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 1⁄2 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 parents—especially her mother—about 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 and questions on p 517. 498

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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

The conference on which this article is based took place at the Medical Grand Rounds at Children’s 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, Children’s 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, Children’s Hospital Boston, Division of Endocrinology, 300 Longwood Ave, Boston, MA 02115 (david.ludwig 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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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 it’s 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 didn’t work. Then for 3 days, I tried the acai berry pill and it didn’t do anything so I stopped taking that. I participated in some activities as well. I would go to Weight Watchers, but I wouldn’t really stay on track. Over the summer and the fall, I tried to do field hockey but my ankle got hurt so I couldn’t keep doing that. My mom usually prepares the meals. There are huge fights between us if I’d want to eat something and it wasn’t healthy. My parents would say, “No, give that back; no, you can’t have that; no, you’re going to gain weight.” For example, if I want 1 bowl of chips before dinner, then I’d be told, “No, you can’t have that.” If we went out to dinner, they just keep looking at whatever I was eating and I just think it’s 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 I’ve been through. However, about 2 weeks ago, another kid that I’ve never met—I’ve never seen him—messaged me calling me those mean names again. Things have gotten a little better than before though. I really think that it’s 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 won’t 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 that’s what really brought me to where I am now. MS K’S 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 doesn’t 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. That’s 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. Patient’s Growth Chart

Ms K’s 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 Child’s psychosocial issues

Societal costs costs, including CHILD H OOD OBESIT Y

Increasing health care costs Decreasing economic productivity


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

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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 epidemic’s 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 in©2012 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 child’s 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)


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)


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 hormone–binding 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 K’s 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


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 K—who has gained approximately 15 lb a year beyond that associated with growth since age 7 years—has 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 abundance—the end of World War II until the 1970s in the United States, for example—without 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


Study Design


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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weight loss and cardiovascular disease risk reduction, at least in adults (B).80,81 From this perspective, Ms K’s attempts to consume “good” junk foods—characteristically highly processed, energydense, nutrient-poor products with modest reductions of fat, sugar, salt, or portion size—may 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 K’s 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 K’s mother’s 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 K’s 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 506

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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 Children’s Hospital Boston and career award K24DK082730 from the National Institute of Diabetes and Digestive and Kidney Diseases. Role of the Sponsors: Neither Children’s 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, Children’s Hospital Boston, for providing a critical review of the manuscript. Dr Fleischman received no financial compensation for her review.

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