Obesity is perhaps the most pervasive medical problem faced by medical providers today. It is a common condition in any patient population in countries with a western diet and lifestyle, affects disease burden in virtually every medical specialty, has broad exposure in the media and popular press, and is the subject of intense research in biomedical, epidemiologic, sociologic, and psychological fields. Americans display a multitude of beliefs about the root causes of obesity, often drawn from personal experience, the popular press, marketing initiatives, or one portion of the medical research on the subject. Yet each such theory falls short of explaining the full spectrum of disease and its resistance to treatment. Although most physicians and their patients recognize that obesity is a major health problem, long-term treatment success is rare.

Against these odds, pediatric providers can still take action in several important ways:

• Equip yourself with an understanding of what is known in the field and -- equally important -- what is not known.
• Provide targeted anticipatory guidance for all patients to help them prevent obesity.
• Identify patients at particular risk for obesity, and provide additional guidance to help prevent or attenuate the problem in these individuals.
• Be alert for the medical and emotional consequences of obesity and treat these accordingly.
• Treat obesity and obesity-related disease with the best tools as they become available, if supported by sound research.
• Be a leader in promoting the cultural changes that can help prevent obesity and that will be required before the obesity epidemic can be reversed.

Any definition of obesity is useful only if it predicts medical disability or complications. Because most medical complications of obesity are associated with body fat and not muscle mass, measures of obesity represent an attempt to estimate the adipose compartment. At present, there is no precise clinically practical method to measure body fat, so most methods rely on measurements of body weight as a surrogate for adiposity.

Body mass index (BMI), which is defined as weight in kilograms divided by height in meters squared (kg/m²), has been established as a useful standard measure of overweight and obesity. Although BMI does not directly measure body fat, it provides a reasonable estimate of adiposity which, in turn, also predicts risks for current or future medical complications of obesity.^[1] BMI in children is correlated not only with other measures of body fat but also with blood pressure,^[2,3] lipid levels,^[4,5] and insulin levels.^[6]

Because BMI naturally increases with increasing age, and also varies by pubertal stage^[7] and gender, BMI percentiles are used to define degrees of overweight and obesity. The BMI-for-age growth charts, released by the Centers for Disease Control and Prevention (CDC) in 2000, show healthy reference standards for BMI during childhood and adolescence, and provide a practical way of tracking an individual's changes in BMI over time. The 85th percentile on the CDC standard charts, which defines children and adolescents "at risk for overweight," also corresponds approximately to a BMI of 25 kg/m² by age 18, the adult definition of overweight. The 95th percentile on the standard chart, defining children and adolescents as "overweight," corresponds to about 30 kg/m² by age 18 years, the standard adult definition of obesity.

Currently, 14% of children and adolescents in the United States are overweight and 20% are at risk for overweight (above the 95th and 85th percentiles for age and gender, respectively, based on the new CDC standards).^[8] Since the 1960s, the prevalence of obesity in children and adolescents has tripled. Similar but more gradual trends are seen worldwide. African American and Mexican American children are disproportionately affected (See the sidebar, "Managing Overweight in Underserved Pediatric Populations.") Recent estimates suggest that obesity and physical inactivity are responsible for 400,000 deaths annually in the United States; thus, it is close to overtaking tobacco as the leading cause of preventable death.^[9]

Determining the specific causes of this rapid increase in obesity rates is clearly important yet remarkably complex. Both genetic and environmental factors have been shown to contribute significantly to this problem. In general, genetic factors explain a large part of the variation of body weight within a given population in a common environment, whereas environmental factors tend to explain changes in obesity over time in that population. Importantly, there is also increasing evidence that obesity and metabolic diseases may be permanently influenced by environmental factors early in development. Adaptive responses to environmental conditions in gestation are proposed to produce a "thrifty phenotype" or metabolic program that affords an individual a better chance for survival. However, when that individual is then exposed to plentiful nutrition after birth, the metabolic program may be inappropriate for the new conditions and cause disease.

Genetic Influences on Obesity

Both animals and humans have a strong tendency to maintain a stable body weight over time owing to a close but sometimes imperfect matching of energy intake with energy expenditure. Animal studies in which energy intake is manipulated reveal powerful influences from homeostatic mechanisms defending body weight.^[10] Similarly, the poor long-term results of weight reduction therapies in humans (about 95% of adults regain all weight after dieting) suggest that there are mechanisms that defend a highly individualized "set point" for body weight. When an individual has a heritable or acquired susceptibility to positive energy balance superimposed on these native homeostatic mechanisms, he or she has a tendency to become obese.

Studies of twins and adoptees provide useful estimates of the role of heritable factors in determining an individual's body weight (see Bouchard's 1997 summary of relevant articles on heritability^[11]). Adoption studies tend to generate the lowest heritability estimates (30%), whereas twin studies provide the highest heritability estimates (70%). The variability in these estimates of heritability depends in part on definitions of obesity: more severe obesity tends to have a greater heritability factor than lesser variations in BMI.^[12]

Any of the genes encoding a component of the mechanism for regulating body weight homeostasis could be considered a candidate gene for a predisposition or resistance to obesity. Specific mutations in a few of these genes have been shown to cause obesity in rare kindreds. Mutations with strong effects were found in the leptin gene,^[13] the leptin receptor gene,^[14] the propiomelanocortin (POMC) gene,^[15] the prohormone convertase gene (PCSK1),^[16] and the melanocortin 4 receptor gene (MC4R).^[17] The latter is the most common gene in which specific mutations cause obesity, but it is still rare (42 mutations in 130 individuals published by 2003).^[18]

Many other genes known to be involved in pathways regulating body weight, appetite, or energy expenditure have been analyzed for association with obesity within specific populations. By 2003, polymorphisms linked to 90 candidate genes had been shown to have some association with obesity phenotypes,^[18] including ghrelin,^[19] peroxisome proliferation-activated receptor gamma,^[20] uncoupling proteins,^[21] and the beta3-adrenoreceptor genes.^[22]

Linkage studies in large populations have identified many chromosomal loci with associations to a variety of obesity-related phenotypes, including BMI, leptin levels, fat distribution, and hyperlipidemia.^[23] One hundred thirty-nine such loci have been identified as of the 2003 gene map update,^[18] some of which appear to represent the chromosomal regions of previously identified candidate genes such as the leptin or MC4 receptors. For many other regions or quantitative trait loci, the biologic mechanisms for the apparent linkage with obesity phenotypes remain unclear.

Syndromic obesity is rare but important to recognize because it may be associated with specific medical complications, possibly with predictable responses to treatment. For example, Prader-Willi syndrome has been associated with gastric rupture, and may respond in part to treatment with growth hormone.^[24] Many of these syndromes, including Prader-Willi syndrome, are characterized by short stature, developmental delay, dysmorphic features, and hypogonadism. The coincidence of several of these features should prompt specific workup for syndromic obesity. Conversely, a child with normal cognitive function and good linear growth is very unlikely to have syndromic obesity.

Environmental Influences on Obesity

Epidemiologists have used cohort studies and case-control designs to determine which environmental factors may contribute to obesity. Such studies have pointed to dietary trends, sedentary lifestyle, decreases in structured physical activity, and psychosocial stressors as likely contributors to the obesity epidemic.^[25] Several dietary factors have been proposed to play important roles. These include the easy availability and high caloric content of fast foods, general trends toward consumption of foods that are highly processed and contain high carbohydrates and/or total calories (including sugary beverages), decreased consumption of fiber and low-density foods, and the strong marketing techniques of the fast food industry. Other factors include decreases in structured physical activity, particularly for children, and decreasing lifestyle activity (occupations and transportation require less movement than in the past) and increasing sedentary activities (particularly television viewing and computer use). While each of these dietary or activity factors has been temporally related to trends of increasing obesity, causal relationships are difficult to prove. The most convincing studies are short-term intervention trials of decreasing television-viewing time,^[26] decreasing caloric density (increasing water content) of food,^[27] and decreasing glycemic index of foods.^[28] It is important to note that, to date, no single factor among these has been shown to play a pivotal role in the increasing prevalence of obesity.

Developmental Influences on Obesity

The concept of metabolic programming first arose from epidemiologic studies in which it was observed that infants with low birthweight had a higher risk of developing diabetes and heart disease during adulthood,^[29-31] suggesting that environmental factors early in development may have a permanent effect on the metabolic profile of an individual. Other epidemiologic studies support the idea that the combination of low birthweight and accelerated growth during childhood confers the greatest risk for diabetes.^[32,33] Remarkably, observed associations between maternal hyperglycemia (and consequent unusually high birthweight)^[34] and later development of metabolic syndrome suggest that a variety of abnormal conditions during gestation can have parallel effects on offspring.

Studies of the Dutch famine provide evidence that nutritional factors in utero have a causal relationship with subsequent metabolic phenotype. The Dutch population was abruptly subjected to famine conditions for 5 months in the winter of 1944-45. Children who were exposed to the famine in utero had higher risks of glucose intolerance and type 2 diabetes later in life, compared with infants who were in utero just before or after the famine.^[35] Comparison with other famines suggests that abrupt restoration of adequate nutrition after birth further increases the risk for metabolic disease.^[36]

Animal studies lend further support to the idea of metabolic programming. In rats, a variety of experimental conditions that restrict nutrition during gestation predispose the offspring to develop elements of the metabolic syndrome during maturity. In particular, the combination of maternal protein deprivation followed by plentiful nutrition during suckling causes increased appetite, insulin resistance, and shortened lifespan.^[37,38] Similar effects are seen in animals exposed to cold ambient temperatures during gestation or early life. Offspring of low-protein-fed dams have proportionally smaller livers, and these livers have fewer but larger lobules than normal.^[39] These animals also have increased hepatic gluconeogenesis and decreased ketogenesis, which are features of several experimental models of fatty liver.

Together, these studies in humans and animals present intriguing evidence that fetal malnutrition (either under-nutrition or some other perturbation of maternal-fetal metabolism) combined with over-nourishment during childhood may create a dangerous "metabolic program" predisposing to the metabolic syndrome. Which metabolic features of the intrauterine environment are most important and the timing of the critical period of over-nutrition during childhood are yet to be determined. However, it is reasonable to conclude that infants with low birthweight are at increased risk for developing the metabolic syndrome, particularly if obesity develops later in life, and that moderate rates of weight gain for these individuals during childhood may attenuate the effect of the gestational programming.

Overview

Because environmental and developmental factors play important roles in the development of obesity in genetically susceptible individuals, the pediatric provider and parents can play critical roles in obesity prevention. Certainly, some parts of our culture and environment are beyond the individual's control. Computers and technology are prominent parts of the educational and work environment in many fields, reducing physical activity in daily life. The individual family has little control over the restaurants, services, and public facilities available in their neighborhood, or over the physical education available in their school, and much food-related advertising cannot be avoided.

Nonetheless, several specific areas of lifestyle can be useful for obesity prevention and can be controlled by the family. The pediatric provider can play an important role in identifying these lifestyle targets and supporting healthy lifestyle habits for all families in their practice, as recommended in a recent policy statement by the American Academy of Pediatrics.^[40] These recommendations are appropriate whether or not a child or family is at risk for obesity. Table 1 outlines some important targets for anticipatory guidance to prevent obesity. The relevance of each of these targets is supported by multiple association studies (eg, breastfeeding, intake of sugared beverages, physical activity), and some are also supported by small intervention studies (eg, family-based behavioral modification techniques, television reduction). Large-scale intervention studies for the prevention of obesity in the family setting are currently lacking.

Table 1. Universal Anticipatory Guidance for Obesity Prevention

Pregnancy

Obesity prevention begins with the obstetrician encouraging good nutrition and glycemic control during pregnancy, and providing anticipatory guidance to encourage breastfeeding. (See "Developmental Influences on Obesity," above.)

Infancy

The pediatric provider continues the process by encouraging continued breastfeeding (and minimizing formula supplements) for as long as possible. Multiple studies in a variety of populations have shown a weak but consistent protective effect of breastfeeding on the development of obesity after adjusting for appropriate possible confounders, including race and maternal education.^[41-43] Moderate rates of weight gain are probably ideal, particularly in infants of low birthweight, because rapid catch-up growth is associated with higher rates of the metabolic syndrome.^[33] (See "Developmental Influences on Obesity," above.)

Toddlerhood

Focused counseling about how to introduce new foods and overcome the picky eating of toddlers can be valuable in preparing them for healthy eating as they grow older. Involving toddlers in food preparation (mixing dips for vegetables), introducing new foods in familiar contexts (soups, stews, and other mixes of old and new), and practicing patience and persistence will often help. Minimizing intake of sweet beverages (including 100% fruit juice) is appropriate, because intake of these drinks is often responsible for large amounts of excessive calories and replaces foods with more balanced macronutrient content.

To establish an appreciation of physical activity, encourage families to spend time together in active play, which is easily accomplished with frequent visits to a playground. Toddlerhood is an important time to establish firm limits on television viewing, before it becomes a habit. Ask the family to limit viewing to 1 hour or less daily for all family members. Keeping the television out of plain sight, if possible, will minimize the child's interest and help avoid conflict over this issue. Since television often distracts from natural signals of hunger and satiety and also encourages overeating through advertising, ask the family to uncouple eating from television by establishing separate times and spaces for snacking and television watching.

To keep food out of the arena of emotions and power struggles, parents should avoid using food as a reward or punishment. To help toddlers learn to respond to natural signals of hunger and satiety, parents should not push the child to eat beyond his or her appetite. Encourage the family to establish regular mealtimes and to eat together whenever possible, and to serve the family's meal to the toddler even if it is sometimes rejected. Parental modeling of healthy eating, physical activity, and low television-viewing habits is essential. Although these lifestyle habits may present a challenge to some families, establishing healthy rules and habits is usually easier when the child is young.

School Age

Most of the same principles above can and should be continued into childhood. Children should now be ready for more structured forms of physical activity, and the pediatric provider can often prompt families to take advantage of local resources. These resources will vary among communities, but local YMCAs, Boys' and Girls' Clubs, as well as town- or school-sponsored sports leagues are often available. If possible, parents should offer the child some choice of activity, but with the goal of participating in at least 1 activity each season of the year. Whenever possible, parents should become involved in the activities or sports, through recreational practice, coaching, or by developing additional interests in family sports for leisure time.

In addition to the behavioral approaches mentioned above, families can help support a positive body image in their child by emphasizing and praising strength and health rather than weight or appearance.

Adolescence

As children reach adolescence and become more independent, the family will have less direct control over eating habits and physical activity. As with many adolescent issues, relinquishing some control is appropriate and healthy, but some basic standards can still be maintained. Eating take-out or fast food with friends may have some social value and appeal, but it is reasonable to limit the frequency of these habits. Concerns about weight and/or busy schedules may prompt teenagers into patterns of meal skipping or eating inadequate meals, which often leads to compensatory over-eating or bingeing. Adolescents should be made aware that meal skipping is both ineffective and unhealthy as a form of dieting. If calorie restriction seems appropriate, then attention to regularizing meal patterns, self-monitoring, and selective decreases in calorie-dense foods are important first steps. (See "Treatment," below.)

Many children, including those with obesity, maintain reasonably high levels of physical activity during childhood. However, recent studies have shown substantial decreases in physical activity for many boys and girls as they reach adolescence,^[44,45] increasing the disparity between active and inactive youth. Important determinants of physical activity are family involvement,^[46] access to local resources and programs,^[47] and self-esteem,^[48] suggesting that each of these factors is an important target in the effort to boost physical activity levels in youth.

Identifying patients at particular risk for developing obesity allows for more intense preventative measures and counseling (Table 2). In early childhood, the obesity status of the parents is the best predictor of the child's risk for obesity in the future; the child's own weight is a weak predictor of his or her future risk. If both parents have obesity, the child's risk of becoming obese in adulthood is 15-fold greater than the risk of a child whose parents are not obese.^[49] By late childhood (6 years or older), the child's own obesity status becomes the stronger predictor of future risk, and can be used to select families for additional counseling. Other factors to consider are the family's diet and level of physical activity. The family history of obesity-associated medical problems such as type 2 diabetes and heart disease can help identify individuals who would be at increased risk for these problems, particularly if they also develop obesity. Finally, a history of low birthweight or very rapid "catch-up" weight gain in early childhood may predict risks for metabolic syndrome. (See "Developmental Influences on Obesity," above.)

Table 2. Identifying Children at Increased Risk for Future Obesity and Related Medical Problems

Raising the Subject

Because obesity has traditionally been blamed on the patient, raising the issue of weight gain in the office can be tricky (Table 3). Many individuals with obesity have come to expect criticism and blame, lectures about the faults in their lifestyle, or avoidance of the subject in their physician's offices. However, the subject can be raised in ways that invite a dialogue and collaboration with lifestyle change, without sacrificing a sense of urgency or importance.

By asking whether the child has, or whether other family members have, a tendency to "gain weight easily," the provider can raise the subject without placing blame on the family or child, and this may lead to more open communication. This or similar language acknowledges the genetic or developmental contributors to obesity, while leaving room for work on the modifiable lifestyle factors. By inquiring about the parents' weight patterns during childhood and early adulthood, parents can be invited to share their perspective on their own weight, and fears or expectations for their child's weight. When recording the family history of the major obesity-related comorbidities, the provider can appropriately focus the discussion on the health implications of obesity rather than on cosmetic concerns. These initial areas of inquiry provide some common ground on which a collaborative action plan can be built.

Table 3. Approaches to Raising the Issue of Obesity in the Office

Obesity is associated with more than 40 different medical or psychological problems, touching virtually every organ system. Even when weight control itself is challenging, the pediatric provider can contribute to the health of a young patient with obesity by being alert for these complications and treating them accordingly. By also addressing future risks for disease -- through discussions about the family history of obesity-associated comorbidities and by screening for risk factors such as hypercholesterolemia -- the pediatric provider helps the patient and family focus on obesity as a health issue rather than a cosmetic problem. At the same time, we must recognize that young patients may not be truly motivated by long-term health concerns, and may be feeling more acutely the psychosocial burdens of obesity.

The comorbidities associated with obesity can be conceptually divided into 5 categories: metabolic, anatomic, psychological, degenerative, and neoplastic (Table 4), although some of these disorders have mixed etiologies. Most of these problems are seen primarily in adulthood, but many are increasingly found in children and adolescents with obesity.

Table 4. Comorbidities

*Also appears in children or adolescents.

Medical Complications

Metabolic syndrome. Insulin resistance and type 2 diabetes are increasingly found in adolescents and even children with obesity. About 25% of children or adolescents with obesity have insulin resistance, and 4% have silent type 2 diabetes (Figure 1).^[50] As in adults, insulin resistance and diabetes are associated with other elements of the metabolic syndrome, including hypertension and abdominal fat distribution. Studies in children have shown a relationship among fasting insulin and lipids,^[51] blood pressure,^[52-54] and BMI.^[55,56] Left ventricular hypertrophy is associated with obesity in children, likely due to hypertension.^[57] An autopsy study showed that blood pressure, lipid levels, and BMI were positively correlated with aortic and coronary atherosclerosis in both children and adults (2-34 years), suggesting that the metabolic syndrome starts before adulthood.^[58] Because obesity in children is associated with all of these cardiovascular risk factors, it is not surprising that adults with obesity have greater morbidity and mortality if their obesity began in childhood.^[59]

Figure 1. Prevalence of insulin resistance and type 2 diabetes in US adolescents.^[50]

Although there are many similarities between the findings of the metabolic syndrome in children and adults, it is important to recognize that children have a different hormonal milieu than adults, especially during puberty. All children become more insulin resistant at the time of puberty compared with either before or after puberty.^[60] Increased body fat and BMI correlate strongly with fasting insulin levels and insulin resistance, and have been proposed as potential mediators of the pubertal changes in insulin resistance.^[61-63] However, insulin resistance can also occur during puberty in the absence of changes in BMI, coinciding with a period of rapid growth during puberty.^[62]

Fatty liver disease. Nonalcoholic fatty liver disease (NAFLD) represents a spectrum of liver disease associated with obesity in children and adults.^[64,65] Microscopic analysis of fatty liver disease reveals either accumulation of fat alone (steatosis) or fat accompanied by inflammation and fibrosis (steatohepatitis); the latter findings are generally termed nonalcoholic steatohepatitis (NASH). Up to 75% of adults with obesity have NAFLD,^[66] and these rates are even higher in patients with severe obesity (Figure 2). Only a minority of patients with steatosis develop progressive liver disease, but the incidence of severe NASH is increasing in parallel with increasing rates of obesity. The prevalence of fatty liver disease in children is unknown, but estimates from noninvasive diagnostic techniques suggest that it is also increasing in parallel with obesity. Strauss and colleagues^[65] used serum aminotransferase measures to estimate that 10% of obese adolescents living in the United States may have NAFLD, whereas other authors using ultrasonographic measures of fatty liver have estimated rates of 25% to 50% among children and adolescents evaluated in obesity programs in the United States and other countries.^[64,67,68] Although rare, several cases of cirrhosis associated with NASH in obese children have been described.^[69,70]

Figure 2. Prevalence of fatty liver disease in US adults^[71] and adolescents.^[65,68]

No treatments for NAFLD have been well established to date, but investigators have explored several possible targets. Consistent with the observed associations between obesity, insulin resistance, and fatty liver disease, weight loss is usually recommended, although the long-term efficacy of this approach is difficult to measure with intervention studies because of the difficulty achieving significant and sustained weight loss in a study population. Studies of weight loss for NAFLD in children have been small and without histologic outcomes,^[71,72] but have suggested some efficacy. Progression of simple fatty liver to more severe steatohepatitis in children has not been demonstrated, but there is evidence that obesity can potentiate other insults to the liver, such as alcohol and hepatitis C virus infection. Thus, weight control may make the liver less susceptible to such insults,^[73] and such considerations are particularly relevant in a young population.

The finding of progressive NAFLD in many adults and some adolescents calls for active pursuit of therapeutic options, including pharmacotherapy. Insulin-sensitizing agents such as metformin and thiazolidinediones have shown some promise in small uncontrolled trials in adults,^[74-76] but trials of these agents for fatty liver disease in children have not yet been reported. Oxidative injury is thought to be an important mechanism of injury in steatohepatitis, and antioxidants have been considered as treatments. Indeed, vitamin E showed some potential for treatment of NAFLD in a small, uncontrolled trial in adolescents.^[77] Like trials of metformin and atorvastatin^[78] in adults, the pediatric NAFLD treatment trials are limited by small sample size, nonrandomized design, and/or a lack of histologic outcomes. A large, multicenter, randomized trial is in progress to evaluate metformin or vitamin E vs placebo in adolescents with fatty liver disease. Under the auspices of the NASH Clinical Research Network, this trial will provide valuable data on the natural history of NAFLD in children and adolescents, as well as outcomes of these 2 promising treatment approaches.^[79]

Sleep apnea. Obstructive sleep apnea is perhaps the most acutely dangerous medical complication of obesity, and is underdiagnosed in all age groups. Sleep apnea is associated with obesity in adults and children (Figure 3), although in children there may be strong contributions from obstructing tonsils and adenoids. It can cause significant hypoxia, heart strain, and reduced daytime functioning, including poor school performance. Clinical criteria for diagnosis include daytime somnolence and consistent snoring; if found in concert with either significant obesity or tonsillar hypertrophy, further workup is indicated.^[80] The diagnosis is best made with a sleep study, and treatment can be initiated with continuous positive airway pressure and/or tonsillectomy, if indicated.

Figure 3. Prevalence of obstructive sleep apnea in US adults^[148,149] and children.^[150]

Other medical complications. Other consequences of obesity seen in childhood are cholelithiasis, pseudotumor cerebri, gastroesophageal reflux disease, polycystic ovary disease, and orthopaedic problems, including Blount disease^[81] and slipped capital femoral epiphysis.^[82] Screening for these and other medical problems is described in Table 5. In addition to these complications, obesity in adults is associated with debilitating or life-threatening degenerative problems (axial arthritis and cardiovascular and cerebrovascular disease),^[64,65] as well as with increased risk of certain neoplasias (breast, ovarian, prostate, and colon cancers).^[66]

Table 5. Initial Screening for Medical Complications of Obesity in Children and Adolescents

ALT = alanine aminotransferase; AST = aspartate aminotransferase; GERD = gastroesophageal reflux disease; HDL = high-density lipoprotein; LDL = low-density lipoprotein; PCOS = polycystic ovary syndrome; SCFE = slipped capital femoral epiphysis; TG = triglycerides

Psychological Complications

The psychosocial complications of obesity are more subjective and difficult to measure in a standard fashion but undoubtedly represent one of the greatest burdens of obesity in children and adolescents. In many cases, psychosocial issues are best understood as consequences of the disease, brought on by feelings of discouragement and criticism by family, peers, or self. In other instances, the psychological issues precede or exacerbate obesity.^[83] Regardless of the causality, it is important to acknowledge and assess these behavioral and psychological issues in each individual to best target treatment.

Depressive symptoms,^[84,85] anxiety,^[86,87] binge-eating disorder,^[88,89] decreased self-esteem,^[90,91] and problems with social interactions^[92] have generally been found more frequently in obese children and adolescents than in their lean peers. Negative psychosocial associations also persist into early adulthood, when obesity is associated with lower educational attainment and household income (independent of baseline education and aptitude) and lower rates of marriage.^[93] Many of these problems can be attributed to the widespread and culturally entrenched bias against obese individuals in our society.^[93,94]

Assessment of the psychosocial issues contributing to and stemming from obesity in a particular patient has not been established and varies greatly among providers. Whether or not standardized instruments are used, some effort should be made to assess mood, motivation, school and social performance, self-image, and eating attitudes and behaviors. When discussions with the adolescent or parent raise concerns about depression, screening for specific symptoms is warranted. Symptoms include persistent sad or irritable mood, loss of enjoyment of activities once enjoyed, feelings of worthlessness or inappropriate guilt, and recurrent thoughts of death or suicide.^[95] The Children's Depression Inventory^[96] is a useful standard tool for depression screening in children 7 to 17 years old. When clinical judgment and/or the depression screen raises a question of childhood depression, steps should be taken to ensure that there is no acute suicidal intent, and referral should be made to an appropriate mental health professional for further evaluation. It is also important to assess these issues in parents or close caretakers of the patient, because factors such as motivation, mood disorders, and eating disorders in a parent will have a substantial impact on the child's attitudes, behaviors, and ability to respond to treatment.^[97] Treatment of depression, eating disorder, or other mental illness should be initiated before efforts can be turned to weight control.

A "stages of change" model may be helpful in establishing the readiness of the patient and family for making lifestyle changes (Table 6).^[98] If the patient or family is in an early stage of change (pre-contemplation or contemplation), efforts should focus on helping them forward into the next stage, perhaps using motivational interviewing techniques.

Table 6. Stages of Change

Adapted from Prochaska, 1992.^[98]

Nutritional Therapy

Many studies have addressed obesity in preadolescents and adolescents using a variety of approaches to alter diet and physical activity. However, the majority of studies still do not provide long-term data, and many issues, such as optimal macronutrient composition of diets and strategies to change food preference, have not been adequately studied. A few studies have suggested that structured exercise increases weight loss compared with diet alone,^[99,100] and treatments focusing on increasing lifestyle exercise and reducing sedentary behaviors have also shown beneficial effects.^[101-103] In general, regimens that combine hypocaloric diets with exercise and behavior modification have been particularly effective.^[102-104] Epstein and colleagues have shown a medically significant long-term effect of an 8-month family-based behavioral intervention for families with children 6 to 11 years old. The improvement persisted 10 years after the intervention was completed.^[105] The design of this study supports the conclusion that the behavioral intervention was a critical component of success.

For dietary treatment of obesity for adults and children, the American Academy of Nutrition and other governmental agencies recommend reduction in dietary fat and energy intake as a balanced, hypocaloric diet.^[106,107] Specific recommendations include limiting beverages and foods with high caloric density and low nutritional value, including sugary beverages and full-fat or low-fat baked goods and candies, and encouraging intake of whole grains, fruits, and vegetables. Simple behavioral measures such as meal planning and label reading during grocery shopping are also generally encouraged to support the implementation of these nutrition guidelines.

The "traffic-light diet" provides a structured, balanced hypocaloric diet in a simple format and has been used effectively for preadolescent^[105] and preschool children.^[108] It uses a simple color-coding scheme to categorize foods into categories for free consumption (low-density foods, "green"), moderate consumption (moderate-density and protein-containing foods, "yellow"), and very limited consumption (foods with high caloric density and/or with high sugar or fat content, "red"). The prescribed caloric content of the diet is generally between 900 and 1300 kcal daily.

The protein-sparing modified fast (PSMF) diet provides high-quality lean protein while strictly limiting total calories. It has been used to treat severe obesity in a variety of settings, including hospitalized patients and school-based interventions. This diet has been effectively used in settings in which short-term weight loss is medically necessary, but there are no data to suggest that the diet reliably improves obesity in the long term. This diet generally prescribes a total energy intake of 600-800 kcal daily, with 2 g/kg/day protein. This is given for 12 weeks, then followed by a maintenance diet.^[109] Of note, one study reported an 11.2-kg weight loss after 10 weeks of a PSMF diet, which was substantially more than that achieved by less restrictive measures, but at the 15- month follow-up, the weight loss achieved by the 2 groups was similar.^[110] Potential complications of the diet include protein losses, hypokalemia, inadequate calcium intake, cholelithiasis, and intravascular volume depletion with orthostatic hypotension.

Although the caloric content of a diet has been shown to relate to treatment success at 1 year,^[111] there is little evidence to suggest that alterations in specific macronutrients yield long-term weight reduction. A variety of popular diets have arisen around alterations of specific macronutrients, with or without limitations on total caloric intake. Many of these show good short-term weight loss, but whether these diets achieve long-term effects on obesity is unclear because no adequate long-term studies (with 5 or more years of follow-up) in representative adult or pediatric populations have been published. Freedman and colleagues^[112] reviewed the available evidence of benefits and risk associated with popular diets in adults. Diets that specifically limit fat intake, which were popularized by Dean Ornish, were the subject of a recent review of studies with 6 to 18 months of follow-up.^[113] The authors of that review concluded that fat-restricted diets are no better than calorie-restricted diets in achieving long-term weight loss in overweight or obese people.

Diets that focus on limiting carbohydrates, with or without restrictions on fat intake, have been touted in the popular press for decades with minimal scientific support. New versions of these diets have enjoyed recent popularity, with increasing but still tenuous scientific support. Careful analysis reveals that in the short term, low-carbohydrate diets cause a greater loss of body water than body fat. If the diet is maintained in the long term, it results in the loss of body fat. There are few long-term data regarding the overall efficacy of these low-carbohydrate diets. High-fat, low-carbohydrate diets such as the Atkins diet are nutritionally inadequate and require supplementation of calcium and water-soluble vitamins.^[112]

Caution should be used when considering the results of studies such as these that focus on adult populations, because there is compelling evidence that at least some "lifestyle" approaches to obesity are substantially more effective in children than they are in adults.^[114] Some dietary approaches might prove to have long-term results in children even if none can be demonstrated for adults.

Diets that include a low glycemic index/load approach or higher consumption of calcium are currently under investigation^[115,116] and will require long-term study before any useful conclusions can be drawn. A trial of increasing the fiber content of a hypocaloric diet in children yielded no better short-term results than a hypocaloric diet alone.^[117] Medical guidance is important because there are ongoing concerns about medical complications, including dyslipidemias arising from the use of some popular diets and from the use of dietary supplements for weight loss, including in children. As many as 80% of children using unsupervised diets from popular magazines had medical problems resulting from these diets.^[118]

As rates of obesity rise, obese children represent an increasing proportion of hospital inpatients.^[119] Whether or not the child is hospitalized for an obesity-related condition such as gallstones, diabetes, sleep apnea, or orthopaedic problems, nutritional needs must be considered. It is particularly important to recognize that the obesity is a chronic problem and will not resolve by attempting weight loss acutely during the inpatient stay. Moreover, acute severe caloric restriction is inappropriate and can lead to metabolic problems, including refeeding syndrome, despite the child's adequate energy stores. Guidelines for nutritional care of obese adult inpatients have been developed,^[120] but this issue has not been examined in children. It may be appropriate to prescribe a modest reduction in caloric intake, guided by indirect calorimetry or by calculations based on adjusted body weights and using a stress factor that is appropriate to the child's condition. The inpatient stay may also present an opportunity for nutritional education and for engaging the patient and family in a therapeutic plan to address the obesity beyond the hospital stay.

Behavior Therapy

As discussed above, some interventions in childhood have demonstrated long-term improvement of obesity with 5^[121] or 10 years^[105] of follow-up; thus, children appear to have a more consistent and durable response to therapy than adults in the same family^[102] or adult populations in general. The importance of including behavior therapy in the treatment of obesity in children has been demonstrated, at least in a family-based setting.^[122] Although many interventions use combinations of dietary, exercise, and behavioral interventions, it is notable that the few studies with long-term results have had a rigorous and structured behavioral component.^[123]

Commonly used techniques include self-monitoring of food intake and weight, modeling, positive reinforcement (praise), contingency management (certain behaviors are paired with predictable, reinforcing responses), and stimulus control (learning to avoid situations that are cues to overeat). Some studies have tested specific elements of these behavioral techniques. These have shown the superiority of family-based over patient-focused treatment,^[105] of gradual behavioral treatment (8 sessions over 15 weeks) over rapid behavioral treatment (8 sessions over 4 weeks),^[124] and of positive reinforcement over restrictive or critical approaches.^[125] Thus, there is ample evidence to support the use of behavioral-modification techniques in the treatment and possibly the prevention of obesity in children. Behavior therapy should be thought of as a tool to achieve long-term changes in diet and exercise. By contrast, there are few data to support the use of behavior "micromanaging" techniques such as the rate of eating and bite size.

Weight-Loss Drugs

Many of the drugs used for the treatment of obesity in adults in the past are characterized by unproven claims, highly variable efficacy, or dangerous side effects. Nonetheless, the incomplete but growing understanding of the mechanisms underlying the homeostatic control of body weight and the increased rigor applied to clinical drug trials hold promise for the development and use of pharmacologic agents to treat this chronic disease. In the short term, drugs can be helpful for a patient whose medical condition requires acute weight loss. Drugs may also have a role in treating the chronic component of obesity. Modification of the environmental and societal pressures contributing to obesity should be thought of as the ultimate goal, but the use of drugs to promote weight loss may keep an individual patient engaged in the lifestyle component of treatment. Thus, pharmacotherapy for obesity is not at odds with lifestyle-changing approaches. As increasingly specific drugs are developed, efficacy and safety should improve, and pharmacotherapy may ultimately be an important tool to treat an otherwise refractory and devastating disease. Whether pharmacologic treatment is cost-effective depends in large part on whether it prevents the medical complications of obesity and associated costs of medical care.

Current options for the pharmacologic treatment of obesity are limited but may have some clinical utility. In general, the drugs demonstrate only modest efficacy but minimal side effects. Sibutramine, an appetite suppressant, acts mainly through enhancement of both norepinephrine and serotonin signaling. Weight loss is typically modest (5% to 8%, about 4% more than placebo),^[126] and generally is regained after the drug is stopped. Side effects include increases in blood pressure and heart rate, dry mouth, constipation, and insomnia. Orlistat inhibits gastrointestinal lipases, reducing fat digestion and absorption by about 30%. Side effects are related to fat malabsorption (steatorrhea with high-fat meals and modest decreases in serum levels of fat-soluble vitamins). With orlistat, weight loss is also typically modest (3.2% more than with placebo).^[125]

A randomized trial of sibutramine in adolescents with concurrent behavioral therapy demonstrated significantly more weight loss than placebo (7.8 vs 3.2 kg). Adverse effects were similar to those seen in adults, and prompted reduction or discontinuation of medication in more than one third of subjects.^[127] A large, multicenter, randomized, placebo-controlled trial of sibutramine in adolescents is in progress and will provide better assessment of the safety and efficacy of these drugs in adolescents. A small, open-label pilot study in adolescents suggested that orlistat enhanced weight loss compared with diet and exercise alone.^[128] A large, randomized clinical trial of orlistat in adolescents has been completed, and led to Food and Drug Administration (FDA) approval for this indication, but the trial has not yet been published.^[129] A smaller trial revealed decreases in vitamin D levels after 3-6 months of treatment, suggesting that vitamin D should be monitored and possibly supplemented during treatment with orlistat. Serum levels of other fat-soluble vitamins were not significantly altered in this small trial.^[130]

The modest weight loss achieved by the use of current available drugs in conjunction with reduced calorie diets is not adequate to treat individuals with severe life-threatening complications of obesity, but the drugs may be considered to boost weight loss, assist weight-loss maintenance, and reinforce lifestyle change. Whether phenotypic or genotypic analysis can be used to select for patients who respond relatively well to these agents is a subject for future study.

Metformin improves insulin sensitivity and also promotes modest weight loss in adults.^[131] In contrast to other antihyperglycemic agents, metformin does not increase insulin secretion but decreases hepatic glucose production and improves insulin sensitivity in both diabetic and nondiabetic adults.^[132] Small open-label trials of metformin have suggested that it may be useful in ameliorating psychotropic drug-induced weight gain in children.^[133] A small randomized trial of metformin in adolescents with hyperinsulinemia and a family history of diabetes showed improved glucose tolerance and a modest decrease in BMI.^[134] Larger trials of metformin in adolescents are in progress. Careful review of these results will be necessary before pharmacotherapy outside of clinical trials can be recommended in adolescents or children.

Phentermine, diethylpropion, phendimetrazine, and benzphetamine are noradrenergic agents with appetite-suppressant effects, but they have been studied and approved for short-term use only in adults (generally 12 weeks or less).^[135] The latter 2 drugs are considered to have some potential for abuse and are listed in Schedule III of the US Drug Enforcement Agency. The use of any agent with only short-term goals for weight loss in children and adolescents, particularly one with any potential for abuse, is highly questionable.

Dietary "supplements" or herbal medicines are popular, and consumers spend more than $1 billion on these products annually in the United States.^[125] However, they are unregulated and relatively untested. Supplements that could be used with caution in adults include conjugated linoleic acid, ginseng, chromium, hydroxycitric acid, dehydroepiandrosterone, hydroxymethylbutyrate, chitosan, and St. John's wort, but there is little evidence of the effectiveness of these drugs. The once-popular supplement ephedra (or ma huan) has been banned for sale in the United States by the FDA. Other substances that have questionable safety and should be discouraged include horsetail, herbal laxatives, and some forms of caffeine and fiber.^[136,137] There are no well-designed studies supporting the use of dietary supplements for weight loss in children, and no supplements for weight loss can be recommended or even considered with caution.

Weight-Loss Surgery

During the past 15 years, surgically induced weight loss has emerged as an important option for adults with severe obesity. In contrast to poor long-term success rates for nonsurgical treatments of obesity, surgical approaches generally produce durable and substantial weight loss. More than 80% of patients lose at least half of their excess body weight during the first year.^[138] Weight generally stabilizes 12 to 24 months after surgery, and 10% to 20% of patients regain a significant portion of the lost weight. If a patient maintains weight loss for 5 years, there is an excellent likelihood that the weight loss will persist for at least 14 years.^[139] Studies have shown improvement or resolution of many of the medical complications of obesity, including diabetes mellitus, hypercholesterolemia, and obstructive sleep apnea.^[140]

The jejunoileal bypass was an early surgical procedure for weight loss and caused global malabsorption. It caused frequent and unacceptable side effects, including intractable diarrhea, nutrient deficiencies, kidney stones, and hepatic failure. The most common operation performed today is the Roux-en-Y gastric bypass, which reduces the gastric capacity to restrict caloric intake and bypasses the majority of the stomach. In contrast to the jejunoileal bypass, this operation does not cause significant malabsorption, and the safety profile is substantially better. The mechanism through which this operation causes weight loss is not fully understood, although recent studies suggest that it may suppress gastric production of ghrelin, thereby reducing appetite.^[141] About 10% of patients have important complications of the procedure, which include anastomotic strictures, incisional hernias, and gallstone formation requiring cholecystectomy. Anastomotic leaks, staple line disruptions, and dumping syndrome can occur but have been reduced to 1% to 2% each by modifications in surgical technique.^[142] Although protein-calorie malabsorption is rare, malabsorption of selected micronutrients, particularly iron, calcium, and vitamin B₁₂, is common and requires postoperative monitoring and treatment.

Laparoscopic approaches to the gastric bypass are increasingly used for adults and have also been reported for adolescents.^[143] The adjustable laparoscopic gastric band has been used extensively in adults with obesity in Australia and Europe.^[144] These series and the most recent US series^[145] suggest somewhat less weight loss than with the gastric bypass, but few major complications. Whether this device is appropriate for use in adolescents with obesity will depend on assessment of long-term weight loss and complication rates compared with those of the gastric bypass through objective studies in the United States and elsewhere.

Weight-loss surgery is thus an appropriate treatment option for adults with medically significant obesity, but there is still significant uncertainty regarding optimal patient selection. To date, no psychological or physiologic factors have been defined that will determine which patients are most likely to suffer weight regain after surgery (approximately 20% of patients regain most or all of their lost weight) or to suffer medical or psychological complications of surgery. Similarly, there are limited data on the outcomes of weight-loss surgery in adolescent patients. A few series have been published,^[146,147] and these suggest that short- and long-term outcomes and complications in adolescents are probably similar to those seen in adults.

Weight-loss surgery may therefore be appropriate in selected severely obese adolescents. Guidelines for selection and management of adolescents for weight-loss surgery have been proposed,^[148] and these are appropriately more conservative than those used for adults. Given the limited data available on outcomes in this age group, these procedures should be limited to patients who have exhausted other management approaches and have significant medical complications of their obesity. To optimize long-term outcomes, any concomitant psychiatric disorders should be carefully assessed and under good control before surgery, and measures should be taken to ensure long-term follow-up for medical, surgical, and nutritional issues, ideally in the setting of a multidisciplinary obesity treatment center with substantial experience in surgical treatment of obesity. Due to significant risks of morbidity and mortality, particularly in inexperienced hands, only centers with substantial experience in performing weight-loss surgery should be considered.

The treatment and prevention of obesity in individual patients and families will be important over the coming decades, but is unlikely to reverse the obesity epidemic. Major changes in some aspects of western culture will be necessary to change the high rates of obesity in the population at large. As voices in the interest of preventative medicine and child health, pediatric providers can lead the way in these essential cultural changes. To be most effective, we need to focus our energy on public policies and interventions that are solidly supported by evidence-based research. Where evidence is lacking, the pediatric community should support and participate in new research to establish which specific public interventions are effective.

Currently, there is adequate evidence to suggest that public programs to increase physical activity in children are likely to be helpful in preventing obesity and/or its long-term consequences. The pediatric healthcare community should strongly support increases in physical education in schools and through community-sponsored programs. To maximize participation and to help establish life-long habits of physical activity, such programs should find creative ways to meet the needs of children with a variety of physical abilities, encourage lifetime sports, and support recreational physical activity and family participation. Communities should plan and aggressively fund recreational facilities, including playgrounds and pools, and urban planning should aim to create safe and encouraging environments for pedestrians and bicycles.

Schools can play a key role in maintaining physical activity and good nutrition for children in the community. Schools should be held responsible for providing a consistently healthy nutritional environment, and the community must be willing to support this goal even when it creates short-term cost increases. Schools need to make more progress in providing food that is palatable yet low in excess calories from sugar and fat, despite common budgetary constraints. Local educational systems can support each other by sharing successful approaches for meeting these goals. Approaches that compromise the nutritional environment, such as allowing vending machines with soft drinks, candy, and snacks in school, should be rejected.

Community-based childcare and after-school programs constitute another important element of our children's environment. By setting high standards for healthy nutrition, and providing play and recreational physical activity as an alternative to after-school television viewing and sedentary activity, such programs can be a critical component of a healthy environment for children with parents who work outside the home. Pediatric healthcare providers, parents, educators, and policy makers should collaborate to support these programs by encouraging their use, finding creative financing of programs and facilities, and setting high standards of care.

References

1. Dietz WH, Robinson TN. Use of the body mass index (BMI) as a measure of overweight in children and adolescents. J Pediatr. 1998;132:191-193.  
2. Lauer RM, Clarke WR, Witt J. Childhood risk factors for high adult blood pressure: the Muscatine study. Pediatrics. 1989;84:633-641.  
3. Gutin B, Basch C, Shea S, et al. Blood pressure, fitness, and fatness in 5-and 6-year-old children. JAMA. 1990;264:1123-1127.  
4. Laskarzewski P, Morrison JA, Mellies MJ, et al. Relationships of measurements of body mass to plasma lipoproteins in schoolchildren and adults. Am J Epidemiol. 1980;111:395-406.  
5. Zwiauer K, Widhalm K, Kerbl B. Relationship between body fat distribution and blood lipids in obese adolescents. Int J Obes Relat Metab Disord. 1990;14:271-277.
6. Ronnemaa T, Knip M, Lautala P, et al. Serum insulin and other cardiovascular risk indicators in children, adolescents and young adults. Ann Intern Med. 1991;23:67-72.
7. Horlick M. Body mass index in childhood: measuring a moving target. J Clin Endocrinol Metab. 2001;86:4059-4060.  
8. Ogden CL, Flegal KM, Carroll MD, Johnson CL. Prevalence and trends in overweight among US children and adolescents, 1999-2000. JAMA. 2002;288:1728-1732.  
9. Mokdad AH, Marks JS, Stroup DF, Gerberding JL. Actual causes of death in the United States, 2000. JAMA. 2004;2911238-1245.
10. Weigle DS. Appetite and the regulation of body composition. FASEB J. 1994;8:302-310.  
11. Bouchard C. Genetics of human obesity: recent results from linkage studies. J Nutr. 1997;127:1887S-1890S.  
12. Katzmarzyk PT, Perusse L, Rao DC, Bouchard C. Familial risk of obesity and central adipose tissue distribution in the general Canadian population. Am J Epidemiol. 1999;149:933-942.  
13. Montague CT, Farooqi IS, Whitehead JP, et al. Congenital leptin deficiency is associated with severe early-onset obesity in humans. Nature. 1997;387:903-908.  
14. Clement K, Vaisse C, Lahlou N, et al. A mutation in the leptin receptor gene causes obesity and pituitary dysfunction. Nature. 1998;392:398-401.  
15. Krude H, Biebermann H, Luck W, et al. Severe early-onset obesity, adrenal insufficiency and red hair pigmentation caused by POMC mutations in humans. Nat Genet. 1998;19:155-157.  
16. Jackson RS, Creemers JW, Ohagi S, et al. Obesity and impaired prohormone processing associated with mutations in the human prohormone convertase 1 gene. Nat Genet. 1997;16:303-306.  
17. Yeo GS, Farooqi IS, Aminian S, et al. A frameshift mutation in MC4R associated with dominantly inherited human obesity. Nat Genet. 1998;20:111-112.  
18. Snyder EE, Walts B, Pérusse L, et al. The human obesity gene map: the 2003 update. Obes Res. 2004;12:369-439.  
19. Ukkola O, Ravissun E, Jacobson P, et al. Mutations in the preproghrelin/ghrelin gene associated with obesity in humans. J Clin Endocrinol Metab. 2001;86:3996-3999.  
20. Hasstedt SJ, Ren QF, Teng K, Elbein SC. Effect of the peroxisome proliferator-activated receptor-gamma 2 pro(12)ala variant of obesity, glucose homeostasis, and blood pressure in members of familial type 2 diabetic kindreds. J Clin Endocrinol Metab. 2001;86:536-541.  
21. Esterbauer H, Schneitler C, Oberkofler H, et al. A common polymorphism in the promoter of UCP2 is associated with decreased risk of obesity in middle-aged humans. Nat Genet. 2001;28:178-183.  
22. Oizumi T, Daimon M, Saitoh T, et al. Genotype Arg/Arg, but not Trp/Arg, of the Trp64Arg polymorphism of the b3 adrenergic receptor is associated with type 2 diabetes and obesity in a large Japanese sample. Diabetes Care. 2001;24:1579-1583.  
23. Tershakovec AM, Jawad AF, Stallings VA, et al. Age-related changes in cardiovascular disease risk factors of hypercholesterolemic children. J Pediatr. 1998;132:414-420.  
24. Carrel AL, Myers SE, Whitman BY, Allen DB. Benefits of long-term GH therapy in Prader-Willi syndrome: a 4-year study. J Clin Endocrinol Metab. 2002;87:1581-1585.  
25. McLellan F. Obesity rising to alarming levels around the world. Lancet. 2002;359:1412.
26. Robinson TN. Reducing children's television viewing to prevent obesity: a randomized controlled trial. JAMA. 1999;282:1561-1567.  
27. Bell EA, Rolls BJ. Energy density of foods affects energy intake across multiple levels of fat content in lean and obese women. Am J Clin Nutr. 2001;73:1010-1018.  
28. Ebbeling CB, Leidig MM, Sinclair KB, Hangen JP, Ludwig DS. A reduced-glycemic load diet in the treatment of adolescent obesity [see comment]. Arch Pediatr Adolesc Med. 2003;157:773-779.  
29. Barker DJP. Fetal origins of coronary heart disease. BMJ. 1995;311:171-174.  
30. Barker DJP, Hales CN, Fall CH, Osmond C, Phipps K, Clark PM. Type 2 (non-insulin-dependent) diabetes mellitus, hypertension and hyperlipidaemia (syndrome x): relation to reduced fetal growth. Diabetologia. 1993;36:62-67.  
31. Rich-Edwards JW, Stampfer MJ, Manson JE, et al. Birthweight and risk of cardiovascular disease in a cohort of women followed up since 1976. BMJ. 1997;315:396-400.  
32. Bhargava SK, Sachdev HS, Fall CHD, et al. Relation of serial changes in childhood body mass index to impaired glucose tolerance in young adulthood. N Engl J Med. 2004;350:865-875.  
33. Vanhala M, Vanhala P, Kumpusalo E, Halonen P, Takala J. Relation between obesity from childhood and the metabolic syndrome: population-based study. Br Med Bull. 1998;317:319.
34. Van Assche, Holemans K, Aerts L. Long-term consequences for offspring of diabetes during pregnancy. Br Med Bull. 2001;60:173-182.  
35. Ravelli ACJ, van der Meulen JHP, Michels RPJ et al. Glucose tolerance in adults after prenatal exposure to famine. Lancet. 1998;351:173-177.  
36. Hales CN, Barker DJP. The thrifty phenotype hypothesis. Br Med Bull. 2001;60:5-20.  
37. Ozanne SE. Hales CN. Lifespan: catch-up growth and obesity in male mice. Nature. 2004;427:411-412.
38. Hales CN, Desai M, Ozanne SE, Crowther NJ. Fishing in the stream of diabetes: from measuring insulin to the control of fetal organogenesis. Biochem Soc Trans. 1996; 24:341-350.  
39. Burns SP, Desai M, Cohen RD, et al. Gluconeogenesis, glucose handling, and structural changes in livers of the adult offspring of rats partially deprived of protein during pregnancy and lactation. J Clin Invest. 1997;100:1768-1774.  
40. Committee on Nutrition, American Academy of Pediatrics. Policy Statement: Prevention of Pediatric Overweight and Obesity. Pediatrics. 2003;112:424-430.  
41. Gillman MW, Rifas-Shiman SL, Camargo CA Jr, et al. Risk of overweight among adolescents who were breastfed as infants. JAMA. 2001;285:2461-2467.  
42. von Kries R, Koletzko B, Sauerwald T, et al. Breast feeding and obesity: cross sectional study. BMJ. 1999;319:147-150.  
43. Toschke AM, Vignerova J, Lhotska L, Osancova K, Koletzko B, von Kries R. Overweight and obesity in 6- to 14-year-old Czech children in 1991: protective effect of breast-feeding. J Pediatr. 2002;141:764-769.  
44. McMurray RG, Harrell JS, Bangdiwala SI, Hu J. Tracking of physical activity and aerobic power from childhood through adolescence. Med Sci Sports Exerc. 2003;35:1914-1922.  
45. Kimm SYS, Glynn NW, Kriska AM, et al. Decline in physical activity in black girls and white girls during adolescence. N Engl J Med. 2002;347:709-715.  
46. Taylor WC, Baranowski T, Sallis JF. Family determinants of childhood physical activity: a social-cognitive model. In: Dishman RK, ed. Advances in Exercise Adherence. Champaign, Ill: Human Kinetics; 1994:319-342.
47. Greendorfer SL, Ewing ME. Race and gender differences in children's socialization into sport. Res Q Exerc Sport. 1981;52:301-310.  
48. Strauss RS, Rodzilsky D, Burack G, Colin M. Psychosocial correlates of physical activity in healthy children. Arch Pediatr Adolesc Med. 2001;155:897-902.  
49. Whitaker RC, Wright JA, Pepe MS, Seidel KD, Dietz WH. Predicting obesity in young adulthood from childhood and parental obesity. N Engl J Med. 1997;337:869-873.  
50. Sinha R, Fisch G, Teague B, et al. Prevalence of impaired glucose tolerance among children and adolescents with marked obesity. N Engl J Med. 2002;346:802-810.  
51. Jiang X, Srinivasan SR, Webber LS, et al. Association of fasting insulin level with serum lipid and lipoprotein levels in children, adolescents, and young adults: The Bogalusa Heart Study. Arch Intern Med. 1995;155:190-196.  
52. Raitakari OT, Porkka KVK, Ronnemaa T, et al. The role of insulin in clustering of serum lipids and blood pressure in children and adolescents. Diabetologia. 1995;38:1042-1050.  
53. Sinaiko AR, Donahue RP, Jacobs, DR, Prineas RJ. Relation of rate of growth during childhood and adolescence to fasting insulin, lipids, and systolic blood pressure in young adults. Circulation. 1999;99:1471-1476.  
54. Jiang X, Srinivasan S, Bao W, Berenson G. Association of fasting insulin with blood pressure in young individuals: The Bogalusa Heart Study. Arch Intern Med. 1993;153:323-328.  
55. Srinivasan SR, Sathanur R, Myers L, Berenson GS. Predictability of childhood adiposity and insulin for developing insulin resistance syndrome (Syndrome X) in young adulthood: The Bogalusa Heart Study. Diabetes. 2002;51:204-209.  
56. Daniels SR, Morrison JA, Sprecher DL, et al. Association of body fat distribution and cardiovascular risk factors in children and adolescents. Circulation. 1999;99:541-545.  
57. Hanevold C, Waller J, Daniels S, Portman R, Sorof J. The effects of obesity, gender, and ethnic group on left ventricular hypertrophy and geometry in hypertensive children: a collaborative study of the International Pediatric Hypertension Association. Pediatrics. 2004;113:328-333.  
58. Berenson GS, Srinivasan SR, Bao W, et al. Association between multiple cardiovascular risk factors and atherosclerosis in children and young adults. N Engl J Med. 1998;338:1650-1656.  
59. Must A, Jacques PF, Dallal GE, et al. Long-term morbidity and mortality of overweight adolescents: a follow-up of the Harvard Growth Study of 1922 to 1935. N Engl J Med. 1992;327:1350-1355.  
60. Moran A, Jacobs D, Steinberger DR, et al. Insulin resistance during puberty: Results from clamp studies in 357 children. Diabetes. 1999;48:2039-2044 .  
61. Arsalnian S, Suprongsin C. Insulin sensitivity, lipids, and body composition in childhood: Is "Syndrome X" present? J Clin Endocrinol Metab. 1996;81:1058-1062.
62. Cook JS, Hoffman RP, Stene MA, Hansen JR. Effects of maturational stage on insulin sensitivity during puberty. J Clin Endocrinol Metab.1993;77:725-730.  
63. Travers JH, Jeffers BW, Bloch CA, et al. Gender and tanner stage differences in body composition and insulin sensitivity in early pubertal children. J Endocrinol Metab. 1995;80:172-178.
64. Kinugasa A, Tsunamoto K, Furukawa N, et al. Fatty liver and its fibrous changes found in simple obesity of children. J Pediatr Gastroenterol Nutr. 1984;3:408-414.  
65. Strauss RS, Barlow SE, Dietz WH. Prevalence of abnormal serum aminotransferase values in overweight and obese adolescents. J Pediatr. 2000;136:727-733.  
66. McCullough AJ. Update on nonalcoholic fatty liver disease. J Clin Gastroenterol. 2002;34:255-262.  
67. Fishbein MH, Miner M, Mogren C, Chalekson J. The spectrum of fatty liver in obese children and the relationship of serum aminotransferases to severity of steatosis. J Pediatr Gastroenterol Nutr. 2003;36:54-61.  
68. Franzese A, Vajro P, Aregenziana A, et al. Liver involvement in obese children: ultrasonography and liver enzyme levels at diagnosis and during follow-up in an Italian population. Dig Dis Sci. 1997;42:1428-1432.  
69. Molleston JP, White F, Teckman J, Fitzgerald JF. Obese children with steatohepatitis can develop cirrhosis in childhood. Am J Gastroenterol. 2002;97:2460-462.  
70. Rashid M, Roberts EA. Nonalcoholic steatohepatitis in children. J Pediatr Gastroenterol Nutr. 2000;30:48-53.  
71. Wanless IR, Lentz JS. Fatty liver hepatitis (steatohepatitis) and obesity: an autopsy study with analysis of risk factors. Hepatology. 1990;12:1106-1110.  
72. Vajro P, Fontanella A, Perna C, Orso G, Tedesco M, De Vincenzo A. Persistent hyperaminotransferasemia resolving after weight reduction in obese children. J Pediatr. 1994;125:239-241.  
73. Bellentani S, Saccoccio G, Masutti F, et al. Prevalence of and risk factors for hepatic steatosis in Northern Italy. Ann Intern Med. 2000;132:112-117.  
74. Marchesini G, Brizi M, Bianchi G, et al. Metformin in non-alcoholic steatohepatitis. Lancet. 2001;358:893-894.  
75. Caldwell SH, Hespenheide EE, Redick JA, Iezzoni JC, Battle EH, Sheppard BL. A pilot study of a thiazolidinedione, troglitazone, in nonalcoholic steatohepatitis. Am J Gastroenterol. 2001;96:519-525.  
76. Promrat K, Lutchman G, Uwaifo GI, A pilot study of pioglitazone treatment for nonalcoholic steatohepatitis. Hepatology. 2004;39:188-196.  
77. Lavine JE. Vitamin E treatment of non-alcoholic steatohepatitis in children: a pilot study. J Pediatr. 2000;136:734-738.  
78. Harlander JC, Kwo PY, Cummings OW. Atorvastatin for the treatment of NASH. Gastroenterology. 2001;120A:2767.
79. Lavine J. Pediatric initiatives within the nonalcoholic steatohepatitis - clinical research network (NASH-CRN). J Pediatr Gastroenterol Nutr. 2003;37:220-221.  
80. American Academy of Pediatrics, Section on Pediatric Pulmonology, Subcommittee on Obstructive Sleep Apnea Syndrome. Clinical practice guideline: diagnosis and management of childhood obstructive sleep apnea syndrome. Pediatrics. 2002;109:704-712  
81. Dietz WH, Gross WL, Kirkpatrick JA Jr. Blount disease (tibia vara): another skeletal disorder associated with childhood obesity. J Pediatr. 1982;101:735-737.  
82. Loder RT Aronson DD, Greenfield ML. The epidemiology of bilateral slipped capital femoral epiphysis. A study of children in Michigan. J Bone Joint Surg Am. 1993;75:1141-1147.  
83. Goodman E, Whitaker RC. A prospective study of the role of depression in the development and persistence of adolescent obesity. Pediatrics. 2002;110:497-504.  
84. Erickson SJ, Robinson TN, Haydel KF, Killen JD. Are overweight children unhappy?: body mass index, depressive symptoms, and overweight concerns in elementary school children. Arch Pediatr Adolesc Med. 2000;154:931-935.  
85. Pine DS, Goldstein RB, Wolk S, Weissman MM. The association between childhood depression and adulthood body mass index. Pediatrics. 2001;107:1049-1056.  
86. Becker ES, Margraf J, Turke V, et al. Obesity and mental illness in a representative sample of young women. Int J Obes Relat Metab Disord. 2001;25(Suppl 1):S5-S9.  
87. Morgan CM, Yanovski SZ, Nguyen TT, et al. Loss of control over eating, adiposity, and psychopathology in overweight children. Int J Eat Disord. 2002;31:430-441.  
88. Berkowitz R, Stunkard AJ, Stallings VA. Binge-eating disorder in obese adolescent girls. Ann N Y Acad Sci. 1993;699:200-206.  
89. Maloney MJ, McGuire J, Daniels SR, Specker B. Dieting behavior and eating attitudes in children. Pediatrics. 1989;84:482-489.  
90. Stunkard A, Burt V. Obesity and the body image. II. Age at onset of disturbances in the body image. Am J Psychiatry. 1967;123:1443-1447.  
91. French SA, Story M, Perry CL. Self-esteem and obesity in children and adolescents: a literature review. Obes Res. 1995;3:479-490.  
92. Epstein LH, Wisniewski L, Wing R. Child and parent psychological problems influence child weight control. Obes Res. 1994;2:509-515.
93. Gortmaker SL, Must A, Perrin JM, et al. Social and economic consequences of overweight in adolescence and young adulthood. N Engl J Med. 1993;329:1008-1012.  
94. Canning H, Mayer J. Obesity -- its possible effect on college acceptance. N Engl J Med. 1966;275:1172-1174.
95. National Institute of Mental Health. Depression in Children and Adolescents: A Fact Sheet for Physicians. 2000. Available at:
    www.nimh.nih.gov/publicat/depchildresfact.cfm#18.
96. Children's Depression Inventory. Developed by M Kovacs. Available from Multi-Health Systems, 65 Overlea Blvd. Suite 10, Toronto, Ontario, Canada M4H1P1.
97. Epstein LE, Myers MD, Anderson K. The association of maternal psychopathology and family socioeconomic status with psychological problems in obese children. Obes Res. 1996;4:65-74.  
98. Prochaska J, DiClemente C, Norcross J. In search of how people change. Applications to addictive behaviors. Am Psychol. 1992;47:1102.
99. Becque MD, Katch VL, Rocchini AP, et al. Coronary risk incidence of obese adolescents: reduction by exercise plus diet intervention. Pediatrics. 1988;81:605-612.  
100. Epstein LH, Wing RR, Penner BC, Kress MJ. Effect of diet and controlled exercise on weight loss in obese children. J Pediatr. 1985;107:358-361.  
101. Epstein LH, Wing RR, Koeske R, et al. A comparison of lifestyle change and programmed aerobic exercise on weight and fitness changes in obese children. Behav Ther. 1982;13:651-665.
102. Epstein LH, Valoski, AM, Vara LS, et al. Effects of decreasing sedentary behavior and increasing activity on weight change in obese children. Health Psychol. 1995;14:109-115.  
103. Epstein LH, Saelens BE, Myers MD, Vito D. The effects of decreasing sedentary behaviors on activity choice in obese children. Health Psychol 1997;16:107-113.
104. Epstein LH, Paluch RA, Gordy CC, Dorn J. Decreasing sedentary behaviors in treating pediatric obesity. Arch Pediatr Adolesc Med. 2000;154:220-226.  
105. Epstein LH, Valoski A, Wing RR, McCurley J. Ten-year follow-up of behavioral, family-based treatment for obese children. JAMA. 1990;264:2519-2523.  
106. Committee on Nutrition, American Academy of Pediatrics. Obesity in children. In: Pediatric Nutrition. Oak Grove, Ill: American Academy of Pediatrics; 1998:423-458.
107. Ikeda JP, Mitchell RA. Dietary approaches to the treatment of the overweight pediatric patient. Pediatr Clin North Am. 2001;48:955-968.  
108. Epstein LH, Valoski A, Koeske R, Wing RR. Family-based behavioral weight control in obese young children. J Am Diet Assoc. 1986;86:481-484.  
109. Yanovski JA. Intensive therapies for pediatric obesity. Pediatr Clin North Am. 2001;48:1041-1053.  
110. Figueroa-Colon R, von Almen TK, Franklin FA, et al. Comparison of two hypocaloric diets in obese children. Am J Dis Child. 1993;147:160-166.  
111. Amador M, Ramos LT, Morono M, Hermelo MP. Growth rate reduction during energy restriction in obese adolescents. Exp Clin Endocrinol. 1990;96:73-82.  
112. Freedman MR, King J, Kennedy E. Popular diets: a scientific review. Obes Res. 2001;9(1 Suppl):1S-40S.
113. Pirozzo S, Summerbell C, Cameron C, Glasziou P. Advice on low-fat diets for obesity. Cochrane Database Syst Rev. 2002;2.
114. Epstein LH, Valoski AM, Kalarchian MA, McCurley J. Do children lose and maintain weight easier than adults: a comparison of child and parent weight changes from six months to ten years. Obes Res. 1995;3:411-417.  
115. Ludwig DS, Peterson KE, Gortmaker SL. Relation between consumption of sugar-sweetened drinks and childhood obesity: a prospective, observational analysis. Lancet. 2001;357:505-508.  
116. Zemel MB. Regulation of adiposity and obesity risk by dietary calcium: mechanisms and implications. J Am Coll Nutr. 2002;21(Suppl 2):S146-S151.
117. Gropper SS, Acosta PB. The theraputic effect of fiber in treating obesity. J Am Coll Nutr. 1987;6:533-535.  
118. Wang G, Dietz WH. Economic burden of obesity in youths aged 6 to 17 years: 1979-1999. Pediatrics. 2002;109:E81-1.  
119. Choban PS, Flanebaum L. Nourishing the obese patient. Clin Nutr. 2000;19:305-311.  
120. Knip M, Nuutinen O. Long-term effects of weight reduction on serum lipids and plasma insulin in obese children. Am J Clin Nutr. 1993;54:490-493.
121. Epstein LH, Wing RR, Steranchak L, et al. Comparison of family-based behavior modification and nutrition education for childhood obesity. J Pediatr Psychol. 1980;5:25-36.  
122. Epstein LH, Paluch RA, Gordy CC, Dorn J. Decreasing sedentary behaviors in treating pediatric obesity. Arch Pediatr Adolesc Med. 2000;154:220-226.  
123. Senediak C, Spence SH. Rapid versus gradual scheduling of therapeutic contact in a family-based behavioural weight control programme for children. Behav Psychother. 1985;13:265-287.
124. Epstein LH, Saelens BE, Myers MD, Vito D. The effects of decreasing sedentary behaviors on activity choice in obese children. Health Psychol. 1997;16:107-113.  
125. Yanovski SZ, Yanovski JA. Obesity. N Engl J Med. 2002;346:591-602.  
126. Berkowitz RI, Wadden TA, Tershakovec AM, Cronquist JL. Behavior therapy and sibutramine for the treatment of adolescent obesity: a randomized controlled trial. JAMA. 2003;289:1805-1812.  
127. McCann S, McDuffie J, Nicholson J, et al. A pilot study of the efficacy of orlistat in overweight adolescents. North American Association for the Study of Obesity annual meeting; 8(Suppl 1): A179.
128. Roche Pharmaceuticals. FDA approves labeling for use of Xenical (Orlistat) in management of obesity in adolescent patients aged 12 to 16 years. Press release, December 15, 2003. Available at:
     http://www.rocheusa.com/newsroom/current/2003/pr2003121501.html. Accessed June 2, 2004.
129. McDuffie JR, Calis KA, Booth SL, Uwaifo GI, Yanovski JA. Effects of orlistat on fat-soluble vitamins in obese adolescents. Pharmacotherapy. 2002;22:814-822.  
130. Lee A, Morley JE. Metformin decreases food consumption and induces weight loss in subjects with obesity with type 2 non insulin-dependent diabetes. Obes Res. 1998;6:47-53  
131. Kirpichnikov D, McFarlane S, Sowers JR. Metformin: an update. Ann Intern Med. 2002;137:25-33.  
132. Morrison JA, Cottingham EM, Barton BA. Metformin for weight loss in pediatric patients taking psychotropic drugs. Am J Psychiatry. 2002;159:655-657.  
133. Freemark M, Bursey D. A therapeutic trial of metformin in obese adolescents predisposed to type 2 diabetes mellitus. Pediatr Res. 2000;47:755.
134. Eisenberg DM, Davis RB, Ettner SL, et al. Trends in alternative medicine use in the United States, 1990-1997: results of a follow-up national survey. JAMA. 1998;280:1569-1575.  
135. Cohen MH, Eisenberg DM. Potential physician malpractice liability associated with complementary and integrative medical therapies. Ann Intern Med. 2002;136:596-603.  
136. Allison DB, Fontaine KR, Heshka S, et al. Alternative treatments for weight loss: a critical review. Crit Rev Food Sci Nutr. 2001;41:1-28.  
137. Capella JF, Capella RF. The weight reduction operation of choice: vertical banded gastroplasty or gastric bypass? Am J Surg. 1996;171:74-79.  
138. Pories WJ, Swanson MS, MacDonald KG, et al. Who would have thought it? An operation proves to be the most effective therapy for adult-onset diabetes mellitus. Ann Surg. 1995;222:339-352.  
139. Schauer PR, Ikramuddin S, Gourash W, et al. Outcomes after laparoscopic Roux-en-Y gastric bypass for morbid obesity. Ann Surg. 2000;232:515-529.  
140. Cummings DE, Weigle DS, Frayo RS, et al. Plasma ghrelin levels after diet-induced weight loss or gastric bypass surgery. N Engl J Med. 2002;346:1623-1630.  
141. Kellum JM, DeMaria EJ, Sugarman HJ. The surgical treatment of morbid obesity. Curr Probl Surg. 1998;35:791-858.  
142. Garcia VF, Langford L, Inge TH. Application of laparoscopy for bariatric surgery in adolescents. Curr Opin Pediatr. 2003;15:248-255.  
143. O'Brien PE, Dixon JB. Weight loss and early and late complications--the international experience. Am J Surg. 2002;184(6B):42S-45S.
144. Rubenstein RB. Laparoscopic adjustable gastric banding at a U.S. center with up to 3-year follow-up. Obes Surg. 2002;12:380-384.  
145. Strauss RS, Bradley LJ, Brolin RE. Gastric bypass surgery in adolescents with morbid obesity. J Pediatr. 2001;138:499-504.  
146. Anderson AE, Soper RT, Scott DH. Gastric bypass for morbid obesity in children and adolescents. J Pediatr Surg. 1980;15:876-881.  
147. Inge TH, Garcia V, Daniels S, et al. A multidisciplinary approach to the adolescent bariatric surgical patient. J Pediatr Surg. 2004;39:442-447.  
148. Vgontzas AN, Tan TL, Bixler EO, Martin LF, Shubert D, Kales A. Sleep apnea and sleep disruption in obese patients. Arch Intern Med. 1994;154:1705-1711.  
149. Young T, Palta M, Dempsey J, Skatrud J, Weber S, Badr S. The occurrence of sleep-disordered breathing among middle-aged adults. N Engl J Med. 1993;328:1230-1235.  
150. Redline S, Tishler PV, Schluchter M, Aylor J, Clark K, Graham G. Risk factors for sleep-disordered breathing in children. Associations with obesity, race, and respiratory problems. Am J Respir Crit Care Med. 1999;159(5 Pt 1):1527-1532.

Prevalence

As the prevalence of childhood overweight has increased dramatically in the United States in recent years,^[1-3] the prevalence of overweight among African American and Hispanic children has increased disproportionately compared with non-Hispanic whites.^[2] Recent data from a nationally representative sample of US children aged 4 to 12 years reported that within a 12-year period, the prevalence of overweight increased to 21.5% among African-Americans, 21.8% among Hispanics, and 12.3% among non-Hispanic whites.^[2] In another national study of US children that examined prevalence of overweight in children aged 6 to 11 years and adolescents aged 12 to 17 years, significant ethnic disparities and distinct age-related patterns of overweight emerged.^[4] In childhood, Hispanics and African Americans were more likely to be overweight than whites. In adolescence, however, Hispanics and Asian/Pacific Islanders had higher rates of overweight.^[4] Haas and colleagues also found disparities in the prevalence of overweight based on socioeconomic status. In particular, children of parents with fewer years of education or lower household income were more likely to be overweight. Furthermore, lack of health insurance was positively associated with prevalence of overweight among adolescents.

The reasons for racial/ethnic variation in the prevalence of overweight are complex and may include differences in level of acculturation,^[5] cultural beliefs and practices, and ethnicity-based differences in body image (Figure). Lack of knowledge about nutrition and physical activity among parents with low educational attainment may also influence the quality of their children's diet and activity patterns.

Figure. Potential determinants of childhood overweight among underserved populations.

Determinants of Overweight

Both epidemiologic and experimental evidence from the past decade indicates that television viewing and consumption of sugar-sweetened beverages and fast food are important determinants of childhood overweight. Multiple cross-sectional and longitudinal observational studies document the impact of television,^[6-10] sugar-sweetened beverages,^[11-14] and fast food^[15-17] on overweight. These observational studies have been corroborated by randomized controlled trials designed to reduce levels of television viewing^[18-21] and consumption of sugar-sweetened beverages^[22] and to reduce overweight.

Available data on older children and adolescents suggest that many do not participate in regular physical activity at recommended levels; participation declines throughout the adolescent years, and racial and ethnic disparities are substantial.^[6,23,24] Data from the 2003 Youth Risk Behavior Surveillance System showed that the prevalence of participation in sufficient vigorous physical activity was higher among white (65.2%) than among African American (54.8%) and Hispanic (59.3%) students.^[23] In addition, the prevalence of having watched television >/= 3 hours/day was higher among African American (67.2%) and Hispanic (45.9%) than among white (29.3%) students. Neighborhood crime and safety, lack of access to recreational facilities, social support, self-efficacy in overcoming barriers, parental activity levels, acculturation, body image, and self-esteem have all been found to be correlates of physical activity among children and adolescents.^[25]

Racial and ethnic differences in dietary fat intake parallel ethnic differences in weight, with African-American and Hispanic girls showing higher percentages of energy from dietary fat. Whole milk, in particular, has been found to be the single largest source of saturated fat in the diets of children studied in a national sample and in a low-income sample of Latino children.^[26,27]

Prevention

Prevention of overweight and obesity should place emphasis on the modification of dietary and physical activity behaviors. Better knowledge of the behavioral, social-cultural, and environmental determinants of obesity among low-income and minority populations is needed to inform the design of effective obesity prevention interventions.^[28] In addition, evidence is needed about which interventions and settings have the highest feasibility and the greatest potential impact. Two settings in particular -- physician practices and school or child care centers -- may provide prime opportunities for parental health education in physical activity and healthful diets. Every year, about 80% of children and adolescents visit a physician, with an estimated 76 million annual contacts.^[29] Clinical practice-based interventions can be effective in changing patients' eating behaviors and levels of physical activity.^[30,31] Furthermore, with the rise in out-of-home child care, there are new opportunities to use this as a venue for health education.

Case Presentation

Below is an illustrative case of a typical patient seen in the One Step Ahead Program at Children's Hospital Boston (Boston, Massachusetts). One Step Ahead is a multidisciplinary, pediatric overweight prevention and early management program that serves a large minority population of inner-city Boston.

C.T. is a 10-year-old, first-generation Dominican-American male being seen by his primary care provider for assessment of overweight. C.T. is accompanied by his mother, who speaks only Spanish and is also overweight. On brief review of his eating and physical activity patterns, C.T. reports that he skips breakfast almost every weekday morning. Weekend breakfasts usually consist of eggs, chorizos (Spanish sausage), mashed plantains, and whole milk. During the day, he consumes about 2 cans of Pepsi during lunch and about 4 cups of Hawaiian Punch when he gets home from school. On the way home from school, he stops at the local convenience store and buys potato chips or cookies as a snack. He reports usually eating fast food about 2-3 times on weekend days. For dinner, his family eats a traditional Caribbean meal consisting of rice, beans, stewed beef (cooked in lard), fried plantains, and a small green salad.

He reports little physical activity, which his mother attributes to lack of neighborhood safety. He enjoys swimming but is embarrassed to take off his shirt while swimming because of gynecomastia related to his overweight. He views about 3 hours of television on weekdays and a "marathon" of television on the weekends.

His weight is 56 kg (123.5 lb), height is 145 cm (4 ft, 9 in), and BMI is 26.6 kg/m² (> 95th percentile for age and gender). His exam is notable for acanthosis nigricans over his neck folds and mild pain in his right knee with weight bearing.

Evaluation and Treatment

The American Academy of Pediatrics recommends that pediatricians calculate and plot BMI once a year in all children and adolescents and use changes to identify rate of excessive weight gain.^[32] In addition, several comprehensive guidelines suggest approaches to the treatment of childhood overweight.^[33,34] The surge in diversity of our nation has led to a greater recognition of the importance of providing both culturally and linguistically appropriate care and providing health services that are sensitive to patients' race/ethnicity, education, family income, place of birth, and insurance coverage. Several strategies can aid clinicians in the treatment of overweight among underserved, diverse pediatric populations:

Provide culturally and linguistically appropriate care. A complete diet history should assess traditional ethnic foods and meals eaten at home or in ethnic restaurants, cooking methods, ingredients of meals prepared at home, and frequency/timing of meals. As illustrated in the case above, traditional ethnic foods, ingredients, and cooking methods are common among first-generation immigrant families and are often accompanied by eating habits that children have acquired through acculturation. Nutrition counseling should provide simple, practical, linguistically appropriate educational materials on nutritious habits and instructions on goals. These suggestions should recognize and respect the normative ethnic and cultural framework of the patient population and should provide families with healthy alternatives within their cultural framework, for example, replacing lard with olive oil or baking instead of frying plantains.

Physical activity options should also include alternatives that will ensure buy-in from diverse populations, including Latin dance and hip hop.

Provide coordinated services or family-based treatment. Multidisciplinary programs that include dieticians, MDs/nurse practitioners, social workers, and/or behavioral psychologists can help families access services for overweight children. In the One Step Ahead program, families are also seen by a physical activity coordinator who links them to physical activity resources within their own communities.

As illustrated in the case above, children are often accompanied by parents or caregivers who have significant health problems of their own. Family-centered care or partnerships with adult obesity treatment programs can aid clinicians in treating overweight in children and motivate the family to make changes as a whole to improve their nutrition and physical activity practices.

Provide health services that aim to uncouple socioeconomic factors from adverse health outcomes. Overweight treatment programs should ensure that families who have limited proficiency in English obtain aid from qualified, trained medical interpreters to review nutritional and physical activity education. Written instructions should be available in several languages commonly spoken by families in surrounding communities and written at the average population reading level. Programs should provide extended office hours to improve access to care for the working poor, who might have difficulty attending appointments during work hours. Finally, programs should provide extended social support for help with:

• application for state/federal assistance for food stamps and subsidized school lunches;
• referral to local food pantries;
• transportation to the clinic for preventive services; and
• referral to after-school programs and other community-based physical activity resources.

Here is the initial treatment plan for C.T.:

Healthy, culturally appropriate alternatives to current diet. For example:

• Replace lard with olive oil;
• Bake or boil plantains; and
• Serve larger portions of salad with evening meal.

Referral to local community resources for physical activity:

• Referred to local after-school program;
• Free swimming lessons in local community center, which will allow him to keep his shirt on while swimming; and
• Encouraged to walk for 15-30 minutes with his mother around the local pond.

Psychosocial support:

• Hospital van helps with transportation to and from the hospital for nutritional counseling and visits with the subspecialists involved in his care;
  
  
• Follow-up appointments with the One Step Ahead team (MD/NP, dietician, physical activity coordinator, and social worker) to assess maintenance of nutrition and activity goals are scheduled either after school or after 5 PM when parents get off from work; and
  
  
• Social worker provides ongoing motivational interviewing and family-centered counseling.

Referral of parents to adult obesity treatment program. C.T.'s parents are overweight, and, as mentioned, partnerships with adult obesity treatment programs can motivate the family to achieve nutrition and activity goals.

References

1. Ogden CL, Flegal KM, Carroll MD, Johnson CL. Prevalence and trends in overweight among US children and adolescents, 1999-2000. JAMA. 2002;288:1728-1732.
2. Strauss RS, Pollack HA. Epidemic increase in childhood overweight, 1986-1998. JAMA. 2001;286:2845-2848.
3. Troiano RP, Flegal KM, Kuczmarski RJ, Campbell SM, Johnson CL. Overweight prevalence and trends for children and adolescents. The National Health and Nutrition Examination Surveys, 1963 to 1991. Arch Pediatr Adolesc Med. 1995;149:1085-1091.
4. Haas JS, Lee LB, Kaplan CP. The association of race, socioeconomic status, and health insurance status with the prevalence of overweight among children and adolescents. Am J Public Health. 2003;93:2105-2110.
5. Gordon-Larsen P, Harris KM, Ward DS, Popkin BM, National Longitudinal Study of Adolescent H. Acculturation and overweight-related behaviors among Hispanic immigrants to the US: the National Longitudinal Study of Adolescent Health. Soc Sci Med. 2003;57:2023-2034.
6. Andersen RE, Crespo CJ, Bartlett SJ, Cheskin LJ, Pratt M. Relationship of physical activity and television watching with body weight and level of fatness among children: results from the Third National Health and Nutrition Examination Survey. JAMA. 1998;279:938-942.
7. Crespo CJ, Smit E, Troiano RP, Bartlett SJ, Macera CA, Andersen RE. Television watching, energy intake, and obesity in US children: results from the third National Health and Nutrition Examination Survey, 1988-1994. Arch Pediatr Adolesc Med. 2001;155:360-365.
8. Dennison BA, Erb TA, Jenkins PL. Television viewing and television in bedroom associated with overweight risk among low-income preschool children. Pediatrics. 2002;109:1028-1035.
9. Dietz WH, Gortmaker SL. Do we fatten our children at the TV set? Obesity and television viewing in children and adolescents. Pediatrics. 1985;75:807-812.
10. Gortmaker SL, Must A, Sobol AM, Peterson K, Colditz GA, Dietz WH. Television viewing as a cause of increasing obesity among children in the United States, 1986-1990. Arch Pediatr Adolesc Med. 1996;150:356-362.
11. Giammattei J, Blix G, Marshak HH, Wollitzer AO, Pettitt DJ. Television watching and soft drink consumption: associations with obesity in 11- to 13-year-old schoolchildren. Arch Pediatr Adolesc Med. 2003;157:882-886.
12. Ludwig DS, Peterson KE, Gortmaker SL. Relation between consumption of sugar-sweetened drinks and childhood obesity: a prospective, observational analysis. Lancet. 2001;357:505-508.
13. Harnack L, Stang J, Story M. Soft drink consumption among US children and adolescents: nutritional consequences. J Am Diet Assoc. 1999;99:436-441.
14. American Academy of Pediatrics Committee on School H. Soft drinks in schools. Pediatrics. 2004;113(1 Pt 1):152-154.
15. Bowman SA, Gortmaker SL, Ebbeling CB, Pereira MA, Ludwig DS. Effects of fast-food consumption on energy intake and diet quality among children in a national household survey. Pediatrics. 2004;113(1 Pt 1):112-118.
16. Thompson OM, Ballew C, Resnicow K, et al. Food purchased away from home as a predictor of change in BMI z-score among girls. Int J Obes Relat Metab Disord. 2004;28:282-289.
17. Paeratakul S, Ferdinand DP, Champagne CM, Ryan DH, Bray GA. Fast-food consumption among US adults and children: dietary and nutrient intake profile. J Am Diet Assoc. 2003;103:1332-1338.
18. Robinson TN. Reducing children's television viewing to prevent obesity: a randomized controlled trial. JAMA. 1999;282:1561-1567.
19. Ford BS, McDonald TE, Owens AS, Robinson TN. Primary care interventions to reduce television viewing in African-American children. Am J Prev Med. 2002;22:106-109.
20. Epstein LH, Valoski AM, Vara LS, et al. Effects of decreasing sedentary behavior and increasing activity on weight change in obese children. Health Psychol. 1995;14:109-115.
21. Gortmaker SL, Peterson K, Wiecha J, et al. Reducing obesity via a school-based interdisciplinary intervention among youth: Planet Health. Arch Pediatr Adolesc Med 1999;153:409-418.
22. James J, Thomas P, Cavan D, Kerr D. Preventing childhood obesity by reducing consumption of carbonated drinks: cluster randomised controlled trial. BMJ. 2004;328:1237-1240.
23. Centers for Disease Control and Prevention, Surveillance Summaries. Youth Risk Behavior Surveillance - United States, 2003. MMWR. 2004;53(SS02):1-96.
24. Kimm SYS, Glynn NW, Kriska AM, Barton BA, Kronsberg SS, Daniels SR, Crawford PB, Sabry ZI, Liu K. Decline in physical activity in black girls and white girls during adolescence. N Engl J Med. 2002;347:709-715.
25. Sallis JF, Prochaska JJ, Taylor WC. A review of correlates of physical activity of children. Med Sci Sports Exerc. 2000;32:963-9