4
pig, 223, 225 premium, 29
pilot study, 40, 49, 163, 168, 204, 246, 250, 346, preparation, xiii, 29, 243, 245, 273
349, 367 preparedness, 142, 214
placebo, xi, 60, 61, 134, 234, 235, 237, 238, 239, prepubertal, 169
240, 241, 242, 247, 248, 249, 250, 251, 252, 253, pressure, 17, 50, 72, 104, 125, 160, 171, 172, 174,
254, 294, 331, 333, 334, 335, 336, 338, 340, 341, 178, 181, 219, 265, 266, 268, 269, 271, 299, 310
342, 343, 345, 346, 347, 348, 350, 351, 352, 353, prevention, 64, 67, 72, 73, 95, 98, 104, 152, 164,
354, 355, 356, 357, 358, 359, 360, 361, 362, 364, 180, 204, 218, 227, 229, 242, 245, 247, 251, 316,
365, 366, 367 334, 356, 360, 365
planning, 87, 93, 96, 110, 142, 218, 243, 279, 296, primary care, 250, 268, 360, 367
316, 317, 318, 323 priming, 214
plasma, 35, 40, 51, 334, 337, 346, 350 priorities, 83, 142, 145, 193
plasma levels, 337 privacy, 302
platelet, 21, 50 private, ix, 115, 198
play, 4, 5, 8, 9, 10, 19, 25, 31, 34, 39, 174, 189, 194, private practice, ix
195, 196, 202, 215, 222, 266, 269, 299, 308, 310, probability, 212
339 proband, 21
plurality, viii probands, 21, 50, 61
political, 72 probe, 7, 16
polymorphism, 42 problem behavior, 282
poor, 2, 5, 9, 27, 28, 35, 36, 87, 89, 90, 103, 115, problem solving, 4, 35, 93, 96, 145, 164, 276, 285,
131, 149, 162, 163, 178, 234, 242, 292, 367 292
procedures, 60, 202, 235, 236, 248, 261, 270
388 Index
processing deficits, 12 psychological phenomena, 24

prodromal symptoms, 25, 26, 49 psychological problems, 64, 198
producers, 79 psychological variables, ix
production, 129, 233, 235 psychological well-being, 88, 145
professions, 83 psychologist, 164
progesterone, 134 psychologists, 120, 145, 242, 277
prognosis, 2, 27, 36, 96, 131, 152, 162, 164, 167, psychology, 13, 325
172, 177, 178 psychometric properties, 63, 68
prognostic value, 177 psychopathology, 3, 12, 27, 28, 38, 44, 48, 52, 57,
program, x, 36, 37, 62, 87, 88, 89, 90, 93, 97, 99, 58, 59, 62, 63, 69, 116, 146, 147, 155, 159, 160,
101, 102, 107, 108, 109, 110, 114, 115, 116, 117, 162, 165, 166, 212, 238, 249, 258, 272, 307, 312,
118, 121, 122, 124, 125, 127, 132, 133, 144, 146, 323, 325, 326, 327, 333, 336, 338, 365
150, 152, 154, 155, 164, 165, 168, 176, 179, 190, psychopharmacology, 102, 349
203, 243, 278, 290, 303, 308, 332, 335, 338, 340, psychosis, 42, 109, 125, 126
341, 342, 353, 358 psychosocial, 19, 42, 45, 53, 66, 88, 90, 164, 180,
programming, 288 209, 306, 333, 335, 364
progressive, 103, 209, 284 psycho-social, ix, 38
prolactin, 48, 131, 132, 339, 348 psychosocial factors, 19, 90
proliferation, 68 psychosocial functioning, 66
promote, 8, 9, 28, 78, 80, 81, 82, 83, 104, 146, 165, psychosocial stress, 88
193, 234, 279, 283, 285, 316 psychotherapeutic, 115, 149, 162, 176, 259, 260,
protein, 3, 124, 220, 280 276, 314, 357
protocol, 87, 114, 128, 177, 178, 207, 273, 287, 296, psychotherapy, ix, x, xi, 45, 87, 95, 98, 102, 113,
312, 324, 343 114, 117, 144, 145, 147, 161, 163, 183, 187, 188,
protocols, 6, 79, 88, 103, 200, 293 190, 193, 194, 196, 197, 200, 201, 202, 203, 204,
prototype, vii 205, 210, 220, 221, 227, 228, 233, 249, 256, 257,
proximal, 193 272, 273, 274, 275, 288, 289, 290, 305, 318, 325,
proxy, 143, 278 326, 332, 333, 335, 341, 342, 355, 359, 361, 362,
psychiatric disorder, 22, 23, 40, 41, 44, 46, 51, 52, 363, 365, 367
57, 63, 97, 117, 139, 209, 219, 263, 297, 345, 362 psychotic, 90, 93, 97, 103, 174, 177, 190
psychiatric disorders, 22, 23, 40, 41, 44, 51, 52, 57, psychotic symptoms, 90, 93
63, 97, 117, 139, 219, 263, 297, 345 psychotropic medications, 149
psychiatric hospitals, 131 PTSD, 26, 27, 28, 32, 36, 38, 40, 43
psychiatric illness, 1, 9, 88, 107, 115, 141, 143, 166 pubertal development, 44
psychiatric morbidity, 26, 250 puberty, 31, 45, 47, 138, 140, 142, 143
psychiatric patients, 29 public, 64, 72, 102, 178, 190, 231, 249
psychiatrist, 54, 89, 97, 114, 363 public health, 64, 72, 231, 249
psychiatrists, 89, 114, 120 PubMed, 55
psychiatry, viii, 42, 64, 103, 117, 185, 334 pulse, 89, 125, 126, 132, 150
psychoanalysis, 12, 13 punishment, 222
psychological, ix, 1, 2, 10, 11, 19, 24, 28, 34, 44, 53,
54, 63, 64, 88, 95, 98, 121, 123, 125, 127, 133,
Q
139, 140, 141, 143, 144, 145, 147, 149, 164, 172,
175, 188, 190, 193, 196, 198, 200, 201, 202, 205,
QTc, 91, 339, 348
211, 212, 216, 217, 220, 223, 227, 228, 236, 239,
quality of life, 53, 79, 284, 336, 345, 364
241, 246, 249, 250, 253, 270, 271, 272, 273, 274,
quality of life, 284
292, 298, 305, 312, 324, 327, 338, 342, 347, 351,
Quebec, 346
352, 353, 354, 357, 358, 359, 362, 364
questioning, 300, 308
psychological distress, 143, 146
questionnaire, 178, 253
psychological health, 53
questionnaires, 33, 55, 216
Index 389
quetiapine, 338, 339, 347 reinforcers, 92, 104, 105

rejection, 6
relapse, 5, 13, 15, 36, 50, 105, 106, 114, 135, 164,
R
173, 179, 180, 181, 188, 202, 204, 218, 229, 242,
245, 247, 259, 262, 267, 316, 322, 323, 334, 335,
race, 38, 45, 50, 63
356, 357, 358, 360, 362, 365
radical, 214, 276
relapses, 64, 93, 96, 97, 323
range, ix, 22, 25, 54, 57, 71, 79, 82, 83, 90, 91, 93,
relationship, 8, 12, 14, 18, 23, 24, 27, 28, 31, 34, 41,
96, 102, 106, 108, 110, 121, 138, 142, 175, 187,
44, 48, 50, 51, 52, 56, 57, 63, 64, 68, 81, 82, 96,
188, 189, 192, 194, 198, 238, 239, 240, 242, 248,
113, 116, 128, 151, 163, 166, 191, 193, 194, 195,
270, 297, 298, 313, 335, 337, 339
196, 197, 199, 201, 210, 217, 221, 246, 253, 263,
rape, 27
264, 266, 271, 272, 288, 297, 299, 310, 311, 312,
rating scale, 336, 337, 338
325, 328, 332, 347
ratings, 7, 46, 167, 237, 259, 333, 342, 344
relationships, 8, 10, 39, 41, 43, 44, 47, 64, 79, 108,
rationality, 173
142, 191, 192, 198, 199, 258, 262, 263, 264, 265,
rats, 185
266, 268, 269, 270, 285, 312, 314, 346
reactivity, 26, 51, 353
relatives, 21, 22, 23, 50, 61, 166, 169
reading, 33
relaxation, 305
reality, viii, 123, 125, 149, 174, 194, 213, 276
relevance, 31, 75, 76, 82, 164, 184, 196, 263, 311,
real-time, 311
313, 349, 362
reasoning, 174, 175, 213, 221
religious, 10, 348
rebel, 96
religious belief, 348
recall, 7
religious beliefs, 348
receptor agonist, 352
remission, 15, 60, 237, 238, 241, 242, 248, 294, 299,
receptor sites, 343
356, 357, 360, 361, 362, 364
receptors, 182, 333, 349, 361
renal, 130
reciprocity, 263
repair, 287
recognition, 16, 82, 115, 149, 190, 228, 245, 345
replication, 3, 189, 241
recovery, xi, 4, 6, 13, 14, 15, 17, 18, 21, 34, 37, 39,
representative samples, 56
41, 46, 47, 49, 93, 104, 107, 110, 125, 135, 145,
research, vii, viii, ix, x, xi, 1, 3, 8, 10, 11, 17, 23, 31,
147, 149, 172, 173, 175, 180, 191, 193, 194, 195,
32, 39, 55, 56, 57, 58, 59, 61, 71, 72, 73, 74, 75,
197, 198, 201, 202, 257, 298, 304, 316, 317, 324,
76, 77, 78, 79, 80, 81, 82, 83, 84, 87, 88, 90, 97,
325, 346, 347, 348
101, 106, 110, 115, 137, 139, 146, 152, 154, 156,
recreational, 145
166, 171, 181, 184, 185, 187, 200, 202, 203, 208,
recruiting, 303
231, 242, 247, 248, 253, 258, 261, 271, 272, 278,
red light, 362
279, 284, 287, 290, 291, 293, 307, 308, 309, 310,
reduction, 3, 18, 133, 148, 166, 236, 239, 246, 248,
311, 313, 323, 327, 328, 333, 345, 346, 352, 354,
251, 316, 337, 352, 360, 362, 363
355, 357, 361, 362, 363, 364
refining, 73
Research and Development, 253
reflection, 269, 322
research design, 76, 80, 82
refractory, 177, 337
research funding, 82, 203
regional, 343, 344
researchers, xiii, 5, 6, 26, 62, 64, 71, 72, 73, 74, 75,
regression, 33, 108, 296, 299
76, 77, 79, 80, 81, 83, 84, 138, 209, 215, 275,
regular, 2, 54, 62, 76, 105, 114, 115, 123, 129, 146,
276, 353, 355, 360
150, 197, 217, 266, 280, 297, 300, 301, 319
resection, 94
regulation, 2, 6, 17, 64, 159, 189, 191, 210, 215, 220,
resentment, 301
226, 275, 276, 277, 285, 310, 327, 328, 336
residential, 36, 88, 155, 162, 163, 164, 165, 300
rehabilitation, 3, 92, 98, 113, 119, 122, 123, 124,
resistance, ix, x, 72, 75, 105, 110, 121, 165, 171,
134, 143, 145, 151, 320, 332, 333, 345
175, 179, 180, 184, 218, 312, 319
rehabilitation program, 92, 333
resolution, 30, 191, 193, 196, 199, 202, 265
reinforcement, 184, 211, 222, 287
390 Index
resources, 74, 75, 77, 82, 89, 90, 147 scarcity, 264
respiratory, 235, 255 scheduling, 304
respiratory problems, 235 schema, 7, 8
responsibilities, 96, 201, 269 schemas, 7, 36
responsiveness, 33, 60 schizophrenia, 23, 331, 339, 349
restaurant, 244, 280, 285, 301, 303 Schmid, 254
restaurants, 303 school, 23, 30, 33, 42, 45, 77, 97, 108, 113, 132,
restoration, 88, 89, 91, 92, 97, 105, 110, 114, 115, 135, 141, 144, 145, 150, 151, 168, 181, 190, 191,
123, 129, 143, 147, 174, 180, 184, 189, 190, 194, 192, 200, 232, 268, 303
202, 291, 293, 294, 295, 296, 299, 332, 334, 342, school achievement, 191
348, 350 school performance, 192
restructuring, 93, 164, 166, 218, 245 school work, 145, 190
resuscitation, 140, 143, 144, 150, 151 science, viii, 72, 83, 191, 308, 325, 326, 327, 332
retention, 105, 224, 247, 275, 295, 343 scientific, viii, 55, 59, 76, 84, 101, 145, 237, 249
returns, 224 scientists, 73, 76, 307, 308
rewards, 173, 184, 244, 304 scores, 8, 25, 28, 48, 63, 160, 237, 238, 241, 338,
rhinitis, 356 352, 353, 354, 355, 359, 360
rigidity, 298 scripts, 320
risk, ix, 1, 2, 4, 8, 9, 10, 11, 12, 13, 14, 16, 20, 21, search, 72, 184, 205, 212, 279, 302, 345
22, 23, 24, 25, 26, 27, 29, 30, 31, 32, 36, 43, 44, searching, xi, 345
45, 46, 47, 48, 51, 57, 60, 64, 87, 93, 94, 96, 102, seasonal affective disorder, 362
128, 131, 135, 143, 166, 173, 174, 175, 177, 179, second generation, 332
192, 193, 196, 199, 204, 205, 217, 219, 233, 234, secret, 108
245, 248, 251, 255, 261, 262, 267, 284, 301, 308, sedation, 241, 333, 338, 341, 353, 354
309, 310, 313, 332, 334, 339, 340, 357 seizures, 94, 125, 126, 128, 130, 178, 354, 361
risk factors, ix, 1, 2, 4, 8, 9, 11, 12, 14, 24, 26, 27, selecting, 58, 101
29, 31, 32, 44, 45, 48, 51, 166, 173, 204, 205, selective memory, 7
234, 309 selective serotonin reuptake inhibitor, 237, 351, 352
risks, 44, 89, 143, 174, 201, 249 self, 16, 24, 44, 50, 189, 211, 213, 218, 231, 243,
risperidone, 338, 339, 347 305, 306, 316, 320, 326, 357, 360
road map, x, 71, 73, 77, 80, 81 self esteem, 21, 189
role playing, 78 self monitoring, 280
Rome, 53 self-awareness, 326
routines, 94, 197, 200 self-care, 154, 306
Royal Society, 169 self-concept, 25, 45, 93, 185
RTI International, 250 self-confidence, 93, 180
self-control, 108, 279, 314
self-destructive behavior, 108
S
self-discrepancy, 314
self-doubt, 198
SAD, 362
self-efficacy, 196, 278
sadness, 113, 244, 308
self-enhancement, 15
safeguard, viii
self-esteem, 5, 8, 9, 10, 24, 25, 26, 35, 36, 38, 42, 46,
safety, 110, 351, 352, 354, 355, 356, 357
59, 63, 93, 104, 108, 113, 145, 167, 168, 189,
sample, 3, 7, 8, 14, 21, 24, 25, 28, 30, 31, 41, 44, 45,
190, 192, 196, 198, 204, 207, 208, 209, 211, 214,
47, 49, 52, 56, 57, 58, 59, 67, 139, 152, 156, 157,
215, 219, 220, 246, 258, 259, 265, 272, 273, 308,
168, 169, 188, 189, 260, 294, 307, 310, 311
313
sampling, 311, 327
self-expression, 93
satisfaction, 144, 302
self-help, 148, 149, 210, 252, 261, 294, 352, 360,
saturated fat, 132
366
Scandinavia, 49
Index 391
self-improvement, 80 short-term, 37, 123, 144, 154, 168, 169, 178, 185,
self-management, 164 198, 228, 231, 234, 237, 242, 243, 257, 270, 345,
self-monitoring, 201, 213, 216, 217, 218, 219, 220, 350, 352, 353, 361, 362, 365
244, 246, 279 shy, 332
self-mutilation, 6 shyness, 164
self-regulation, 191 sibling, 107, 192, 303
self-report, 55, 241 siblings, 22, 107, 142, 152, 193, 294, 297, 301, 302,
self-view, 321 303
self-worth, 8, 189, 214, 219 Sibutramine, 234, 240, 242, 251
semantic, 123 side effects, 234, 235, 241, 332, 333, 336, 338, 340,
semantics, 123 342, 345, 351, 353, 354, 357, 359, 360, 361, 362,
sensation, 5, 21, 26, 38, 41 363, 364
sensation seeking, 21, 26, 38, 41 sign, 178, 268
sensations, 6, 28, 224, 244, 284 signals, 236
sensitivity, 35, 173, 185, 304 signs, 91, 93, 96, 113, 127, 132, 280
separation, 59, 71, 301 similarity, 141, 163
sequelae, 362 simulation, 78, 81
sequencing, 203, 212, 362 sites, 50, 106
series, 60, 113, 119, 122, 139, 161, 162, 163, 180, skills, xi, 6, 30, 35, 78, 96, 108, 143, 145, 195, 208,
314, 316, 317, 334, 336, 339 210, 245, 246, 275, 277, 278, 279, 281, 282, 284,
serotonergic, 3, 21, 33 285, 286, 287, 288, 291, 292, 299, 302, 303, 307,
serotonin, 2, 12, 14, 21, 34, 35, 40, 45, 46, 50, 96, 316, 319, 322, 323
234, 310, 324, 326, 327, 333, 334, 343, 346, 348, skills training, 96, 278, 284, 285
349, 352, 355, 367 skin, 178
Serotonin, 46, 237, 326, 346 sleep, 92, 110, 193, 232, 336, 354
sertraline, 237, 239, 251, 253, 355, 360, 364, 366 sleep apnea, 232
serum, 34, 45, 91, 94, 95, 96, 251, 255, 339, 340, sleep disturbance, 92, 354
343, 348 sleeve gastrectomy, 236
serum bicarbonate, 94 small intestine, 235, 236
services, 101, 103, 109, 281 smoking, 205, 235
severity, 28, 34, 59, 60, 61, 62, 66, 69, 97, 102, 106, smoking cessation, 235
115, 121, 125, 139, 140, 164, 170, 177, 203, 232, sobriety, 114
237, 238, 239, 240, 241, 273, 279, 300, 354, 356 social, ix, 4, 5, 9, 11, 17, 19, 21, 25, 27, 28, 29, 31,
sex, 4, 8, 9, 56, 63, 123, 124, 125, 126, 129, 163, 35, 41, 44, 49, 50, 62, 64, 77, 78, 88, 94, 95, 108,
165, 173, 236, 335, 337, 338, 341, 342 120, 139, 145, 172, 175, 190, 191, 192, 197, 198,
sex ratio, 56 201, 216, 219, 222, 232, 242, 244, 246, 258, 259,
sex steroid, 4 263, 277, 292, 299, 311, 314, 316, 325, 327, 336,
sexual abuse, 10, 34, 36, 48, 50, 51, 52, 145 337, 363
sexual assault, 27 social adjustment, 49
sexual behavior, 163 social anxiety, 190
sexually abused, 36 social behavior, 197
shame, 6, 36, 39, 48, 211, 244, 247, 268, 363 social change, 11, 31
shape, vii, 7, 8, 9, 13, 14, 16, 33, 59, 62, 63, 123, social cognition, 325
140, 141, 144, 145, 148, 150, 157, 166, 189, 190, social comparison, 9
196, 204, 207, 208, 209, 211, 212, 213, 214, 215, social competence, 28
216, 219, 220, 238, 244, 246, 258, 262, 267, 270, social contract, 201
272, 277, 287, 298, 299, 308, 317, 332, 363, 365 social development, 139
sharing, xi social environment, 219
short period, 90 social events, 190
short term memory, 145 social factors, 19
392 Index
social group, 219 standard deviation, 129

social information processing, 325 standard operating procedures, 104
social insecurity, 336 standards, 8, 75, 220, 314
social isolation, 35, 191, 363 starvation, 3, 5, 8, 9, 10, 31, 35, 46, 102, 109, 130,
social life, 95, 263 145, 173, 174, 201, 204, 217, 223, 224, 299, 305,
social network, 263 306
social phobia, 4, 25, 41 statistics, 76, 120, 131
social relations, 192 stereotypes, 8
social relationships, 192 sterile, 321
social situations, 244 stigma, 64, 121
social skills, 44, 95 stigmatized, 299
social stress, 88 stimulant, 95
social support, 27, 44, 88, 242, 246 stimulus, 242, 287
social support network, 88 stock, 73
social transition, 29 stomach, 99, 223, 235, 236, 244
social withdrawal, 258, 314 strain, 190
social work, 120, 145, 277 strategic, 198, 266, 271, 292, 293, 298
social workers, 120, 145, 277 strategies, vii, 6, 71, 72, 73, 77, 78, 79, 80, 81, 82,
socially, 132, 150, 172, 190, 191, 303 83, 108, 164, 181, 189, 191, 192, 197, 199, 210,
society, 78 218, 231, 244, 245, 246, 249, 261, 270, 275, 276,
sociocultural, vii, 1, 2, 9, 28, 192, 214, 310 277, 279, 283, 284, 312, 324
socioeconomic, 28, 122 strength, 221
socioeconomic status, 28, 122 stress, 6, 42, 46, 51, 64, 78, 148, 164, 166, 191, 194,
sociological, 8 196, 210, 212, 214, 219, 242, 244, 262, 268, 286,
sodium, 90, 91, 94, 97 327
softener, 92, 95 stressors, 35, 38, 160, 214
software, 77 striatum, 344
solutions, 72, 74, 266, 282 stroke, 251
somatic complaints, 141 structural changes, 83
somatic symptoms, 139, 140 student populations, 77
somatization, 160 students, 8, 30, 42, 43, 48
South Africa, 47, 168 stupor, 126
South Carolina, 19 subgroups, 160, 241, 255, 311
Spain, 154, 155, 156, 164 subjective, 7, 48, 58, 158, 174, 280, 300
specialists, 119 substance abuse, 5, 26, 27, 39, 57, 90, 93, 94, 96,
specificity, 1, 12, 45 103, 109, 143, 173, 216, 258, 298
SPECT, 3, 344, 347 substance use, 24, 27, 28, 35, 64, 109, 173, 174, 355
spectrum, viii, x, 38, 50, 54, 102, 106, 115, 139, 189, suburban, 114, 122
209 success rate, 248
speculation, 222 sucrose, 344
speed, 145 suffering, 9, 88, 203, 264, 275, 284, 288, 292
spine, 132 sugar, 214
sports, 122, 128 suicidal, 6, 94, 97, 103, 114, 125, 126, 153, 174,
spouse, 107, 180, 252 261, 276, 282, 283, 284, 286, 334, 357
stability, 12, 60, 61, 93, 96, 109, 332, 343 suicidal behavior, 153, 261, 286
stabilization, 87, 89, 90, 97, 106, 123, 124, 177 suicidal ideation, 94, 103, 125, 126, 283
stabilize, 235 suicide, 6, 26, 93, 96, 236, 283
stages, 78, 80, 101, 127, 145, 180, 195, 197, 199, summaries, 81
200, 201, 202, 203, 284, 288 summer, 113, 132, 300, 321
stakeholders, 78, 79 superiority, 124, 333
Index 393
supervision, 75, 78, 80 teenagers, 121

supplemental, 216, 362 teens, 149
supplements, 89, 91, 105 telecommunications, 165
supply, 180 telephone, 278, 286, 287, 289
suppression, 310 television, 8, 11, 33, 39, 133, 280, 281
surgeons, 351 temperament, 21, 26, 40, 167, 169, 227, 328
surgery, 66, 67, 99, 233, 236, 248, 249, 252, 253, temporal, 3, 12, 24, 25, 31
254, 255, 256 temporal lobe, 3
surgical, 232, 233, 235, 236, 248, 249, 251 tension, ix, x, 72, 73, 75, 77, 83, 180, 194, 277, 297
surgical intervention, 249 testosterone, 91
surprise, 128, 149, 303 text messaging, 231, 247
survival, 98, 226 theoretical, 2, 6, 49, 51, 77, 144, 187, 189, 266, 277,
susceptibility, vii, 14, 142, 147 283, 293, 324, 333
swallowing, 121 theory, 1, 13, 19, 20, 38, 40, 73, 77, 78, 81, 83, 209,
swelling, 127 242, 244, 270, 273, 276, 278, 289, 292, 309, 312,
switching, 358 325, 326, 327, 328
Switzerland, 18 therapeutic, vii, viii, 43, 55, 101, 104, 114, 115, 144,
symbolic, 193 148, 151, 161, 163, 164, 167, 171, 172, 175, 178,
symmetry, 17 179, 180, 181, 185, 192, 193, 194, 195, 196, 197,
symptomology, 328 201, 219, 221, 242, 244, 247, 271, 276, 277, 278,
syndrome, 9, 20, 27, 48, 54, 58, 61, 62, 66, 68, 69, 287, 288, 298, 312, 316, 320, 332, 333, 343, 358,
119, 121, 122, 124, 126, 127, 134, 135, 138, 177, 367
251, 341 therapeutic approaches, 161, 163
synergistic, 355 therapeutic goal, 181, 276, 288
synthesis, 73, 277, 334, 346 therapeutic interventions, 271
systematic, vii, 66, 81, 115, 117, 118, 152, 154, 166, therapeutic process, 244, 278
167, 169, 229, 250, 254, 261, 293, 306, 367 therapeutic relationship, 193, 194, 195, 287, 298,
systematic review, 66, 81, 117, 118, 152, 154, 166, 312, 316
167, 169, 229, 250, 254, 261, 306, 367 therapeutics, 250
systems, 2, 34, 64, 83, 127, 153, 343 therapists, viii, 64, 154, 193, 194, 195, 197, 198,
systolic blood pressure, 125 199, 200, 201, 202, 210, 267, 268, 277, 278, 286,
292, 298
thinking, 7, 38, 81, 93, 122, 124, 144, 194, 208, 212,
T
213, 214, 215, 218, 219, 220, 224, 225, 233, 242,
243, 265, 267, 268, 270, 271, 309, 334, 337, 346
tactics, 180
threat, 176, 181, 283, 300
tangible, 193
threatened, 89, 191
tardive dyskinesia, 336
threatening, 6, 94, 102, 106, 121, 143, 276, 279, 283,
target behavior, 277, 282
322
targets, 180, 198, 214, 283, 313, 316, 322, 355
threatening behavior, 279, 283
task demands, 297
three-dimensional, 59
task force, 54, 83
three-dimensional model, 59
taste, 350
threshold, 62, 90
taxonomy, 14, 45, 54, 204
thrombocytopenia, 91, 130
teachers, xiii, 77, 145
thyroid, 90, 129, 131, 132
teaching, 6, 76, 96, 140, 179, 210, 275
timing, 31, 32, 44, 145
team members, 286
tissue, 18, 130
technician, 165
title, 55, 198
technological, 247
toddlers, 121
technology, 1, 77, 231, 248, 311
tolerance, 96, 246, 285, 313
Technology Assessment, 250
394 Index
top-down, 71, 72 type 2 diabetes, 57, 64, 235, 247, 254, 255
Topiramate, 239, 253, 367 type 2 diabetes mellitus, 64, 254
total parenteral nutrition, 105
toxic, 37
U
toxicology, 95, 302
trabecular bone, 134
ubiquitous, 9, 37, 79, 180, 189
tradition, 39
UK, 98, 140, 253, 261, 294
training, 17, 71, 75, 76, 77, 78, 80, 82, 87, 95, 184,
ulceration, 236
278, 284, 288, 289
uncertainty, 163, 165, 177, 265
training programs, 82
undergraduate, 8, 9, 30
trait anxiety, 344
uniform, 76
traits, 4, 10, 13, 21, 24, 29, 38, 160, 168, 169, 347
uniformity, vii, 74
transactions, 320
unilateral, 3
transcript, 317, 321
United Kingdom, 107, 118, 153, 177, 184, 247, 257
transfer, 71, 78, 81, 97, 101, 109, 110, 127
United States, 26, 43, 87, 89, 98, 107, 120, 122, 125,
transition, 93, 96, 109, 117, 143, 150, 151, 179, 267,
167, 177, 231, 253
303
univariate, 24, 25
transitions, 10, 210, 261, 264, 265, 297
universality, 72, 83, 164
translation, 71
universities, 30
translational, 81
university students, 30
transmission, 21, 51, 355
urban, 56, 67, 122, 133
transparent, 181
urban population, 56, 67
transportation, 108, 243
urinary, 341
trauma, 11, 12, 13, 26, 27, 28, 40, 50, 52, 96, 193
urine, 91, 92, 95
traumatic experiences, 19, 32, 49
users, 78, 79
treatment methods, 72, 363
treatment programs, 53, 88, 91, 95, 115, 200, 279
treatment-resistant, 44, 186, 350 V
tremor, 340
trend, 158 vacation, 113, 363
trial, viii, 61, 68, 98, 113, 117, 134, 146, 147, 153, validation, 10, 65, 68, 276, 328
154, 188, 204, 227, 228, 229, 237, 250, 251, 252, validity, 27, 58, 59, 60, 63, 66, 80
253, 254, 255, 272, 274, 288, 289, 290, 294, 306, values, 75, 79, 80, 82, 95, 122, 123, 124, 129, 175,
313, 333, 334, 336, 337, 342, 346, 347, 349, 350, 197, 218
353, 354, 356, 357, 358, 359, 360, 361, 365, 366, variability, vii, 58, 161, 311, 313
367 variable, 22, 30, 32, 124, 132, 140, 359
tricyclic antidepressant, 237, 241, 333, 350, 351, variables, 1, 4, 14, 18, 29, 30, 36, 43, 48, 83, 117,
352, 364 165, 236, 308, 309, 312, 313
tricyclic antidepressants, 237, 241, 333, 350, 351, variance, 21, 24
352 variation, 49, 210, 312
triggers, 208, 218, 224, 233, 244, 271, 323 vein, 362
triglycerides, 234 ventricles, 3
trust, 83, 113, 180, 201, 297, 303 ventricular, 91
tryptophan, 41, 46, 49, 50, 52, 310, 326, 334, 346, venue, 76
347, 350 veterans, 169
tuition, 176 victimization, 27, 40, 43
turnover, 103 vignette, 150, 233
twin studies, 2, 24 violence, 42
Twin studies, 21, 42 violent, 36, 49, 300
twins, 25, 26, 29, 31, 44, 60 violent behavior, 300
Index 395
Virginia, 60 Western culture, 9, 20, 37

visible, 104, 185 wheat, 280
visual, 3, 7, 16, 242 white women, 56
visual processing, 3 winter, 23, 365
vitamin D, 129 wisdom, xi, 21, 59
vitamins, 236 withdrawal, 114, 342
vocabulary, 198 witness, viii
voice, 266, 303 women, 8, 9, 11, 12, 14, 15, 16, 20, 21, 22, 23, 25,
vomiting, vii, 5, 22, 23, 32, 33, 91, 94, 95, 121, 122, 30, 32, 36, 37, 40, 41, 42, 44, 46, 47, 48, 49, 50,
127, 128, 130, 131, 132, 139, 140, 141, 165, 173, 51, 52, 54, 56, 57, 58, 60, 61, 62, 63, 65, 66, 67,
178, 207, 208, 211, 214, 217, 220, 223, 236, 268, 68, 120, 138, 155, 157, 158, 161, 164, 165, 167,
270, 277, 284, 300, 303, 308, 327, 353, 354, 355, 170, 185, 188, 229, 232, 235, 237, 246, 250, 252,
356, 357, 358, 359, 360, 361, 363 255, 260, 274, 326, 327, 328, 344, 346, 348, 350,
vulnerability, 2, 19, 20, 21, 24, 36, 38, 173, 190, 353, 359, 360, 362, 365, 366
214, 277, 282 workers, 78, 224
World Health Organization (WHO), 54, 64, 69, 69
World War, 126, 201, 223
W
worry, 222
writing, 7, 81, 115, 284
walking, 233, 244
war, 150
warrants, 63, 235, 361 X
Washington, 11, 39, 65, 70, 84, 85, 98, 117, 133,
185, 205, 273, 288, 290, 325, 326, 327, 328 x-ray, 95, 129
water, 88, 92, 97, 128, 224 x-rays, 95
Watson, 174, 177, 178, 181, 186, 197, 205, 212, 308,
328, 336, 348
Y
weakness, 94
wealth, 281
yes/no, 248
weight changes, 127, 170
yield, 31
weight control, vii, 33, 53, 57, 67, 122, 157, 189,
yogurt, 197
217, 242, 243, 244, 245, 253, 309
young adults, x, 51, 119, 120, 122, 123, 133, 134,
weight gain, 3, 31, 37, 57, 91, 92, 104, 105, 106,
149, 152, 334, 357
111, 114, 116, 121, 122, 124, 127, 130, 132, 139,
young men, 169
140, 144, 145, 146, 147, 167, 174, 175, 176, 179,
young women, 9, 11, 16, 17, 20, 50, 59, 66, 101,
180, 181, 190, 193, 202, 214, 219, 220, 222, 232,
120, 134, 138, 153, 198
238, 242, 295, 297, 299, 300, 302, 308, 331, 332,
younger children, 138, 140
333, 334, 335, 336, 337, 338, 340, 342, 343, 345,
346, 347
weight loss, 19, 29, 31, 37, 38, 39, 53, 56, 58, 63, 69, Z
89, 90, 103, 104, 105, 113, 121, 125, 129, 130,
132, 133, 138, 140, 141, 142, 150, 163, 192, 201, Zen, 277
202, 214, 233, 234, 235, 237, 238, 240, 241, 242, Zimbabwe, 45
243, 244, 245, 246, 247, 248, 249, 251, 252, 253, zinc, 340, 341, 342, 346, 348
254, 255, 256, 300 ziprasidone, 339
weight management, 63, 66, 217, 242, 243, 245, 291,
308
weight reduction, 14
weight status, 334
well-being, 144, 232, 236
Western countries, 62

Ida F. Dancyger, Ida F. Dancyger, Victor M. Fornari - Evidence Based Treatments For Eating Disorders - Children, Adolescents, and Adults-Nova Kroshka Books (2009)

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EVIDENCE-BASED TREATMENTS FOR

EATING DISORDERS: CHILDREN,

IDA F. DANCYGER AND

Nova Science Publishers, Inc.

NOTICE TO THE READER

Library of Congress Cataloging-in-Publication Data

Published by Nova Science Publishers, Inc.  New York

Foreword A Book Reflecting the Kaleidoscopic Nature of the Treatment of

Chapter VIII Evidence-Informed Care of Children with Eating Disorders 137

A Book Reflecting the Kaleidoscopic

Interpersonal psychotherapy to treat patients with EDs is described by Murphy, Straebler,

Judith D. Banker, MA, LLP, FAED

Dara Bellace, PhD

Devra Lynn Braun, MD

Timothy D. Brewerton, MD, DFAPA, FAED

Amanda Joelle Brown, BA

Kimberly A. Brownley, PhD

Cynthia M. Bulik, PhD

Zafra Cooper, DPhil, DipPsych

Janelle W. Coughlin, PhD

Ida F. Dancyger, PhD

Scott G. Engel, PhD

Christopher G. Fairburn, DM, FMedSci, FRCPsych

Anita Federici, MSc

Fernando Fernández-Aranda, PhD, FAED

Kathleen Kara Fitzpatrick, PhD

Susana Jiménez-Murcia, PhD

Allan S. Kaplan, MD FRCP(C)

Kelly L. Klump, PhD, FAED

James Lock, MD, PhD

Sloane Madden, MB BS (Hons) FRANZCP

Rebecca Murphy, DClinPsych

Kathleen M. Pike, PhD

James D. Roerig, PharmD, BCPP

Jennifer Shapiro, PhD

Kristine Steffen, PharmD

Suzanne Straebler, APRN-Psychiatry, MSN

Walter Vandereycken, MD, PhD

Mark Warren, MD, MPH

Lucene Wisniewski, PhD, FAED

Steve A. Wonderlich, PhD

Overview of the Biopsychosocial Risk

Anita Federici1 and Allan S. Kaplan2

Changes in Brain Structure/Cerebral Blood Flow

Prenatal and Perinatal Factors

II. Psychological Factors

Cognitive models have been particularly influential in providing a theoretical framework

result of core disturbances in thinking, perception, and memory. Individuals with AN

Family Systems and Environmental Risk Factors

Overview of Evidence on the

Predisposing Biological Underpinnings

Gender is an indisputable characteristic of BN. One of the most consistent findings in

Trait-Related Biological Differences

Biological differences that appear to be related to specific personality traits linked to BN

Ethnicity and Race

Published by Nova Science Publishers, Inc.  New York