archived

Evidence Summary

Obesity in Children and Adolescents: Screening, July 2005

July 12, 2005

Recommendations made by the USPSTF are independent of the U.S. government. They should not be construed as an official position of the Agency for Healthcare Research and Quality or the U.S. Department of Health and Human Services.

Screening and Interventions for Childhood Overweight: A Systematic Review for the U.S. Preventive Services Task Force

By Evelyn P Whitlock, MD, MPH; Selvi B. Williams, MD; Rachel Gold, PhD, MPH; Paula R. Smith, RN, BSN; Scott A. Shipman, MD, MPH

The information in this article is intended to help clinicians, employers, policymakers, and others make informed decisions about the provision of health care services. This article is intended as a reference and not as a substitute for clinical judgment.

This article may be used, in whole or in part, as the basis for the development of clinical practice guidelines and other quality enhancement tools, or as a basis for reimbursement and coverage policies. AHRQ or U.S. Department of Health and Human Services endorsement of such derivative products may not be stated or implied.

Return to Table of Contents

Obesity/overweight has been declared an epidemic1-3 and a “public health crisis” among children worldwide4 due to an alarming increase in its prevalence. Overweight in children (defined by experts as a body mass index (BMI) > 95th percentile for age and sex)5,6 aged 2 and older has at least doubled in the last 25 years (Figure 1). The age- and sex-specific mean BMI and the proportion of children with BMI > 95th percentile increased markedly in children from the mid-1970s to the 1990s, with almost all of this increase occurring in children in the upper half of the BMI distribution.7 Thus, about 50% of children appear to have “obesity susceptibility genes” that environmental changes have acted upon in the last 25 years.8

Since increases in mean BMI have occurred primarily due to increases in the upper half of the BMI distribution,7,9 weight-related health consequences will become increasingly common in children. Childhood overweight and obesity’s health consequences include pulmonary, orthopedic, gastroenterological, neurological, and endocrine conditions and cardiovascular risk factors.4,10-15 Tables 1 and 2 contain the limited prevalence data for key morbidities and risk factors available from recent summaries. Rarely, severe childhood obesity is associated with immediate morbidity from conditions such as slipped capital femoral epiphysis,16 while steatohepatitis and sleep apnea are more common.17-21 Medical conditions new to this age group, such as Type 2 diabetes mellitus,22 represent “adult” morbidities that are now more frequently seen among overweight adolescents.23 Most medical complications, however, do not become clinically apparent for decades.10

Overweight is associated with a higher prevalence of intermediate metabolic consequences and risk factors, such as insulin resistance, elevated blood lipids, increased blood pressure, and impaired glucose tolerance.24-29 Perhaps the most significant short-term morbidities for overweight/obese children are psychosocial and include social marginalization, self-esteem, and quality of life.30-33 Risk factors for developing childhood overweight include increased parental adiposity, low parental education, social deprivation, and perhaps, infant feeding patterns, early or more rapid puberty, extreme birth weights, gestational diabetes, and various social and environmental factors, such as childhood diet or time spent in sedentary behaviors.4

Prior U.S. Preventive Services Task Force (USPSTF) Recommendations

The USPSTF makes recommendations about clinical preventive services to assist primary care clinicians using an explicit, evidence-based approach. In 1996, the USPSTF recommended periodic height and weight measurement for all patients (B recommendation).34 Comparing height and weight measures against appropriate age and sex norms to determine further evaluation, intervention, or referral was recommended, using BMI (> 85th percentile) in adolescents, and weight and height (or length as appropriate) plotted on growth charts or compared to average weight tables for age, sex, and height in younger children. The USPSTF has not previously made separate recommendations about screening criteria or specific interventions for overweight or obesity in childhood populations. To assist the USPSTF in making its recommendation, the Oregon Evidence-based Practice Center undertook a systematic review and summary of the strength of the evidence concerning screening and interventions for overweight in childhood populations. We combined the findings of prior fair- or good-quality35 systematic evidence reviews with fair- to good-quality studies not covered in these reviews or published subsequently.

Return to Table of Contents

Terminology

Since BMI is the primary clinical measure and a measure of relative weight, we have adopted the use of the term “overweight” in children as opposed to obesity.7 Considering the limitations of BMI in defining adiposity and concerns about labeling (stigma or concern resulting from being labeled “obese”) overweight is more accurate than obesity when the designation is based on a BMI value alone. Using accepted conventions, we use “overweight” to describe those with > 95th percentile BMI for age and sex, and “at risk for overweight” to describe those in the 85th to 95th percentile for age and sex.5,6

Key Questions and Analytic Framework

We developed an analytic framework (Figure 2) and seven key questions (KQs), using USPSTF methods, to guide our literature search.35 The first KQ examined direct evidence that screening to identify and treat overweight in children and adolescents improves age-appropriate behavioral, anthropometric, or physiologic measures. Because we found no evidence addressing this key question, we searched for indirect evidence for KQs 2 through 6 to estimate the benefits and harms of overweight screening and interventions. KQ2 concerned appropriate standards for overweight in children and adolescents, the overweight prevalence based on appropriate standards, and validity of clinical screening tests for predicting poorer health outcomes and obesity in adulthood. KQ3 examined adverse effects of screening for overweight. KQs 4 and 5 examined the efficacy of behavioral counseling, pharmacotherapeutic, and surgical interventions for improving age-appropriate anthropometric, physiologic, and health outcomes, and KQ6 addressed intervention-associated harms. The relationship between intervention-associated improvements in intermediate health measures and decreased morbidity in childhood or adulthood (KQ7) was examined only in the presence of adequate evidence for intervention efficacy (KQs 4 and 5). We did not examine KQ7 due to limited and inconsistent evidence for KQs 4 and 5.

Review methods are summarized below and further detailed elsewhere.36

Literature Search Strategy

We developed literature search strategies and terms for each KQ and conducted four separate literature searches (for KQs 1 and 2; for KQs 4, and 5; for KQ 3; and for KQ 6) in Medline, PsycINFO, CINAHL, and the Cochrane library, to update the literature from previous good-quality systematic reviews (KQs 4, 5, and 6) or to comprehensively examine literature from 1966 to the present (KQs 1, 2, and 3). Literature searches were extensively supplemented with source material from experts in the field, bibliographies of included trials, and other reviews. We also conducted limited hand searching of pediatric obesity-focused editions of selected journals. A single investigator reviewed abstracts. A second investigator reviewed all excluded abstracts for all KQs, except KQ2. Due to this search’s large yield, we conducted blinded dual review for a random subset (27%), with acceptable agreement (97.5%) between reviewers. Inter-reviewer discrepancies were resolved by consensus.

Article Review and Data Abstraction

Using pre-specified inclusion criteria36 we reviewed 2,162 abstracts and 353 complete articles for KQ1 and 2, 949 abstracts and 198 complete articles for KQs 4 and 5, and 1,176 abstracts and 36 complete articles for KQs 3 and 6. We included 0 articles for KQ1, 41 articles for KQ2, 0 articles for KQ3, 22 articles for KQs 4 and 5, and 4 articles for KQ6. Two investigators quality rated all included articles and those excluded for quality reasons, using the USPSTF criteria.35

One primary reviewer abstracted relevant information from included studies into standardized evidence tables.36 To be within the USPSTF scope, interventions needed to be conducted in primary care or feasible for primary care conduct or referral (defined elsewhere),36 and were categorized as pharmaceutical, surgical, or behavioral counseling interventions. Abstracted behavioral counseling intervention details included setting, type of professional delivering the intervention, parent/family participation, intervention components, number and type of contacts, and intervention duration.37 Comprehensive behavioral treatments were those using a combination of behavioral modification (e.g., self-monitoring, stimulus control, cognitive-behavioral techniques), dietary modification (e.g., Traffic Light Diet,38 reduced glycemic load, reduced fat or kilocalorie diets), and physical activity components (broadly specified as aerobic, callisthenic, lifestyle, or decreased sedentary behaviors).37

Studies had to report weight outcomes, preferably as BMI or BMI percentile changes, to be included. We also recorded all reported behavioral, physiological, and health outcomes specified on our analytic framework (Figure 2).

Literature Synthesis

There were insufficient homogeneous studies for any key question to allow quantitative synthesis. To better illustrate the study participants’ degree of overweight and the treatment impact of clinical interventions on overweight, we converted baseline measures and outcomes to BMI percentiles and plotted results on CDC growth charts. Treatment effects that were typical of interventions in this age group (10-20% reduction in percent overweight after one year) were modeled and plotted for 8, 10, and 12 year old girls. We plotted reported mean BMI treatment effects at 6 or more months for six trials in adolescents included in our review (one adolescent trial did not report BMI or percent overweight outcomes). These methods are described in more detail elsewhere.36 Using the USPSTF approach,35 we summarized the overall quality of the evidence for each key question.

Return to Table of Contents

Key Question 1. Is there direct evidence that screening (and intervention) for overweight in children/adolescents improves ageappropriate behavioral or physiologic measures, or health outcomes?

Our searches found no studies addressing this key question, nor did examination of all individual trials included in previous systematic evidence reviews.39-43

Key Question 2a. What are appropriate standards for overweight in children/adolescents and what is the prevalence of overweight based on these?

Eight nationally representative health examination surveys that included children have been conducted in the United States since 1963.44,45 These surveys have gathered a variety of anthropometric measures on a range of ages (2 months to 18 years), providing growth references46 and trend analyses of changes within the population over time. In order to provide useful trend analyses, measures must be valid, gathered consistently in surveys, and must use a single source for comparison. Due to these limitations, almost all data on prevalence and trends in US children are based on BMI measures calculated from standardized weight and height information.47

BMI measurements for an individual, or to determine population prevalence, must be compared to a reference population to determine the age- and sex-specific percentile ranking. Although multiple reference datasets to determine childhood BMI percentiles are available, where possible we used the CDC’s 2000 gender-specific BMI growth charts (for ages 2-19 years).48 Prevalence estimates and trend information are taken primarily from the NHANES program conducted from 1971-2000 which provides the most comprehensive data available on boys and girls aged 6 months through 19 years, with recent over-sampling of black and Mexican American children. These prevalence estimates use the CDC 2000 gender-specific BMI growth charts as their reference dataset to assign BMI percentiles.

Prevalence

Using BMI > 95th percentile, overweight prevalence in 1999-2002 was 10% in two- to five-year- olds and 16% in those six years and older49 (Figure 3). For children two to five years of age, the prevalence was similar between all racial/ethnic subgroups and both sexes, but was lower than the prevalence in older children in the same racial/ethnic subgroups. Among children 6 to 11 years, differences were seen between racial/ethnic subgroups, with significantly more Mexican American (21.8%) and non-Hispanic black (19.8%) children categorized as overweight compared with non-Hispanic whites (13.5%) (p<.05). Sex-specific differences were also apparent, with the highest prevalence of overweight in 6- to 11-year-olds among Mexican American boys (26.5%), which was significantly higher than non-Hispanic black boys (17%), non-Hispanic white boys (14%), and Mexican American girls (17.1%), and similar to that of non-Hispanic black girls (22.8%). Among youth aged 12 to 19 years, significantly more non- Hispanic black (21.1%) and Mexican American (22.5%) children had overweight BMI measurements than non-Hispanic whites (13.7%) (p<.05), with no differences between males and females.

Key Question 2b. What clinical screening tests for overweight in childhood are reliable and valid in predicting obesity in adulthood?

We found 19 fair- or good-quality longitudinal cohort studies (in 20 publications) that reported on BMI and other weight status measurements in childhood and adulthood.50-69 BMI measurements in childhood and adulthood correlated with each other as well as, or better than, childhood and adult correlations for other overweight measures, such as Ponderal Index or skinfold measurements. Table 3 illustrates that BMI tracking from childhood to adulthood varies by age.50-52,55,62,63 Single BMI measures track reasonably well from childhood and adolescence (ages 6 to 18) into young adulthood (ages 20 to 37), as evidenced by longitudinal studies showing low to moderate (r = 0.2-0.4) or moderate to high (0.5-0.8) correlations between childhood and adult BMI measures. Increased tracking (r > 0.6 or elevated odds of adult obesity) is seen in older children (after age eight),55 particularly with sexual maturity,70,71 in younger children (ages 6 to 12) who are more overweight (usually above the 95th or 98th percentile),36,72 and in children with an obese parent.12,56 Data on tracking for children before the age of 12 are not extensive. Sex differences in tracking are not consistent across ages or within age categories. Limited data are available comparing white and black children. Table 4 illustrates the probability of adult obesity (BMI ≥ 30 kg/m2) at various BMI percentiles in children of various ages taken from our larger report.36 A 50% or greater probability of adult obesity is generally seen for children age 13 or older with BMI measures > 95 percentile. Combining younger and older children in these analyses may obscure the increased probability of adult obesity with older age of childhood overweight.

Key Question 2c. What clinical screening tests for overweight in childhood are reliable and valid in poor health outcomes in adulthood?

Although many (n=11) US studies50,54,57,65-67,73-77 examined the risk associated with childhood overweight and adult outcomes – including socioeconomic outcomes, mortality, and a range of adult cardiovascular risk factors and morbidities – studies rarely controlled for adult BMI, a critical confounder.36 In one that did, the apparent association between elevated BMI at age 10 and several elevated adult cardiovascular risk factors (total cholesterol, LDL and HDL cholesterol, insulin, systolic and diastolic blood pressure) in the Bogalusa Heart cohort study was eliminated after controlling for adult BMI.57

Key Question 3. Does screening have adverse effects, such as labeling or unhealthy psychological or behavioral consequences?

We found no direct evidence on the harms of screening. Potential harms include labeling, induced self-managed dieting with its negative sequelae, poorer self-concept, poorer health habits, disordered eating, or negative impacts from parental concerns.5,13,32,78-84

Key Question 4. Do interventions (behavioral counseling, pharmacotherapy, or surgery) that are feasible to conduct in primary care settings or available for primary care referral lead to improved intermediate behavioral or physiologic measures with or without weight-related measures?

Behavioral counseling interventions

The most extensive treatment literature for childhood overweight involves behavioral counseling interventions. Behavioral counseling interventions included behavioral modification, special diets, and/or activity components delivered to children and/or parents as individuals or in groups by primary care clinicians or related healthcare staff to help patients adopt, change, or maintain health behaviors affecting overweight and related outcomes.85

We considered all trials published since 1985 from Western industrialized nations (n = 22 from 23 publications) that addressed interventions feasible for primary care conduct or primary care referral (including one that combined comprehensive behavioral treatment with pharmacotherapy, described separately below) (Table 5).86-108 We limited our search to post- 1985 trials given the dramatic increases in overweight in children that occurred during the 1980s and 1990s, suggesting a very different treatment environment.1,8,109 A previous good-quality systematic review including 16 of these trials concluded that this behavioral counseling treatment literature is limited, due to marginal quality trials employing small sample sizes of primarily white, school-age children receiving short-term, non-comparable, non-generalizable interventions.40 These trials typically tested intensive, often family-based, interventions conducted in specialty obesity clinic settings to address overweight in school-aged children who were about 40-50% above ideal weight. Figure 4 models the short-term (1 year) results from these types of studies when translated to BMI percentiles.

Figure 5 demonstrates results from all behavioral counseling studies in adolescents86,88,104,105,107,108 that reported, or could be translated into, BMI percentiles. Most studies addressed extremely overweight patients, with short-term results showing modest to no change in BMI percentiles. Only two good-quality studies in adolescents were particularly relevant to primary care.105,108

One short-term, primary care conducted trial used a computer-based approach to generate tailored plans for counseling obese (above the adult BMI cutoff of 30) adolescents (ages 12 to 16) showed small, but significant improvements105 (Figure 5). Another internet-based, shortterm trial targeting 57 overweight (mean BMI 36.37 kg/m2), non-Hispanic black, females aged 11 to 15 years with at least one obese biological parent resulted in statistically significant differences in weight and BMI.108 Although both trials showed small but statistically significant benefits in BMI measures at 6-12 months, it is not clear that these BMI changes would have clinical benefits.

Considering other intermediate outcomes in addition to weight, over half (n=13) of fair- or good-quality trials86,88-94,97,99,104,105,108 reported intermediate behavioral (n=11) or physiological (n=7) measures (Table 5). Two good-quality trials105,108 reported behavioral changes, but no physiological outcomes. While one108 indicated reduced total daily energy intake in the active treatment group, neither indicated changes in physical activity. One fair-quality study reported reductions in targeted dietary components (fat or glycemic load of diet) but not kilocalories,88 while other fair-quality studies89-94,99,104 measured changes in eating behaviors, physical activity, and sedentary behaviors, but did not provide a clear picture due to differences in subjects, interventions, and measures.

No good-quality trials of behavioral treatment reported intermediate physiologic outcomes, such as lipids or lipoproteins, glucose tolerance, or blood pressure or physical fitness measures. Only one trial of at least fair-quality reported intermediate physiologic measures. An intensive six-month behavioral weight-control program comparing a reduced glycemic load (RGL) diet with a reduced fat (RF) diet, increased insulin resistance scores (measured by the homeostatic model) significantly less in the RGL than RF group (-0.4 +/- 0.9 vs. 2.6 +/- 1.2, p=0.03).88 Insulin resistance increases with sexual maturation, however, which was not assessed. These results are further limited by baseline differences between groups and lack of consideration of physical activity as a confounder. Among the fair-quality studies that measured physical work capacity or physical fitness, most reported some improvement when physical activity or sedentary behaviors were addressed in the intervention.89,90,93,94

Pharmacotherapy

One randomized placebo-controlled trial of sibutramine within a comprehensive behavioral treatment program in adolescents showed superior weight change outcomes after six months (4.6 kg greater weight loss, 95% CI 2.0-7.4 kg) in an intent-to-treat analysis86 (Figure 5). With continued use, weight loss at six months was maintained through 12 months. It is not clear that the additional short-term weight change achieved by adding sibutramine to a comprehensive behavioral treatment program in adolescents86 would provide a net benefit, since changes in serum lipids, serum insulin, serum glucose, and HOMA (homeostatic model of insulin sensitivity) did not differ between groups. Among all trial completers (63-76% of all participants) at 12 months, significant improvements from baseline were seen in high-density lipoprotein cholesterol, serum insulin, and HOMA. Blood pressure was not improved, and in some cases increased blood pressure was a reason for discontinuation. The rate of adverse effects and discontinuation was fairly high (12% discontinued and 28% reduced the medication) (see also KQ 6).

We found no evidence for metformin use for weight loss/disease prevention in normoglycemic obese adolescents with weight outcomes after more than three months, nor did we find acceptable evidence on alternative or complementary therapies.

Surgery

No acceptable quality evidence is available in adolescents evaluating surgical approaches to overweight. There are no controlled treatment outcome data on bariatric surgery approaches in adolescents.

Key Question 5. Do interventions lead to improved adult health outcomes, reduced childhood morbidity, and/or improved psychosocial and functional childhood outcomes?

Behavioral counseling interventions

Few (n = 3) studies reported health outcomes as defined in our analytic framework,94,104,107 and only two were rated at least fair-quality (Table 5). In one fair-quality trial, depression scores measured using reliable and valid instruments showed improvement from baseline in treated adolescent girls but not controls, while reliably measured self-esteem scores improved from baseline in both groups.104 In a second fair-quality study, significantly fewer children aged 8-12, receiving comprehensive behavioral treatment, had elevated total behavior problem scores or elevated internalizing behavior problem scores at 24 months’ follow-up than at baseline.95

Key Question 6. Do interventions have adverse effects, such as stigmatization, binging or purging behaviors, eating disorders, suppressed growth, or exercise-induced injuries?

Adverse effect reporting for behavioral counseling interventions was limited to 3 of 22 intervention trials.

Behavioral counseling interventions

Potential eating problems or weight management behaviors were the only harms addressed in two trials. One good-quality trial reported no adverse effects on problematic eating (using validated measures for dietary restraint, eating disinhibition, problematic weight management behaviors, weight concerns, and eating disorder psychopathology) after primary care-based comprehensive behavioral treatment in 37 of 44 adolescent trial completers.105 One fair-quality trial reported no effect on eating disorder symptoms, weight dissatisfaction, or purging/restricting behaviors in 47 8-12 year-olds in a family-based comprehensive behavioral treatment program, using a reliable measure (Kids’ Eating Disorder Survey).95,110 Differences between boys (no effect) and girls (elevated total scores) were not significant, but may be revealed in studies with larger sample sizes.

Pharmacotherapy

In the placebo-controlled phase of the sibutramine trial,86 44% (19/43) of patients in the active medication group reduced or discontinued the medication due to elevated blood pressure, pulse rate, or both, which were the main adverse events reported.

Surgery

We attempted to estimate the rate of harms from the uncontrolled cohort literature, but found loss to follow-up (25-60% at 4-24 months),111-113 and inadequate reporting prevented us from making reasonable estimates of surgery-associated harms.

Return to Table of Contents

Table 6 summarizes the overall quality of evidence, according to USPSTF criteria,35 for each key question addressed in this review (see Appendix). The overall evidence is poor for the direct effects of screening (and intervention) programs (KQ1), screening harms (KQ3), and bariatric surgery (KQs 4, 5). The overall evidence is fair-to-poor for behavioral counseling interventions (KQs 4, 5) due to small, non-comparable, short-term studies with limited generalizability that rarely report health or intermediate outcomes, such as cardiovascular risk factors. Trials are particularly inadequate for non-whites and children aged two-five. Fair-topoor evidence is available for behavioral counseling intervention harms due to very limited reporting (KQ6). Fair evidence supports childhood BMI as a risk factor for adult overweight, although data are limited in non-whites (KQ2b), and data addressing BMI as a risk factor for adult morbidities generally do not control for confounding by adult BMI (KQ2c). Good evidence is available for overweight prevalence based on BMI measures in all groups, except Native Americans and Asians (KQ2a).

Return to Table of Contents

Overweight has at least doubled in children and adolescents in the US over the last 25 years, and is particularly common among racial/ethnic minorities. This increase represents a major public health concern with the potential for future health risks and growing burdens on the healthcare system. In terms of evidence, however, little has changed since a 1998 Journal of Pediatrics editorial concluded that, “In the case of obesity, the primary care physician is left in the uncomfortable (but familiar) position of needing to do something now for the patient and family seeking help, regardless of the uncertainty about the nature of the disease and the absence of a cure.”114 Given the nature of the problem, effective solutions will likely require substantial collaboration between the medical and public health communities.115 Further understanding of how to expand the appropriate role of the clinician in community public health, such as through advocating necessary environmental and political changes, would be helpful.116,117

A major limitation to clinicians addressing overweight in children, most of whom are not morbidly overweight, is the uncertain criteria for determining clinically significant overweight. Although BMI is the best clinically available measure of overweight, uncertainty in its application to individual patients remains due to limited knowledge of BMI’s current and future health impacts and the possible limits in the applicability of current BMI cut-points, particularly for minority race/ethnicity. Understanding normal variations in body composition with age, sex, race/ethnicity, sexual maturity, and other factors will be critical to accurately defining unhealthy excess fat or other components of overweight, and appropriate measurement methods. Similarly, as has been done elsewhere, examining the sensitivity and specificity of BMI percentile cutoffs for identifying overweight children using large, representative samples of US children of all ages and races/ethnicities would increase our understanding of BMI as a screening tool.118

The risk for overweight children becoming overweight or obese adults has been judged as the best available criterion to judge the clinical validity of BMI in the pediatric age group.119 Adult BMI has been clearly associated with morbidity and mortality – particularly at higher BMI levels – although there is no single threshold for increased health risks.120 Adolescents who are at or above the 95th percentile for age- and sex-specific BMI clearly have an increased probability of adult obesity, and early interventions would be potentially very beneficial. Recent intervention research targeting this age group primarily addresses those who are very overweight, with some studies showing short-term (6-12 month) weight-related improvements. The treatment evidence in this age group could be strengthened by larger trials testing generalizable interventions that can demonstrate sustained effects on overweight status and on weight-related outcomes. Many trials in adolescents have specifically targeted minorities107,108 or enrolled reasonable proportions in their studies,86,102,105 and this should continue. Trials among mildly overweight adolescents, as well as those more severely affected, are needed. With limited to no evidence available, experts agree that surgical approaches should be considered only in adolescents with extreme and morbid obesity, and pharmacologic approaches should be limited to a second-tier approach after failed behavioral counseling.111,121

In contrast, current data suggests that a substantial proportion of children under age 12 or 13, even with BMIs above the 95th percentile, will not develop adult obesity. Children aged 8-12 have been the most studied for behavioral overweight treatment, but we still have very limited information about interventions that would be applicable to primary care. No current randomized controlled trial for clinical interventions of any type is available in children two to five years old.

For all ages, there is very limited evidence for behavioral or other overweight treatment that is feasible for primary care delivery or referral. Few studies have taken place in primary care — most have been conducted in research or specialty obesity clinics using intensive, comprehensive behavioral treatment. Experts have cautioned that behavioral therapy represents an expertisedriven approach to improving diet and physical activity using behavioral principles, and not simply an add-on to a diet and exercise plan.122 If larger studies confirm that behavioral skills and approaches are key to treatment success, creating referral clinics or involvement of clinic team members with behavioral medicine/psychology weight management expertise will be critical.

Experts recommend referring certain children to pediatric obesity treatment centers for expert management. These include children who are massively overweight (defined through clinical judgment)5 or who have BMI exceeding the 95th percentile with associated severe morbidities that require immediate weight loss. In asymptomatic children with a BMI > 95th percentile, experts also recommend an in-depth medical assessment to detect treatable causes of obesity, risk factors, and co-morbidities. For children whose BMI falls between the 85th and 95th percentiles for age and sex, they also recommend clinical evaluations for secondary effects of overweight, such as hypertension and hyperlipidemia. We did not find adequate evidence meeting our criteria to address the impact of BMI screening and/or treatment of overweight (or at risk for overweight) on any of these risks factors or morbidities.

Experts emphasize talking to families about energy balance behaviors that may help prevent obesity and would also promote other aspects of health and likely cause no harms.123 These behaviors include limiting television viewing, encouraging outdoor play, and limiting the consumption of sugar-sweetened soft drinks. For the interested clinician, pragmatic approaches for all children (particularly young children) that emphasize the “healthy lifestyle prescription” approach over targeting overweight identification seem appropriate since we found limited evidence for secondary prevention or treatment. However, clinicians should be aware that others have found limited evidence for the effectiveness of primary prevention in clinical settings.124

Given the current evidence, BMI measurement in older adolescents may provide an early and reasonable indication of future adult health risks due to obesity. BMI measurement in younger children should be performed as a growth-monitoring tool that may indicate future risk for adult overweight and its attendant morbidities, with reduced emphasis on defining current overweight. Children, particularly those under the age of 13, without clinical weight-related morbidities would not necessarily be labeled overweight, but might be considered “at risk” or “at high risk” depending on the BMI level. Experts recommend regular longitudinal monitoring and careful documentation of BMI in children and adolescents.125 Such monitoring will likely prove even more valuable as our understanding grows about the predictive value of levels and patterns of growth and overweight status change over time and about effective ways to address patterns that indicate overweight that impacts current health or a high future risk of adult overweight.

Limitations of the Literature

In the absence of direct evidence of screening’s impact on improved weight and health outcomes in children and/or adults, we have evaluated indirect evidence for screening and intervention. In the current literature, evidence linkages between screening and intervention are hampered by divergent definitions of overweight. It is important that a consistent definition of overweight be accepted to encourage rapid progress in our understanding of how to address this critical problem.

Limited evidence on normal body composition in children and adolescents, and lack of criterion standards for adiposity in children, hampered our ability to determine the test characteristics (sensitivity and specificity) of clinically feasible screening tests. Valid, feasible body composition measures in children are becoming established,126 which should allow the examination of sensitivity and specificity of BMI percentiles and overweight in US populations, as elsewhere.118 Similarly, clearly establishing current or future health consequences of elevated BMI (and other overweight measures) for boys and girls of all ages and racial/ethnic origins will enable future diagnostic research. By confining our review of childhood BMI and adult health consequences to longitudinal US studies, we gained some advantages from more similar overweight definitions, measurements, and reference standards,72 but may have unnecessarily eliminated applicable data. Since the reviewed research was primarily in non-Hispanic whites, its applicability to minorities, in whom the prevalence of overweight is particularly increasing, may be limited.

We did not locate adequate longitudinal data relating childhood weight status to childhood health outcomes, and thus did not review it formally. Current literature is primarily crosssectional, presents relative risks without absolute risks, or reports on the relationship of growth measures (or changes in them over time) to intermediate measures, such as blood pressure or lipids, rather than health outcomes.

Although we made an effort to comprehensively review several areas of the literature, some areas were not reviewed. We did not review any evidence on children under the age of two, although this is an active area for research. We did not attempt to examine risk factors for childhood overweight, but note that others have recently done so.71 Similarly, research on changing children’s daily life habits that might also affect or prevent pediatric overweight—such as changing dietary intake, increasing physical activity or limiting activities such as television viewing—that did not directly address weight effects were beyond our scope.

Future Research

There are critical research gaps in answering the most basic questions needed to enable clinicians to engage strategies to prevent current and future weight-related morbidities in children. Despite the fact that many of these gaps were pointed out over 10 years ago,127 little subsequent research has addressed the most clinically relevant questions. In addition to the clinical research already underway to address childhood overweight prevention and treatment, we strongly urge the research community to prioritize research studies that will supply needed evidence to address the key questions formulated for this report in order to inform pragmatic clinical, as well as public health, prevention strategies. Some of these studies could involve reporting from existing good-quality cross-sectional and longitudinal cohort studies in addition to new studies and clinical trials. For a more complete list of research recommendations, please consult the full review.36

Return to Table of Contents

This evidence summary was funded by the Agency for Healthcare Research and Quality (AHRQ) for the U.S. Preventive Services Task Force (USPSTF). The investigators acknowledge the contributions of Daphne Plaut, M.L.S.; Tracy Beil, M.S.; Betsy Garlitz, M.D.; and Kevin Lutz, M.F.A., for their assistance in the preparation of this manuscript. The authors also acknowledge the reviewers of the full evidence report for their contributions to this project. The authors also relied on guidance from the USPSTF members at key points throughout the review process: Janet Allan, Ph.D., R.N., C.S., FAAN; Mark Johnson, M.D., M.P.H.; Jonathan Klein, M.D., M.P.H.; Virginia Moyer, M.D., M.P.H.; Judith Ockene, Ph.D.; and Steven Teutsch, M.D., M.P.H.; and former USPSTF member, C. Tracy Orleans, Ph.D.

This study was conducted by the Oregon Evidence-based Practice Center under contract to the Agency for Healthcare Research and Quality (AHRQ) Contract No. 290-02-0024, Rockville, MD.

Return to Table of Contents

1. Flegal KM. The obesity epidemic in children and adults: current evidence and research issues. Med Sci Sports Exerc 1999; 31(11 Suppl):S509-S514.
2. Kohn M, Booth M. The worldwide epidemic of obesity in adolescents. Adolescent Medicine State of the Art Reviews 2003; 14(1):1-9.
3. Sokol RJ. The chronic disease of childhood obesity: the sleeping giant has awakened. J Pediatr 2000; 136(6):711-3.
4. Lobstein T, Baur L, Uauy R. Obesity in children and young people: a crisis in public health. Obes Rev 2004; 5 Suppl 1:4-85.:4-85.
5. Barlow SE, Dietz WH. Obesity evaluation and treatment: Expert Committee recommendations. The Maternal and Child Health Bureau, Health Resources and Services Administration and the Department of Health and Human Services. Pediatrics 1998; 102(3):E29.
6. Himes JH, Dietz WH. Guidelines for overweight in adolescent preventive services: recommendations from an expert committee. The Expert Committee on Clinical Guidelines for Overweight in Adolescent Preventive Services. Am J Clin Nutr 1994; 59(2):307-16.
7. Troiano RP, Flegal KM. Overweight children and adolescents: description, epidemiology, and demographics. Pediatrics 1998; 101(3 Pt 2):497-504.
8. Koplan JP, Dietz WH. Caloric imbalance and public health policy. JAMA 1999; 282(16):1579-81.
9. Dwyer JT, Stone EJ, Yang M, Webber LS, Must A, Feldman HA, et al. Prevalence of marked overweight and obesity in a multiethnic pediatric population: findings from the Child and Adolescent Trial for Cardiovascular Health (CATCH) study. J American Dietetic Association 2000; 100(10):1149-56.
10. Must A, Strauss RS. Risks and consequences of childhood and adolescent obesity. Int J Obes Relat Metab Disord 1999; 23 Suppl 2:S2-11.:S2-11.
11. Must A. Morbidity and mortality associated with elevated body weight in children and adolescents. Am J Clin Nutr 1996; 63(3 Suppl):445S-447S.
12. Reilly JJ, Methven E, McDowell ZC, Hacking B, Alexander D, Stewart L, et al. Health consequences of obesity. Arch Dis Child 2003; 88(9):748-52.
13. Zametkin AJ, Zoon CK, Klein HW, Munson S. Psychiatric aspects of child and adolescent obesity: a review of the past 10 years. J Am Acad Child Adolesc Psychiatry 2004; 43(2):134-50.
14. Must A, Anderson SE. Effects of obesity on morbidity in children and adolescents. Nutr Clin Care 2003; 6(1):4-12.
15. Rodriguez MA, Winkleby MA, Ahn D, Sundquist J, Kraemer HC. Identification of population subgroups of children and adolescents with high asthma prevalence: findings from the Third National Health and Nutrition Examination Survey. Arch Pediatr Adolesc Med 2002; 156(3):269-75.
16. Kelsey JL. Epidemiology of slipped capital femoral epiphysis: a review of the literature. Pediatrics 1973; 51(6):1042-50.
17. Silvestri JM, Weese-Mayer DE, Bass MT, Kenny AS, Hauptman SA, Pearsall SM. Polysomnography in obese children with a history of sleep-associated breathing disorders. Pediatr Pulmonol 1993; 16(2):124-9.
18. Mallory GB, Jr., Fiser DH, Jackson R. Sleep-associated breathing disorders in morbidly obese children and adolescents. J Pediatr 1989; 115(6):892-7.
19. Tominaga K, Kurata JH, Chen YK, Fujimoto E, Miyagawa S, Abe I, et al. Prevalence of fatty liver in Japanese children and relationship to obesity. An epidemiological ultrasonographic survey. Dig Dis Sci 1995; 40(9):2002-9.
20. Franzese A, Vajro P, Argenziano A, Puzziello A, Iannucci MP, Saviano MC, et al. Liver involvement in obese children. Ultrasonography and liver enzyme levels at diagnosis and during follow-up in an Italian population. Dig Dis Sci 1997; 42(7):1428-32.
21. Chan DF, Li AM, Chu WC, Chan MH, Wong EM, Liu EK, et al. Hepatic steatosis in obese Chinese children. Int J Obes Relat Metab Disord 2004.
22. Rosenbloom AL, Joe JR, Young RS, Winter WE. Emerging epidemic of type 2 diabetes in youth. Diabetes Care 1999; 22(2):345-54.
23. Dabelea D, Hanson RL, Bennett PH, Roumain J, Knowler WC, Pettitt DJ. Increasing prevalence of Type II diabetes in American Indian children. Diabetologia 1998; 41(8):904-10.
24. Sinha R, Fisch G, Teague B, Tamborlane WV, Banyas B, Allen K, et al. Prevalence of impaired glucose tolerance among children and adolescents with marked obesity. N Engl J Med 2002; 346(11):802-10.
25. Freedman DS, Srinivasan SR, Berensen GS. Risk of cardiovascular complication. In: Burniat W, Cole T, Lissau I, Poskitt EME, editors. Child and Adolescent Obesity Causes and Consequences, Prevention and Management. Cambridge: Cambridge University Press, 2002: 221-39.
26. Cook S, Weitzman M, Auinger P, Nguyen M, Dietz WH. Prevalence of a metabolic syndrome phenotype in adolescents: findings from the third National Health and Nutrition Examination Survey, 1988-1994. Arch Pediatr Adolesc Med 2003; 157(8):821-7.
27. Weiss R, Dziura J, Burgert TS, Tamborlane WV, Taksali SE, Yeckel CW, et al. Obesity and the metabolic syndrome in children and adolescents. N Engl J Med 2004; 350(23):2362-74.
28. Dietz WH. Health consequences of obesity in youth: childhood predictors of adult disease. Pediatrics 1998; 101(3 Pt 2):518-25.
29. Figueroa-Colon R, Franklin FA, Lee JY, Aldridge R, Alexander L. Prevalence of obesity with increased blood pressure in elementary school-aged children. South Med J 1997; 90(8):806-13.
30. Dietz WH. Childhood weight affects adult morbidity and mortality. J Nutrition 1998; 128(2 Suppl):411S-414S.
31. French SA, Story M, Perry CL. Self-esteem and obesity in children and adolescents: a literature review. Obesity Res 1995; 3(5):479-90.
32. Strauss RS. Childhood obesity and self-esteem. Pediatrics 2000; 105(1):e15.
33. Strauss RS, Pollack HA. Social marginalization of overweight children. Arch Pediatr Adolesc Med 2003; 157(8):746-52.
34. U.S. Preventive Services Task Force. Guide to Clinical Preventive Services, 2nd ed. Washington, DC: Office of Disease Prevention and Health Promotion; 1996.
35. Harris RP, Helfand M, Woolf SH, Lohr KN, Mulrow CD, Teutsch SM, et al. Current methods of the U.S. Preventive Services Task Force: a review of the process. Am J Prev Med 2001; 20(3 Suppl):21-35.
36. Whitlock EP, Williams SB, Gold R, Smith P, Shipman S. Screening and Interventions for Childhood Overweight: A Systematic Review for the U.S. Preventive Services Task Force. Systematic Evidence Review, 2005. Rockville, MD, Agency for Healthcare Research and Quality. Available at https://www.uspreventiveservicestaskforce.org.
37. Haddock CK, Shadish WR, Klesges RC, Stein RJ. Treatments for childhood and adolescent obesity. Ann Behav Med 1994; 16(3):235-44.
38. Epstein LH, Roemmich JN, Raynor HA. Behavioral therapy in the treatment of pediatric obesity. Pediatr Clin North Am 2001; 48(4):981-93.
39. Glenny AM, O'Meara S, Melville A, Sheldon TA, Wilson C. The treatment and prevention of obesity: a systematic review of the literature. Int J Obes Relat Metab Disord 1997; 21(9):715-37.
40. Summerbell CD, Ashton V, Campbell KJ, Edmunds L, Kelly S, Waters E. Interventions for treating obesity in children. Cochrane Database of Systematic Reviews 2003;(1).
41. Reilly JJ, Wilson ML, Summerbell CD, Wilson DC. Obesity: diagnosis, prevention, and treatment; evidence based answers to common questions. Arch Dis Child 2002; 86(6):392-4.
42. Reilly JJ, McDowell ZC. Physical activity interventions in the prevention and treatment of paediatric obesity: systematic review and critical appraisal. Proceedings of the Nutrition Society 2003; 62(3):611-9.
43. McLean N, Griffin S, Toney K, Hardeman W. Family involvement in weight control, weight maintenance and weight-loss interventions: a systematic review of randomised trials. Int J Obes Relat Metab Disord 2003; 27(9):987-1005.
44. Kuczmarski RJ. Trends in body composition for infants and children in the U.S. Crit Rev Food Sci Nutr 1993; 33(4-5):375-87.
45. Ogden CL, Flegal KM, Carroll MD, Johnson CL. Prevalence and trends in overweight among U.S. children and adolescents, 1999-2000. JAMA 2002; 288(14 Oct 9):1728-32.
46. Use and interpretation of anthropometric indicators of nutritional status. WHO Working Group. Bull World Health Organ 1986; 64(6):929-41.
47. Ogden CL, Carroll MD, Flegal KM. Epidemiologic trends in overweight and obesity. Endocrinology & Metabolism Clinics of North America 2003; 32(4):741-60, vii.
48. Kuczmarski RJ, Ogden CL, Guo SS, Grummer-Strawn LM, Flegal KM, Mei Z, et al. 2000 CDC Growth Charts for the United States: methods and development. Vital Health Stat 11 2002;(246):1-190.
49. Hedley AA, Ogden CL, Johnson CL, Carroll MD, Curtin LR, Flegal KM. Prevalence of overweight and obesity among US children, adolescents, and adults, 1999-2002. JAMA 2004; 291(23):2847-50.
50. Freedman DS, Khan LK, Serdula MK, Dietz WH, Srinivasan SR, Berenson GS. Inter-relationships among childhood BMI, childhood height, and adult obesity: the Bogalusa Heart Study. Int J Obes Relat Metab Disord 2004; 28(1):10-6.
51. Hulman S, Kushner H, Katz S, Falkner B. Can cardiovascular risk be predicted by newborn, childhood, and adolescent body size? An examination of longitudinal data in urban African Americans. J Pediatrics 1998; 132(1):90-7.
52. Wattigney WA, Webber LS, Srinivasan SR, Berenson GS. The emergence of clinically abnormal levels of cardiovascular disease risk factor variables among young adults: the Bogalusa Heart Study. Preventive Medicine 1995; 24(6):617-26.
53. Garn SM, Lavelle M. Two-decade follow-up of fatness in early childhood. Am J Dis Child 1985; 139(2):181-5.
54. Lauer RM, Clarke WR, Burns TL. Obesity in childhood: the Muscatine Study. Chung-Hua Min Kuo Hsiao Erh Ko i Hsueh Hui Tsa Chih 1997; 38(6):432-7.
55. Guo SS, Roche AF, Chumlea WC, Gardner JD, Siervogel RM. The predictive value of childhood body mass index values for overweight at age 35 y. Am J Clin Nutr 1994; 59(4):810-9.
56. Whitaker RC, Wright JA, Pepe MS, Seidel KD, Dietz WH. Predicting obesity in young adulthood from childhood and parental obesity. N Engl J Med 1997; 337(13):869-73.
57. Freedman DS, Khan LK, Dietz WH, Srinivasan SR, Berenson GS. Relationship of childhood obesity to coronary heart disease risk factors in adulthood: the Bogalusa Heart Study. Pediatrics 2001; 108(3):712-8.
58. Guo SS, Wu W, Chumlea WC, Roche AF. Predicting overweight and obesity in adulthood from body mass index values in childhood and adolescence. Am J Clin Nutr 2002; 76(3):653-8.
59. Freedman DS, Shear CL, Burke GL, Srinivasan SR, Webber LS, Harsha DW, et al. Persistence of juvenile-onset obesity over eight years: the Bogalusa Heart Study. American JPublic Health 1987; 77(5):588-92.
60. Casey VA, Dwyer JT, Coleman KA, Valadian I. Body mass index from childhood to middle age: a 50-y follow-up. Am J Clin Nutr 1992; 56(1):14-8.
61. Lauer RM, Lee J, Clarke WR. Factors affecting the relationship between childhood and adult cholesterol levels: the Muscatine Study. Pediatrics 1988; 82(3):309-18.
62. Lauer RM, Clarke WR. Childhood risk factors for high adult blood pressure: the Muscatine Study. Pediatrics 1989; 84(4):633-41.
63. Clarke WR, Lauer RM. Does childhood obesity track into adulthood? Crit Rev Food Sci Nutr 1993; 33(4-5):423-30.
64. Valdez R, Greenlund KJ, Wattigney WA, Bao W, Berenson GS. Use of weight-for-height indices in children to predict adult overweight: the Bogalusa Heart Study. Int J Obes Relat Metab Disord 1996; 20(8):715-21.
65. Sinaiko AR, Donahue RP, Jacobs DR, Jr., Prineas RJ. Relation of weight and rate of increase in weight during childhood and adolescence to body size, blood pressure, fasting insulin, and lipids in young adults. The Minneapolis Children's Blood Pressure Study. Circulation 1999; 99(11):1471-6.
66. Gortmaker SL, Must A, Perrin JM, Sobol AM, Dietz WH. Social and economic consequences of overweight in adolescence and young adulthood. N Engl J Med 1993; 329(14):1008-12.
67. Srinivasan SR, Bao W, Wattigney WA, Berenson GS. Adolescent overweight is associated with adult overweight and related multiple cardiovascular risk factors: the Bogalusa Heart Study. Metabolism: Clinical & Experimental 1996; 45(2):235-40.
68. Lauer RM, Clarke WR, Mahoney LT, Witt J. Childhood predictors for high adult blood pressure. The Muscatine Study. Pediatric Clinics of North America 1993; 40(1):23-40.
69. Webber LS, Cresanta JL, Croft JB, Srinivasan SR, Berenson GS. Transitions of cardiovascular risk from adolescence to young adulthood—the Bogalusa Heart Study: II. Alterations in anthropometric blood pressure and serum lipoprotein variables. J Chronic Diseases 1986; 39(2):91-103.
70. Power C, Lake JK, Cole TJ. Body mass index and height from childhood to adulthood in the 1958 British born cohort. Am J Clin Nutr 66(5):1094-101, 1997.
71. Parsons TJ, Power C, Logan S, Summerbell CD. Childhood predictors of adult obesity: a systematic review. Int J Obes Relat Metab Disord 1999; 23 Suppl 8:S1-107.
72. Power C, Lake JK, Cole TJ. Measurement and long-term health risks of child and adolescent fatness. Int J Obes Relat Metab Disord 1997; 21(7):507-26.
73. Must A, Jacques PF, Dallal GE, Bajema CJ, Dietz WH. 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(19):1350-55.
74. Nieto FJ, Szklo M, Comstock GW. Childhood weight and growth rate as predictors of adult mortality. Am J Ep 1992; 136(2):201-13.
75. Lauer RM, Lee J, Clarke WR. Predicting adult cholesterol levels from measurements in childhood and adolescence: the Muscatine Study. Bulletin of the New York Academy of Medicine 1989; 65(10):1127-42.
76. Srinivasan SR, 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(1):204-9.
77. Bao W, Srinivasan SR, Wattigney WA, Bao W, Berenson GS. Usefulness of childhood low-density lipoprotein cholesterol level in predicting adult dyslipidemia and other cardiovascular risks. The Bogalusa Heart Study. Arch Int Med 1996; 156(12):1315-20.
78. Kaplan KM, Wadden TA. Childhood obesity and self-esteem. J Pediatrics 1986; 109(2):367-70.
79. Davison KK, Birch LL. Weight status, parent reaction, and self-concept in five-year-old girls. Pediatrics 2001; 107(1):46-53.
80. Cameron JW. Self-esteem changes in children enrolled in weight management programs. Issues in Comprehensive Pediatric Nursing 1999; 22(2-3):75-85.
81. Erickson SJ, Robinson TN, Haydel KF, Killen JD. Are overweight children unhappy?: Body mass index, depressive symptoms, and overweight concerns in elementary school children [comment]. Arch Pediatr Adolesc Med 2000; 154(9):931-35.
82. Berkey CS, Rockett HR, Gillman MW, Field AE, Colditz GA. Longitudinal study of skipping breakfast and weight change in adolescents. Int J Obes Relat Metab Disord 2003; 27(10):1258-66.
83. Strauss RS, Mir HM. Smoking and weight loss attempts in overweight and normal-weight adolescents. Int J Obes Relat Metab Disord 2001; 25(9):1381-5.
84. Fulkerson JA, French SA. Cigarette smoking for weight loss or control among adolescents: gender and racial/ethnic differences. J Adolescent Health 2003; 32(4):306-13.
85. Whitlock EP, Orleans CT, Pender N, Allan J. Evaluating primary care behavioral counseling interventions: an evidence-based approach. Am J Prev Med 2002; 22(4):267-84.
86. 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(14):1805-12.
87. Duffy G, Spence SH. The effectiveness of cognitive self-management as an adjunct to a behavioural intervention for childhood obesity: a research note. J Child Psychol Psychiatry 1993; 34(6):1043-50.
88. Ebbeling CB, Leidig MM, Sinclair KB, Hangen JP, Ludwig DS. A reduced-glycemic load diet in the treatment of adolescent obesity. Arch Pediatr Adolesc Med 2003; 157(8):773-9.
89. Epstein LH, Wing RR, Koeske R, Valoski A. A comparison of lifestyle exercise, aerobic exercise, and calisthenics on weight loss in obese children. Behavior Therap 1985; 16(4):356.
90. Epstein LH, Wing RR, Penner BC, Kress MJ. Effect of diet and controlled exercise on weight loss in obese children. J Pediatr 1985; 107(3):358-61.
91. Epstein LH. Effects of family-based behavioral treatment on obese 5-to-8-year-old children. Behavior Therapy 16(2):Mar 1985;212.
92. Epstein LH, McKenzie SJ, Valoski A, Klein KR, Wing RR. Effects of mastery criteria and contingent reinforcement for family-based child weight control 3838. Addictive Behaviors 1994; 19(2):135-45.
93. Epstein LH, Valoski AM, Vara LS, McCurley J, Wisniewski L, Kalarchian MA, et al. Effects of decreasing sedentary behavior and increasing activity on weight change in obese children 3814. Health Psychology 1995; 14(2):109-15.
94. Epstein LH, Paluch RA, Gordy CC, Dorn J. Decreasing sedentary behaviors in treating pediatric obesity. Arch Pediatr Adolesc Med 2000; 154(3):220-6.
95. Epstein LH, Paluch RA, Gordy CC, Saelens BE, Ernst MM. Problem solving in the treatment of childhood obesity. J Consult Clin Psychol 2000; 68(4):717-21.
96. Epstein LH, Paluch RA, Raynor HA. Sex differences in obese children and siblings in family-based obesity treatment. Obesity Res 2001; 9(12):746-53.
97. Flodmark CE, Ohlsson T, Ryden O, Sveger T. Prevention of progression to severe obesity in a group of obese schoolchildren treated with family therapy. Pediatrics 1993; 91(5):880-4.
98. Golan M, Weizman A, Apter A, Fainaru M. Parents as the exclusive agents of change in the treatment of childhood obesity. Am J Clin Nutr 1998; 67:1130-35.
99. Graves T, Meyers AW, Clark L. An evaluation of parental problem-solving training in the behavioral treatment of childhood obesity. J Consult Clin Psychol 1988; 56(2):246-50.
100. Israel AC, Shapiro LS. Behavior problems of obese children enrolling in a weight reduction program. J Pediatr Psychol 1985; 10(4):449-60.
101. Israel AC, Guile CA, Baker JE, Silverman WK. An evaluation of enhanced self-regulation training in the treatment of childhood obesity. J Pediatric Psychology 1994; 19(6):737-49.
102. Gutin B, Barbeau P, Owens S, Lemmon CR, Bauman M, Allison J, et al. Effects of exercise intensity on cardiovascular fitness, total body composition, and visceral adiposity of obese adolescents. Am J Clin Nutr 2002; 75(5):818-26.
103. Kang HS, Gutin B, Barbeau P, Owens S, Lemmon CR, Allison J, et al. Physical training improves insulin resistance syndrome markers in obese adolescents. Medicine & Science in Sports & Exercise 2002; 34(12):1920-7.
104. Mellin LM, Slinkard LA, Irwin CE, Jr. Adolescent obesity intervention: validation of the SHAPEDOWN program 3987. J American Dietetic Association 1987; 87(3):333-8.
105. Saelens BE, Sallis JF, Wilfley DE, Patrick K, Cella JA, Buchta R. Behavioral weight control for overweight adolescents initiated in primary care. Obesity Res 2002; 10(1):22-32.
106. Senediak C, Spence SH. Rapid versus gradual scheduling of therapeutic contact in a family based behavioural weight control programme for children. Behavioural Psychotherap 1985; 13(4):287.
107. Wadden TA, Stunkard AJ, Rich L, Rubin CJ, Sweidel G, McKinney S. Obesity in black adolescent girls: a controlled clinical trial of treatment by diet, behavior modification, and parental support 3928. Pediatrics 1990; 85(3):345-352.
108. White MA. Mediators of weight loss in an internet-based intervention for African-American adolescent girls (Dissertation). Baton Rouge: Louisiana State University, 2003.
109. Strauss RS, Pollack HA. Epidemic increase in childhood overweight, 1986-1998. JAMA 2001; 286(22):2845-8.
110. Epstein LH, Paluch RA, Saelens BE, Ernst MM, Wilfley DE. Changes in eating disorder symptoms with pediatric obesity treatment. J Pediatrics 2001; 139(1):58-65.
111. Inge TH, Garcia V, Daniels S, Langford L, Kirk S, Roehrig H, et al. A multidisciplinary approach to the adolescent bariatric surgical patient. J Pediatric Surger 2004; 39(3):442-7; discussion 446-7.
112. Stanford A, Glascock JM, Eid GM, Kane T, Ford HR, Ikramuddin S, et al. Laparoscopic Roux-en-Y gastric bypass in morbidly obese adolescents. J Pediatric Surger 2003; 38(3):430-3.
113. Strauss RS, Bradley LJ, Brolin RE. Gastric bypass surgery in adolescents with morbid obesity. J Pediatr 2001; 138(4):499-504.
114. Charney E. Childhood obesity: the measurable and the meaningful. J Pediatr 1998; 132(2):193-5.
115. Institute of Medicine (U.S.). Committee on Prevention of Obesity in Children and Youth. Preventing Childhood Obesity: Health in the Balance. Washington, D.C.: National Academies Press, 2005.
116. Stettler N. Comment: the global epidemic of childhood obesity: is there a role for the paediatrician? Obes Rev 2004; 5 Suppl 1:1-3.:1-3.
117. Gruen RL, Pearson SD, Brennan TA. Physician-citizens—public roles and professional obligations. JAMA 2004; 291(1):94-8.
118. Reilly JJ, Dorosty AR, Emmett PM. Identification of the obese child: adequacy of the body mass index for clinical practice and epidemiology. Int J Obes Relat Metab Disord 2000; 24(12):1623-7.
119. Dietz WH, Robinson TN. Use of the body mass index (BMI) as a measure of overweight in children and adolescents. J Pediatr 1998; 132(2):191-3.
120. Pi-Sunyer FX. Medical hazards of obesity. Ann Intern Med 1993; 119(7 Pt 2):655-60.
121. Daniels S. Pharmacological treatment of obesity in paediatric patients. Paediatric Drugs 2001; 3(6):405-10.
122. Stunkard A. Diet, exercise and behavior therapy: A cautionary tale. Obes Res 1996; 4:293-94.
123. Whitaker RC. Obesity prevention in pediatric primary care: four behaviors to target. Arch Pediatr Adolesc Med 2003; 157(8):725-7.
124. Campbell K, Waters E, O'Meara S, Kelly S, Summerbell C. Interventions for preventing obesity in children. Cochrane Database of Systematic Reviews 2003;(1).
125. Krempf M, Louvet JP, Allanic H, Miloradovich T, Joubert JM, Attali JR. Weight reduction and long-term maintenance after 18 months treatment with orlistat for obesity. Int J Obes Relat Metab Disord 2003; 27(5):591-7.
126. Sopher AB, Thornton JC, Wang J, Pierson RN, Jr., Heymsfield SB, Horlick M. Measurement of percentage of body fat in 411 children and adolescents: a comparison of dual-energy X-ray absorptiometry with a four-compartment model. Pediatrics 2004; 113(5):1285-90.
127. Robinson TN. Defining obesity in children and adolescents: clinical approaches. Critical Reviews in Food Science & Nutrition 1993; 33(4-5):313-20.

Return to Table of Contents

This document is in the public domain within the United States.

Requests for linking or to incorporate content in electronic resources should be sent via the USPSTF contact form.

Source: U.S. Preventive Services Task Force. This article first appeared in Pediatrics 2005;116(1)125-44. Available at: www.pediatrics.org/cgi/content/full/116/1/e125.

Return to Table of Contents

The graph has percentages as its vertical axis—from 0% to 20% in 5% increments. The horizontal axis is years: 1963-1965, 1966-1970, 1971-1974, 1976-1980, 1988-1994, and 1999-2002. Three lines represent children 2-5 years, children 6-11 years, and children 12-19 years.  Overall, the graph indicates that overweight in children (defined by experts as a body mass index (BMI) > 95th percentile for age and sex)5,6 aged 2 and older has at least doubled in the last 25 years.   The line for children 2-5 years of age indicates that the proportion of children with BMI at or more than the 95th percentile was 5% in the periods 1971-1974 and 1976-1980. By 1988-1994, the proportion of children 2-5 years with BMI at or more than the 95th percentile was approximately 7% and by 1999-2002 it was approximately 10%.  The line for children 6-11 years of age indicates that the proportion of children with BMI at or more than the 95 percentile was approximately 4% in 1963-1965, approximately 3% in 1971-1974, approximately 7% in 1976-1980, approximately 11% in 1988-1994, and approximately 15% in 1999-2002.  The line for children 12-19 years indicates that the proportion of children with BMI at or more than the 95th percentile was approximately 5% in the 1966-1970 period, approximately 7% in the 1971-1974 period, approximately 5% in the 1976-1980 period, approximately 10% in the 1988-1994 period, and approximately 15% in the 1999-2002 period.

Source: Ogden CL, Flegal KM, Carroll MD, Johnson CL. Prevalence and trends in overweight among US children and adolescents, 1999-2000. JAMA 2002;288(14Oct 9):1728-1732.

Return to Table of Contents

The analytic framework diagram starts with a three-item list: pre-school children (2-5 years), latency age children (6-11 years), and adolescents (12-18 years). The arrow goes to "screening" where it branches to arrow 1 and arrow 2. Arrow 1 is "Is there direct evidence that screening (and intervention) for overweight in childhood improves age appropriate behavioral or physiologic measures, or health outcomes?" Arrow 2 is a) "What are appropriate standards for overweight in childhood and what is the prevalence of overweight based on these?," b) "What clinical screening tests for overweight in childhood are reliable and valid in predicting poor health outcomes in adulthood?" and c) "What clinical screening tests for overweight in childhood are reliable and valid in predicting poor health outcomes in adulthood?"  Arrow 1 goes directly to the end of the diagram on the far right, to "decreased childhood morbidity from diabetes mellitus, slipped capital femoral epiphysis, sleep apnea, hypertension," "improved childhood functioning," and "reduced adult morbidity and mortality." Arrow 2 forks. One fork goes to arrow 3 ("What are the adverse effects of screening, including labeling? Is screening acceptable to patients?") The other fork goes to "overweight" and "at risk for overweight" and proceeds to arrow 4: "Do weight control interventions (behavioral counseling, pharmacotherapy, surgery) lead to improved intermediate outcomes, including behavioral, physiologic, or weight-related measures?" a) "What are common behavioral and health system elements of efficacious interventions?" and b) "Are there differences in efficacy between patient subgroups?"  Arrow 4 forks in three directions. One fork goes to arrow 6: "What are the adverse effects of interventions? Are interventions acceptable to patients?"  The second fork goes to Arrow 5: "Do weight control interventions lead to improved health outcomes, including decreased morbidity, and/or improved functioning (school attendance, self esteem, and other psychosocial indicators?" then directly to "decreased childhood morbidity from diabetes mellitus, slipped capital femoral epiphysis, sleep apnea, hypertension," "improved childhood functioning," and "reduced adult morbidity and mortality."  The third fork goes to "increased physical activity, dietary improvement, sedentary behavior," "stabilized or reduced BMI-for-age" and "improved glucose tolerance, blood pressure, lipid disorders, and physical fitness." From there, the arrow proceeds to arrow 7, shown as a dotted line: "Are improvements in intermediate outcomes associated with improved health outcomes? (Only evaluated if there is no direct evidence for arrow 1 or arrow 5 and if there is sufficient evidence for arrow 4)." This arrow continues to "decreased childhood morbidity from diabetes mellitus, slipped capital femoral epiphysis, sleep apnea, hypertension," "improved childhood functioning," and "reduced adult morbidity and mortality."

Key Questions:
Arrow 1: Is there direct evidence that screening (and intervention) for overweight in childhood improves age-appropriate behavioral or physiologic measures, or health outcomes?
Arrow 2: a. What are appropriate standards for overweight in childhood and what is prevalence of overweight based on these?
b. What clinical screening tests for overweight in childhood are reliable and valid in predicting obesity in adulthood?
c. What clinical screening tests for overweight in childhood are reliable and valid in predicting poor health outcomes in adulthood?
Arrow 3: What are the adverse effects of screening, screening, including labeling? Is screening acceptable to patients?
Arrow 4: Do weight control interventions (behavioral counseling, pharmacotherapy, surgery) lead to improved intermediate outcomes, including behavioral, physiologic or weight-related measures?
a. What are common behavioral and health system elements of efficacious interventions?
b. Are there differences in efficacy between patient subgroups?
Arrow 5: Do weight control interventions lead to improved health outcomes, including decreased morbidity, and/or improved functioning (school attendance, self-esteem and other psychosocial indicators)?
Arrow 6: What are the adverse effects of interventions? Are interventions acceptable to patients?
Arrow 7: Are improvements in intermediate outcomes associated with improved health outcomes? (Only evaluated if there is no direct evidence for KQ1 or KQ5 and if there is sufficient evidence for for KQ4.)

Return to Table of Contents

Figure 3 has two titles, one over each half of the figure: "Prevalence of Overweight or at Risk for Overweight, 1999-2002—% with BMI equal to or greater than 85% with standard error bars" and "Prevalence of Overweight or at Risk for Overweight, 1999-2002—% with BMI Equal to or Greater than 85% with Standard Error Bars." These two titles indicate mirrored bar charts with differences only in BMI. Clusters of horizontal bars indicate "non-Hispanic white"; "non-Hispanic black," and "Mexican Americans". Each cluster of bars includes an "all", a "male" and a "female" bar. Bars are divided into "2-5 years old," "6-11 years old" and "12-19 years old."   Using BMI ≥ 95th percentile, overweight prevalence in 1999-2002 was 10% in two- to five-year-olds and 16% in those six years and older.49 For children 2 to 5 years of age, the prevalence was similar between all racial/ethnic subgroups and both sexes, but was lower than the prevalence in older children in the same racial/ethnic subgroups. Among children 6 to 11 years, significantly more Mexican American (21.8%) and non-Hispanic black (19.8%) children categorized as overweight compared with non-Hispanic whites (13.5%) (p < .05). The highest prevalence of overweight was in 6- to-11-year-olds among Mexican American boys (26.5%), which was significantly higher than non-Hispanic black boys (17%), non-Hispanic white boys (14%), and Mexican American girls (17.1%), and similar to that of non-Hispanic black girls (22.8%). Among youth aged 12 to 19 years, significantly more non-Hispanic black (21.1%) and Mexican American (22.5%) children had overweight BMI measurements than non-Hispanic whites (13.7%) (p<.05), with no differences among males and females.

NHW = Non-Hispanic white; NHB = Non-Hispanic black; MA = Mexican American

Source: Hedley AA, Ogden CL, Johnson CL, Carroll MD, Curtin LR, Flegal KM. Prevalence of overweight and obesity among US children, adolescents, and adults, 1999-2002. JAMA. 2004;291(23):2847-2850.

Return to Table of Contents

Figure 4 models the short-term (1 year) results when translated to BMI percentiles.  On the graph, the horizontal axis is age in years and goes from 2 through 20. The vertical axis is BMI (kg/m2) numbered from 12 at the bottom to 36 at the top, in even-number intervals. A second vertical axis on the right indicates the percentiles. At age 20:  The 5th percentile is at BMI 18. The 10th percentile is at approximately BMI 18.5. The 25th percentile is at approximately BMI 20. The 50th percentile is at BMI 22. The 75th percentile is at approximately BMI 24.5. The 85th percentile is at approximately BMI 26.5. The 90th percentile is at BMI 28. The 95th percentile is at BMI 32.  Lines on the graph show the percentiles from age 2 through age 20.  A horizontal dotted line at BMI 25 indicates the overweight threshold for adults. Another horizontal dotted line at BMI 30 indicates the obesity threshold for adults.   Three circles indicate the mean BMI of study participants at a given age at the time of entry into a typical behavioral counseling weight loss trial. The bracket to the right of each circle indicates the typical range of mean participant BMI one year after trial entry. Top and bottom bars of brackets indicate a 10% or 20% reduction in percent overweight converted to BMI, respectively, which was the typical amount of weight lost.  One circle indicates a mean BMI of approximately 23.75 at age 8. The corresponding bracket indicates a typical range 1 year later from BMI 21 to BMI 22.5.   A second circle indicates a mean BMI of 25 at age 10. The corresponding bracket indicates a typical range 1 year later from approximately BMI 22.5 to BMI 24.  A third circle indicates a mean BMI of 27 at age 12. The corresponding bracket indicates a typical range 1 year later from BMI 24.5 to BMI 26.5.

Published May 30, 2000.
Source: Developed by the National Center for Health Statistics in collaboration with the National Center for Chronic Disease Prevention and Health Promotion (2000).

Note: Large black circles indicate the mean BMI of study participants at a given age at the time of entry into a typical behavioral counseling weight loss trial. The bracket to the right of each circle indicates the typical range of mean participant BMI one year after trial entry. Top and bottom bars of brackets indicate a 10% or 20% reduction in percent overweight converted to BMI, respectively, which was the typical amount of weight lost.

Return to Table of Contents

86,88,104,105,107,108 that reported, or could be translated into, BMI percentiles. Most studies addressed extremely overweight patients, with short-term results showing modest to no change in BMI percentiles. On the graph, the horizontal axis is age in years and goes from 2 through 20. The vertical axis is BMI (kg/m2) numbered from 12 at the bottom to 36 at the top, in even-number intervals. A second vertical axis on the right indicates the percentiles. At age 20: The 5th percentile is at BMI 18. The 10th percentile is at approximately BMI 18.5. The 25th percentile is at approximately BMI 20. The 50th percentile is at BMI 22. The 75th percentile is at approximately BMI 24.5. The 85th percentile is at approximately BMI 26.5. The 90th percentile is at BMI 28. The 95th percentile is at BMI 32. Lines on the graph show the percentiles from age 2 through age 20. A horizontal dotted line at BMI 25 indicates the overweight threshold for adults. Another horizontal dotted line at BMI 30 indicates the obesity threshold for adults. Black boxes represent mean BMI at entry for each behavioral counseling intervention trial. (A white box indicates a study of behavioral counseling plus sibutramine.) Numbers inside boxes identify studies in the reference list. Arrows from the boxes indicate the mean change in BMI at study followup six months or later. No arrow indicates that the mean BMI for the treatment group did not change significantly. The white box, reference number 86, sits above the body of the graph, at approximately BMI 38. An arrow indicates a change in BMI to approximately 34.5. Black box numbers 107 and 108 sit BMI 35 with no arrows, indicating the mean BMI did not change significantly. Black Box 88 also sits at BMI 35 but has an arrow indicating a change in BMI to approximately 33.75. Black box 105 sits at BMI 31 with no arrow." src="/Home/GetImage/1/17002/chovfig5/gif" style="width: 732px; height: 867px;" />

Published May 30, 2000.
Source: Developed by the National Center for Health Statistics in collaboration with the National Center for Chronic Disease Prevention and Health Promotion (2000).

Figure 5. Boxes represent mean BMI at entry for each behavioral counseling intervention trial. The white box indicates a study of behavioral counseling plus sibutramine. Numbers inside boxes identify studies in the reference list. Arrows indicate the mean change in BMI at study follow-up six months or later. No arrow indicates that the mean BMI for the treatment group did not change significantly.

Return to Table of Contents

Health Condition Population Source (Number) Age/Race- Ethnicity/Gender Level of Overweight Prevalence % Reference Cited in Source Bibliography
Diabetes Mellitus
Diabetes Mellitus Type II Community
N=2066
PIMA NA*     Dabelea, 199823
-ages 15-19 yrs
girls
boys

5.31
3.78
-ages 10-14 yrs
girls
boys

2.88
1.4
Community
N=142
Navajo NA
-ages 12-19
  1.41 Lobstein, 20044
NHANES III
N=2867
NHW, NHB, MA adolescents
-ages 12-19
  .04 (includes Type I DM as well)  
Diabetes Mellitus Type II Obesity clinic
N=55
Multi-ethnic boys and girls
-ages 4-10 years
BMI > for age & sex (95%ile) 0 Sinha, 200224
Obesity clinic
N=112
Multi-ethnic boys and girls
-ages 11-18 years
BMI > 95%ile 4 (all were NHB or H)  
Asthma
Parental report of doctor diagnosed asthma in child NHANES III
Subset of children with family history of parental asthma
N=625
Ages 10-16 years, multiethnic girls and boys BMI ≥ 85
BMI < 85
31
14.5
Rodriguez, 200215
Sleep Apnea (SA)
Sleep-associated abnormal breathing tests Obese children referred for history of sleep disordered breathing
N=32
Ages 2.7-13.8 years, multiethnic boys and girls Mean IBW = 196 ± 45% 40-90 Silvestri, 199317
1 or more abnormal polysomnography test Obesity clinic
N=222
Children and adolescents
-ages 3-20 years
"Severe obesity" - >150% IBW, mean = 208% IBW 6.8 (calc) Mallory, 198918
Severely abnormal tests (severe SA) 1 (calc)
1 or more abnormal polysomnography test Obesity clinic patients with history of sleep disordered breathing
N=41
Children and adolescents
-ages 3-20 years
"Severe obesity" - >150% IBW, mean = 208% IBW 32 Mallory, 198918
Severely abnormal tests (severe SA) 5
Nonalcoholic Fatty Liver Disease
Steatosis by U.S. General pediatric
N=810
Japanese school boys and girls
-ages 4-12 years
Population sample 3 Tominaga, 199519
Steatosis by U.S. Obesity clinic
N=72
Italian boys and girls
-ages 4.5-15.9 years
Obese > 120% IBW 53 Franzese, 199720
Steatosis and elevated transaminases (presumptive NASH) Of these, 32% had elevated transaminases (calc)
Steatosis by U.S. Obesity clinic
N=84
Chinese children, mean age 12 BMI > 95th percentile for age and sex 77 Chan, 200421
Steatosis and elevated transaminases (presumptive NASH) 24
Slipped Capital Femoral Epiphysis       3.4 per 100,000 children (50-70% are "obese") Kelsey, 197316

* The highest risk population in the world (Dabelea D. Endo and Metab clinic 1999).
Notes: Calc: calculated number.
Childhood morbidities discussed in reviews without reporting prevalence: Binge-eating disorders, low self-esteem.

Return to Table of Contents

Risk Factor Population Source (Number) Age/Race- Ethnicity/Gender Level of Overweight
(percentile of BMI for age and sex if given)
Prevalence % Reference Cited in Source Bibliography
Impaired glucose tolerance
Impaired glucose tolerance Obesity clinic
N=55
Multi-ethnic boys and girls
-ages 4-10 years
> 95 25 Sinha, 200224
Obesity clinic
N=112
Multi-ethnic boys and girls
-ages 11-18 years
> 95 21 Sinha, 200224
Hyperinsulinemia
(Insulin levels above the 95%ile) Bogalusa Heart Study Black and white boys and girls aged 5-10 years < 95
95-97
> 97
< 4
10
27
Freedman, 200225
Metabolic Syndrome
Hypertension, hypertriglyceridemia, low HDL cholesterol, hyperinsulinemia NHANES Adolescent boys and girls aged 12-19 years < 85
85-95
> 95
0.1
6.8
28.7
Cook, 200326
With at least three of: SBP or DBP > 95%ile, triglycerides > 95%ile, 2 hr. GTT > 140 mg/dl, BMI z score > 2.0 (97%ile), HDL cholesterol < 5%ile Obese sample
N=439
41% white, 31% black, 27% Hispanic
-ages 4-20 years.
-z-score 2-2.5
-z-score >2.5
38.7
49.7 overall (39 in blacks)
Weiss, 200427
Hypertension
Hypertension Population based Multiethnic boys and girls
-ages 5-11
Obese Up to 30 Figueroa-Colon, 199729
Hypertension Muscatine Heart Study (>6600) 5-18 years Community distribution 1 (60% of these had relative wt >120%) Dietz, 199828
Increased systolic blood pressure measures >95%ile Bogalusa Heart Study Black and white boys and girls aged 5-10 years < 95
95-97
> 97
2-7
12
22
Freedman, 200225
Increased diastolic blood pressure >95%ile Bogalusa Heart Study Black and white boys and girls aged 5-10 years < 95
95-97
> 97
2-7
9
14
Freedman, 200225
Dyslipidemia
LDL cholesterol > 130 mg/dl Bogalusa Heart Study Black and white boys and girls aged 5-10 years < 85

85-94
95-97
> 97
8-10 across all percentiles
18
12
23
Freedman, 200225
HDL cholesterol < 35 mg/dl Bogalusa Heart Study Black and white boys and girls aged 5-10 years < 85

85-94
95-97
> 97
5-8 & non-linear
8
7
18
Freedman, 200225
TG levels > 130 mg/dl Bogalusa Heart Study Black and white boys and girls aged 5-10 years < 85
85-94
95-97
> 97
2-6
10
10
21
Freedman, 200225

Note: Risk factors discussed in reviews without reporting prevalence: Menstrual disorders, polycystic ovarian syndrome, early maturation (girls), late maturation (boys).

Return to Table of Contents

Effect of age on the correlation of childhood with young adult BMI

Reference Population Childhood Age, Years Males Females
Guo 199455 100% White (n=555) 3 .18 .22
Lauer 198962 100% White (n=109 observations) 7 to 8 .57 .45
Lauer 198962 100% White (n=603 observations) 9 to 10 .63 .61
Clarke 199363 100% White (n=1286 observations) 9 to 10 .61 .59
Lauer 198962 100% White (n=1018 observations) 11 to 12 .67 .65
Guo 199455 100% White (n=555) 13 .5 .65
Lauer 198962 100% White (n=1041 observations) 13 to 14 .64 .68
Clarke 199363 100% White (n=1104 observations) 13 to 14 .7 .7
Lauer 198962 100% White (n=615 observations) 17 to 18 .74 .73
Clarke 199363 100% White (n=631 observations) 17 to 18 .81 .72

Effect of race on the correlation of childhood with young adult BMI

Reference Population Childhood Age, Years Males Females
Hulman 199851 100% Black (n=137) 13 .37
Wattigney 199552 100% Black (n=147) 13 to 17 .69 .72
Wattigney 199552 100% White (n=327) 13 to 17 .63 .48
Freedman, 200225 67% White (n=2212) 14 to 17 .76 .73
Return to Table of Contents

Study ID Overweight Measure in Childhood, BMI percentile Child's Age When Measured Adult's Age when Measured Probability of Adult Overweight
(Male & Female combined)
Probability of Adult Overweight
(Males)
Probability of Adult Overweight
(Females)
Gortmaker, 199366
(n=10,039)
80% White, 14% Black, 6% Hispanic 51% Female
> 95 16-24 23-31 - .77* .66*
Freedman, 200157
(n=2617)
67% White, 32% Black, 57% Female
< 50 5-27 18-37 .07 - -
Freedman, 200157
(as above)
85-94 5-27 18-37 .51 - -
Freedman, 200157
(as above)
≥ 95 5-27 18-37 .77 - -
Guo 200258
(n=347)
100% White, 52% female
≥ 75
≥ 85
≥ 95
3 35 -
-
.1
.1
.2
.14
.17
.24
Guo 200258
(as above)
≥ 75
≥ 85
≥ 95
8 35 - .1
.1
.2
.16
.23
.46
Guo 200258
(as above)
≥ 75
≥ 85
≥ 95
13 35 - .2
.2
.5
.16
.27
.64
Guo 200258
(as above)
≥ 75
≥ 85
≥ 95
18 35 - .2
.3
.8
.15
.26
.68

*In this study adult overweight was defined as >95%ile on NHANES.

Return to Table of Contents

Study Reference N Randomized
Country
Age
% Male
% Non-white
Baseline Measure of Overweight  Intervention Characteristics*
Components
Comprehensive?
Parent participation?
Group vs. Indiv.
Time period
# of Sessions
Session length
Total contact time (min)
Berkowitz, 2003[[86]]  82 adolescents
USA
13-17
33%
45%
BMI 37.8 kg/m2 (3.8);
BMI z-score: 2.4 (0.2)
BM,D,E
yes
yes
G
6 mo (phase I)
19 (phase I)
NR
NR
Duffy, 199387 29 children
Australia
7-13
21%
NR, Australian
48.4% overweight BM,D,E
yes
yes
NR
8 wk
8
90 in
720 min
Ebbeling, 200388  16 adolescents
USA
13-21
31%
19%
BMI 34.9 kg/m2 (reduced glycemic group);
 37.1 kg/m2 (reduced fat diet group)
BM,D
No
No
NR
12 mo
14
NR
NR
Epstein, 198589 41 families
USA
8-12
40%
NR
 48% overweight BM,D,E
yes
yes
NR
12 mo
18
NR
NR
Epstein, 198590  23 children
USA
8-12
0%
NR
48 % overweight  BM,D,E
yes
yes
NR
12 mo
NR
NR
NR
Epstein, 198591   24 children
USA
5-8
0%
NR
39-42% overweight BM,D,E
yes
yes
G, unclear if I
12 mo
unclear, approx 26
NR
NR
Epstein, 199492   44 families
USA
8-12
26%
NR
59.6% over the 50th%ile for BMI  BM,D,E
yes
yes
unclear
1 yr
32
NR
NR
Epstein, 199593  61 families
USA
8-12
27%
4%
51.8% overweight BM,D,E
yes
yes
I + G
6 mo
18
NR
NR
Epstein, 200094  90 families
USA
8-12
32%
NR
62% overweight BM,D,E
yes
yes
I + G
6 mo
20
45-60 min
900-1200 min
Epstein, 200095/
Epstein, 200196
67 children
USA
NR, mean (sd) 10.3 (1.1) yrs
48%
4% 
BMI 27.4 kg/m2(3.2) BM,D,E
yes
yes
I + G
6 mo
18
45-60 min
810-1080 min
Epstein, 200196  67 families
USA
8-12
52%
NR
60.2% overweight (compared to the 50%ile BMI for age and sex);
BMI 27.4 kg/m2 (3.6 kg/m2)
BM, D,E
yes
yes
I + G
6 mo
20
30 min
600 min
Flodmark, 199397 44 children (plus 50 matched controls)
Sweden
10-11
48%
NR (Swedish)
24.7 kg/m2 (family therapy group);
25.5 kg/m2 (conventional treatment group);
 25.1 kg/m2 (control group)
D,E
no
yes
I
14-18 mo
5 + 6 family therapy sessions
NR
NR
Golan, 199898 60 children
Israel
6-11
38%
NR (Israeli)
39.1% overweight  (conventional group);
39.6% (parents agents of change group)
BM,D,E
yes
noa
G+I
1 yr
30
60 min
1800 min
Graves, 198899  40 children
USA
6-12
NR
NR
52%-56% overweight  BM,D,E
yes
yes
G
8 wk
8
60 min
480 min
Israel, 1985100 33 children
USA
8-12
30%
NR
45.88% overweight (parent training group);
53.13%  (BT only); 56.02% (controls)
BM,D,E
yes
yes
G
12 mo
17
same +2-60 min sessions
>930 min
Israel, 1994101 36 families
USA
8-13
NR
NR
48.1% overweight (enhanced child involvement group); 46.0% (standard treatment group) BM,D,E
yes
yes
G
26 wk
17
90 min
1530 min
Kang, 2002103/
Gutin, 2002102 
80
USA
13-16
33%
69%
40.7% body fat (white boys); 45.8% body fat (white girls); 43.9% body fat (black boys); 45.2% body fat (black girls) BM,E
no
no
G
8 mo
160
60 min for LSE,
variable for PA
NR
Mellin, 1987104  66 adolescents
USA
12-18
21%
22%
30-37% overweight BM,D,E
yes
yes
G
14 wk
16
90 min
1440 min
Saelens, 2002105  44
USA
12-16
59%
30%
BMI 30.7 kg/m2 (3.1) BM,D,E
yes
no
I
4 mo
13
10-20 min for TC, NR for visit
NR, > 200 min
Senediak, 1985106  45 children
USA
6-13
approximately 66%
NR
37.22% overweight BM,D,E
yes
yes
G
4 wk
8
90 min
720 min
Wadden, 1990107  47 girls
USA
12-16
0%
100% black
95.1 kg; BMI 35.6 kg/m2 BM,D,E
yes
yes
G
10 mo
22
60 min (first 16 sessions), others NR
>960 min
White, 2003108/
Williamson, unpublished data
57 adolescents
USA
11-15
0%
100%
BMI 36.34 kg/m2; 98.3 BMI %ile BM,D,E
yes
yes
I  
6 mo
4 + weekly Web site logins
NR
NR

Table 5 (continued)

Study Reference Group Units of Measure Study Duration Outcome at Latest Followup Time P Value for Comparisons Between Groups** Other Outcomes USPSTF Quality Grade
Berkowitz, 200386  Sibutramine change in BMI (% change from entry BMI) 6 months -8.5% p = 0.001 P, A Good
Placebo -4.0%
Duffy, 199387 BT + cognitive self-management % overweight change 6 months -8.9% n.s. B Fair-to-Poor
BT + relaxation placebo -9.2%
Ebbeling, 200388  Reduced glycemic load diet absolute change in BMI 12 months -1.2 kg/m2 p < 0.05 B, P Fair
Reduced fat diet 0.6 kg/m2
Epstein, 198589 Lifestyle PA % overweight change 24 months -18.0% <0.05, lifestyle PA vs. Aerobic PA;
<0.05, lifestyle PA vs. calisthenics PA
B, P Fair
Aerobic PA -6.8%
Low-intensity calisthenics PA -7.2%
Epstein, 198590  Diet + PA % overweight change 12 months -25.4% n.s. B, P Fair
Diet alone -18.7%
Epstein, 198591   BT % overweight change 12 months -26.3% <0.05 B Fair
Education only -11.2%
Epstein, 199492 Mastery criteria & contingent reinforcement group % overweight change 24 months -15.4% n.s. B Fair
Comparison group -10.6%
Epstein, 199593  Combined % overweight change 12 months -8.7% p < 0.05, combined vs. increased PA B, P Fair
Decreased SB -10.3%
 Increased PA -18.7%
Epstein, 200094  Decreased SB high dose % overweight change 24 months -14.3% n.s. B, P Fair
Decrease SB low dose -11.6%
PA high dose -13.2%
PA low dose -12.4%
Epstein, 200095/
Epstein, 200196
PS to parent and child change in BMI z-score 24 months -0.5 p < 0.05, PS to parent and child vs. no PS;
p < 0.05, PS to parent and child vs. PS to child only 
H, A Fair
PS to child only -0.9
No PS -1.1
Epstein, 200196  Increased PA change in absolute BMI (statistical comparisons done on percent overweight change) 12 months girls: -0.27 kg/m2;
boys: -0.65 kg/m2
p < 0.01, interaction of group by sex;
p < 0.001, boys in combined group vs. girls in combined group
p < 0.05, boys in combined group vs. girls in increased PA group
none Fair
Combined increased PA + decreased SB  girls: 1.0 kg/m2; boys: -1.76 kg/m2
Flodmark, 199397 Family therapy change in BMI (kg/m2) 26-30 months 1.1 kg/m2 p < 0.05, family therapy vs. untreated controls P Fair
Conventional treatment 1.6 kg/m2
Matched controls, untreated 2.8 kg/m2
Golan, 199898 Conventional: children responsible for own wt loss % overweight change 12 months -8.1% p < 0.05 none Fair
Parents exclusive agents of change -14.7%
Graves, 198899  BT + parent PS % overweight change 6 months -24.5% p < 0.05, PS vs BT only;
p < 0.05, PS vs. instruction only
B Fair
BT only -10.2%
Instruction only -9.5%
Israel, 1985100 BT + parent training in child management % overweight change 12 months -10.2% p < 0.001 per NHS review B Fair-to-Poor
BT only -1.3%
Wait list controls NR
Israel, 1994101 Enhanced child involvement % overweight change 36 months -4.8% n.s. none Fair-to-Poor
Standard treatment (parents primarily responsible) 6.4%
Kang, 2002103/
Gutin, 2002102 
LSE + high intensity PA change in % body fat 8 months -2.9% n.s. B, P Fair-to-Poor
LSE + moderate PA -1.4%
LSE -0.1%
Mellin, 1987104  SHAPEDOWN group (Cognitive, behavioral, affective treatment) % overweight change 15 months -9.9% Between group comparison NR
(15 months vs. baseline: p < 0.01, SHAPEDOWN; n.s., control group)
B, H Fair
No treatment controls -0.1%
Saelens, 2002105  Healthy habits intervention % overweight change & change in BMI (statistical analyses on BMI z-scores) 7 months -2.4%, 0.1 kg/m2 n.s. B, A Good
Typical care 4.1%, 1.4 kg/m2
Senediak, 1985106  Rapid schedule BT % overweight change 6 months -14.7%  p < 0.05, rapid and gradual schedule BT groups combined vs. non-specific controls;
 (comparison of rapid vs. gradual schedule BT groups n.s.)
B Fair-to-Poor
Gradually decreasing schedule BT -18.3%
Non-specific treatment controls -10.9%
 Wait list controls NR
Wadden, 1990107  Mother and child together change in weight 6 months 1.7 kg n.s. P, H Fair-to-Poor
Child alone 3.0 kg
Mother and child separate 3.5 kg
White, 2003108/
Williamson, unpublished data
Behavioral change in % body fat; change in BMI 6 months -1.12%; -0.19 kg/m2 p < 0.05 (% body fat); p < 0.05 (change in BMI) B Good
Education only 0.43%; 0.65 kg/m2

*a For most intensive intervention which is listed first.
**If multiple comparisons, then presented only if p < 0.05.
Notes: Intervention characteristics: BM = behavior modification; D = special diet; E = exercise program; G = group; I = individual.
Other outcomes: B = behavioral; p = physiological; H = childhood health outcomes; A = adverse effects.

Return to Table of Contents

Key Question Study Hierarchy Overall USPSTF Quality
1. Screening - Poor
2a. Prevalence II-2 Good, but lacking for specific non-White racial/ethnic subgroups.
2b,c. Screening tests as a risk factor II-2 Fair. Data for BMI as a risk factor for adult overweight from childhood overweight are the most valid but are very limited for non-Whites. Data for BMI as a risk factor for adult morbidities generally do not control for confounding by adult BMI.
3. Screening harms - Poor. Due to lack of screening studies, possible harms can only be inferred from other sources.
4,5. BCI Interventions I Fair-to-poor. Data are limited by very small samples, non-comparable interventions & not using intent-to-treat analyses. Little reporting of intermediate outcomes—including risk factor changes, or changes in health outcomes. Poor generalizability due to specialist interventions not widely available and addressing mostly 8-12 yrs. No data in 2-5. Few trials include non-Whites.
4,5. Pharmacology with BCI I Fair. One good quality trial in adolescents.
4,5. Surgery - Poor
6. Intervention harms I, II-2 Fair-to-Poor. Very limited reporting of harms for BCI interventions.
Return to Table of Contents

Hierarchy of Research Design

I:   Properly conducted randomized controlled trial (RCT).
II-1:   Well-designed controlled trial without randomization.
II-2:   Well-designed cohort or case-control analytic study.
II-3:   Multiple time series with or without the intervention; dramatic results from uncontrolled experiments.
III:   Opinions of respected authorities, based on clinical experience; descriptive studies or case reports; reports of expert committees.

Design-Specific Criteria and Quality Category Definitions

Systematic Reviews

Criteria:

  • Comprehensiveness of sources considered/search strategy used.
  • Standard appraisal of included studies.
  • Validity of conclusions.
  • Recency and relevance are especially important for systematic reviews.
Case-Control Studies

Criteria:

  • Accurate ascertainment of cases.
  • Nonbiased selection of cases/controls with exclusion criteria applied equally to both.
  • Response rate.
  • Diagnostic testing procedures applied equally to each group.
  • Measurement of exposure accurate and applied equally to each group.
  • Measurement of exposure accurate and applied equally to each group.
  • Appropriate attention to potential confounding variables.
Randomized Controlled Trials and Cohort Studies

Criteria:

  • Initial assembly of comparable groups:
    • For RCTs: adequate randomization, including first concealment and whether potential confounders were distributed equally among groups.
    • For cohort studies: consideration of potential confounders with either restriction or measurement for adjustment in the analysis; consideration of inception cohorts.
  • Maintenance of comparable groups (includes attrition, cross-overs, adherence, contamination).
  • Important differential loss to followup or overall high loss to followup.
  • Measurements: equal, reliable, and valid (includes masking of outcome assessment).
  • Clear definition of the interventions.
  • All important outcomes considered.
Diagnostic Accuracy Studies

Criteria:

  • Screening test relevant, available for primacy care, adequately described.
  • Study uses a credible reference standard, performed regardless of test results.
  • Reference standard interpreted independently of screening test.
  • Handles indeterminate result in a reasonable manner.
  • Spectrum of patients included in study.
  • Sample size.
  • Administration of reliable screening test.
Return to Table of Contents