CLINICAL CROSSROADS

CLINICIANS CORNER

CONFERENCES WITH PATIENTS AND DOCTORS

Weight Loss Strategies for Adolescents

A 14-Year-Old Struggling to Lose Weight
David S. Ludwig, MD, PhD, Discussant
DR SHIP: Ms K is an obese 14-year-old girl who is struggling with weight loss. She lives in the greater metropolitan Boston area. Ms K began to gain excess weight at age 8
years. Over the past 7 years, her weight has increased by 20
to 30 lb annually (FIGURE 1). Her peak weight is 256 lb, giving her a body mass index of 40. Her menarche was at age
11 years and her menstrual periods are regular. She reports
trying various weight loss programs but either she did not
follow through or they did not work. She has never lost more
than 5 lb with any focused effort.
On a typical day, Ms K skips breakfast, so her school lunch
is her first meal of the day. She eats whatever is served there,
often something greasy, with a small salad and chocolate
milk. When she comes home from school, she begins to snack
on good junk food. Over the course of the afternoon, she
might have several of the following: baked chips, a cereal
bar or 2, 2 or more 100-calorie packs, a glass of (1% fat)
milk, crackers, or pasta with cheese. She eats dinner with
her parents, which is often fried chicken, pasta with cheese,
or a hamburger. There are rarely vegetables on the plate.
After dinner, she will routinely eat more, ingesting 1 to 3
snacks while working on her computer. She does not routinely eat dessert at dinner and does not drink sugarsweetened beverages. She does not watch television regularly. She used to ride a horse several times a week but has
not done so in several years. Her only regular activity is walking home from school, about 12 mile daily.
Ms K was told by her pediatrician that she needed to lose
weight or she might develop diabetes. She has experienced
harassment at school and online related to her obesity. There
has also been significant tension between Ms K and her parentsespecially her motherabout her eating habits and
progressive weight gain.
Ms K was adopted at birth. Her biological father is obese.
Her adoptive parents are overweight. She does not drink alcohol, use recreational drugs, or smoke cigarettes.
She has had no hospitalizations or surgery. On examination, Ms K weighs 248 lb and is 5 ft, 6 in tall. Her blood
pressure is 131/83 mm Hg, repeated at 118/70 mm Hg.
CME available online at www.jamaarchivescme.com
and questions on p 517.
498

JAMA, February 1, 2012Vol 307, No. 5

With prevalence approaching 20% in the United States, adolescent obesity has become a common problem for patients,
parents, and clinicians. Obese adolescents may experience
physical and psychosocial complications, as illustrated by
the case of Ms K, a 14-year-old girl with a body mass index
of 40. Unfortunately, the effectiveness of pediatric obesity
treatment is modest in younger children and declines in older
children and adolescents, and few interventions involving
adolescents have produced significant long-term weight loss.
Nevertheless, novel strategies to alter energy balance have
shown preliminary evidence of benefit in clinical trials, including a diet focused on food quality rather than fat restriction and a lifestyle approach to encourage enjoyable physical activity throughout the day rather than intermittent
exercise. Parents can have an important influence on weightrelated behaviors in adolescents despite typically complicated emotional dynamics at this age, especially through the
use of noncoercive methods. A key parenting practice applicable to children of all ages is to create a protective environment in the home, substituting nutritious foods for unhealthful ones and facilitating physical activities instead of
sedentary pursuits. Other behaviors that may promote successful long-term weight management include good sleep
hygiene, stress reduction, and mindfulness. Ultimately, the
obesity epidemic can be attributed to changes in the social
environment that hinder healthful lifestyle habits, and prevention will require a comprehensive public health strategy.
JAMA. 2012;307(5):498-508

www.jama.com

The conference on which this article is based took place at the Medical Grand
Rounds at Childrens Hospital Boston, Boston, Massachusetts, on February 23, 2011.
Author Affiliations: Dr Ludwig is Director of the Optimal Weight for Life (OWL)
Program and the New Balance Foundation Obesity Prevention Center, Childrens
Hospital Boston, Professor of Pediatrics, Harvard Medical School, and Professor
of Nutrition, Harvard School of Public Health, Boston, Massachusetts.
Corresponding Author: David S. Ludwig, MD, PhD, Childrens Hospital Boston,
Division of Endocrinology, 300 Longwood Ave, Boston, MA 02115 (david.ludwig
@childrens.harvard.edu).
Clinical Crossroads at Beth Israel Deaconess Medical Center is produced and edited by Risa B. Burns, MD, series editor; Tom Delbanco, MD, Howard Libman, MD,
Eileen E. Reynolds, MD, Marc Schermerhorn, MD, Amy N. Ship, MD, and Anjala
V. Tess, MD.
Clinical Crossroads Section Editor: Margaret A. Winker, MD, Deputy Editor and
Online Editor, JAMA.

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CLINICAL CROSSROADS

The only other abnormal examination finding was dermatological changes on her neck, diagnosed as acanthosis
nigricans.
MS K: HER VIEW
When I turned 8, I started realizing that other kids would
look at me different. I think when you are a kid its kind of
hard to monitor what you eat because your friends would
be asking what kind of things you are doing and why.
I tried a few different diets. I tried a cottage cheese diet
but that didnt work. Then for 3 days, I tried the acai berry
pill and it didnt do anything so I stopped taking that. I participated in some activities as well. I would go to Weight
Watchers, but I wouldnt really stay on track. Over the summer and the fall, I tried to do field hockey but my ankle got
hurt so I couldnt keep doing that.
My mom usually prepares the meals. There are huge fights
between us if Id want to eat something and it wasnt healthy.
My parents would say, No, give that back; no, you cant
have that; no, youre going to gain weight.
For example, if I want 1 bowl of chips before dinner, then
Id be told, No, you cant have that. If we went out to dinner, they just keep looking at whatever I was eating and I
just think its kind of hard to go anywhere without being
yelled at. I mean, we always have healthy foods at home.
Mostly everything in our house is reduced fat, light, no sugar,
but if I just wanted a snack there usually is some sort of disagreement.
I have had some difficulties at school. About a month and
a half ago, there were a few kids from a different town and
online, on Facebook, who were repeatedly calling me very
mean names. One kid even texted me the word fat about
25 times. He then called me and I kept ignoring it and I decided to change my number because it was really bad. We
actually ended up calling the police. I think that was the worst
Ive been through. However, about 2 weeks ago, another kid
that Ive never metIve never seen himmessaged me calling me those mean names again. Things have gotten a little
better than before though.
I really think that its important to be ready to lose the
weight. If you have your parents pressuring you and saying
you need to do this or doctors saying you need to do this, it
wont be as motivating. I first realized it when I was at the
store; I just wanted to be able to fit in all the clothes that
my friends were buying and it really hurt me at that moment. It was at that moment I said I need to change and I
think thats what really brought me to where I am now.
MS KS MOTHER: HER VIEW
Probably the biggest challenge that I and my husband have
had is backing off. I constantly watch her, correct her, and
stop her from doing things. I am almost obsessive about what
she eats, what she doesnt eat. My husband and I went to a
counselor locally, and he was the one to tell us we need to
back off because it is making things worse. Thats been the

biggest challenge. I think I feel like I am the food police sometimes.

AT THE CROSSROADS:
QUESTIONS FOR DR LUDWIG
What is the definition of childhood obesity and how has its
prevalence changed since the mid-20th century? What are the
long-term implications of the childhood obesity epidemic to
society? What are the immediate medical and psychological
consequences of obesity in children? Why is childhood obesity so difficult to treat? What are the therapeutic options? What
parenting strategies can be used to promote long-term behavior change? What do you recommend for Ms K?
DR LUDWIG: In this article, the GRADE system1 is used
to describe the strength of the evidence.
A. High quality: Further research is very unlikely to change
confidence in the estimate of effect.
B. Moderate quality: Further research is likely to have an
important impact on confidence in the estimate of effect and
may change the estimate.
Figure 1. Patients Growth Chart

Ms Ks height and weight throughout childhood on growth curves from the Centers for Disease Control and Prevention.

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Figure 2. Conceptual Model of Cycle of Childhood and Adult

Obesity

Duration of excessive weight gain

Obesity-promoting lifestyle
Obesity-promoting biological changes
Childs psychosocial issues

Societal costs
costs, including
CHILD H OOD
OBESIT Y

Increasing health care costs

Decreasing economic productivity

ADULT
OBESI TY

Morbidity
Shortened life expectancy

In utero metabolic programming

Parental modeling of obesity-promoting lifestyle
Normalized perception of excess weight
Parental psychosocial issues

Childhood obesity may lead to adult obesity because of greater duration of excessive weight gain; the tendency for obesity-promoting diet and physical activity
habits to track into adulthood8; persistence of biological changes that promote obesity involving, for example, fat cell size, number, or distribution9; and psychosocial
issues that cause weight gain and/or antagonize weight loss, including poverty
and depression.10 Adult obesity, in turn, may cause childhood obesity through in
utero metabolic programming as discussed in the text; parental modeling of obesitypromoting diet and physical activity habits11; normalized perception of excess weight,
wherein obesity in a child may be unrecognized or encouraged12; and parental psychosocial issues. Medical and economic costs for society will likely escalate unless
this cycle can be arrested.

C. Low quality: Further research is very likely to have an

important impact on confidence in the estimate of effect and
is likely to change the estimate.
D. Very low quality: Any estimate of effect is very uncertain.
DEMOGRAPHICS
Body composition and its relationship to disease risk change
with growth and sexual maturation. For this reason, absolute values for body mass index (BMI; calculated as weight
in kilograms divided by height in meters squared) cannot
be used to define excessive weight in the pediatric age group.
Instead, weight status is classified according to age- and sexspecific BMI percentiles. These percentiles are based on population surveys conducted predominantly in the 1960s and
1970s, before onset of the obesity epidemic.2 According to
current consensus, a BMI greater than or equal to the 85th
but less than the 95th percentiles is considered overweight, and a BMI greater than or equal to the 95th percentile is considered obese.3 However, these arbitrary cut points,
corresponding to adult BMI cut points of 25 and 30, respec500

JAMA, February 1, 2012Vol 307, No. 5

tively, underestimate the true effects of excessive adiposity, as demonstrated by long-term prospective data showing associations between childhood body weight and adult
cardiovascular disease that extend well into the normal range
for BMI percentile (B).4
After remaining relatively stable for many years, the prevalence of obesity began to increase rapidly in about 1980
among children of all age and racial/ethnic groups in the
United States. Today in the United States, adolescent obesity rates range from 16.1% in non-Hispanic whites to 23.9%
in Mexican Americans.5 Approximately 1 in 3 adolescents
is excessively heavy, with a BMI at or above the 85th percentile. Of particular concern, the proportion of children
like Ms K with extreme obesity, at or above the 99th
percentile, has increased dramatically.6 A nationally representative survey reported no overall change in obesity prevalence among boys or girls between 2007-2008 and 20092010,5 although it is too soon to know whether these data
indicate a true plateau or a statistical aberration.
LONG-TERM EFFECTS OF THE EPIDEMIC
Even without further increases in prevalence, the effects of
obesity may continue to mount for many years, as successive stages of the epidemic unfold. In the first stage, prevalence increased rapidly as discussed above. However, it may
take many years for an obese child to develop complications such as diabetes or fatty liver (second stage) and additional time for weight-related complications to result in
a life-threatening event such as myocardial infarction, stroke,
or kidney failure (third stage). Indeed, early evidence of the
epidemics progression may already exist. In a nationwide
survey of hospitalizations from 1995 to 2008, the incidence of ischemic stroke among children and young adults
increased by approximately 30%, and the most common coexisting conditions included obesity, diabetes, hypertension, and dyslipidemias.7 A fourth stage of the epidemic may
involve transgenerational propagation.
As depicted in FIGURE 2, childhood obesity may cause
adult obesity and, conversely, adult obesity may cause childhood obesity through several genetic and nongenetic mechanisms. Recently, a potential biological basis for transgenerational propagation has been elucidated. When female rats
were made obese by overfeeding before and during pregnancy, their offspring became fatter and had higher blood
glucose concentration than offspring of females who were
not overfed, despite having the same genetic background.13 In humans, high prepregnancy BMI or pregnancy weight gain is associated with higher birth weight and
childhood BMI, controlling for genetic influences.14,15 Thus,
obesity during pregnancy may create a metabolically abnormal intrauterine environment that programs the developing fetus for an increased lifetime risk of obesity and
related diseases.16 These biological, behavioral, and psychosocial influences create a vicious cycle that may accelerate
obesity-related disease, shorten life expectancy,17 and in2012 American Medical Association. All rights reserved.

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crease annual health care expenditures by several hundred

billion dollars in the United States in the next few decades.18,19
COMPLICATIONS OF CHILDHOOD OBESITY
In addition to its long-term sequelae, obesity may affect
virtually every organ system of a childs body, as summarized in TABLE 1 and discussed elsewhere.3,20 Ms K has several of these complications. Acanthosis nigricans is a common dermatological sign of insulin resistance in obese
children indicating elevated risk of type 2 diabetes. Type 2

diabetes, once virtually unknown in adolescents, now

accounts for more than half of all new cases of diabetes
among most racial/ethnic groups.21 Ms K may also have
hypertension, a major, often undiagnosed cardiovascular
risk factor. 22 The prevalence of high blood pressure
increased among children between 1963 and 2002, and
this secular trend can be primarily attributable to the obesity epidemic.23 As a component of the metabolic syndrome, hypertension is associated with hypertriglyceridemia, low serum high-density lipoprotein cholesterol,
glucose intolerance, chronic systemic inflammation, coag-

Table 1. Medical Complications of Childhood Obesity a

Diagnosis
Complications
Neurological
Pseudotumor cerebri
Skin
Acanthosis nigricans
Musculoskeletal
Slipped capital femoral epiphysis
Tibia vara (Blount disease)
Flat feet
Cardiovascular
Metabolic syndrome

Pulmonary
Sleep apnea

Exercise intolerance
Gastrointestinal
Gastroesophageal reflux

History
Headache, visual changes, vomiting

Precocious puberty
Polycystic ovarian syndrome
(in girls)

Hypogonadism (in boys)

Nutritional deficiencies
Vitamin D
Psychosocial (eating disorders,
anxiety, depression, poor
self-esteem)

Papilledema

Evaluation b
Head magnetic resonance imaging

Dark, velvety skin in

intertriginous areas
Hip pain, difficulty walking
Progressive bowing of one or both legs
Foot pain with walking

Decreased range of motion, limp

Characteristic deformity
Decreased or absent foot arch

Hip radiography
Leg radiography

Acanthosis nigricans, high blood

pressure

Fasting glucose, insulin, triglycerides,

high-density lipoprotein
cholesterol, C-reactive protein

Gasping for air and mouth breathing

during sleep, snoring, daytime
somnolence, fatigue, behavioral
changes
Shortness of breath with physical
exertion

Sleep study, electrocardiography

Burning pain in the upper abdomen or

chest, asthma, difficulty swallowing

Upper endoscopy, pH monitoring

study (severe cases)
Liver transaminases, liver ultrasound;
rule out other causes

Fatty liver
Endocrine
Type 2 diabetes

Physical Examination

Rule out cardiac and pulmonary

disease (severe cases)

Hepatomegaly

Polyuria, polydipsia

Urinalysis, fasting glucose, oral

glucose tolerance test,
hemoglobin A1c, pancreatic
autoantibodies, C-peptide
Rule out other causes

Early breast or pubic hair development,

rapid growth
Irregular menstrual periods or
amenorrhea, excess hair growth,
acne

Advanced sexual development,

tall stature

Lack of secondary sexual characteristics

Delayed sexual development

Usually none

Manifestations of rickets
(severe cases)

Vitamin D, calcium, phosphate

Emotional lability, behavioral changes,

social withdrawal, suicidal ideation

Evidence of self-harming
behaviors (eg, scars from
self-inflicted knife cuts)

Psychiatric and/or social services

assessment

Acanthosis nigricans, hirsutism,

acne, clitoromegaly

Luteinizing hormone,
follicle-stimulating hormone,
free testosterone, sex
hormonebinding globulin,
17-hydroxyprogesterone; pelvic
examination; rule out other causes
Testosterone; rule out other causes

a This overview is not intended to be exhaustive; more comprehensive reviews are referenced in the text.
b The following laboratory tests are recommended for all obese adolescents in view of the prevalence of related complications and the medical consequences of missed diagnosis: fasting

blood glucose or hemoglobin A1c, fasting serum lipids, liver transaminases (especially alanine aminotransferase), and vitamin D level. Other evaluations are recommended if indicated by
positive findings on history or physical examination.

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ulopathy, hypercortisolemia, elevated oxidative stress,

endothelial dysfunction, and fatty liver. Laboratory testing
would likely identify some of these other complications in
Ms K.24 Nonalcoholic fatty liver disease merits special
attention as another serious, underdiagnosed metabolic
abnormality. Fatty liver occurs in an estimated 1 of 3 obese
children,25 and less than half of affected individuals have
elevated serum liver enzymes. Excess liver fat appears to
play a central pathophysiological role in development of
the metabolic syndrome26 and may cause hepatitis, cirrhosis, and liver failure in some cases.27
Psychosocial difficulties frequently comprise the most
troublesome complications for an adolescent. Obese children and adolescents commonly experience teasing, anxiety,
depression, disordered eating, and poor self-esteem.28-31 Ms
K has been subjected to recurrent online harassment, and
cyber bullying of this nature may have tragic consequences (as highlighted by recent suicides among teenagers32). Social stigmatization of obese children appears to start
at a young age. When fifth- and sixth-grade students were
shown drawings of children with obesity, various physical
disabilities, or no disability, they indicated liking the obese
child least.33 According to one study, childhood obesity may
affect quality of life as severely as a diagnosis of cancer.34
Adults who were obese during adolescence tend to complete fewer years of school, to have higher rates of poverty,
and to be less often married compared with those who were
of normal weight during adolescence.35
MEDICAL EVALUATION
As the fifth vital sign,36 BMI should be routinely measured at regular medical visits. Body mass index higher than
the 85th percentile or showing a persistent upward trend

warrants attention, and BMI at or above the 95th percentile requires full evaluation. The main goals of the medical
evaluation are to identify treatable complications (Table 1)
and causes (TABLE 2) of obesity; assess motivation and obstacles to behavioral change (including psychological problems); and evaluate modifiable lifestyle factors affecting body
weight (ie, diet, physical activity and inactivity habits, sleep
patterns, and stress). Ms Ks normal linear growth (Figure 1),
long-term excessive weight gain, regular menstrual cycles,
and obesity-associated lifestyle factors argue against the presence of an etiologic endocrinopathy or genetic disease. The
report of an expert committee, comprising representatives
from 15 national organizations, provides comprehensive, evidence-based guidelines for the history, physical examination, and laboratory assessment of obesity in childhood (B).3
TREATMENT STRATEGY
Almost every drug used to treat obesity in the last century
has been found to have unacceptable adverse effects, typically cardiovascular in nature. The removal of sibutramine
from the US market in 2010 leaves only orlistat with US Food
and Drug Administration approval for adolescents. This drug,
which blocks intestinal fat absorption, has very modest effectiveness, producing about a 2.5-kg weight loss compared with placebo in 1 year,37 and concerns about longterm safety remain.38 (Metformin is indicated for treatment
of type 2 diabetes but not obesity.) Recently, interest in bariatric surgery has increased, with evidence that these procedures may reverse type 2 diabetes and prolong survival
in severely obese adults39 and preliminary reports of efficacy in adolescents.40 Nevertheless, the long-term safety and
effectiveness of bariatric surgery in the pediatric age range
is unknown, and life-threatening complications may oc-

Table 2. Medical Etiologies of Childhood Obesity a

Diagnosis
Etiologies
Endocrinopathy (hypothyroidism,
Cushing syndrome)

History
Slow growth, fatigue, low muscular
strength, cold intolerance,
constipation, menstrual
abnormalities (in girls)

Hypothalamic obesity (brain tumor,

head injury, ROHHAD
syndrome)

Rapid onset of weight gain, voracious

appetite, headache, visual
defects, vomiting, temperature
instability, hypoventilation

Medications (eg, olanzapine,

carbamazapine,
glucocorticoids, insulin)

Psychiatric illness, past and current

medication use

Genetic disease (eg, MCR4

mutations, POMC mutations,
leptin deficiency, Prader-Willi
syndrome, Bardet-Biedl
syndrome) b

Early onset of obesity, voracious

appetite and/or unusual
food-seeking behavior, sexual
and/or developmental delay

Physical Examination

Evaluation

Short stature, central distribution of

body fat, delayed pubertal
development, hyporeflexia
(hypothyroidism), moon facies and
buffalo hump (Cushing syndrome)

Thyroid function tests,

urinary cortisol
excretion

Papilledema, bitemporal hemianopsia

Head magnetic
resonance imaging,
pituitary hormone
levels, serum
electrolytes

Severe obesity, short stature,

hypogonadism, dysmorphic
features

Genetic analysis, serum

leptin, adrenal
stimulation test

Abbreviations: MC4R, melanocortin 4 receptor; POMC, pro-opiomelanocortin; ROHHAD, rapid-onset obesity with hypothalamic dysfunction, hypoventilation, and autonomic dysregulation.
a This overview is not intended to be exhaustive; more comprehensive reviews are referenced in the text.
b Presentations are variable, depending on specific etiology.

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cur.41 Thus, lifestyle modification constitutes the mainstay

of pediatric obesity treatment.
Ultimately, weight loss requires establishment of a negative energy balance, though for growing children and adolescents, maintenance of a neutral energy balance will produce favorable changes in body composition. The magnitude
of change in diet and physical activity level needed to treat
severe obesity has been a subject of debate. According to
the conventional model, a decrease in the balance between
energy intake and expenditure of 10 kcal/d will produce a
1-lb weight loss (about 3500 kcal) per year.42 This simple,
linear model suggests that Ms Kwho has gained approximately 15 lb a year beyond that associated with growth since
age 7 yearshas a daily energy gap averaging only about
150 kcal, equivalent to 1 cup of grape juice or a 30-minute
walk. However, calorie expenditure increases significantly
with weight gain, in part because it takes more energy to
maintain and move the extra body mass. Taking this compensatory mechanism into account, more sophisticated models reveal the energy gap to be about 500 kcal/d for obese
adults and 1000 kcal/d for severely obese adolescents.43,44
Thus, successful weight management necessitates major, not
modest, changes in diet and physical activity level.
THERAPEUTIC CHALLENGES
In 1998, Epstein et al45 reviewed 32 clinical trials and found
that most pediatric obesity interventions are marked by small
changes in relative weight or adiposity and substantial relapse. In 2008, a review by McGovern at al46 concluded that
[t]he long-term efficacy and safety of pediatric obesity treatments remain unclear. The results of other recent metaanalyses of treatment and prevention are not much more
encouraging, especially with regard to adolescents.47-49 Even
these modest effects may overestimate outcomes that can
be achieved in the clinical setting because research participants tend to be more motivated and receive more intensive intervention than patients. Moreover, randomized controlled trials involving individual and/or family-based
treatment for adolescent obesity often have methodological problems, including limited statistical power, short duration of follow-up, lack of attention to treatment fidelity,
high dropout rates, or failure to conduct an intention-totreat analysis. This disappointing situation notwithstanding, a few randomized controlled trials in an outpatient,
school, or community setting have obtained clinically significant improvements in body weight. The most recent
Cochrane meta-analysis of childhood obesity treatment49
identified 9 nonpharmacological trials involving adolescents that fulfilled all quality criteria (TABLE 3), several of
which demonstrated decreases in BMI, in absolute terms or
relative to a control, of 2 to 3.
One explanation for the poor overall outcome of conventional treatment relates to biology. According to the thrifty
gene theory,59 food scarcity during human evolution led
to selection of genetic variants that promote weight gain and

improve survival during famine. However, in the modern

era of food abundance, these genes cause excessive weight
gain and antagonize weight loss efforts. Clearly, genetic factors influence individual predisposition to obesity, as demonstrated by genome-wide association studies.60 Nevertheless, human populations have lived for many years amid food
abundancethe end of World War II until the 1970s in the
United States, for examplewithout experiencing rapid
weight gain. Moreover, the genetic makeup of children in
the United States has not likely changed much since emergence of the obesity epidemic.
A second explanation for the poor success rates of obesity treatment is a toxic environment that undermines
behavior and overwhelms the biological regulators of body
weight, leading to a vicious cycle of weight gain. These
ubiquitous adverse environmental influences counteract
individual efforts to improve diet quality and physical
activity level. Thus, the solution to the obesity epidemic
will require fundamental changes in the social environment to support a healthful lifestyle, as has been widely
recognized.61,62
A third explanation, of more immediate relevance to the
clinical management of obesity, is that conventional treatment has often lacked efficacy. Most intervention studies
involving diet have focused on restriction of a single macronutrient, typically fat,63 whereas research shows that macronutrient ratio has little effect on body weight.64,65 Other
studies emphasized bouts of exercise, even though many children are unable to achieve a substantive change in energy
balance through this approach.47,66,67 Fortunately, alternative, potentially more efficacious strategies to reduce energy intake and increase energy expenditure are available
that, when used in combination with proper parenting strategies, offer the possibility of improved outcome for clinical
treatment.
DIET
Many aspects of diet quality appear to affect body weight
and risk of obesity-related disease to a greater extent
than relative macronutrient quantity. Sugar-sweetened beverages,68 fast food,69 refined grain products,70 glycemic
load,71,72 energy density,73 and industrial (ie, partially hydrogenated or trans) fat74 affect it in an adverse manner, and
fruits and vegetables,70,75 whole grains,70 dietary fiber,76 and
vegetable protein and fat70,77 do so in a protective manner.
Traditional eating patterns based on whole or minimally processed foods, such as the Mediterranean diet, typically incorporate most of the protective but few of the adverse individual dietary factors. Whole and minimally processed
foods tend to take longer to consume and digest, elicit hormonal and metabolic responses that promote a high
degree of satiety, and have a high nutrient-to-calorie ratio.78,79 Indeed, numerous clinical trials and prospective observational studies support the superiority of the Mediterranean diet compared with a conventional low-fat diet for

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Table 3. Randomized Controlled Trials of Lifestyle Interventions for Adolescent Obesity a

Study
Diet b
Ebbeling
et al,50
2003

Participants

Study Design

Results

N = 16
Aged 13-21 y; mean age, 16.1 y
Sex: 69% female
Mean weight: 103.5 kg
(experimental) vs 104.7 kg
(control)
Setting: clinical research center

Groups: ad libitum
low-glycemic-load diet
(experimental) vs
energy-restricted low-fat
diet (control)
Duration: 6-mo intervention with
follow-up through 12 mo

Completion rate: 87%

BMI decreased in the
experimental group (1.3 vs
0.7).
Insulin resistance was lower in the
experimental group.

N = 81
Aged 11-16 y; mean age, 13 y
Sex: 56% female
BMI 98th percentile
Setting: outpatient clinic,
research center

Groups: exercise therapy vs

equal contact exercise
placebo vs usual care
control
Duration: 8-wk intervention with
follow-up through 6 mo

Completion rate: 88%

No significant difference in BMI
Exercise group reported improved
self-esteem.

N = 41; 95% black or Hispanic

Aged 10-14 y, mean age, 12.6 y
Sex: 63% female
Mean BMI: 35.8 (experimental)
vs 37.0 (control)
Setting: school

Groups: nutrition education and

exercise training with coping
skills vs without coping skills
Duration: 4-mo intervention with
follow-up through 10 mo

Jelalian et al,53
2006

N = 76
Aged 13-16 y
Sex: 71% female
Mean BMI: 32.5
Setting: outpatient clinic

Groups: cognitive behavioral

treatment with either
adventure therapy
(experimental) or aerobic
exercise (control)
Duration: 4-mo intervention with
follow-up through 10 mo

Johnston
et al,54
2007

N = 71; Mexican American

Aged 10-14 y
Sex: 52% female
Mean BMI z score: 1.86
(experimental) vs 1.64
(control)
Setting: school
N = 60; Mexican American
Aged 10-14 y; mean age, 12.4 y
Sex: 45% female
Mean BMI z score: 1.6
(experimental) vs 1.7
(control)
Setting: school
N = 44
Aged 12-16 y; mean age, 14.2 y
Sex: 41% female
Mean BMI: 31.0 (experimental)
vs 30.7 (control)
Setting: primary care

Groups: behavioral family

treatment (experimental) vs
self-help (control)
Duration: 6-mo intervention

Completion rate: 78%

No significant change in absolute
BMI or differences between
groups
Experimental group showed
trends in improvement in
health-related behaviors.
Completion rate: 74%
Mean weight loss at 10 mo
(experimental, 3.4 kg vs
control, 0.7 kg) did not differ
significantly between groups.
Older adolescents appeared to
respond better to the
experimental treatment.
Completion rate: 93%
BMI z score decreased at 6 mo in
experimental group (0.11 vs
0.03).

Savoye et al,57
2007

N = 209
Aged 8-16 y
Sex: 61% female
Mean BMI: 35.8 (experimental)
vs 36.2 (control)
Setting: outpatient clinic

Williamson
et al,58
2006

N = 57; black
Aged 11-15 y; mean age, 13.2 y
Sex: 100% female
Mean BMI: 98.3 percentile
Setting: community

Groups: intensive, family-based

weight management
(experimental) vs usual care
(control); a third group
(structured meal plan) was
discontinued because of
high dropout rate
Duration: 12-mo intervention
Groups: interactive behavioral
Internet program
(experimental) vs Internet
health education program
(control)
Duration: 24-mo intervention

Physical activity b
Daley et al,51
2006

Behavior b
Grey et al,52
2004

Johnston
et al,55
2007

Saelens et al,56
2002

Groups: behavioral family

treatment (experimental) vs
self-help (control)
Duration: 6-mo intervention

Completion rate: 95%

BMI z score decreased at 6 mo in
the experimental group (0.16
vs 0.05).
Total cholesterol was lower in the
experimental group.

Groups: multiple-component
behavioral weight control
intervention (experimental)
vs usual care (control)
Duration: 4-mo intervention with
follow-up through 7 mo

Completion rate: 84%

BMI z score decreased slightly in
experimental group at 4 mo.
Change in BMI at 7 mo did
not differ (experimental, 0.1 vs
control, 0.4).
Behavioral measures related to
weight loss did not differ.
Completion rate: 52%
BMI decreased in experimental
group (1.7 vs 1.6) at 12
mo.
Insulin resistance improved in
experimental group.

Completion rate: 70%

Change in BMI did not differ at 24
mo (experimental, 0.7 vs
control, 1.2).
Body fat percentage decreased in
experimental vs control
groups at 6 mo.

Abbreviation: BMI, body mass index, calculated as weight in kilograms divided by height in meters squared.
a Studies targeting adolescents and fulfilling all quality criteria in the most recent Cochrane meta-analysis of childhood obesity treatment49 (excluding pharmacological trials).
b Primary focus of intervention as characterized by the Cochrane meta-analysis.

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CLINICAL CROSSROADS

weight loss and cardiovascular disease risk reduction, at least

in adults (B).80,81
From this perspective, Ms Ks attempts to consume good
junk foodscharacteristically highly processed, energydense, nutrient-poor products with modest reductions of
fat, sugar, salt, or portion sizemay be misguided. Although the energy content of a single 100-calorie pack is
small, its satiety value is arguably smaller still, often leading to consumption of several portions, as occurs with Ms
K. More important, such products displace inherently more
nutritious, whole foods from the diet, with serious consequences to overall health.
PHYSICAL ACTIVITY
A typical adolescent in the United States spends more than
6 hours a day in sedentary pursuits like television and
computer use and only 12 minutes a day engaged in vigorous physical activity.82 Among girls aged 16 to 17 years in
the Growth and Health Study, half reported no habitual
physical activities of any kind outside of gym class, a lifestyle exemplified by Ms K.83 In view of these statistics,
measures to increase energy expenditure would seem
essential for successful long-term weight management.
However, interventions based exclusively on physical
activity (typically exercise) produce only modest changes
in body composition and no significant weight loss.47,66,67
For example, Daley et al51 randomly assigned 81 obese
adolescents to a moderate-intensity aerobics exercise
therapy group, an equal-contact control group, or usual
care for 8 weeks. Participants in the exercise group showed
improvements in several measures of psychological wellbeing but no significant change in BMI.
The failure of exercise-based interventions can be attributed to an intuitively evident aspect of human metabolism:
in the modern environment, energy intake occurs much more
easily than expenditure. Adolescents may consume more than
1800 kcal in a single fast-food meal,84 but to expend those
calories would require running 2.5 miles per day for a full
week, assuming about 100 kcal/mile. Moreover, most adolescents (and many adults) have difficulty maintaining an
exercise regimen over the long term. A promising alternative approach involves deemphasizing exercise, with the focus placed on reducing sedentary time and encouraging fun,
social activities like sports, skating, dancing, and active
play.85-87 Television viewing warrants special emphasis because this sedentary behavior not only displaces physical
activities but also undermines diet quality, primarily through
the influence of food advertising.88,89 Several pilot interventions aimed exclusively at television viewing have produced significant improvements in body weight or adiposity (C).63,90,91
SLEEP AND STRESS
For children and adults, sleep deprivation or emotional
stress may undermine motivation to adhere to healthful

eating and a physical activity plan.92,93 In addition, inadequate sleep or stress may dysregulate circadian hormone
patterns and metabolism, leading to fat deposition. For
these reasons, treatment of related conditions (eg, sleep
apnea, mental health disorders), establishment of good
sleep hygiene habits, stress reduction practices, and attention to maintaining a peaceful home environment can be
crucial to obesity treatment (C).
BEHAVIORAL STRATEGIES
Several theoretical models have been proposed to promote
lifestyle change in obesity,94 including social cognitive theory,
transtheoretical model (providing a framework for motivational interviewing),95,96 and behavioral economics, though
none have clearly documented superiority. Each may have
utility, depending on the clinical considerations, especially
in the context of ongoing treatment by a behavioral medicine specialist. For clinicians without specialized training
in behavior modification, basic principles of child psychological development may help guide treatment.
Young children have an innate preference for sweetness,
the primary flavor of breast milk, and a reluctance to try new
foods (ie, neophobia). However, they are developmentally
programmed to learn about new foods from adults, especially their parents, and require clear guidance. In contrast, adolescents tend to be more influenced by peers than
parents and need increasing autonomy.97
Some parents respond to this developmental sequence in
reverse order, raising young children without adequate guidance regarding diet and physical activity. In the absence of
clear parental guidance, poor diet quality (influenced by pervasive junk food marketing) and a sedentary lifestyle may
become ingrained, increasing the likelihood of excessive
weight gain in childhood. If obesity emerges in adolescents, parents, like Ms Ks mother, may complicate an already difficult situation with coercive behavior change methods, including pressure to eat some foods (eg, vegetables),
excessive restriction of other foods, criticism, nagging, or
punishment. The adverse effects of these coercive parenting methods at any age have been well documented. For example, when young children were pressured to eat 1 of 2
soups, they consumed less of the targeted soup.98 Conversely, 5-year-old girls whose mothers restricted food tended
to eat in the absence of hunger later in childhood.99 With
Ms K, excessive parental oversight of diet may have contributed to conflict at home, poor self-esteem, and counterproductive behaviors.
An age-appropriate behavioral strategy to prevent and
treat obesity would therefore involve establishing a
parent-directed system with young children that provides
progressively increasing autonomy to the child over time.
A key parenting practice applicable to all ages is to create
a protective environment in the home by substituting
nutritious foods for unhealthful ones and physical activities (eg, dance, active play) for sedentary pursuits (eg,

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television). By applying equally to everyone, this practice

avoids stigmatizing obese children and supports the
health of the whole family. Other noncoercive behavior
change methods applicable to adolescence include praise,
self-monitoring, goal setting, contingency management,
anticipating obstacles, and mindfulness (the practice of
bringing attention to the present moment in a nonjudgmental manner) (B).20,97,100-103 Although treatment of obesity in adolescents tends to be more complicated and less
successful compared with younger children, parents can
continue to have an important influence on weightrelated behaviors at this age.
RECOMMENDATIONS FOR MS K
AND HER MOTHER
Adolescent obesity is a remarkably frustrating condition for
patients, parents, and clinicians because of its major physical and emotional morbidities and the limited effectiveness
of conventional treatment. However, Ms K. and her mother
may find some solace in the knowledge that they are not
alone: several million adolescents and their families in the
United States struggle with obesity. Moreover, new and potentially more effective treatment options provide some
grounds for optimism.
Ms Ks mothers decision to relinquish her role as food
police was an important first step and may have helped her
daughter become ready to pursue a weight management program. With guidance, if needed, from her own therapist or
a family-based weight management program, her mother can
develop her capacity to provide support and encouragement while avoiding judgmental comments and coercive supervision. Special emphasis should be placed on modeling
healthful behaviors and maintaining a health-promoting
home environment. She can offer to help her daughter practice constructive coping strategies to deal with teasing.29 In
addition, she should work with school officials and, if necessary, the police to protect Ms K from bullying and harassment.
Ms Ks acknowledgment of her weight problem and
awareness of the need to find internal motivation for
change augur well for success. In view of her complicated
medical and psychosocial issues, close support from a
comprehensive pediatric weight management program,
including a pediatrician, a dietitian, and a behavioral medicine specialist, would be warranted. Focus should be
placed on sustainable lifestyle changes rather than rapid
weight loss, as improved diet and physical activity level
reduce long-term risk of chronic disease independent of
body weight. Regarding nutrition, Ms K should increase
intake of nonstarchy vegetables, fruits, and legumes (eg,
pinto, red, or black beans); consume grains in their least
processed state possible (eg, steel-cut oats, brown rice, and
100% whole-grain breads prepared from stone-ground
flour); choose healthful (primarily plant-based) sources of
protein and fat; limit consumption of sugar, including
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JAMA, February 1, 2012Vol 307, No. 5

sugar-sweetened beverages; and avoid skipping breakfast.104 In addition, she may benefit from measurement of
serum 25-hydroxyvitamin D concentration and vitamin D
supplementation, in view of the high prevalence of deficiency of this micronutrient among obese adolescents.105
Ms K should also attend to good sleep hygiene, participate
in moderate physical activities (such as walking, swimming, or dancing) on a daily basis, and use stress reduction methods and mindful eating practices (to support
good decision making about what and how much to eat).
Finally, physicians and other health care professionals who
treat patients like Ms K have a special opportunity, by virtue of their credibility and expertise, to advocate for local
and national policy changes to create a more healthful social environment for all children.61
QUESTIONS AND DISCUSSION
QUESTION: I understand that bariatric surgery programs for
adolescents have been established. Would you describe what
kind of individual would be a candidate for this procedure?
DR LUDWIG: Some children and adolescents above the 99th
percentile for BMI develop severe complications, including type 2 diabetes. Inadequate management of obesityrelated complications and the underlying weight problem
can place these individual at risk of irreversible harm and
death. In such situations, a range of more invasive options
should be considered, including institutionalization for medically supervised weight loss; state intervention (eg, financial assistance, parenting training, in-home social supports, counseling, and, perhaps, in extreme circumstances,
foster care)106; and bariatric surgery. The selection criteria
for bariatric surgery generally include prolonged failure of
medical treatment, a minimum age of 13 years for girls and
15 years for boys (when skeletal maturation is nearly complete), and a willingness and ability to adhere to a demanding postoperative dietary regimen.107 Unfortunately, psychiatric illness, major behavioral issues, and parental neglect
may contribute to the development of severe obesity, and
the presence of these problems would tend to make affected individuals poor surgical candidates.
Conflict of Interest Disclosures: The author has completed and submitted the ICMJE
Form for Disclosure of Potential Conflicts of Interest. Dr Ludwig reports receiving
grants from the National Institutes of Health and foundations for obesity-related
research, mentoring, and patient care and royalties from a book about childhood
obesity.
Funding/Support: Dr Ludwig is supported in part by an endowment from Childrens Hospital Boston and career award K24DK082730 from the National Institute of Diabetes and Digestive and Kidney Diseases.
Role of the Sponsors: Neither Childrens Hospital Boston nor the National Institute of Diabetes and Digestive and Kidney Diseases had any role in the collection,
management, analysis, and interpretation of the data; or preparation, review, or
approval of the manuscript.
Disclaimer: The content of this article is solely the responsibility of the author and
does not necessarily represent the official views of the National Institute of Diabetes and Digestive and Kidney Diseases or the National Institutes of Health.
Additional Contributions: We thank the patient and her mother for sharing their
stories and for providing permission to publish them. Dr Ludwig thanks Amy Fleischman, MD, Childrens Hospital Boston, for providing a critical review of the manuscript. Dr Fleischman received no financial compensation for her review.

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CLINICAL CROSSROADS
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