REVIEW
Review of Childhood Obesity: From
Epidemiology, Etiology, and Comorbidities to
Clinical Assessment and Treatment
Seema Kumar, MD, and Aaron S. Kelly, PhD
Abstract
Childhood obesity has emerged as an important public health problem in the United States and other
countries in the world. Currently 1 in 3 children in the United States is afflicted with overweight or
obesity. The increasing prevalence of childhood obesity is associated with emergence of comorbidities
previously considered to be “adult” diseases including type 2 diabetes mellitus, hypertension, nonalcoholic
fatty liver disease, obstructive sleep apnea, and dyslipidemia. The most common cause of obesity in
children is a positive energy balance due to caloric intake in excess of caloric expenditure combined with a
genetic predisposition for weight gain. Most obese children do not have an underlying endocrine or single
genetic cause for their weight gain. Evaluation of children with obesity is aimed at determining the cause of
weight gain and assessing for comorbidities resulting from excess weight. Family-based lifestyle interventions, including dietary modifications and increased physical activity, are the cornerstone of weight
management in children. A staged approach to pediatric weight management is recommended with
consideration of the age of the child, severity of obesity, and presence of obesity-related comorbidities in
determining the initial stage of treatment. Lifestyle interventions have shown only modest effect on weight
loss, particularly in children with severe obesity. There is limited information on the efficacy and safety of
medications for weight loss in children. Bariatric surgery has been found to be effective in decreasing
excess weight and improving comorbidities in adolescents with severe obesity. However, there are limited
data on the long-term efficacy and safety of bariatric surgery in adolescents. For this comprehensive review, the literature was scanned from 1994 to 2016 using PubMed using the following search terms:
childhood obesity, pediatric obesity, childhood overweight, bariatric surgery, and adolescents.
ª 2016 Mayo Foundation for Medical Education and Research
C
hildhood obesity has emerged as one
of the most important public health
problems in the United States and
other countries in the world.1,2 The increasing
prevalence of childhood obesity has led to the
emergence of multiple serious obesity-related
comorbidities3 that not only threaten the
health of those affected but also promise to
place a large strain on the health care system.
In addition, obesity in childhood tracks
strongly into adulthood, particularly in those
with severe obesity and/or a strong family history of obesity.4,5 For this comprehensive review, the literature was scanned from 1994
to 2016 using PubMed using the following
search terms: childhood obesity, pediatric
obesity, childhood overweight, bariatric surgery,
and adolescents.
n
Mayo Clin Proc. 2017;92(2):251-265
DEFINITION OF CHILDHOOD OBESITY
The term obesity refers to an excess of fat.
Because of the unavailability and high cost of
techniques that directly measure body fat,
body mass index (BMI), derived from the
body weight and height, has emerged as the
accepted clinical standard measure of overweight and obesity for children 2 years and
older. Body mass index is calculated by
dividing the body weight in kilograms by the
height in meters squared. In general, BMI provides a reasonable estimate of adiposity in the
healthy pediatric population.6 However, BMI
may slightly overestimate fatness in children
who are short or who have relatively high
muscle mass and may underestimate adiposity
in a substantial proportion of children, such as
those with reduced muscle mass due to low
Mayo Clin Proc. n February 2017;92(2):251-265 n http://dx.doi.org/10.1016/j.mayocp.2016.09.017
www.mayoclinicproceedings.org n ª 2016 Mayo Foundation for Medical Education and Research
From the Division of Pediatric Endocrinology and
Metabolism, Mayo Clinic,
Rochester, MN (S.K.); and
Department of Pediatrics
and Department of Medicine, University of Minnesota, Minneapolis (A.S.K.).
251
MAYO CLINIC PROCEEDINGS
ARTICLE HIGHLIGHTS
d
d
d
d
d
d
Childhood obesity has increased in epidemic proportions both
in the United States and worldwide. We discuss the epidemiology of childhood obesity including the trend toward increasing
prevalence of severe obesity in children.
Children with obesity are at high risk for multiple comorbidities
previously considered to be “adult” diseases. We discuss the
association of childhood obesity with type 2 diabetes mellitus,
hypertension, dyslipidemia, obstructive sleep apnea, nonalcoholic fatty liver disease, and other diseases.
Lifestyle modifications including dietary changes aimed at
decreasing total caloric intake, increasing physical activity and
decreasing sedentary time are crucial for weight management.
Pharmacotherapy may have a role in the treatment of pediatric
obesity, but evidence is scant.
Bariatric surgery is effective in achieving weight loss and
improving comorbidities in adolescents with severe obesity. We
discuss the indications for bariatric surgery in adolescents and
the data on the efficacy and safety of these procedures.
We discuss the components of family-based lifestyle interventions for weight loss.
levels of physical activity.7 Therefore, BMI
should be viewed as a surrogate measure of
adiposity and its strengths and limitations
should be considered when used in clinical
and research settings. For children younger
than 2 years, weight for length is the accepted
measure of overweight and obesity.
Waist circumference and waist-to-hip ratio
can be used to assess abdominal obesity,
whereas skinfold thickness is helpful as an indicator of adiposity.8-11
Because children experience constant
fluidity in height and weight as a result of
normal growth and development, the norms
for the absolute level of BMI in children vary
with age and sex. In 2000, the National Center
for Health Statistics and the Centers for Disease Control and Prevention (CDC) published
BMI reference standards for children between
2 and 20 years of age.12 Similarly, the World
Health Organization (WHO)13 developed
growth standards through the WHO Multicentre Growth Reference Study to describe
normal child growth from birth to 5 years
252
Mayo Clin Proc.
n
under optimal environmental conditions.
Although probably not ideal for all segments
of the pediatric population, these standards
have been applied to all children everywhere,
regardless of ethnicity, socioeconomic status,
and type of feeding. The CDC recommends
using curves based on the WHO child growth
standards for infants and toddlers younger
than 2 years and the CDC/National Center
for Health Statistics growth references for children 2 years and older.12
The following BMI-based definitions are
used for overweight and obesity for children
and adolescents between 2 and 20 years of
age:
d
d
d
Overweight: BMI at or greater than 85th to
less than 95th percentile for age and sex
Obesity: BMI at or greater than 95th percentile for age and sex
Severe obesity: BMI at or greater than 120% of
the 95th percentile, or BMI at or above 35 kg/m2
(whichever is lower).14,15 This corresponds to
approximately the 99th percentile, or BMI z
score at or above 2.3 above the mean.16,17
Some experts recommend classifying obesity
in 3 classes: class I obesity (BMI at or above
95th percentile to less than 120% of the
95th percentile), class II (BMI at or above
120% to less than 140% of the 95th percentile, or BMI at or above 35 kg/m2), and class
III (BMI at or above 140% of the 95th percentile, or BMI at or above 40 kg/m2).15
EPIDEMIOLOGY
Prevalence
Currently, about one-third of children and adolescents in the United States are classified as
either overweight or obese.1 The prevalence
of overweight or obesity increases with
advancing age: 22.8% of preschool children
(age, 2-5 years), 34.2% of school-aged children (age, 6-11 years), and 34.5% of adolescents (age, 12-19 years) are afflicted with
overweight or obesity1 and 8.4% of preschool
children (age, 2-5 years), 17.7% of schoolaged children (age, 6-11 years), and 20.5%
of adolescents (age, 12-19 years) have obesity.1
The prevalence of obesity varies by racial,
ethnic, and socioeconomic factors. Childhood
obesity is more common in African Americans,
February 2017;92(2):251-265
n
http://dx.doi.org/10.1016/j.mayocp.2016.09.017
www.mayoclinicproceedings.org
CHILDHOOD OBESITYdAN UPDATE
American Indians, and Mexican Americans
than in non-Hispanic whites.1,14,18 Obesity is
also more prevalent in low-income populations.19,20 Hereditary factors have a strong
effect on the prevalence of obesity in children.
Obesity in 1 parent increases the risk of
obesity in the child by 2- to 3-fold, and up
to 15-fold if both parents have obesity.4
Trends
The prevalence of obesity has increased
dramatically in school-aged children (age,
6-11 years) and adolescents (age, 12-19 years)
between 1976 and 1980 and between 2009
and 2010 (from 6.5% to 18.0% in children
and from 5.0% to 18.4% in adolescents).21,22
However, the percentage of children and adolescents in each weight category remained
almost stable between 2000 and 2012.1 In
addition, limited evidence suggests that obesity
prevalence may have decreased in preschoolaged children (age, 2-5 years) from 13.9% in
2004 to 8.4% in 2011 and 2012.1 However,
this isolated finding has yet to be replicated
and will need to be monitored over time to
engender confidence about whether this is
truly representative of a real trend.
Despite the recent plateau in the overall
prevalence of childhood obesity in the United
States, the prevalence of severe obesity in children aged 2 to 19 years has continued to increase. In 2012, 5.9% of children had severe
obesity (defined in this report as BMI 120%
of the 95th percentile, or BMI 35 kg/m2).15
Tracking of Childhood Obesity Into
Adulthood
Unfortunately, a high percentage of children
with obesity carry their adiposity into adulthood.
The tracking of obesity into adulthood is affected
by age of the child,23,24 severity of obesity,25 and
presence of parental obesity.4 Older age is associated with greater persistence of obesity into
adulthood, and therefore most adolescents with
obesity will continue to be obese during adult
life.24,26 The severity of obesity is also important:
71% of adolescents with severe obesity in 1
study27 continued to have severe obesity in
adulthood compared with only 8% of adolescents with nonsevere obesity. In addition,
parental obesity has been shown to increase
the risk of adult obesity by more than 2-fold in
children younger than 10 years.4
Mayo Clin Proc. n February 2017;92(2):251-265
www.mayoclinicproceedings.org
n
ETIOLOGY
Childhood obesity is the consequence of an
interaction among a complex set of factors
that are related to the environment, genetics,
and ecological effects such as the family, community, and school.
Environmental Factors
The etiological factors for childhood are
extremely complex.28 Psychosocial and
emotional distress contribute to excess weight
gain in children via maladaptive coping strategies such as eating to suppress negative emotions, appetite up-regulation, and low-grade
inflammation.28,29 Eating behaviors in children
and risk of childhood obesity have been shown
to be associated with parental feeding styles,
stress, and depression.30 Other crucial proposed
effects include perinatal factors,26,27 birth size,31
catch-up growth,32 breast-feeding status,33 antibiotic use,34 environmental chemicals,35 microbiota,36,37 and adverse life experiences.38
Several factors in the current “obesogenic”
environment have resulted in increased caloric
consumption, such as increasing use of sugarsweetened beverages, sweet snacks, fast foods
containing excess fat, large portion sizes, and
high glycemic foods.39-42 Consumption of
sugar-sweetened beverages (including fruit
juice) has been postulated as an important
contributor to the development of obesity in
children.43,44 In nationally representative surveys of children in the United States, sugarsweetened beverages supplied an average of
270 kcal/d, representing 10% to 15% of the
total caloric intake.42 Consumption of fast
food has also been purported to contribute
to the increasing prevalence of obesity.45
The changes in the environment contributing to increased caloric intake have been
accompanied by factors predisposing to
decreased caloric expenditure such as reduced
levels of physical activity and increasing time
spent in sedentary activities such as use of
television, computers, phones, and tablets.46,47 The amount of time spent watching
television and the presence of a television in
a child’s bedroom have been shown to be
directly related to the prevalence of obesity
in children and adolescents.48,49 This association can be explained by several potential
mechanisms including displacement of physical activity and adverse effects on the quality
http://dx.doi.org/10.1016/j.mayocp.2016.09.017
253
MAYO CLINIC PROCEEDINGS
and quantity of foods consumed.50,51 The use
of electronic games has also been associated
with obesity during childhood.52 As children
spend a substantial amount of time and
consume a considerable proportion of their
daily calories at school, the school environment has an effect on the development of
childhood obesity.53,54
Genetic Factors
Heritable factors appear to be responsible for
30% to 50% of the variation in adiposity.55
Although polygenetic obesity is by far the
most commonly observed, several single gene
defects and syndromes associated with obesity
have been identified (Table 1). However, these
account for less than 1% of childhood obesity
in tertiary care centers.56,57 Children with
genetic syndromes associated with obesity
typically have early-onset obesity and characteristic features on physical examination,
such as short stature, dysmorphic features,
developmental delay, or intellectual disability
(mental retardation), retinal changes, or deafness. Prader-Willi syndrome is the most common syndrome associated with obesity, and
TABLE 1. Secondary Causes of Pediatric Obesity
Monogenic disorders
Melanocortin 4 receptor
haploinsufficiency
Leptin deficiency
Leptin receptor deficiency
Proopiomelanocortin deficiency
Proprotein convertase 1
Syndromes
Prader-Willi
Bardet-Biedl
Cohen
Alström
Albright hereditary
osteodystrophy
Beckwith-Wiedemann
Carpenter
Neurologic
Brain injury
Brain tumor
After cranial irradiation
Hypothalamic obesity
Endocrine
Hypothyroidism
Glucocorticoid excess (Cushing syndrome)
Growth hormone deficiency
Pseudohypoparathyroidism
Psychological
Depression
Eating disorders (binge eating disorder and night
eating disorder)
Drug induced
Tricyclic antidepressants
Glucocorticoids
Antipsychotic drugs
Antiepileptic drugs
Sulfonylureas
Hypothalamic causes
Tumor
After brain surgery/radiation (craniopharyngioma)
ROHHAD/ROHHADNET syndrome
ROHHAD ¼ rapid-onset obesity with hypothalamic dysfunction, hypoventilation, and autonomic
dysregulation; ROHHADNET ¼ rapid-onset obesity with hypothalamic dysfunction, hypoventilation, and autonomic dysregulation with neural crest tumors.
254
Mayo Clin Proc.
n
children have hypotonia and feeding difficulties during infancy (often with failure to
thrive), followed by hyperphagia and subsequent development of obesity.
The most common single gene defect
currently identified in children with obesity
is mutations in the melanocortin 4 receptor.58,59 Other gene defects include those in
leptin, leptin receptor, proopiomelanocortin,
and proprotein convertase. Mutations causing
deficiencies in leptin and leptin receptor genes
are rare, and only a few cases of leptin or leptin receptor mutations have been reported,
most from consanguineous families.60
There is also increasing evidence for the
role of epigenetic factors in the development
of obesity. These epigenetic factors may
modify the interaction of environment, microbiome, and nutrition in promoting weight
gain.37
Endocrine Disorders
Endocrine causes of weight gain are identified
in less than 1% of children and adolescents
with obesity.56,57 Most children with endocrine disorders resulting in weight gain have
poor linear growth, short stature, and/or
hypogonadism.57 The endocrine disorders
causing weight gain include either endogenous
or exogenous glucocorticoid excess (the use of
corticosteroid medication or Cushing syndrome), hypothyroidism, growth hormone
deficiency, and pseudohypoparathyroidism
type 1a (Albright hereditary osteodystrophy)
(Table 1).
Sleep
There is increasing evidence for an association
between shortened sleep duration and/or poor
sleep quality and obesity.61,62 Sleep may also
have an association with decreased insulin
sensitivity, independent of the association
with adiposity.63
Medications
Several medications can contribute to weight
gain such as glucocorticoids,64 antipsychotic
drugs including risperidone and olanzapine,65
and antiepileptic drugs.66
Hypothalamic Obesity
Acquired hypothalamic lesions such as craniopharyngioma, particularly after surgery and/or
February 2017;92(2):251-265
n
http://dx.doi.org/10.1016/j.mayocp.2016.09.017
www.mayoclinicproceedings.org
CHILDHOOD OBESITYdAN UPDATE
cranial radiation, and diencephalic tumors can
present with weight gain. Patients may have
symptoms of increased intracranial pressure
such as headache and vomiting and may also
have symptoms of panhypopituitarism.
Weight gain may also be seen in patients after
cranial trauma or inflammatory disease
affecting the hypothalamus.
COMORBIDITIES OF CHILDHOOD OBESITY
Childhood obesity is associated with comorbidities affecting almost every system in the
body including, but not limited to, the endocrine, gastrointestinal, pulmonary, cardiovascular, and musculoskeletal systems. Many of
the comorbidities encountered in youth with
obesity, including type 2 diabetes mellitus
(T2DM), dyslipidemia, obstructive sleep apnea
(OSA), and steatohepatitis, used to be previously considered “adult” diseases. The severity
of these comorbidities typically increases with
the severity of obesity.67
Cardiometabolic and Cardiovascular
Children with obesity are at an increased risk
of hyperinsulinemia, insulin resistance, prediabetes, and subsequently T2DM.68-71 The prevalence of prediabetes and T2DM varies with
severity of obesity, race, ethnicity, and age of
the child. Those who present with T2DM
during adolescence appear to have more rapid
deterioration of glycemic control and progression of diabetes-related complications such as
microalbuminuria, dyslipidemia, and hypertension as compared with those who present
later in life.72-74 Children with obesity also
have a high prevalence of other cardiometabolic risk factors including elevated blood
pressure,75,76 low levels of high-density lipoprotein cholesterol, and elevated levels of triglycerides.76-78 Echocardiographic findings
include left ventricular hypertrophy, increased
left ventricular and left atrial diameter, and
systolic and diastolic dysfunction.79,80
Endocrine
Obesity may be associated with early onset of
sexual maturation in girls and with accelerated
linear growth and advanced skeletal maturation.81,82 Adolescent girls are also at higher
risk of developing hyperandrogenism and
polycystic ovary syndrome. Manifestations of
Mayo Clin Proc. n February 2017;92(2):251-265
www.mayoclinicproceedings.org
n
polycystic ovary syndrome can include menstrual irregularities, acne, and hirsutism.82
Pulmonary
Children with obesity have a considerably
higher prevalence of OSA than do healthy
weight children.83 The prevalence and severity
of OSA increase with increasing BMI.84 Children with severe obesity may also have
alveolar hypoventilation associated with severe
oxygen desaturation.85 Childhood obesity has
also been shown to be associated with
asthma.86
Gastrointestinal
Nonalcoholic fatty liver disease (NAFLD) in
children is strongly associated with obesity.
The spectrum of NAFLD can range from
simple steatosis to progressive steatohepatitis
and cirrhosis.87,88 Nonalcoholic fatty liver disease is now the most common cause of liver
disease in children.89 Although most patients
with NAFLD are asymptomatic, laboratory abnormalities include elevations in levels of liver
transaminases (alanine aminotransferase and
aspartate aminotransferase), alkaline phosphatase, and gamma-glutamyl transpeptidase.90,91
Imaging may confirm the presence of fatty
liver, indicated by increased echogenicity on
ultrasonography, but liver biopsy is the only
way to reliably distinguish between simple
steatosis, steatohepatitis, and fibrosis and can
also be helpful in excluding other causes of
elevated levels of serum aminotransferases.
Musculoskeletal
Childhood obesity increases the risk of various
musculoskeletal problems including impairment in mobility, increased prevalence of fractures, lower extremity joint pain, and lower
extremity malalignment.92,93 Obesity is also a
risk factor for unilateral or bilateral slipped
capital femoral epiphysis and for tibia
vara.94,95
Psychosocial
Psychosocial consequences of childhood
obesity are common and include poor selfesteem, anxiety, depression, and decreased
health-related quality of life.96-98 Children
with obesity are more likely to become victims
of bullying and discrimination.99 Women who
had obesity during adolescence have been
http://dx.doi.org/10.1016/j.mayocp.2016.09.017
255
MAYO CLINIC PROCEEDINGS
noted to have lower family income, lower rates
of marriage, and higher rates of poverty as
compared with their normal weight peers.100
Dermatologic
Acanthosis nigricans, a marker of insulin resistance, is a common finding in children with
obesity.101 Other skin abnormalities include
intertrigo, hidradenitis suppurativa, furunculosis, and stretch marks.101
Neurologic
Childhood obesity is associated with a higher
risk of idiopathic intracranial hypertension
(pseudotumor cerebri). Clinical symptoms
include headache, vomiting, retro-ocular eye
pain, and visual loss.102
Long-Term Risks
Children whose obesity persists into adulthood have a significantly increased risk of
T2DM, hypertension, dyslipidemia, and
carotid-artery atherosclerosis than do adults
who were never afflicted with obesity.5 Higher
BMI during childhood has also been associated with an increased risk of fatal and
nonfatal cardiovascular events during adulthood in both men and women, though this
may be partially mediated by the association
between childhood obesity and adult
obesity.103
CLINICAL EVALUATION OF THE CHILD WITH
OBESITY
The clinical evaluation of the obese child is
directed at identifying the cause of obesity
and obesity-related comorbidities. The evaluation includes a complete history and physical
examination.104,105
A complete history and physical examination are usually sufficient in determining the
cause of childhood obesity. Dietary history
should consist of details of eating habits
including frequency, content, and location of
meals and snacks as well as intake of caloriedense foods such as fruit juice and soda. Physical activity assessment should include details
of time spent in unstructured play, organized
sports, school recess, and physical education
as well as screen time (television, video games,
mobile phones, and tablets). Medical history
should include details about medications that
may cause weight gain such as glucocorticoids,
256
Mayo Clin Proc.
n
antipsychotic drugs, and antiepileptic drugs. A
developmental history is important as developmental delay may point toward a chromosomal
or genetic cause for obesity. A complete review
of systems is helpful in determining an underlying etiology for the weight gain, such as
Cushing syndrome or hypothalamic tumor.
The review of symptoms is also helpful in
screening for obesity-related comorbidities
such as OSA. Family history of obesity and
obesity-related comorbidities is a predictor of
persistence of obesity into adulthood. Performing a comprehensive psychosocial screening
including collecting details related to depression, peer relationships, and disordered eating
habits is crucial.
Physical examination should include measurement of height and assessment for dysmorphic features suggestive of a chromosomal or
monogenic cause and for Cushingoid features.
Most children with exogenous obesity are tall,
whereas children with genetic and endocrine
causes of obesity tend to have short stature.
Blood pressure should be measured with an
appropriate sized cuff.106
There is lack of standardization and
consensus on when to screen and the types
of laboratory screening tests to perform in
children with obesity. Most experts recommend that children afflicted with overweight,
that is, BMI between the 85th and 95th percentiles, who are free from risk factors should
have measurement of a fasting lipid profile.105
These children should also undergo measurement of fasting blood glucose or hemoglobin
A1c and aspartate aminotransferase and
alanine aminotransferase levels if they are 10
years and older and have 1 or more of the
following risk factors: elevated blood pressure,
elevated lipid levels, currently using tobacco,
or have a family history of obesity-related diseases.105 A fasting lipid profile is recommended for all children with BMI 95th
percentile even in the absence of risk factors.105 In addition, transaminases and fasting
blood glucose or hemoglobin A1c are recommended for all children with BMI 95th
percentile starting at 10 years of age even in
the absence of risk factors.105 If the results of
the fasting lipid profile are normal, repeat
screening is recommended every 2 years. If
the results are borderline, repeat screening in
1 year is recommended, and if the results are
February 2017;92(2):251-265
n
http://dx.doi.org/10.1016/j.mayocp.2016.09.017
www.mayoclinicproceedings.org
CHILDHOOD OBESITYdAN UPDATE
abnormal, repeat screening in 2 weeks to
3 months is recommended.107 A fasting lipid
profile should be repeated every 2 years in
children 10 years or older if their BMI is
85th percentile in the presence of risk factors
or if their BMI is 95th percentile regardless
of risk factors.105 In 2011, the US National
Heart, Lung, and Blood Institute expert panel
recommended universal screening between 9
and 11 years of age and again between 17
and 21 years of age and selective screening
at other ages.107 The universal screening
guidelines, however, remain controversial,
with concerns related to lack of data on the
effect of early detection of dyslipidemia on cardiovascular disease during adulthood, fear
about psychological effect of early diagnosis
of dyslipidemia, and low predictive value of
childhood lipid screening.108
Children with signs and symptoms suggestive of a genetic or endocrine cause for the
weight gain may need specific testing. In addition, children with signs and symptoms suggestive of comorbidity such as OSA may
need specific testing such as an overnight
polysomnogram.
CLINICAL INTERVENTIONS FOR THE
TREATMENT OF CHILDHOOD OBESITY
The Expert Committee on the Assessment, Prevention, and Treatment of Child and Adolescent
Overweight and Obesity recommends a staged
approach to weight management in children.
(Table 2).109 Stage 1 (Prevention Plus) includes
specific dietary and physical activity recommendations, such as encouraging fruit and vegetable
consumption and limiting sedentary activities
such as watching television, playing video
games, and using computers. If there is no
improvement in BMI in 3 to 6 months, stage 2
(Structured Weight Management) should be
considered. This stage includes recommendations on loweenergy-dense, balanced diet;
structured meals; supervised physical activity
of at least 60 min/d; 1 hour or less of screen
time per day; and self-monitoring through
food and physical activity recording. Referral
to dietitians is needed for this stage. Monthly
contact is recommended and should be tailored
to the needs of the patient and family. Advancement to the next stage (stage 3, Comprehensive
Multidisciplinary Intervention) is recommended depending on responses to treatment with
Mayo Clin Proc. n February 2017;92(2):251-265
www.mayoclinicproceedings.org
n
TABLE 2. Suggested Staged Approach to Weight Management in Children and
Adolescents
d
d
d
d
Stage 1 (Prevention Plus) can be implemented in a primary care office setting, 5 or
more servings of fruits and vegetables per day, minimize or eliminate consumption
of sugar-containing beverages, <2 hours of screen time and >1 hour of physical
activity per day
Stage 2 (Structured Weight Management) can be implemented in a primary care
office with a dietitian, includes stage 1 guidelines plus increased structure of meals
and snacks with attention to energy density of foods
Stage 3 (Comprehensive Multidisciplinary Intervention) can be implemented in a
primary care office with a multidisciplinary team and outside facilities for structured
physical activity, includes stage 2 guidelines plus increased structured physical activity
and dietary program
Stage 4 (Tertiary Care Intervention) can be ideally implemented in a pediatric weight
management center with a multidisciplinary team with expertise in pediatric obesity,
includes in addition to stage 3 recommendations, medications, extremely structured
dietary regimens, or bariatric surgery
stage 2, age, health risks, and motivation of
the patient and family. Stage 3 is characterized
by more frequent patient-provider contact and
more active use of behavioral strategies and
monitoring. Weekly visits for the first 8
and 12 weeks, followed by monthly contact,
are recommended as being most efficacious.
Moderate to strong parental involvement is recommended for children younger than 12 years.
This stage requires a multidisciplinary team with
expertise in childhood obesity, including a
behavioral counselor (eg, social worker, psychologist, and trained nurse practitioner), registered dietitian, and exercise specialist. Primary
care offices with dietitians and behavioral counselors can deliver these services with community
partners such as public health programs, local
schools, Head Start, Young Men’s Christian Association and Boys and Girls Club. Children
with inadequate response to stage 3 treatment,
health risks, and motivation should be considered for stage 4 (Tertiary Care Intervention).
This stage often includes the use of meal replacement, low-energy diets, medications, and/or
surgery. Stage 4 requires a multidisciplinary
team with expertise in childhood obesity at a pediatric weight management center that has specific clinical and research protocols for the
assessment of outcomes and risks.
The weight loss goals are determined by
the child’s age and severity of obesity and
related comorbidities.109,110 Weight maintenance might be an appropriate goal for children who have mild obesity because BMI
http://dx.doi.org/10.1016/j.mayocp.2016.09.017
257
MAYO CLINIC PROCEEDINGS
will decrease as children gain height. In
contrast, weight loss is recommended in children with severe obesity and those with
comorbidities. It has been suggested that a
weight loss of 1 lb/mo is safe in children between 2 and 11 years of age whereas weight
loss of up to 2 lb/wk is safe in adolescents
with severe obesity and comorbidities. However, it should be noted that little to no evidence
supports these specific recommendations;
rather, they represent expert opinion.110
Behavioral strategies targeted at decreasing
overall caloric intake, decreasing sedentary
time, and increasing physical activity are the
cornerstone of pediatric weight management
(Table 3). Family-based behavioral approaches
that include the child’s parents or caregivers are
recommended.110-112
Exclusive
parental
participation has been shown to be effective
in the treatment of childhood obesity113-115
and noted to give better results as compared
with participation of the child only.114 Motivational interviewing is a nonjudgmental and
patient-centered counseling technique that
entails reflective listening and addresses a
patient’s ambivalence to change and uses the
patient’s values to resolve that ambivalence.
This technique has been shown to be a useful
tool in the treatment of pediatric obesity.116,117
Obtaining accurate assessments of barriers
to healthy eating and physical activity,
including those that are financial and cultural,
is crucial to identify specific behaviors to
target for change. Behavioral modification
TABLE 3. Behavioral Treatment Strategies for Obesity During Childhood and
Adolescence
Dietary approaches
1. Encourage intake of 5 servings of fruits and vegetables daily
2. Decrease intake of calorie-dense foods such as saturated fats, salty snacks, and
high glycemic foods such as candy
3. Minimize intake of sugar-containing beverages
4. Minimize eating outside home and fast food in particular
5. Eat breakfast daily
6. Avoid skipping meals
Physical activity
1. Decrease sedentary behavior such as watching television, surfing the Internet, and
playing video games to <2 h/d
2. Engage in fun and age-specific exercise that is appropriate to the individual’s
abilities
3. Increase intensity, frequency, and duration of exercise gradually as tolerated
4. More than 1 h of physical activity daily
258
Mayo Clin Proc.
n
interventions include self-monitoring of food
and physical activity as well as control of stimuli that contribute to or elicit unhealthy behaviors.118 Appropriate goals for healthy behavior
should be “SMART,” specific, measurable,
attainable, realistic, and timely.119
There is lack of consensus on what the best
structured dietary strategies for weight loss are
in children. Diets with modified carbohydrate
intake such as low glycemic index diets and
low carbohydrate diets have been shown to
be as effective as standard portion-controlled
diets for weight management in children with
obesity.120,121 However, adherence to the
modified carbohydrate diets may be low and
children may be unable to follow these types
of regimens, particularly in the long term.122
Some programs use the “traffic light” format
that labels food as red, yellow, and green on
the basis of the energy density of the foods
(red foods being most calorie dense and green
foods being least calorie dense).50 Children
are encouraged to eat green foods more often
and red foods rarely. The NuVal nutritional
scoring system is another helpful way to obtain
comprehensive nutritional information with a
simple number between 1 and 100, in which
higher scores represent better nutrition
(https://www.nuval.com).
Semistructured dietary approaches that are
aimed at encouraging children and their families to select food groups of lower energy density, such as fats, and decreasing portion size
are best used for weight loss in children.112,118
Physical activity goals should be determined by the child’s age, personal preferences
for the type of physical activity, and exercise
tolerance. It is recommended that children 6
years or older participate in 60 minutes or
more of physical activity per day.123 Toddlers
should be allowed 60 to 90 minutes per 8hour day for moderate- to vigorous-intensity
physical activity, including running; and 90
to 120 minutes are recommended for preschoolers.124 Unstructured physical activity,
including outdoor play, should be encouraged
in younger children, whereas older children
should be encouraged to participate in structured physical activity such as after-school
sports. It is also recommended that “screen
time” (other than homework) be limited to
less than 2 h/d for children older than 2 years,
whereas those younger than 2 years should
February 2017;92(2):251-265
n
http://dx.doi.org/10.1016/j.mayocp.2016.09.017
www.mayoclinicproceedings.org
CHILDHOOD OBESITYdAN UPDATE
avoid “screen time” altogether. Because of the
increasing evidence for an association between
shortened sleep duration and obesity,62,125
good sleep hygiene and adequate amount of
sleep (10-13 hours a night for preschoolers
and 8-10 hours a night for teenagers) should
be recommended. “My Plate” (http://www.
ChooseMyPlate.gov/), Let’s Go! 5-2-1-20
Maine program (http://www.letsgo.org/), and
Let’s Move (http://www.letsmove.gov/) are
excellent resources for promoting healthy
eating and active lifestyle.
Lifestyle interventions of moderate or high
intensity (defined as 26-75 or >75 hours of
provider contact, respectively) are effective in
achieving short-term (up to 12 months) weight
improvements in children, but these may not
be feasible in primary care settings or even
specialty pediatric weight management programs.126 Low-intensity interventions (<25
hours of provider contact, typically spread
over 3-6 months) are feasible in a primary
care setting and are recommended. However,
low-intensity interventions have been shown
to have weak or inconsistent effects.126-128
Behavioral interventions for treating overweight and obesity in children and youth are
associated with a low to moderate treatment
effect. The reported weight loss and BMI reductions have been modest, ranging from 1 to 3
kg/m2 of BMI.3,127-130 In addition, dropout
rates tend to be high.127,129,130
PHARMACOLOGICAL THERAPY
The role of pharmacological therapy in the
treatment of obesity in children and adolescents is limited.14,131 Orlistat is the only medication currently approved by the Food and
Drug Administration for the treatment of
obesity in adolescents (age, 12 years). Orlistat
is a lipase inhibitor that blocks absorption of
about one-third of the fat ingested in a meal.
The recommended dose of orlistat is 120 mg
3 times a day with meals. Orlistat is also available as an over-the-counter medication at a
lower dose of 60 mg 3 times a day. The efficacy
of orlistat is modest: 1-year placebo-subtracted
changes in BMI less than 1 kg/m2.132,133
Adverse effects limiting the use of orlistat
include diarrhea, abdominal pain, flatulence,
and greasy stools. Orlistat blocks absorption
of fat-soluble vitamins and therefore administration of a multivitamin is recommended.
Mayo Clin Proc. n February 2017;92(2):251-265
www.mayoclinicproceedings.org
n
Metformin, a drug approved for the treatment of T2DM in children 10 years and older,
has been used off-label for weight loss in
several trials but results in modest reductions
in BMI only (placebo-subtracted BMI decrease
of 1.1-1.4 kg/m2).134,135
Other medications that have been used
off-label for the treatment of obesity in children include topiramate136 and glucagon-like
peptide-1 analogs such as exenatide.137,138
However, these studies were either uncontrolled or included small sample sizes; therefore, more trials are needed to better
understand the efficacy and safety of these
medications for the treatment of pediatric
obesity.
BARIATRIC SURGERY
Bariatric surgery in adults has been shown to
result in significant and sustained decreases
in BMI and several obesity-related comorbidities as well as reduce mortality.139,140 As a
consequence, bariatric surgery has been performed in adolescents with severe obesity for
several decades. There has been an increase
in the number of bariatric surgery procedures
in adolescents: a 5-fold increase from 1997 to
2003 and a 3-fold increase from 2000 to
2003.141,142 Despite the increasing trend, bariatric surgery is infrequently performed in adolescents. In fact, less than 1% of all bariatric
procedures in the United States are performed
in adolescents. A total of 771 bariatric procedures were performed in 2003142 and 1600
procedures in 2009.143
Types of Bariatric Procedures
Laparoscopic sleeve gastrectomy (LSG) and
Roux-en-Y gastric bypass (RYGB) are the
most commonly performed procedures in the
United States.144 An adjustable gastric band
(AGB) comprises less than 5% of procedures
performed in adolescents. The results of a National Institutes of Healthesponsored study
involving 5 centers (Teen-Longitudinal Assessment of Bariatric Surgery) suggest that
bariatric surgery is safe and effective in adolescents with severe obesity.145,146 The TeenLongitudinal Assessment of Bariatric Surgery
study is one of the first and largest prospective
studies to systematically investigate the shortterm and long-term efficacy and safety of
bariatric surgery in children.
http://dx.doi.org/10.1016/j.mayocp.2016.09.017
259
MAYO CLINIC PROCEEDINGS
FIGURE. A, Sleeve gastrectomy. B, Roux-en-Y gastric bypass. C, Adjustable gastric band.
Laparoscopic sleeve gastrectomy involves
resection of most of the greater curvature of
the stomach, resulting in the creation of a
tubular stomach (Figure A). This procedure
was traditionally performed as the first part
of a 2-stage weight loss procedure for
extremely high-risk obese adults but is now
being used as a stand-alone procedure. Laparoscopic sleeve gastrectomy is an attractive
procedure for adolescents because of a lower
risk of micronutrient deficiencies (because
the procedure does not result in malabsorption) and less complexity of the procedure itself in comparison to RYGB. The RYGB
procedure involves the creation of a small
(<30 mL) proximal gastric pouch that is
divided and separated from the distal stomach
and is anastomosed to a Roux limb of small
bowel 75 to 150 cm in length (Figure B).
This procedure therefore results in restriction
of caloric intake as well as malabsorption of
food along with vitamins and minerals.
Reduced caloric intake due to reduced capacity of the stomach and neuroendocrine
mechanisms such as an increase in postprandial concentrations of total peptide YY after
RYGB are thought to play important roles in
weight loss after bariatric procedures. Dramatic improvements in diabetes and insulin
resistance are seen immediately after RYGB
even before any significant weight loss. These
may be attributed to an increased secretion
of incretins such as glucagon-like peptide-1
or simply as a result of dramatically reduced
caloric intake.147 The AGB is a tight prosthetic
band that is placed around the entrance to the
stomach and therefore compartmentalizes the
stomach (Figure C). The gastric band is not
Food and Drug Administration approved for
adolescents younger than 18 years.
260
Mayo Clin Proc.
n
The following criteria have been recommended by the American Society for Metabolic
and Bariatric Surgery to select adolescents for
bariatric surgery148,149:
1. Body mass index 35 kg/m2 and a severe comorbidity, with significant comorbidity with
short-term effects on health (eg, moderate to
severe OSA [apnea-hypopnea index >15],
T2DM, pseudotumor cerebri, or severe and
progressive steatohepatitis), or BMI 40 kg/m2
or above with more minor comorbidities
2. Physical maturity, defined as completing
95% of predicted adult stature based on
bone age or reaching Tanner stage IV.
This criterion is based on theoretical concerns that rapid weight loss might inhibit
statural growth if an adolescent has not
reached near adult height
3. History of lifestyle efforts to lose weight
through changes in diet and physical activity
4. Ability and motivation of the patient and
family to adhere to recommended treatments pre- and postoperatively, including
vitamin and mineral supplementation
5. Appropriate understanding of the risks and
benefits of surgery on behalf of the adolescents
6. Supportive but not coercive family
According to expert guidelines from the
American Society for Metabolic and Bariatric
Surgery, contraindications for surgical weight
loss procedures in adolescents include148,150
1. Medically correctable cause of obesity
2. An ongoing substance abuse problem
(within the preceding year)
3. A medical, psychiatric, psychosocial, or
cognitive condition that prevents adherence
to postoperative dietary and medication
regimens or impairs decisional capacity
February 2017;92(2):251-265
n
http://dx.doi.org/10.1016/j.mayocp.2016.09.017
www.mayoclinicproceedings.org
CHILDHOOD OBESITYdAN UPDATE
4. Current or planned pregnancy within 12 to
18 months of the procedure
5. Inability on the part of the patient or parent
to comprehend the risks and benefits of the
surgical procedure
Preoperative evaluation of adolescents
before bariatric surgery should be performed
by a multidisciplinary team consisting of a pediatric obesity specialist, experienced bariatric
surgeon, nurse, dietitian, and pediatric psychologist or psychiatrist.
Postoperative
management
includes
advancement of the diet from clear liquids to
a protein-containing liquid diet, then high protein shakes to puree, and subsequently solid,
normal consistency foods over a period of
several months. Lifelong vitamin and mineral
supplementation is recommended to prevent
the development of nutritional deficiencies as
a result of decreased intake and/or malabsorption. The typical supplementation regimen includes a daily standard multivitamin with
folate and iron, calcium, vitamin D, and daily
or monthly vitamin B12. Pregnancy prevention
is recommended for at least 12 to 18 months
after surgery because of the potential adverse
effects of weight loss and micronutrient deficiencies on the mother and fetus.
In a prospective study of 242 adolescents
with severe obesity who underwent bariatric
surgery (predominant RYGB and LSG), at 3
years postoperatively, clinically significant decreases in BMI were seen (in LSG from 50
kg/m2 at baseline to 37 kg/m2 and in RYBG
from 54 kg/m2 at baseline to 39 kg/m2).144
Bariatric surgery also results in a significant
improvement in comorbidities such as
T2DM, elevated blood pressure, dyslipidemia,
markers of inflammation and oxidative stress,
fatty liver disease, and abnormal kidney
function as well as quality of life and
depression.144,151-155
Short-term complications of bariatric surgery include wound infections, leakage at
anastomotic sites, pulmonary embolism, small
bowel obstruction, gastrojejunal strictures,
and gastrogastric fistula.146,153 Complications
of the AGB include band slippage, gastric
obstruction, and pouch dilatation.154 Longterm complications include nutritional deficiencies of iron, vitamin B12, thiamine, and
vitamin D.144 Iron deficiency is the most
Mayo Clin Proc. n February 2017;92(2):251-265
www.mayoclinicproceedings.org
n
common nutritional problem, with prevalence
of low ferritin levels increasing from 5% at
baseline to 57% 3 years after surgery.144 The
adherence to recommendations for nutritional
supplementation has been noted to be poor in
adolescents. Therefore, appropriate patient
selection and long-term follow-up is recommended after bariatric surgery.
CONCLUSION
Childhood obesity has emerged as one of the
most pressing medical and public health problems of our day. The prevalence is unacceptably
high, and the rate of increase in severe obesity
continues to climb. The etiology of the disease
is multifactorial and complex, stemming from
an interaction among genetic and biological
factors, environmental factors, and ecological
effects. Childhood obesity is associated with
several comorbidities that affect physical and
mental health. The multitude of serious comorbidities associated with childhood obesity necessitates effective treatment modalities. A
staged approach to treatment is recommended,
with initial management being implemented in
primary care and with focus on healthy eating
habits and active lifestyle. Those with poor
response to interventions in primary care and
with significant health risks should be managed
by a multidisciplinary team with expertise in
childhood obesity. Pharmacotherapy and/or
bariatric surgery should be considered if there
has been no response to structured weight
management with a multidisciplinary team.
Additional research is needed to evaluate the
efficacy and safety of these modalities.
Abbreviations and Acronyms: AGB = adjustable gastric
band; BMI = body mass index; CDC = Centers for Disease
Control and Prevention; LSG = laparoscopic sleeve gastrectomy; NAFLD = nonalcoholic fatty liver disease; OSA =
obstructive sleep apnea; RYGB = Roux-en-Y gastric bypass;
T2DM = type 2 diabetes mellitus; WHO = World Health
Organization
Potential Competing Interests: Dr Kelly serves as a pediatric obesity consultant for Novo Nordisk but does not
accept personal or professional income for his activities.
He receives research support, in the form of a drug and a
placebo, from AstraZeneca for a clinical trial funded by
the National Institutes of Health.
Correspondence: Address to Seema Kumar, MD, Division
of Pediatric Endocrinology and Metabolism, Mayo Clinic,
200 First St SW, Rochester, MN 55905 (kumar.seema@
mayo.edu).
http://dx.doi.org/10.1016/j.mayocp.2016.09.017
261
MAYO CLINIC PROCEEDINGS
REFERENCES
1. Ogden CL, Carroll MD, Kit BK, Flegal KM. Prevalence of childhood and adult obesity in the United States, 2011-2012.
JAMA. 2014;311(8):806-814.
2. Strauss RS, Bradley LJ, Brolin RE. Gastric bypass surgery in
adolescents with morbid obesity. J Pediatr. 2001;138(4):
499-504.
3. Dietz WH, Robinson TN. Clinical practice: overweight children and adolescents. N Engl J Med. 2005;352(20):2100-2109.
4. Whitaker RC, Wright JA, Pepe MS, Seidel KD, Dietz WH. Predicting obesity in young adulthood from childhood and
parental obesity. N Engl J Med. 1997;337(13):869-873.
5. Juonala M, Magnussen CG, Berenson GS, et al. Childhood
adiposity, adult adiposity, and cardiovascular risk factors.
N Engl J Med. 2011;365(20):1876-1885.
6. Freedman DS, Sherry B. The validity of BMI as an indicator of
body fatness and risk among children. Pediatrics. 2009;
124(suppl 1):S23-S34.
7. Javed A, Jumean M, Murad MH, et al. Diagnostic performance
of body mass index to identify obesity as defined by body
adiposity in children and adolescents: a systematic review
and meta-analysis. Pediatr Obes. 2015;10(3):234-244.
8. Lee S, Bacha F, Gungor N, Arslanian SA. Waist circumference
is an independent predictor of insulin resistance in black and
white youths. J Pediatr. 2006;148(2):188-194.
9. Fernández JR, Redden DT, Pietrobelli A, Allison DB. Waist
circumference percentiles in nationally representative samples
of African-American, European-American, and MexicanAmerican children and adolescents. J Pediatr. 2004;145(4):
439-444.
10. Moreno LA, Rodríguez G, Guillén J, Rabanaque MJ, León JF,
Ariño A. Anthropometric measurements in both sides of
the body in the assessment of nutritional status in prepubertal
children. Eur J Clin Nutr. 2002;56(12):1208-1215.
11. WHO Expert Committee. Physical Status: The Use of and Interpretation of Anthropometry. Geneva: World Health Organization; 1995. WHO Technical Report Series No. 854.
12. Kuczmarski RJ, Ogden CL, Grummer-Strawn LM, et al. CDC
growth charts: United States. Adv Data. 2000;(314):1-27.
13. WHO Multicentre Growth Reference Study Group. WHO
Child Growth Standards based on length/height, weight and
age. Acta Paediatr Suppl. 2006;450:76-85.
14. Kelly AS, Barlow SE, Rao G, et al; American Heart Association
Atherosclerosis, Hypertension, and Obesity in the Young
Committee of the Council on Cardiovascular Disease in the
Young, Council on Nutrition, Physical Activity and Metabolism, and Council on Clinical Cardiology. Severe obesity
in children and adolescents: identification, associated health
risks, and treatment approaches: a scientific statement from
the American Heart Association. Circulation. 2013;128(15):
1689-1712.
15. Skinner AC, Skelton JA. Prevalence and trends in obesity and
severe obesity among children in the United States, 19992012. JAMA Pediatr. 2014;168(6):561-566.
16. Flegal KM, Wei R, Ogden CL, Freedman DS, Johnson CL,
Curtin LR. Characterizing extreme values of body mass
index-for-age by using the 2000 Centers for Disease Control
and Prevention growth charts. Am J Clin Nutr. 2009;90(5):
1314-1320.
17. Gulati AK, Kaplan DW, Daniels SR. Clinical tracking of severely
obese children: a new growth chart. Pediatrics. 2012;130(6):
1136-1140.
18. Anderson SE, Whitaker RC. Prevalence of obesity among US
preschool children in different racial and ethnic groups. Arch
Pediatr Adolesc Med. 2009;163(4):344-348.
19. Eagle TF, Sheetz A, Gurm R, et al. Understanding childhood
obesity in America: linkages between household income,
community resources, and children’s behaviors. Am Heart J.
2012;163(5):836-843.
262
Mayo Clin Proc.
n
20. Pan L, Blanck HM, Sherry B, Dalenius K, Grummer-Strawn LM.
Trends in the prevalence of extreme obesity among US
preschool-aged children living in low-income families, 19982010. JAMA. 2012;308(24):2563-2565.
21. Ogden CL, Carroll MD, Kit BK, Flegal KM. Prevalence of
obesity and trends in body mass index among US children
and adolescents, 1999-2010. JAMA. 2012;307(5):483-490.
22. Ogden CL, Flegal KM, Carroll MD, Johnson CL. Prevalence
and trends in overweight among US children and adolescents,
1999-2000. JAMA. 2002;288(14):1728-1732.
23. Parsons TJ, Power C, Logan S, Summerbell CD. Childhood
predictors of adult obesity: a systematic review. Int J Obes Relat
Metab Disord. 1999;23(suppl 8):S1-S107.
24. Guo SS, Roche AF, Chumlea WC, Gardner JD, Siervogel RM.
The predictive value of childhood body mass index values
for overweight at age 35 y. Am J Clin Nutr. 1994;59(4):
810-819.
25. Power C, Lake JK, Cole TJ. Measurement and long-term health
risks of child and adolescent fatness. Int J Obes Relat Metab
Disord. 1997;21(7):507-526.
26. Davis EF, Lazdam M, Lewandowski AJ, et al. Cardiovascular
risk factors in children and young adults born to preeclamptic
pregnancies: a systematic review. Pediatrics. 2012;129(6):
e1552-e1561.
27. Lau EY, Liu J, Archer E, McDonald SM, Liu J. Maternal weight
gain in pregnancy and risk of obesity among offspring: a systematic review. J Obes. 2014;2014:524939.
28. Incledon E, Wake M, Hay M. Psychological predictors of
adiposity: systematic review of longitudinal studies. Int J Pediatr
Obes. 2011;6(2-2):e1-e11.
29. Hemmingsson E. A new model of the role of psychological
and emotional distress in promoting obesity: conceptual review with implications for treatment and prevention. Obes
Rev. 2014;15(9):769-779.
30. El-Behadli AF, Sharp C, Hughes SO, Obasi EM, Nicklas TA.
Maternal depression, stress and feeding styles: towards a
framework for theory and research in child obesity. Br J
Nutr. 2015;113(suppl):S55-S71.
31. Yu ZB, Han SP, Zhu GZ, et al. Birth weight and subsequent
risk of obesity: a systematic review and meta-analysis. Obes
Rev. 2011;12(7):525-542.
32. Taveras EM, Rifas-Shiman SL, Sherry B, et al. Crossing growth
percentiles in infancy and risk of obesity in childhood. Arch
Pediatr Adolesc Med. 2011;165(11):993-998.
33. Grummer-Strawn LM, Mei Z; Centers for Disease Control
and Prevention Pediatric Nutrition Surveillance System.
Does breastfeeding protect against pediatric overweight?
Analysis of longitudinal data from the Centers for Disease
Control and Prevention Pediatric Nutrition Surveillance System. Pediatrics. 2004;113(2):e81-e86.
34. Schwartz BS, Pollak J, Bailey-Davis L, et al. Antibiotic use and
childhood body mass index trajectory. Int J Obes (Lond). 2016;
40(4):615-621.
35. Warner M, Wesselink A, Harley KG, Bradman A, Kogut K,
Eskenazi B. Prenatal exposure to dichlorodiphenyltrichloroethane and obesity at 9 years of age in the CHAMACOS
study cohort. Am J Epidemiol. 2014;179(11):1312-1322.
36. Kalliomäki M, Collado MC, Salminen S, Isolauri E. Early differences in fecal microbiota composition in children may predict
overweight. Am J Clin Nutr. 2008;87(3):534-538.
37. Chang L, Neu J. Early factors leading to later obesity: interactions of the microbiome, epigenome, and nutrition. Curr Probl
Pediatr Adolesc Health Care. 2015;45(5):134-142.
38. Fuemmeler BF, Dedert E, McClernon FJ, Beckham JC. Adverse
childhood events are associated with obesity and disordered
eating: results from a U.S. population-based survey of young
adults. J Trauma Stress. 2009;22(4):329-333.
39. Banfield EC, Liu Y, Davis JS, Chang S, Frazier-Wood AC. Poor
adherence to US Dietary Guidelines for children and
February 2017;92(2):251-265
n
http://dx.doi.org/10.1016/j.mayocp.2016.09.017
www.mayoclinicproceedings.org
CHILDHOOD OBESITYdAN UPDATE
40.
41.
42.
43.
44.
45.
46.
47.
48.
49.
50.
51.
52.
53.
54.
55.
56.
57.
58.
59.
adolescents in the National Health and Nutrition Examination
Survey population. J Acad Nutr Diet. 2016;116(1):21-27.
Ford CN, Slining MM, Popkin BM. Trends in dietary intake
among US 2- to 6-year-old children, 1989-2008. J Acad
Nutr Diet. 2013;113(1):35-42.
Nicklas TA, Hayes D; American Dietetic Association. Position
of the American Dietetic Association: nutrition guidance for
healthy children ages 2 to 11 years. J Am Diet Assoc. 2008;
108(6):1038-1044, 1046-1047.
Wang YC, Bleich SN, Gortmaker SL. Increasing caloric contribution from sugar-sweetened beverages and 100% fruit juices
among US children and adolescents, 1988-2004. Pediatrics.
2008;121(6):e1604-e1614.
Malik VS, Pan A, Willett WC, Hu FB. Sugar-sweetened beverages and weight gain in children and adults: a systematic review
and meta-analysis. Am J Clin Nutr. 2013;98(4):1084-1102.
DeBoer MD, Scharf RJ, Demmer RT. Sugar-sweetened beverages and weight gain in 2- to 5-year-old children. Pediatrics.
2013;132(3):413-420.
Mancino L, Todd JE, Guthrie J, Lin BH. Food away from home
and childhood obesity. Curr Obes Rep. 2014;3(4):459-469.
Taber DR, Chriqui JF, Powell L, Chaloupka FJ. Association between state laws governing school meal nutrition content and
student weight status: implications for new USDA school
meal standards. JAMA Pediatr. 2013;167(6):513-519.
Nelson MC, Neumark-Stzainer D, Hannan PJ, Sirard JR,
Story M. Longitudinal and secular trends in physical activity
and sedentary behavior during adolescence. Pediatrics. 2006;
118(6):e1627-e1634.
Falbe J, Rosner B, Willett WC, Sonneville KR, Hu FB, Field AE.
Adiposity and different types of screen time. Pediatrics. 2013;
132(6):e1497-e1505.
Gilbert-Diamond D, Li Z, Adachi-Mejia AM, McClure AC,
Sargent JD. Association of a television in the bedroom with
increased adiposity gain in a nationally representative sample
of children and adolescents. JAMA Pediatr. 2014;168(5):
427-434.
Epstein LH, Roemmich JN, Robinson JL, et al. A randomized
trial of the effects of reducing television viewing and computer
use on body mass index in young children. Arch Pediatr
Adolesc Med. 2008;162(3):239-245.
Lipsky LM, Iannotti RJ. Associations of television viewing with
eating behaviors in the 2009 Health Behaviour in School-aged
Children Study. Arch Pediatr Adolesc Med. 2012;166(5):
465-472.
Stettler N, Signer TM, Suter PM. Electronic games and environmental factors associated with childhood obesity in
Switzerland. Obes Res. 2004;12(6):896-903.
Heelan KA, Bartee RT, Nihiser A, Sherry B. Healthier school
environment leads to decreases in childhood obesity: the
Kearney Nebraska Story. Child Obes. 2015;11(5):600-607.
Welker E, Lott M, Story M. The school food environment and
obesity prevention: progress over the last decade. Curr Obes
Rep. 2016;5(2):145-155.
Bouchard C. Genetic determinants of regional fat distribution.
Hum Reprod. 1997;12(suppl 1):1-5.
Reinehr T, Hinney A, de Sousa G, Austrup F, Hebebrand J,
Andler W. Definable somatic disorders in overweight
children and adolescents. J Pediatr. 2007;150(6):618-622,
622e1-622.e5.
Speiser PW, Rudolf MC, Anhalt H, et al; Obesity Consensus
Working Group. Childhood obesity. J Clin Endocrinol Metab.
2005;90(3):1871-1887.
Dubern B, Bisbis S, Talbaoui H, et al. Homozygous null mutation of the melanocortin-4 receptor and severe early-onset
obesity. J Pediatr. 2007;150(6):613-617.e1.
Vaisse C, Clement K, Durand E, Hercberg S, Guy-Grand B,
Froguel P. Melanocortin-4 receptor mutations are a frequent
and heterogeneous cause of morbid obesity. J Clin Invest.
2000;106(2):253-262.
Mayo Clin Proc. n February 2017;92(2):251-265
www.mayoclinicproceedings.org
n
60. Farooqi IS, O’Rahilly S. 20 years of leptin: human disorders of
leptin action. J Endocrinol. 2014;223(1):T63-T70.
61. Jiang F, Zhu S, Yan C, Jin X, Bandla H, Shen X. Sleep and
obesity in preschool children. J Pediatr. 2009;154(6):814-818.
62. Sekine M, Yamagami T, Handa K, et al. A dose-response relationship between short sleeping hours and childhood obesity:
results of the Toyama Birth Cohort Study. Child Care Health
Dev. 2002;28(2):163-170.
63. Koren D, Levitt Katz LE, Brar PC, Gallagher PR, Berkowitz RI,
Brooks LJ. Sleep architecture and glucose and insulin homeostasis in obese adolescents. Diabetes Care. 2011;34(11):24422447.
64. Huscher D, Thiele K, Gromnica-Ihle E, et al. Dose-related patterns of glucocorticoid-induced side effects. Ann Rheum Dis.
2009;68(7):1119-1124.
65. Reekie J, Hosking SP, Prakash C, Kao KT, Juonala M, Sabin MA.
The effect of antidepressants and antipsychotics on weight
gain in children and adolescents. Obes Rev. 2015;16(7):
566-580.
66. Hamed SA. Antiepileptic drugs influences on body weight in
people with epilepsy. Expert Rev Clin Pharmacol. 2015;8(1):
103-114.
67. Skinner AC, Perrin EM, Moss LA, Skelton JA. Cardiometabolic
risks and severity of obesity in children and young adults.
N Engl J Med. 2015;373(14):1307-1317.
68. HEALTHY Study Group; Kaufman FR, Hirst K, Linder B, et al.
Risk factors for type 2 diabetes in a sixth- grade multiracial
cohort: the HEALTHY study. Diabetes Care. 2009;32(5):
953-955.
69. Pinhas-Hamiel O, Dolan LM, Daniels SR, Standiford D,
Khoury PR, Zeitler P. Increased incidence of non-insulindependent diabetes mellitus among adolescents. J Pediatr.
1996;128(5 pt 1):608-615.
70. Molnár D. The prevalence of the metabolic syndrome and
type 2 diabetes mellitus in children and adolescents. Int J
Obes Relat Metab Disord. 2004;28(suppl 3):S70-S74.
71. Sinha R, Fisch G, Teague B, et al. Prevalence of impaired
glucose tolerance among children and adolescents with
marked obesity [published correction appears in N Engl J
Med. 2002;346(22):1756. Dosage error in published abstract;
MEDLINE/PubMed abstract corrected; Dosage error in article
text]. N Engl J Med. 2002;346(11):802-810.
72. Copeland KC, Zeitler P, Geffner M, et al; TODAY Study
Group. Characteristics of adolescents and youth with
recent-onset type 2 diabetes: the TODAY cohort at baseline.
J Clin Endocrinol Metab. 2011;96(1):159-167.
73. TODAY Study Group. Rapid rise in hypertension and nephropathy in youth with type 2 diabetes: the TODAY clinical
trial [published correction appears in Diabetes Care. 2013;
36(8):2448]. Diabetes Care. 2013;36(6):1735-1741.
74. TODAY Study Group; Zeitler P, Hirst K, Pyle L, et al. A clinical
trial to maintain glycemic control in youth with type 2 diabetes. N Engl J Med. 2012;366(24):2247-2256.
75. Sorof J, Daniels S. Obesity hypertension in children: a problem
of epidemic proportions. Hypertension. 2002;40(4):441-447.
76. Friedemann C, Heneghan C, Mahtani K, Thompson M,
Perera R, Ward AM. Cardiovascular disease risk in healthy
children and its association with body mass index: systematic
review and meta-analysis. BMJ. 2012;345:e4759.
77. Weiss R, Dziura J, Burgert TS, et al. Obesity and the metabolic
syndrome in children and adolescents. N Engl J Med. 2004;
350(23):2362-2374.
78. Calcaterra V, Klersy C, Muratori T, et al. Prevalence of metabolic syndrome (MS) in children and adolescents with varying degrees of obesity. Clin Endocrinol (Oxf). 2008;68(6):
868-872.
79. Crowley DI, Khoury PR, Urbina EM, Ippisch HM, Kimball TR.
Cardiovascular impact of the pediatric obesity epidemic:
higher left ventricular mass is related to higher body mass
index. J Pediatr. 2011;158(5):709-714.e1.
http://dx.doi.org/10.1016/j.mayocp.2016.09.017
263
MAYO CLINIC PROCEEDINGS
80. Chinali M, de Simone G, Roman MJ, et al. Impact of obesity
on cardiac geometry and function in a population of adolescents: the Strong Heart Study. J Am Coll Cardiol. 2006;47(11):
2267-2273.
81. Kaplowitz PB, Slora EJ, Wasserman RC, Pedlow SE, HermanGiddens ME. Earlier onset of puberty in girls: relation to
increased body mass index and race. Pediatrics. 2001;108(2):
347-353.
82. Legro RS, Arslanian SA, Ehrmann DA, et al; Endocrine Society.
Diagnosis and treatment of polycystic ovary syndrome: an
Endocrine Society clinical practice guideline. J Clin Endocrinol
Metab. 2013;98(12):4565-4592.
83. Spilsbury JC, Storfer-Isser A, Rosen CL, Redline S. Remission
and incidence of obstructive sleep apnea from middle childhood to late adolescence. Sleep. 2015;38(1):23-29.
84. Kalra M, Inge T. Effect of bariatric surgery on obstructive
sleep apnoea in adolescents. Paediatr Respir Rev. 2006;
7(4):260-267.
85. Verhulst SL, Schrauwen N, Haentjens D, et al. Sleep-disordered breathing in overweight and obese children and adolescents: prevalence, characteristics and the role of fat
distribution. Arch Dis Child. 2007;92(3):205-208.
86. Papoutsakis C, Priftis KN, Drakouli M, et al. Childhood overweight/obesity and asthma: is there a link? A systematic review
of recent epidemiologic evidence. J Acad Nutr Diet. 2013;
113(1):77-105.
87. Feldstein AE, Charatcharoenwitthaya P, Treeprasertsuk S,
Benson JT, Enders FB, Angulo P. The natural history of nonalcoholic fatty liver disease in children: a follow-up study for
up to 20 years. Gut. 2009;58(11):1538-1544.
88. Matteoni CA, Younossi ZM, Gramlich T, Boparai N, Liu YC,
McCullough AJ. Nonalcoholic fatty liver disease: a spectrum
of clinical and pathological severity. Gastroenterology. 1999;
116(6):1413-1419.
89. Lavine JE, Schwimmer JB. Nonalcoholic fatty liver disease in
the pediatric population. Clin Liver Dis. 2004;8(3):549-558,
viii-ix.
90. Huang JS, Barlow SE, Quiros-Tejeira RE, et al; NASPGHAN Obesity Task Force. Childhood obesity for pediatric gastroenterologists. J Pediatr Gastroenterol Nutr. 2013;
56(1):99-109.
91. Franzese A, Vajro P, Argenziano A, et al. Liver involvement in
obese children: ultrasonography and liver enzyme levels at
diagnosis and during follow-up in an Italian population. Dig
Dis Sci. 1997;42(7):1428-1432.
92. Pomerantz WJ, Timm NL, Gittelman MA. Injury patterns in
obese versus nonobese children presenting to a pediatric
emergency department. Pediatrics. 2010;125(4):681-685.
93. Chan G, Chen CT. Musculoskeletal effects of obesity. Curr
Opin Pediatr. 2009;21(1):65-70.
94. Montgomery CO, Young KL, Austen M, Jo CH, Blasier RD,
Ilyas M. Increased risk of Blount disease in obese children
and adolescents with vitamin D deficiency. J Pediatr Orthop.
2010;30(8):879-882.
95. Bhatia NN, Pirpiris M, Otsuka NY. Body mass index in patients
with slipped capital femoral epiphysis. J Pediatr Orthop. 2006;
26(2):197-199.
96. Strauss RS. Childhood obesity and self-esteem. Pediatrics.
2000;105(1):e15.
97. Sawyer MG, Harchak T, Wake M, Lynch J. Four-year prospective study of BMI and mental health problems in young
children. Pediatrics. 2011;128(4):677-684.
98. Schwimmer JB, Burwinkle TM, Varni JW. Health-related quality
of life of severely obese children and adolescents. JAMA. 2003;
289(14):1813-1819.
99. Griffiths LJ, Wolke D, Page AS, Horwood JP; ALSPAC Study
Team. Obesity and bullying: different effects for boys and girls.
Arch Dis Child. 2006;91(2):121-125.
100. Gortmaker SL, Must A, Perrin JM, Sobol AM, Dietz WH.
Social and economic consequences of overweight in
264
Mayo Clin Proc.
n
101.
102.
103.
104.
105.
106.
107.
108.
109.
110.
111.
112.
113.
114.
115.
116.
117.
118.
adolescence and young adulthood. N Engl J Med. 1993;
329(14):1008-1012.
Yosipovitch G, DeVore A, Dawn A. Obesity and the skin: skin
physiology and skin manifestations of obesity. J Am Acad Dermatol. 2007;56(6):901-916; quiz 917-920.
Brara SM, Koebnick C, Porter AH, Langer-Gould A. Pediatric
idiopathic intracranial hypertension and extreme childhood
obesity. J Pediatr. 2012;161(4):602-607.
Baker JL, Olsen LW, Sørensen TI. Childhood body-mass index
and the risk of coronary heart disease in adulthood. N Engl J
Med. 2007;357(23):2329-2337.
Armstrong S, Lazorick S, Hampl S, et al. Physical examination
findings among children and adolescents with obesity: an
evidence-based review. Pediatrics. 2016;137(2):e20151766.
Krebs NF, Himes JH, Jacobson D, Nicklas TA, Guilday P,
Styne D. Assessment of child and adolescent overweight
and obesity. Pediatrics. 2007;120(suppl 4):S193-S228.
Pickering TG, Hall JE, Appel LJ, et al; Subcommittee of Professional and Public Education of the American Heart Association
Council on High Blood Pressure Research. Recommendations
for blood pressure measurement in humans and experimental
animals, Part 1: blood pressure measurement in humans: a
statement for professionals from the Subcommittee of Professional and Public Education of the American Heart Association
Council on High Blood Pressure Research. Hypertension. 2005;
45(1):142-161.
Expert Panel on Integrated Guidelines for Cardiovascular
Health and Risk Reduction in Children and Adolescents; National Heart, Lung, and Blood Institute. Expert panel on integrated guidelines for cardiovascular health and risk reduction
in children and adolescents: summary report. Pediatrics.
2011;128(suppl 5):S213-S256.
Gillman MW, Daniels SR. Is universal pediatric lipid screening
justified? JAMA. 2012;307(3):259-260.
Spear BA, Barlow SE, Ervin C, et al. Recommendations for
treatment of child and adolescent overweight and obesity. Pediatrics. 2007;120(suppl 4):S254-S288.
Barlow SE; Expert Committee. Expert committee recommendations regarding the prevention, assessment, and treatment
of child and adolescent overweight and obesity: summary
report. Pediatrics. 2007;120(suppl 4):S164-S192.
Kitzman-Ulrich H, Wilson DK, St George SM, Lawman H,
Segal M, Fairchild A. The integration of a family systems
approach for understanding youth obesity, physical activity,
and dietary programs. Clin Child Fam Psychol Rev. 2010;13(3):
231-253.
Epstein LH, Valoski A, Wing RR, McCurley J. Ten-year outcomes of behavioral family-based treatment for childhood
obesity. Health Psychol. 1994;13(5):373-383.
Jansen E, Mulkens S, Jansen A. Tackling childhood overweight:
treating parents exclusively is effective. Int J Obes (Lond). 2011;
35(4):501-509.
Golan M, Crow S. Targeting parents exclusively in the treatment of childhood obesity: long-term results. Obes Res.
2004;12(2):357-361.
Janicke DM, Sallinen BJ, Perri MG, et al. Comparison of
parent-only vs family-based interventions for overweight
children in underserved rural settings: outcomes from
project STORY. Arch Pediatr Adolesc Med. 2008;162(12):
1119-1125.
Resnicow K, McMaster F, Bocian A, et al. Motivational interviewing and dietary counseling for obesity in primary care:
an RCT. Pediatrics. 2015;135(4):649-657.
Irby M, Kaplan S, Garner-Edwards D, Kolbash S, Skelton JA.
Motivational interviewing in a family-based pediatric obesity
program: a case study. Fam Syst Health. 2010;28(3):
236-246.
Daniels SR, Hassink SG; COMMITTEE ON NUTRITION. The
role of the pediatrician in primary prevention of obesity. Pediatrics. 2015;136(1):e275-e292.
February 2017;92(2):251-265
n
http://dx.doi.org/10.1016/j.mayocp.2016.09.017
www.mayoclinicproceedings.org
CHILDHOOD OBESITYdAN UPDATE
119. Ross MM, Kolbash S, Cohen GM, Skelton JA. Multidisciplinary
treatment of pediatric obesity: nutrition evaluation and management. Nutr Clin Pract. 2010;25(4):327-334.
120. Ebbeling CB, Leidig MM, Sinclair KB, Hangen JP, Ludwig DS.
A reduced-glycemic load diet in the treatment of adolescent
obesity. Arch Pediatr Adolesc Med. 2003;157(8):773-779.
121. Sondike SB, Copperman N, Jacobson MS. Effects of a lowcarbohydrate diet on weight loss and cardiovascular risk factor
in overweight adolescents. J Pediatr. 2003;142(3):253-258.
122. Kirk S, Brehm B, Saelens BE, et al. Role of carbohydrate modification in weight management among obese children: a randomized clinical trial. J Pediatr. 2012;161(2):320-327.e1.
123. US Department of Health and Human Services. 2008 Physical
Activity Guidelines for Americans: Be Active, Healthy and Happy.
Washington, DC: US Department of Health and Human
Services; 2008.
124. American Academy of Pediatrics, National Resource Center
for Health and Safety in Child Care and Early Education. Caring
for Our Children: National Health and Safety Performance Standards: Guidelines for Early Care and Education Programs. 3rd ed.
Washington, DC: American Public Health Association; 2011.
125. Anderson SE, Whitaker RC. Household routines and obesity
in US preschool-aged children. Pediatrics. 2010;125(3):
420-428.
126. Whitlock EP, O’Connor EA, Williams SB, Beil TL, Lutz KW.
Effectiveness of weight management interventions in children:
a targeted systematic review for the USPSTF. Pediatrics. 2010;
125(2):e396-e418.
127. Peirson L, Fitzpatrick-Lewis D, Morrison K, Warren R, Usman
Ali M, Raina P. Treatment of overweight and obesity in children and youth: a systematic review and meta-analysis.
CMAJ Open. 2015;3(1):E35-E46.
128. August GP, Caprio S, Fennoy I, et al; Endocrine Society. Prevention and treatment of pediatric obesity: an endocrine society clinical practice guideline based on expert opinion. J Clin
Endocrinol Metab. 2008;93(12):4576-4599.
129. Savoye M, Shaw M, Dziura J, et al. Effects of a weight management program on body composition and metabolic parameters in overweight children: a randomized controlled trial.
JAMA. 2007;297(24):2697-2704.
130. Kamath CC, Vickers KS, Ehrlich A, et al. Clinical review: behavioral interventions to prevent childhood obesity: a systematic
review and metaanalyses of randomized trials. J Clin Endocrinol
Metab. 2008;93(12):4606-4615.
131. Kelly AS, Fox CK, Rudser KD, Gross AC, Ryder JR. Pediatric
obesity pharmacotherapy:current status of the field, review
of the literature and clinical trial considerations. Int J Obes
(Lond). 2016;40(7):1043-1050.
132. Chanoine JP, Hampl S, Jensen C, Boldrin M, Hauptman J. Effect
of orlistat on weight and body composition in obese adolescents: a randomized controlled trial [published correction appears in JAMA. 2005;294(12):1491]. JAMA. 2005;293(23):
2873-2883.
133. McGovern L, Johnson JN, Paulo R, et al. Clinical review: treatment of pediatric obesity: a systematic review and metaanalysis of randomized trials. J Clin Endocrinol Metab. 2008;
93(12):4600-4605.
134. McDonagh MS, Selph S, Ozpinar A, Foley C. Systematic review of the benefits and risks of metformin in treating obesity
in children aged 18 years and younger. JAMA Pediatr. 2014;
168(2):178-184.
135. Park MH, Kinra S, Ward KJ, White B, Viner RM. Metformin for
obesity in children and adolescents: a systematic review. Diabetes Care. 2009;32(9):1743-1745.
136. Fox CK, Marlatt KL, Rudser KD, Kelly AS. Topiramate for
weight reduction in adolescents with severe obesity. Clin
Pediatr (Phila). 2015;54(1):19-24.
Mayo Clin Proc. n February 2017;92(2):251-265
www.mayoclinicproceedings.org
n
137. Kelly AS, Rudser KD, Nathan BM, et al. The effect of glucagonlike peptide-1 receptor agonist therapy on body mass index in
adolescents with severe obesity: a randomized, placebocontrolled, clinical trial. JAMA Pediatr. 2013;167(4):355-360.
138. Kelly AS, Metzig AM, Rudser KD, et al. Exenatide as a weightloss therapy in extreme pediatric obesity: a randomized,
controlled pilot study. Obesity (Silver Spring). 2012;20(2):
364-370.
139. Sjöström L, Narbro K, Sjöström CD, et al; Swedish Obese
Subjects Study. Effects of bariatric surgery on mortality in
Swedish obese subjects. N Engl J Med. 2007;357(8):741-752.
140. Sjöström L, Lindroos AK, Peltonen M, et al; Swedish Obese
Subjects Study Scientific Group. Lifestyle, diabetes, and cardiovascular risk factors 10 years after bariatric surgery. N Engl J
Med. 2004;351(26):2683-2693.
141. Schilling PL, Davis MM, Albanese CT, Dutta S, Morton J. National trends in adolescent bariatric surgical procedures and
implications for surgical centers of excellence. J Am Coll Surg.
2008;206(1):1-12.
142. Tsai WS, Inge TH, Burd RS. Bariatric surgery in adolescents:
recent national trends in use and in-hospital outcome. Arch
Pediatr Adolesc Med. 2007;161(3):217-221.
143. Zwintscher NP, Azarow KS, Horton JD, Newton CR,
Martin MJ. The increasing incidence of adolescent bariatric surgery. J Pediatr Surg. 2013;48(12):2401-2407.
144. Inge TH, Courcoulas AP, Jenkins TM, et al; Teen-LABS Consortium. Weight loss and health status 3 years after bariatric
surgery in adolescents. N Engl J Med. 2016;374(2):113-123.
145. Inge TH, King WC, Jenkins TM, et al. The effect of obesity in
adolescence on adult health status. Pediatrics. 2013;132(6):
1098-1104.
146. Inge TH, Zeller MH, Jenkins TM, et al; Teen-LABS Consortium.
Perioperative outcomes of adolescents undergoing bariatric
surgery: the Teen-Longitudinal Assessment of Bariatric Surgery
(Teen-LABS) study. JAMA Pediatr. 2014;168(1):47-53.
147. le Roux CW, Aylwin SJ, Batterham RL, et al. Gut hormone
profiles following bariatric surgery favor an anorectic state,
facilitate weight loss, and improve metabolic parameters.
Ann Surg. 2006;243(1):108-114.
148. Pratt JS, Lenders CM, Dionne EA, et al. Best practice updates
for pediatric/adolescent weight loss surgery. Obesity (Silver
Spring). 2009;17(5):901-910.
149. Michalsky M, Reichard K, Inge T, Pratt J, Lenders C; American
Society for Metabolic and Bariatric Surgery. ASMBS pediatric
committee best practice guidelines. Surg Obes Relat Dis.
2012;8(1):1-7.
150. Inge TH, Krebs NF, Garcia VF, et al. Bariatric surgery for
severely overweight adolescents: concerns and recommendations. Pediatrics. 2004;114(1):217-223.
151. Loux TJ, Haricharan RN, Clements RH, et al. Health-related
quality of life before and after bariatric surgery in adolescents.
J Pediatr Surg. 2008;43(7):1275-1279.
152. Loy JJ, Youn HA, Schwack B, Kurian M, Ren Fielding C,
Fielding GA. Improvement in nonalcoholic fatty liver disease
and metabolic syndrome in adolescents undergoing bariatric
surgery. Surg Obes Relat Dis. 2015;11(2):442-449.
153. Sugerman HJ, Sugerman EL, DeMaria EJ, et al. Bariatric surgery
for severely obese adolescents. J Gastrointest Surg. 2003;7(1):
102-107; discussion 107-108.
154. Dillard BE III, Gorodner V, Galvani C, et al. Initial experience
with the adjustable gastric band in morbidly obese US adolescents and recommendations for further investigation. J Pediatr
Gastroenterol Nutr. 2007;45(2):240-246.
155. Kelly AS, Ryder JR, Marlatt KL, Rudser KD, Jenkins T, Inge TH.
Changes in inflammation, oxidative stress and adipokines
following bariatric surgery among adolescents with severe
obesity. Int J Obes (Lond). 2016;40(2):275-280.
http://dx.doi.org/10.1016/j.mayocp.2016.09.017
265