P h a r m a c o l o g i c Tre a t m e n t o f

Eating D isorders
a,b,
Scott J. Crow, MD *

KEYWORDS
 Eating disorders  Anorexia nervosa  Bulimia nervosa  Binge eating disorder
 Medication  Fluoxetine

KEY POINTS
 Medication plays a very limited role in the treatment of anorexia nervosa.
 Numerous antidepressants can be used to treat bulimia nervosa.
 High-dose fluoxetine (ie, 60 mg/d) is the standard of care medication approach for BN.
 Numerous medications can treat binge eating disorder but tend to bring little change in
weight.

INTRODUCTION

Psychopharmacologic agents can play an important role in the treatment of eating

disorders. However, the role of medication treatment of eating disorders differs
from that seen in other areas of psychiatric treatment. Medications are a key treatment
approach for many psychiatric illnesses (for example, schizophrenia or bipolar illness).
However, they do not play this same role in eating disorders. Generally, medications
follow in importance behind nutritional approaches and psychotherapy. Nonetheless,
there is a longstanding, fairly substantial literature on the impact of medications for
various eating disorder symptoms. Furthermore, there is evidence, at least for bulimia
nervosa (BN), that including medication early in the treatment algorithm in a stepped
care approach may be cost-effective.1
The role of medication varies considerably by eating disorder diagnosis. Carefully
conducted studies examining the impact of medications on anorexia nervosa (AN)
and BN date back to the 1980s, and, in more recent years, the use of medications
for binge eating disorder (BED) has been an active area of inquiry. In the case of BN
and BED, a U.S. Food and Drug Administration (FDA)-approved medication exists
for each, with many other studies showing benefit for a wide variety of other medica-
tions. The treatment of AN differs; the degree of benefit shown in most studies to date
has been quite limited.

Disclosure Statement: None.

a
Department of Psychiatry, University of Minnesota, F282/2A West, 2450 Riverside Avenue,
Minneapolis, MN 55434, USA; b The Emily Program, St Paul, MN 55108, USA
* F282/2A West, 2450 Riverside Avenue, Minneapolis, MN 55454.
E-mail address: crowx002@umn.edu

Psychiatr Clin N Am - (2019) -–-

https://doi.org/10.1016/j.psc.2019.01.007 psych.theclinics.com
0193-953X/19/ª 2019 Elsevier Inc. All rights reserved.
2 Crow

This article reviews the existing literature on medication treatment of AN, BN, and
BED. Options, goals for treatment, and general strategy are examined. The potential
impact of medications on avoidant/restrictive food intake disorder (ARFID) and other
specified eating disorders (OSFED) are also briefly discussed.

GENERAL CONSIDERATIONS AND STRATEGY

When to Consider Medication Treatment
There are several instances in which medication treatment should be considered for
the management of people who have eating disorders. First, medications should
be considered when other treatments (particularly psychotherapy) have not worked
well enough.
Second, medications can be uniquely valuable when geography limits access to
specialized treatment. In many regions, travel of at least several hours is needed to
reach a clinician who can provide specialized eating disorder-focused psychotherapy.
By contrast, pharmacies are nearly everywhere, and medications are readily available
via mail-order pharmacy. Moreover, psychiatrists and primary care providers providing
medication treatment are far more widely distributed than are eating disorder specialist
psychotherapists. These factors render medications to be more widely accessible in
certain areas.
Third, comorbidity is a consideration (particularly mood and anxiety disorders). One
caveat to consider, although, is that successful treatment of eating disorder symp-
toms may relieve comorbid mood and anxiety. This is especially true for weight resto-
ration and AN. For this reason, when weight restoration is ongoing, watchful waiting to
see the extent to which mood and anxiety symptoms resolve is quite defensible. On
the other hand, persistent, mood and anxiety syndromes do co-occur with AN, BN,
and BED, and these may benefit from medications.
Last is the issue of patient choice. People seeking treatment often have specific
views about which treatments they would prefer to receive. Many people prefer psy-
chotherapy, but, for some, medication treatment may feel preferable.

Goals
The general goals of medication treatment deserve careful consideration. In other psy-
chiatric illnesses, various concepts of treatment response are seen. For example,
sometimes syndromal remission of the psychopathology is the goal. Examples would
probably include major depression or panic disorder. In other instances, reduction of
symptoms without full syndromal remission would be the goal; an example would be
medication treatment of schizophrenia. Still another possibility would be the goal of
preventing recurrence, as could be the case in bipolar illness.
Complicating the consideration of goals of pharmacologic treatment of eating dis-
orders, most psychopharmacology studies in eating disorders have involved acute
treatment, typically not lasting beyond 8 or 12 weeks. There is limited work on relapse
prevention in AN, which will be reviewed, and one study attempting to look at long-
term treatment of BN, but, for the most part, the duration of treatment in the existing
literature falls far short of the a typical course of clinical treatment. Given this, longer-
term treatment must proceed with little guiding evidence base.
The likely goals of medication use in AN should be symptom reduction, and perhaps
as a strategy to facilitate other types of treatments. Abstinence seems a reasonable
treatment goal in the treatment of BN and BED, which is seen in a ministry of partic-
ipants in many published studies. On the other hand, there is some reason to think that
this may not usually be full syndromal remission: most studies that have assessed
 Pharmacologic Treatment of Eating Disorders 3

eating behaviors and eating disorder cognitions have found that, when abstinence
from binge eating and purging is achieved, significant eating disorder cognitions
remain, at least in the short term.
Duration of Treatment
The appropriate duration of medication treatment of eating disorders is unknown and
largely untested. A reasonable guide might be the model often used in the treatment of
major depression, in which the goal of a year of stability followed by a slow taper with
careful monitoring is a reasonable and commonly used clinically strategy.

ANOREXIA NERVOSA

The list of agents that have been tried for the treatment of AN is unusually broad
(Table 1). This reflects the fact that AN has been largely nonresponsive to medication
treatments (and, of course, not highly responsive to other treatments as well, at least in
adults). The list includes medications no longer widely used in general psychiatric
practice (for example, tricyclic antidepressants or typical antipsychotic medications).
Furthermore, it includes medications not easily managed in, or tolerated by, individ-
uals at low weight who are prone to dehydration (for example, lithium2 or clonidine3).
Interestingly, tetrahydrocannabinol was examined in a randomized, controlled trial
and did not seem to be beneficial.4 Presently, marijuana-related compounds are
increasingly used for many conditions, but it is important to note that the use of
tetrahydrocannabinol for AN long predates the recent interest in marijuana as a
medical treatment; this should be interpreted as reflecting the challenge inherent in
treating AN.
It is worth reviewing several specific medications in this regard. First, there has been
substantial interest in the role of altered serotonin neurotransmission in the patho-
physiology of AN.5 In keeping with this interest, several trials have examined the
use of fluoxetine. These include acute treatment trials6 in which treatment does not
seem to be beneficial. One might imagine that this represents nutritional lack of sero-
tonin precursors, but Barbarich and colleagues7 found that co-administration of
tryptophan, a precursor to serotonin synthesis, did not potentiate fluoxetine effects.
There has also been interest in the use of fluoxetine as a relapse prevention agent.
An open trial showed no benefit,8 but the first large prospective trial suggested
some benefit of fluoxetine.9 Subsequently, a more definitive multicenter trial using

Table 1
Medications studied in blinded, controlled for AN

Positive
Trial Negative Trial
Olanzapine Pimozide
Sulpiride
Cisapride
Clonidine
Zinc
Tetrahydrocannabinol
Lithium
Cyproheptadine
Amitriptyline
Clomipramine
Nortriptyline
Fluoxetine
4 Crow

fluoxetine as a relapse prevention strategy in AN relapse prevention was conducted.10

This study enrolled 120 participants, who received up to 60 mg of fluoxetine per
day for a year after first achieving a body mass index of at least 19. Placebo and
active medication did not differ in preventing relapse; thus, it seems that selective se-
rotonin reuptake inhibitors (SSRIs) are not effective for AN. It is possible that there may
be selected subgroups that benefit, but these have not been identified in the
completed trials.
The second area of recent interest in medication treatment of AN involves atypical
antipsychotics. A recent multicenter trial examined the use of olanzapine in acute treat-
ment of AN.11 This study of 152 people with AN showed about 1 lb per month greater
weight gain in the olanzapine group. This benefit may be sufficient to justify the use of
olanzapine. In considering these medications, one must consider the potential risks,
including tardive dyskinesia and neuroleptic malignant syndrome, versus the potential
benefits of accelerated weight restoration. Certainly, patient acceptance of this medica-
tion, given its potential for weight gain, is a challenge in using it in this population.
Interestingly, Attia12 have reported that the elevations in lipids and impairments in
glucose tolerance seen in other patient populations (for example, those with schizo-
phrenia or bipolar illness), do not seem to occur in people with AN. At this time, it is un-
clear whether this reflects the unique nutritional status of those with anorexia nervosa,
or represents a different metabolic profile in those with AN, suggested by recent work.13

BULIMIA NERVOSA

As in AN, many studies have looked at medication treatments for BN over the last few
decades. Unlike AN, medications seem to be effective in treating BN (Box 1). The first
medication approved by the FDA for treatment of an eating disorder was fluoxetine
used for treatment of BN.
Early work in this area was often based on alternative conceptualizations of BN
causation and maintenance. At one point, anticonvulsants were used extensively,
reflecting the possibility that the cause of BN was an underlying seizure disorder.14
Subsequently, it was argued that BN might be a manifestation of a mood disorder.15
This led to extensive work with antidepressants. Although BN is no longer thought to
be a mood disorder variant, because of the efficacy shown by initial antidepressant
studies, this work has continued.

Box 1
Medications shown to have efficacy for BN

Fluoxetine
Fluvoxamine
Citalopram
Sertraline
Amitriptyline
Imipramine
Desipramine
Trazodone
Phenelzine
Topiramate
 Pharmacologic Treatment of Eating Disorders 5

Two studies of fluoxetine have led it to be the most-often considered medication for
BN in the treatment of bulimia nervosa. In this instance, there have been 2 large studies
conducted, and these contributed to a great degree to a decision made by the FDA to
approve fluoxetine for the treatment of BN. One of these studies compared 60 mg
fluoxetine with placebo in 482 people16 for 16 weeks. The other was a 3-cell design
with participants randomized to receive either 60 mg/d of fluoxetine, 20 mg/d of fluox-
etine, or placebo.17 In this study with 387 participants, substantial improvements
were seen in binge eating and purging, and substantial rates of abstinence from binge
eating at the end of treatment were described. Sixty mg was clearly more effective
than 20 mg; 20 mg was more effective than placebo on some outcomes but not
others. This has led to the widespread recommendation of fluoxetine as a starting
point of pharmacologic treatment of BN. Furthermore, it is led to the recommendation
for high-dose (ie, 60 or 80 mg) fluoxetine treatment. In at least one instance, a sequen-
tial treatment approach initiated medication treatment with 60 mg/d.18 In that study,
the 60-mg starting dose was actually quite well tolerated. However, it seems likely
that some would respond to lower doses if doses were titrated, and that some
individuals would be likely not to tolerate 60 mg, so typically clinical practice involves
starting at 20 mg with the anticipation that titration to a relatively high dose will likely
be necessary.

Alternative Medication Treatments for Bulimia Nervosa

A wide variety of alternative treatments have been studied and been shown to be
effective. There is support in the literature for the use of other SSRIs, and they typically
represent a second line of treatment. One caveat in this regard, however, is that the
FDA has recognized concerns about prolonged QTc in individuals receiving high
doses of citalopram.19 Given the probable need for high doses of SSRIs for good
response, this limits citalopram (and perhaps escitalopram) for BN treatment.
There is a remarkably deep literature on the use of tricyclic antidepressants for BN.
This spans work using amitriptyline and desipramine, primarily, with several extensive
studies examining desipramine.20–23 Among these, desipramine seems the logical
choice. Desipramine has less anticholinergic side effects, less cardiac effects, less
sedation, and is less likely to induce weight gain than other tricyclics. Furthermore,
there is an ample literature supporting its use in BN. Last, standardized blood levels
are available for depression (which one assumes would generalize to the treatment
of BN, although this is not fully clear).
Trazodone represents an alternative treatment, supported in other trials, although
sedation and orthostasis may limit its use somewhat.24 Monoamine oxidase
(MAO) inhibitors can be used, as noted above.25,26 Finally, topiramate has been
examined in one trial and has been shown to decrease binge eating and purging,
although significant weight loss occurred.27 This may limit its use in BN in patients
with a low-normal weight, and certainly in patients with a history of sub-normal
weight or AN.

Contraindications
Bupropion is contraindicated in the treatment of BN because of an elevated risk for
seizures that was identified in the one study of bupropion that has been conducted
in this area.28 Questions are often raised about whether MAO inhibitors are contrain-
dicated, related to the possibility of dietary violations of a low-tyramine diet leading to
hypertensive crises. This has not been observed in clinical trials of MAO inhibitors
for BN, and in clinical practice it seems to be rare. On the other hand, the introduction
of a low-tyramine diet provides dietary limitations and rules for a group of individuals
6 Crow

who generally have an excessive number of dietary rules to begin with, so this is a
limitation.

BINGE EATING DISORDER

Treatment Goals
The main treatment goal for BED is cessation of binge eating. The other psychological
components of BED enumerated in DSM-5 are also reasonable treatment goals, but
tend to receive less emphasis than diminishment or elimination of binge eating. A sec-
ond treatment goal involves weight loss. This remains a somewhat controversial issue
within the eating disorders field, and is sometimes less of a treatment focus for pro-
viders. On the other hand, it tends to be at least as important to many individuals
with BEDs as the cessation of binge eating itself. It is important to clarify the extent
to which this is a treatment goal, and to clearly lay out the expectations the patient
may have and the expectations that may be reasonable to achieve based on the exist-
ing literature, as these may be quite different.
Agents Studied
Treatment development for BED initially mirrored the path seen in BN. Initial studies
examined tricyclic antidepressants and then moved on to SSRIs. Much of this work
for a long time has focused on antidepressant medications, and at this point an even
wider array of antidepressants has been examined in controlled studies for BED than
for BN (Box 2). These include trials of fluoxetine,29 fluvoxamine,30 citalopram,31 escita-
lopram,32 bupropion,33 duloxetine,34 lamotrigine,35 sertraline,36 and atomoxetine.37
Most of these studies have been positive, showing greater decrease in binge eating
symptoms and/or greater levels of abstinence in binge eating after treatment in those
receiving medications compared with those receiving placebo. An important aspect
of these medication trials, however, has been that the major effect has been on binge
eating. The overall rates of binge eating tend to decrease fairly markedly, and a signif-
icant minority of people receiving medication treatment are abstinent from binge eating
at the end of short-term treatment (although, as in BN, little is known about the long-
term course). Weight loss with antidepressant medications has not typically been
seen, even when major reductions or abstinence from binge eating has been achieved.

Box 2
Medications shown to have efficacy for BED

Fluoxetine
Fluvoxamine
Citalopram
Escitalopram
Sertraline
Duloxetine
Bupropion
Lamotrigine
Topiramate
Zonisamide
Lisdexamfetamine
 Pharmacologic Treatment of Eating Disorders 7

A new direction in binge eating pharmacotherapy, partially driven by concerns

about a need for weight loss, has been the examination of medications that have
direct or indirect effects on appetite. For example, the agent fenfluramine, previ-
ously used for weight loss but now taken off the market because of concerns
about heart valve lesions, was examined and shown to diminish binge eating
(although curiously, not to cause weight loss).38 Subsequently, sibutramine was
studied in several trials39,40 and clearly can diminish binge eating and cause weight
loss, but it too has been removed from the market because of concerns about
elevated blood pressure. The anticonvulsant agents topiramate41–43 and zonisa-
mide44 have also been examined, as each have been noted to diminish appetite;
this was seen as a side-effect in many anticonvulsant trials, but in this instance
is viewed as a desired treatment effect. Treatment with these agents does lead
to significant decreases in BED, and does lead to modest, persisting weight loss;
this has been particularly clear in the case of topiramate. There is one longer-
term study with topiramate43 that suggests that there is persisting effect on binge
eating symptoms.
Finally, the most recent effort in regard to medication treatments for BED has been a
series of studies involving lisdexamfetamine.45–47 In this regard, several large studies
have shown clear evidence of impact on binge eating, with modest impacts on weight.
Numerically, the magnitude of clinical response in these studies seems similar to
that seen with other BED medication treatments. These studies have led to FDA
indication for the use of lisdexamfetamine in the treatment of BED.

AVOIDANT/RESTRICTIVE FOOD INTAKE DISORDER

With the advent of DSM-5, ARFID has received increasing attention. However, behav-
ioral treatments for ARFID in general are only now being worked out,48 and appro-
priate medication treatments are not at all clear. Gray and colleagues49 recently
described a case series of 14 individuals receiving mirtazapine (6 as monotherapy,
8 as combination therapy). This study was uncontrolled, so the impacts attributable
to mirtazapine treatment are not completely clear, but the authors note that the rate
of weight gain exceeded that typically seen in their treatment-as-usual ARFID pro-
gram. They hypothesize that mirtazapine could be beneficial because it increases
appetite, causes weight gain, diminishes nausea and vomiting, and increases rates
of gastric emptying.
Clearly, continued medication development in this area is needed. Our understand-
ing of the underlying psychopathology process in ARFID is growing50 and this may
help guide pharmacologic treatment development.

OTHER SPECIFIED FEEDING OR EATING DISORDER

There currently exist no data on medication treatments for OSFED, including sub-
threshold AN, subthreshold BN, or purging disorder. Clearly development of such
treatments is needed; observational studies of people receiving treatment for OSFED
suggest that remission rates are relatively limited.51 This highlights the need for devel-
opment of new and effective treatments, and certainly raises the possibility that med-
ications may play a role. In clinical practice decisions about medications are
commonly made on a symptom-by-symptom basis, assuming that responses are
relatively similar to those seen in similar symptom presentations. So, for example,
medication strategies seen to be helpful for BN are often used in the treatment of purg-
ing disorder. Similarly, what we know about medication treatments for AN is presumed
by many clinicians to apply to subthreshold AN.
8 Crow

SUMMARY

Medications, at present, play a limited role in treatment of AN, although there is current
interest in the potential utility of atypical antipsychotics. A wide variety of medications,
primarily antidepressants, can be beneficial in BN. Antidepressants are also poten-
tially useful for BED symptoms, and medications that suppress appetite can diminish
or eliminate binge eating as well. The only 2 FDA-approved medications for eating
disorder treatments at present are fluoxetine for BN, and lisdexamfetamine for BED.
This remains an area of active research interest, and one in which substantial further
development is needed.

REFERENCES

1. Crow SJ, Agras WS, Halmi KA, et al. A cost effectiveness analysis of stepped
care treatment for bulimia nervosa. Int J Eat Disord 2013;46(4):302–7.
2. Gross H, Ebert MH, Faden VB, et al. A double-blind trial of delta 9-tetrahydrocan-
nabinol in primary anorexia nervosa. J Clin Psychopharmacol 1983;3(3):165–71.
3. Casper RC, Schlemmer RF Jr, Javaid JI. A placebo-controlled crossover study of
oral clonidine in acute anorexia nervosa. Psychiatry Res 1987;20(3):249–60.
4. Gross HA, Ebert MH, Faden VB, et al. A double-blind controlled trial of lithium
carbonate primary anorexia nervosa. J Clin Psychopharmacol 1981;1(6):
376–81.
5. Kaye WH, Wierenga CE, Bailer UF, et al. Nothing tastes as good as skinny feels:
the neurobiology of anorexia nervosa. Trends Neurosci 2013;36(2):110–20.
6. Attia E, Haiman C, Walsh BT, et al. Does fluoxetine augment the inpatient treat-
ment of anorexia nervosa? Am J Psychiatry 1998;155(4):548–51.
7. Barbarich NC, McConaha CW, Halmi KA, et al. Use of nutritional supplements to
increase the efficacy of fluoxetine in the treatment of anorexia nervosa. Int J Eat
Disord 2004;35(1):10–5.
8. Strober M, Freeman R, DeAntonio M, et al. Does adjunctive fluoxetine influence
the post-hospital course of restrictor-type anorexia nervosa? A 24-month pro-
spective, longitudinal followup and comparison with historical controls. Psycho-
pharmacol Bull 1997;33(3):425–31.
9. Kaye WH, Nagata T, Weltzin TE, et al. Double-blind placebo-controlled adminis-
tration of fluoxetine in restricting- and restricting-purging-type anorexia nervosa.
Biol Psychiatry 2001;49(7):644–52.
10. Walsh BT, Kaplan AS, Attia E, et al. Fluoxetine after weight restoration in anorexia
nervosa: a randomized controlled trial. JAMA 2006;295(22):2605–12.
11. Attia E. Presentation at the Eating Disorders Research Society annual meeting.
New York: 2016.
12. Attia E. Presented at the Eating Disorder Research Society annual meeting.
Sydney (Australia): 2018.
13. Duncan L, Yilmaz Z, Gaspar H, et al. Significant locus and metabolic genetic
correlations revealed in genome-wide association study of anorexia nervosa.
Am J Psychiatry 2017;174(9):850–8.
14. Wermuth BM, Davis KL, Hollister LE, et al. Phenytoin treatment of the binge-
eating syndrome. Am J Psychiatry 1977;134(11):1249–53.
15. Pope HG Jr, Hudson JI. Antidepressant drug therapy for bulimia: current status.
J Clin Psychiatry 1986;47(7):339–45.
16. Goldstein DJ, Wilson MG, Thompson VL, et al. Long-term fluoxetine treatment of
bulimia nervosa. Fluoxetine Bulimia Nervosa Research Group. Br J Psychiatry
1995;166(5):660–6.
 Pharmacologic Treatment of Eating Disorders 9

17. FBNC Study Group. Fluoxetine in the treatment of bulimia nervosa. A multicenter,
placebo-controlled, double-blind trial. Fluoxetine Bulimia Nervosa Collaborative
Study Group. Arch Gen Psychiatry 1992;49(2):139–47.
18. Mitchell JE, Agras WS, Wilson GT, et al. A trial of a relapse prevention strategy in
women with bulimia nervosa who respond to cognitive-behavior therapy. Int J Eat
Disord 2004;35(4):549–55.
19. U.S. Food and Drug Administration. FDA drug safety communication: revised rec-
ommendations for Celexa (citaloprm hydrobromide) related to a potential risk of
abnormal heart rhythms with high doses. 2012. Available at: https://www.fda.
gov/Drugs/DrugSafety/ucm297391.htm. Accessed December 1, 2018.
20. Barlow J, Blouin J, Blouin A, et al. Treatment of bulimia with desipramine: a
double-blind crossover study. Can J Psychiatry 1988;33(2):129–33.
21. Hughes PL, Wells LA, Cunningham CJ, et al. Treating bulimia with desipramine.
A double-blind, placebo-controlled study. Arch Gen Psychiatry 1986;43(2):
182–6.
22. McCann UD, Agras WS. Successful treatment of nonpurging bulimia nervosa with
desipramine: a double-blind, placebo-controlled study. Am J Psychiatry 1990;
147(11):1509–13.
23. Walsh BT, Hadigan CM, Devlin MJ, et al. Long-term outcome of antidepressant
treatment for bulimia nervosa. Am J Psychiatry 1991;148(9):1206–12.
24. Pope HG Jr, Keck PE Jr, McElroy SL, et al. A placebo-controlled study of trazo-
done in bulimia nervosa. J Clin Psychopharmacol 1989;9(4):254–9.
25. Kennedy SH, Piran N, Garfinkel PE. Monoamine oxidase inhibitor therapy for
anorexia nervosa and bulimia: a preliminary trial of isocarboxazid. J Clin Psycho-
pharmacol 1985;5(5):279–85.
26. Walsh BT, Gladis M, Roose SP, et al. Phenelzine vs. placebo in 50 patients with
bulimia. Arch Gen Psychiatry 1988;45(5):471–5.
27. Hoopes SP, Reimherr FW, Hedges DW, et al. Treatment of bulimia nervosa
with topiramate in a randomized, double-blind, placebo-controlled trial, part 1:
improvement in binge and purge measures. J Clin Psychiatry 2003;64(11):
1335–41.
28. Horne RL, Ferguson JM, Pope HG Jr, et al. Treatment of bulimia with bupropion: a
multicenter controlled trial. J Clin Psychiatry 1988;49(7):262–6.
29. Arnold LM, McElroy SL, Hudson JI, et al. A placebo-controlled, randomized trial
of fluoxetine in the treatment of binge-eating disorder. J Clin Psychiatry 2002;
63(11):1028–33.
30. Hudson JI, McElroy SL, Raymond NC, et al. Fluvoxamine in the treatment of
binge-eating disorder: a multicenter placebo-controlled, double-blind trial. Am
J Psychiatry 1998;155(12):1756–62.
31. Merikangas K, Avenevoli S, Costello J, et al. National comorbidity survey replica-
tion adolescent supplement (NCS-A): I. Background and measures. J Am Acad
Child Adolesc Psychiatry 2009;48(4):367–9.
32. Guerdjikova AI, McElroy SL, Kotwal R, et al. High-dose escitalopram in the treat-
ment of binge-eating disorder with obesity: a placebo-controlled monotherapy
trial. Hum Psychopharmacol 2008;23(1):1–11.
33. White MA, Grilo CM. Bupropion for overweight women with binge-eating disorder:
a randomized, double-blind, placebo-controlled trial. J Clin Psychiatry 2013;
74(4):400–6.
34. Guerdjikova AI, McElroy SL, Winstanley EL, et al. Duloxetine in the treatment of
binge eating disorder with depressive disorders: a placebo-controlled trial. Int
J Eat Disord 2012;45(2):281–9.
10 Crow

35. Guerdjikova AI, McElroy SL, Welge JA, et al. Lamotrigine in the treatment of
binge-eating disorder with obesity: a randomized, placebo-controlled monother-
apy trial. Int Clin Psychopharmacol 2009;24(3):150–8.
36. McElroy SL, Casuto LS, Nelson EB, et al. Placebo-controlled trial of sertraline in
the treatment of binge eating disorder. Am J Psychiatry 2000;157(6):1004–6.
37. McElroy SL, Guerdjikova A, Kotwal R, et al. Atomoxetine in the treatment of binge-
eating disorder: a randomized placebo-controlled trial. J Clin Psychiatry 2007;
68(3):390–8.
38. Stunkard A, Berkowitz R, Tanrikut C, et al. d-fenfluramine treatment of binge
eating disorder. Am J Psychiatry 1996;153(11):1455–9.
39. Appolinario JC, Bacaltchuk J, Sichieri R, et al. A randomized, double-blind,
placebo-controlled study of sibutramine in the treatment of binge-eating disorder.
Arch Gen Psychiatry 2003;60(11):1109–16.
40. Wilfley DE, Crow SJ, Hudson JI, et al. Efficacy of sibutramine for the treatment of
binge eating disorder: a randomized multicenter placebo-controlled double-blind
study. Am J Psychiatry 2008;165(1):51–8.
41. McElroy SL, Arnold LM, Shapira NA, et al. Topiramate in the treatment of binge
eating disorder associated with obesity: a randomized, placebo-controlled trial.
Am J Psychiatry 2003;160(2):255–61.
42. McElroy SL, Hudson JI, Capece JA, et al. Topiramate for the treatment of moder-
ate to severe binge eating disorder associated with obesity: a double-blind,
placebo-controlled study. Neuropharmacology 2005;30:S138.
43. McElroy SL, Shapira NA, Arnold LM, et al. Topiramate in the long-term treatment
of binge-eating disorder associated with obesity. J Clin Psychiatry 2004;65(11):
1463–9.
44. McElroy SL, Kotwal R, Guerdjikova AI, et al. Zonisamide in the treatment of binge
eating disorder with obesity: a randomized controlled trial. J Clin Psychiatry 2006;
67(12):1897–906.
45. Hudson JI, McElroy SL, Ferreira-Cornwell MC, et al. Efficacy of lisdexamfetamine
in adults with moderate to severe binge-eating disorder: a randomized clinical
trial. JAMA Psychiatry 2017;74(9):903–10.
46. McElroy SL, Hudson J, Ferreira-Cornwell MC, et al. Lisdexamfetamine dimesylate
for adults with moderate to severe binge eating disorder: results of two pivotal
phase 3 randomized controlled trials. Neuropsychopharmacology 2016;41(5):
1251–60.
47. McElroy SL, Hudson JI, Mitchell JE, et al. Efficacy and safety of lisdexamfetamine
for treatment of adults with moderate to severe binge eating disorder: a random-
ized clinical trial. JAMA Psychiatry 2015;72(3):235–46.
48. Thomas JJ, Wons OB, Eddy KT. Cognitive-behavioral treatment of avoidant/
restrictive food intake disorder. Curr Opin Psychiatry 2018;31(6):425–30.
49. Gray E, Chen T, Menzel J, et al. Mirtazapine and weight gain in avoidant and
restrictive food intake disorder. J Am Acad Child Adolesc Psychiatry 2018;
57(4):288–9.
50. Thomas JJ, Lawson EA, Micali N, et al. Avoidant/restrictive food intake disorder:
a three-dimensional model of neurobiology with implications for etiology and
treatment. Curr Psychiatry Rep 2017;19(8):54.
51. Riesco N, Aguera Z, Granero R, et al. Other specified feeding or eating disorders
(OSFED): clinical heterogeneity and cognitive-behavioral therapy outcome. Eur
Psychiatry 2018;54:109–16.