Published online December 1, 2006
PEDIATRICS Vol. 118 No. 6 December 2006, pp. e1721-e1733 (doi:10.1542/peds.2006-0682)
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ARTICLE

Estimating the Energy Gap Among US Children: A Counterfactual Approach

Y. Claire Wang, MD, ScDa, Steven L. Gortmaker, PhDb, Arthur M. Sobol, AMb and Karen M. Kuntz, ScDa

a Departments of Health Policy and Management
b Society, Human Development, and Health, Harvard School of Public Health, Boston, Massachusetts


    ABSTRACT
 TOP
 ABSTRACT
 METHODS
 RESULTS
 DISCUSSION
 APPENDIX 1: STATISTICAL REVERSAL...
 APPENDIX 2: ADJUSTMENT FOR...
 APPENDIX 3: MEAN-DIFFERENCE...
 REFERENCES
 
OBJECTIVE. Our goal was to quantify the magnitude of energy imbalance responsible for the increase in body weight among US children during the periods 1988–1994 and 1999–2002.

METHODS. We adopted a counterfactual approach to estimate weight gains in excess of normal growth and the implicit "energy gap"—the daily imbalance between energy intake and expenditure. On the basis of Centers for Disease Control and Prevention growth charts, we constructed weight, height, and BMI percentile distributions for cohorts 2 to 4 and 5 to 7 years of age in the 1988–1994 National Health and Nutrition Examination Survey (N = 5000). Under the counterfactual "normal-growth-only" scenario, we assumed that these percentile distributions remained the same as the cohort aged 10 years. Under this assumption, we projected the weight and height distributions for this cohort at 12 to 14 and 15 to 17 years of age on the basis of their baseline weight-for-age and stature-for-age percentiles. We compared these distributions with those for corresponding age groups in the 1999–2002 National Health and Nutrition Examination Survey (N = 3091) ~10 years after the 1988–1994 National Health and Nutrition Examination Survey. We calculated differences between the counterfactual and observed weight distributions and translated this difference into the estimated average energy gap, adjusting for increased total energy expenditure attributable to weight gain. In addition, we estimated the average excess weight accumulated among overweight adolescents in the 1999–2002 National Health and Nutrition Examination Survey, validating our counterfactual assumptions by analyzing longitudinal data from the National Longitudinal Survey of Youth and Bogalusa Heart Study.

RESULTS. Compared with the counterfactual scenario, boys and girls who were aged 2 to 7 in the 1988–1994 National Health and Nutrition Examination Survey gained, on average, an excess of 0.43 kg/year over the 10-year period. Assuming that 3500 kcal leads to an average of 1-lb weight gain as fat, our results suggest that a reduction in the energy gap of 110–165 kcal/day could have prevented this increase. Among overweight adolescents aged 12 to 17 in 1999–2002, results indicate an average energy imbalance ranging from 678 to 1017 kcal/day because of an excess of 26.5 kg accumulated over 10 years.

CONCLUSIONS. Quantifying the energy imbalance responsible for recent changes in weight distribution among children can provide salient targets for population intervention. Consistent behavioral changes averaging 110 to 165 kcal/day may be sufficient to counterbalance the energy gap. Changes in excess dietary intake (eg, eliminating one sugar-sweetened beverage at 150 kcal per can) may be easier to attain than increases in physical activity levels (eg, a 30-kg boy replacing sitting for 1.9 hours with 1.9 hours walking for an extra 150 kcal). Youth at higher levels of weight gain will likely need changes in multiple behaviors and environments to close the energy gap.


Key Words: childhood obesity • lifestyle factors • prevention • public health • weight gain

Abbreviations: CDC—Centers for Disease Control and Prevention • NHANES—National Health and Nutrition Examination Survey • NLSY—National Longitudinal Study of Youth • PAL—physical activity level • FAO—Food and Agriculture Organization • WHO—World Health Organization • BMR—basal metabolic rate

The prevalence of overweight children and youth is rapidly rising in the United States1,2 as well as many other regions in the world.3,4 Over the past 3 decades, the prevalence of overweight has doubled among preschool-aged children and adolescents, and the prevalence increased threefold among children 6 to 11 years of age.2 Approximately 9 million children over the age of 6 are considered overweight, defined as BMI ≥95th percentile on the Centers for Disease Control and Prevention (CDC) growth charts.5 Ethnic disparities in overweight are growing as rates increase faster among black and Hispanic children.6,7 Moreover, adolescents living in lower-income households are more likely to be overweight compared with youth living in higher-income households.8

Many epidemiologic studies document the likely role of excess adiposity in increasing mortality and morbidity,912 including cardiovascular diseases,13 cancer,14,15 and reduced functional status.16 An estimated 60% of overweight children between the ages of 5 and 10 have already developed at least 1 cardiovascular disease risk factor such as hyperinsulinemia, hypertension, and hyperlipidemia, and 25% have ≥2 risk factors.17 The incidence of type 2 diabetes, until recently thought to be almost exclusively an adult-onset disease, has dramatically increased among youth.18,19 Moreover, overweight children and adolescents are more likely than their peers to experience negative social and psychological consequences such as marginalization, low self-esteem, stigmatization, and discrimination.2023

An analysis by Hill et al24 estimated body weight changes in US adults between 20 and 40 years of age during the period of 1992–2000 and quantified the magnitude of energy imbalance that could explain such changes. They asserted that "affecting energy balance by 100 kilocalories [420 kJ] per day could prevent weight gain in the majority of the population." Their findings provide salient and tangible targets for implementing population preventive interventions. However, to provide similar estimates in the youth population requires methodologic adjustments. Throughout adulthood, a positive shift in weight distribution can be reasonably seen as the result of a positive "energy gap" (energy intake exceeding expenditure). The major challenge in estimating energy imbalance in childhood involves the fact that excess energy beyond daily activities is essential for growth. Unlike adults, all children should grow taller and heavier as they age. The issue is how much weight gain would be considered excessive beyond normal growth. Hence, we propose a counterfactual framework to project changes in the weight distribution of a hypothetical population if they only gain weight commensurate with their gain in height. This hypothetical scenario represents "what would have been" if the US youth had not experienced excess weight gain beyond normal growth. We then quantify the population-level deviation of reality from this counterfactual scenario to estimate the average excess weight gain and corresponding energy imbalance for US children during the period of 1988–1994 to 1999–2002. We also aim to address one potential criticism of the Hill et al approach: their calculations do not address the recognized fact that as individuals gain weight, they will also increase energy expenditure because of this extra weight.25,26


    METHODS
 TOP
 ABSTRACT
 METHODS
 RESULTS
 DISCUSSION
 APPENDIX 1: STATISTICAL REVERSAL...
 APPENDIX 2: ADJUSTMENT FOR...
 APPENDIX 3: MEAN-DIFFERENCE...
 REFERENCES
 
Descriptive Analysis
We compared data from children (2–11 years of age) and adolescents (12–17 years of age) in 2 nationally representative population studies: the National Health and Nutrition Examination Survey (NHANES) III (1988–1994) and NHANES 1999–2002. The NHANES is an ongoing series of nationwide surveys and clinical examinations conducted by the National Center for Health Statistics. The surveys use a multistage, clustered, probability sampling strategy to select households and individuals to provide national estimates representative of the civilian noninstitutionalized US population. Beginning in 1999, the NHANES began collecting data every year. This analysis is based on the first 4 years of the continuous NHANES data collection (1999–2002) and NHANES III (1988–1994). Weight and height are measured in mobile clinic settings by using standard NHANES protocols. A complete description of data-collection procedures and analytic guidelines are available on the National Center for Health Statistics Web site (www.cdc.gov/nchs/nhanes.htm).

For all NHANES subjects with complete height and weight measurements, we calculated weight-for-age, stature-for-age, and BMI-for-age percentiles as a function of gender on the basis of the revised CDC growth charts.5,27 Because body composition changes during growth, the distribution of these percentiles, both epidemiologically and clinically, have been widely used to monitor changes in relative body size across gender and age groups. Instead of defining a range of reasonable values for each age, we excluded subjects with BMI more extreme than the 0.5th or 99.5th BMI-for-age percentiles.

Synthetic Cohorts and Counterfactual Weight Trajectory
We created a "synthetic" cohort of children by linking subsets of children between the 2 cross-sectional studies: children 2 to 7 years old in the NHANES III (born between 1981 and 1992) who approximately represent the same birth cohorts as adolescents 12 to 17 years old in the NHANES 1999–2002 (born between 1982 and 1990). The midyear of the NHANES III is 1991, and the midyear of the NHANES 1999–2002 is 2001, so we have 2 "snapshots" of this synthetic cohort ~10 years apart. Although the cross-sectional nature of the surveys precludes the exact matching of birth cohorts, we aim to capitalize on the large sample size and wide geographical coverage in making nationally representative inferences.

We used a counterfactual scenario as the idealized trajectory of weight at the population level. Between 1988–1994 and 1999–2002, the average height of US children and adolescents did not increase significantly (Table 1). Therefore, when we converted the height of our synthetic cohort of children at baseline (1988–1994) into a stature-for-age percentile using the CDC growth charts, we assumed that the distribution remained stable over time.


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TABLE 1 Percent Overweight and Mean Height Among Children and Adolescents in NHANES III (1988–1994) and NHANES 1999–2002

 
Assuming stability in height distributions, we hypothesized that the distribution of weight-for-age percentile in a cohort of children with perfect energy balance (ie, weight gain only in proportion to height gain) should also remain the same as they age. This projection of a weight-distribution shift for the synthetic cohort in the NHANES III 10 years later represents an ideal growth trajectory into adolescence that, although heavier in actual body weight, maintains an identical weight-for-age percentile distribution. The deviation from this counterfactual "normal-growth-only" trajectory of weight distribution of the actual weight distribution among the synthetic cohort in the NHANES 1999–2002 therefore provides us with an estimate of the distribution of excess weight gained during the 10-year period.

Operationally, for each sampled child in the NHANES III synthetic cohort, we calculated the expected body weight for an adolescent 10 years older and of the same weight-for-age percentile. This mapping from a given percentile to corresponding age- and gender-specific weight is accomplished by reversing the statistical procedure that produced percentiles in the construction of the CDC growth charts (Appendix 1).28,29 Finally, we calculated the difference between the counterfactual distribution and the actual weight distribution in the NHANES 1999–2002 as the area enclosed between the 2 cumulative weight-distribution curves (Fig A1).


Figure 2
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FIGURE A1 Estimate excess weight gain from cumulative distribution curves. The area enclosed by the 2 curves represents the average difference in percentile values. Let A stand for the area of interest, Oi for the ith percentile of the observed actual cumulative distribution, and Ci for the ith percentile of the counterfactual cumulative distribution. Then, because the width between each percentile is 1%,

Formula 13

 
Translating Excess Weight Gain to Daily Energy Gap
To estimate the excess energy responsible for fueling the average excess weight gains observed in the NHANES, we assumed that the accumulation of excess weight is linear over the years and that each pound of excess weight gain as fat is associated with 3500 kcal stored.24

In addition to the assumptions described above, similar to Hill et al,24 we assumed 63% efficiency of the conversion of this imbalance of energy intake over expenditure into weight gain, the average efficiency of energy storage from composite diet.3032 We further adjusted for the increase in average energy requirements associated with weight gain. This adjustment aims to reflect the fact that, at a given level of physical activity, greater energy intake is required to move a higher body weight.31 Hence, to sustain a continuing excess-weight trajectory, an energy surplus needs to not only deposit fat mass (as accounted for in the Hill et al approach) but also offset the margin created by elevated energy expenditure.25 We modeled this time-dependent dynamic process using a differential equation to approximate the magnitude of this margin (detailed in Appendix 2) as a linear function of both the realized excess weight gain and average daily physical activity level (PAL).26

We provide 2 sets of adjusted energy-gap estimates: the primary estimates are based on the average age-specific PAL implied by the Food and Agriculture Organization (FAO)/World Health Organization (WHO) energy-requirement recommendations for youth 2 to 17 years of age ("average physical activity")26; the supplemental estimates assume "light physical activity."33

Excess Weight Gained Among Overweight Adolescents
A question of particular concern for pediatricians is the magnitude of the energy gap that leads to overweight status (BMI ≥95th percentile) among adolescents. We validated our counterfactual assumptions using 2 longitudinal samples to study the actual shifts in body size among children who became overweight adolescents. We compared longitudinal changes in weight and BMI in contrast to stature-for-age percentile changes in 2 cohorts: the National Longitudinal Study of Youth (NLSY) and the Bogalusa Heart Study; detailed information on these cohorts3436 has been published elsewhere. Briefly, data were collected every 2 years since 1986 on children born to a nationally representative sample of women enrolled in the NLSY in 1979, from a child’s birth through age 14. To be consistent with the time span of our NHANES analyses, we analyzed the subset of NLSY children who were 2 to 4 years of age in 1990 and had a BMI of ≥95th percentile in 2000 when aged 12 to 14 years (n = 39), and all measurements of weight and height were obtained by the interviewers. The initial Bogalusa Heart Study population consists of all children and young adults living in ward 4 of Washington Parish, Louisiana, which includes the city of Bogalusa. We studied the subset of children from the Bogalusa cohort who were 5 to 7 years of age in 1981–1982 and were considered overweight in 1992–1993 when aged 16 to 18 (n = 40).

The results can indicate the validity of using the simple counterfactual: "what if" their counterfactual weight-for-age percentile would have equaled their height-for-age percentile. We compared these estimates across the NLSY and Bogalusa samples and applied the results to the NHANES data.

Statistical Analysis
All statistical procedures were conducted in SAS 9.1 (SAS Institute, Cary, NC) and SUDAAN 9.0.1 (Research Triangle Institute, Research Triangle Park, NC) software. Age standardization of overweight prevalence and mean height and weight in Table 1 used direct standardization based on the 2000 US census.37,38 All statistics based on the NHANES and the NLSY data were weighted to adjust for unequal probabilities of sampling. Variance estimates from the NHANES analyses were adjusted for the stratified and clustered structure of the national sample using the robust variance estimation method.39


    RESULTS
 TOP
 ABSTRACT
 METHODS
 RESULTS
 DISCUSSION
 APPENDIX 1: STATISTICAL REVERSAL...
 APPENDIX 2: ADJUSTMENT FOR...
 APPENDIX 3: MEAN-DIFFERENCE...
 REFERENCES
 
NHANES Cross-sectional Comparisons
Samples included 6964 children and 2229 adolescents from the NHANES III (1988–1994) and 3260 children and 3091 adolescents from the NHANES 1999–2002. Sample size and the age-standardized prevalence of overweight (BMI ≥ 95th percentile) according to demographic subgroups are summarized in Table 1. As reported previously,2,40 between 1988–1994 and 1999–2002, the overall age-standardized prevalence of overweight significantly increased in children (8% vs 11%; P = .006) and adolescents (10% vs 13%; P = .002) during the 10-year period. Increases occurred among both boys and girls. Among race/ethnicity groups, Mexican American children and adolescents have the highest prevalence of overweight, followed by non-Hispanic black children and adolescents. In addition, although children from lower-income families had a slightly lower prevalence of overweight compared with their higher-income counterparts in the NHANES III, this was reversed in 1999-2002. Adolescents from lower-income families had higher overweight prevalence in both periods, although overweight adolescents from higher-income families increased by 50%. The mean height in all groups of youth remained virtually unchanged during the 2 time periods (Table 1).

Synthetic Cohorts and the Counterfactual Growth Trajectory
Figure 1 illustrates the baseline (age 2–7, NHANES III), counterfactual trajectory (age 12–17), and the actual (age 12–17, NHANES 1999–2002) BMI, weight, and height cumulative frequency distributions for the synthetic cohort (left panels). As expected, the baseline curves are to the left of the others, because they represent the body-size distributions of children much younger in age. Note that for height distributions, the counterfactual trajectory largely overlaps the actual curves in 1999–2002. This close approximation can also be demonstrated on the mean-difference plots (right panels). In these plots, the deviation of the actual distributions from the counterfactual scenario of corresponding percentiles (y-axis) is graphed against the mean of the same percentiles (x-axis) (see Appendix 3). The deviance of height distributions scatters around zero, mirroring the overlapping height-distribution curves and providing strong evidence for our assumption of constant stature-for-age percentile distribution during growth. As a result, the shifts in BMI and weight distributions beyond expectation under normal growth represent excess weight gain during these 10 years. The mean-difference plots indicate that deviation from the normal growth trajectory tends to be more prominent at higher percentiles.


Figure 1
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FIGURE 1 Counterfactual trajectory of growth: 1988–1994 to 1999–2002. Left, Cumulative distributions of BMI (kg/m2), height (cm), and body weight (kg) for the synthetic cohort at baseline (age 2–7, NHANES III, 1988–1994) and ~10 years later (age 12–17, NHANES 1999–2002). Counterfactual distributions are projected on the basis of baseline measurements assuming stable percentile distributions. Right, Mean-difference plots contrasting the counterfactual and the actual distribution in NHANES 1999–2002. Mean values of corresponding percentiles among the 2 distributions are plotted (x-axis) against the differences of the same percentiles (y-axis). A positive difference indicates that the actual distribution in 1999–2002 has a higher value than the counterfactual distribution for the given percentile.

 
We calculated the areas between the 2 curves to estimate the average excess weight gain in kilograms among this synthetic cohort during the 10-year period (see Fig A1 for details). The resulting overall and subpopulation estimates of excess weight gain and corresponding mean energy gap are summarized in Table 2. On the basis of the synthetic cohorts from the NHANES, we estimate that US children between 2 and 7 years of age gained an excess of 4.3 kg beyond normal growth during the 10-year period. Averaged over the 10-year period,24 we calculated that a 0.43-kg annual excess weight gain is fueled by an average of 131 kcal of excess energy intake over expenditure on a daily basis. Because of our assumption of uniform excess weight gain, this energy gap changes over time as the children grow, ranging from 14 kcal/day in the beginning of the first year to 247 kcal/day toward the end of the tenth year.


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TABLE 2 Estimates of Excess Weight Gain and Implied Energy Gap on the Basis of Distributions Derived From Children Aged 2 to 7 in NHANES III (1988–1994) and Adolescents Aged 12 to 17 in NHANES 1999–2002, Dynamically Adjusted for Total Energy Expenditure as a Function of Weight

 
Corresponding estimates indicate a greater energy gap among children who were younger (age 2–4) than who were older (age 5–7) at baseline, children from lower-income families than from higher-income families, and among Mexican American and black compared with non-Hispanic white children. However, estimates of the average daily energy gap for all groups are no larger than 165 kcal/day. If we vary the energy efficiency assumption from 50%, as assumed by Hill et al,24 to an upper bound of 75%,3032 our energy-gap estimate of 131 kcal/day would range from 165 to 110 kcal/day. Furthermore, when we assume a lower age-specific activity level throughout the 10-year period instead of the average level according to the WHO/FAO report,26 the energy-gap estimates decrease by ~13% (to 113 kcal/day, as indicated in Table 2). Finally, we follow the recommendations from the WHO/FAO report to use basal metabolic rate (BMR) prediction equations that assume linear increase in energy expenditure by weight gain. Had we alternatively used the nonlinear equations according to existing evidence suggesting a possible nonlinear relationship,26,32,41 we would have obtained slightly higher energy-gap estimates (~13 kcal higher for a typical boy in the NHANES who gained 4.5 kg of excess weight).

Excess Weight Gain and Energy Gap Among Overweight Adolescents
When weight and height changes were traced for each overweight NLSY adolescent aged 12–14 years at follow-up (n = 39), their average stature-for-age percentile modestly decreased from 66 in 1990 to 61 in 2000, and there were large increases in mean BMI-for-age (58 to 98) and weight-for-age percentiles (67 to 97). Similar results were observed among the Bogalusa Heart Study adolescents aged 16–18 years who were overweight at follow-up in 1992–1993 (n = 40). Over the ~11 years’ time, their mean stature-for-age percentile decreased (63 to 58), and there were large increases in mean BMI-for-age (73 to 98) and weight-for-age percentiles (71 to 97). Compared with these 2 cohorts, the overweight adolescents (n = 299 aged 12–14 and n = 232 aged 15–17) in the NHANES 1999–2002 showed similar distribution of weight, BMI, and height for their age. Among the 12- to 14-year-olds, weight-for-age percentiles averaged 97, whereas height-for-age percentiles averaged to 61 (the same as for those in the NLSY). Similarly, the 15- to 17-year-old overweight NHANES subjects had a mean weight-for-age percentile of 97, in comparison to their mean stature-for-age percentile of 53.

To quantify this disconnection between the growth in weight and height among the overweight NHANES adolescents, we calculated the difference between their actual weight and a hypothetical "ideal weight," which we defined as a weight-for-age percentile equaling their stature-for-age percentile. Under this counterfactual scenario, we estimated that the overweight 12- to 14-year-old NHANES adolescents were, on average, 24 ± 8 kg (median: 26 kg) above their idealized weight. The corresponding NLSY estimate in this analytic scenario would be 30 ± 16 kg (median: 26 kg). As for the older adolescents, we calculate that the overweight 15- to 17-year-old NHANES adolescents accumulated an average of 30 ± 9 kg (median: 29 kg) in excess. The same calculation applied to the Bogalusa Heart Study sample resulted in an average of 31 ± 11 kg (median: 30 kg) of excess gain.

The combined estimate of average excess weight gained among all overweight NHANES adolescents aged 12 to 17 years is 26.5 ± 9.7 kg (median: 26 kg). Following the same calculation that produces 110- to 165-kcal energy-gap estimates for all US adolescents, this average excess weight accumulated over 10 years’ time would indicate a daily imbalance of 678 to 1017 kcal.


    DISCUSSION
 TOP
 ABSTRACT
 METHODS
 RESULTS
 DISCUSSION
 APPENDIX 1: STATISTICAL REVERSAL...
 APPENDIX 2: ADJUSTMENT FOR...
 APPENDIX 3: MEAN-DIFFERENCE...
 REFERENCES
 
In its 2005 report "Preventing Childhood Obesity: Health in the Balance," the Institute of Medicine recommended reporting changes in the mean BMI and the shape of the whole BMI distribution as the benchmarking metric for evaluation of clinical guidelines and pubic health campaigns.42 We believe that estimates of energy imbalance underlying the observed excess shifts in weight distribution can be informative in facilitating communications in clinical, community, and policy settings.

We used a counterfactual approach, which acknowledges the natural changes in BMI distribution associated with growth, to calculate excess weight gains experienced by children in the United States. Between 1988–1994 and 1999–2002, we estimate that the cohort of children between ages 2 and 7 at baseline gained an excess of 4.3 kg over 10 year’s time. This translates to an average energy gap of 110 to 165 kcal/day. Compared with the analysis of adults by Hill et al,24 our estimates are relatively larger, because we take into account the increased energy expenditure resulting from excess weight. Had we not taken into account the excess energy required to maintain the extra weight, the estimated energy gap would have been much smaller (14 kcal/day).

Our findings are limited by the validity of our assumptions, including our estimates of BMR based on body weight, age, and gender. We calculated the energy gap for 2 levels of PAL: both the average and light levels noted in the WHO/FAO report.26 There is some evidence that US children may be in the light range.33 In addition, our assumption of a 63% efficiency of energy deposition from dietary intake represents estimation. Experimental studies have shown variations of this efficiency between fat and fat-free mass, by dietary content, and between individuals.30,43,44 It is also important to note that we assume that the calculated energy gap pertains to excess gain of weight and not to weight loss. Finally, we made inference from a counterfactual framework, which relies on model assumptions instead of controlled experiments. The validity of our estimates depends on the linkage of cohorts from cross-sectional data, which is subject to sampling variability as well as changes in population demographics resulting from immigration or childhood morbidity/mortality. We also stress that the interpretation of our results should be at the population level, not for individual children.

These results suggest that the behavioral modifications required for preventing excess weight accumulation in the US pediatric population are of manageable scale for most children. The accumulation of small lifestyle or environmentally induced changes in diet and physical activity could make significant differences. More importantly, because we show that an increasingly large energy excess must be sustained to continue a trajectory of excess weight gain, early prevention may be crucial. A typical child in the NHANES synthetic cohort aged 2 to 7 years at baseline gains an excess 0.43 kg every year for a decade, accumulating a total excess of 4.3 kg. The excess energy needed to produce this excess weight gain increases from ~40 kcal when the child is only 0.5 kg in excess, to 120 kcal when 2 kg in excess, and finally up to 230 kcal when 4 kg in excess to normal growth (see Fig A2). A possible implication of this scenario is that early recognition of behavioral risks and intervention could be more effective than attempting changes in habits and environments after a weight-gaining pattern has been sustained for years.


Figure 3
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FIGURE A2 Energy-gap estimates over time, adjusting for excess energy expenditure resulting from increasing excess-weight trajectory while compared with normal growth over 10 years. Energy gap (gray) and energy expenditure (1 kcal = 4.2 kJ) resulting from excess weight (dotted line) are plotted on the left y-axis, and excess body weight trajectory (black line) is plotted against the right y-axis.

 
A wide range of behavioral and environmental strategies can be imagined. For example, one strategy would be to increase the daily PAL of children. Using the same approach with BMR and PAL as detailed in Appendix 3, we calculate that a typical 9-year-old boy weighing 30 kg could burn an extra 150 kcal every day by replacing 1.9 hours of sitting with 1.9 hours of walking. Increasing physical education classes for the same child from once a week to 3 times a week can mean a difference of 240 kcal/week (assuming that children are active half of the time in class: 30/60 min in class, with activity intensity equivalent to playing volleyball instead of sitting in class).

Another strategy might be reducing portion size or reducing intake of certain foods. One source of calories associated with overweight in both observational and experimental studies is sugar-sweetened beverages.45,46 Studies suggest that calories from these beverages were often not offset by reduction of intake elsewhere.47,48 Thus, if this same child replaced one 12-oz can of sugar-sweetened beverage per day with water, this change could mean a difference of 150 kcal/day. In addition, eating at fast food restaurants has been associated with an additional 126 kcal/day,49 indicating another intervention target.

Reductions in television-viewing time could be another important strategy. Multiple observational and experimental studies link excess television viewing to increased overweight.5053 If the same 30-kg boy replaces 1 hour of television-watching time with 1 hour of slow walking, the difference in energy expenditure would be ~55 kcal. However, both observational and experimental studies document substantial effects of television-viewing time not only on physical activity but also on dietary intake.5456 Each hour per day decrease in television viewing has been associated with a reduction of total energy intake of 167 kcal/day (95% confidence limits: 136, 197).56 In experimental studies, Epstein et al54,55 found even larger effects. These results suggest that the role of television viewing on energy imbalance from both promoting sedentary behavior and encouraging dietary intake can be substantial.

Previous research has documented that shifts in BMI distribution in children over the past decades are characterized by a disproportionately elongating upper tail.6,57 The largest gains in overweight have thus occurred among those already overweight or at risk of overweight. The health risks associated with elevated BMI are also higher among this group: elevated blood pressure and insulin level are twice as common in children above the 97th percentile as in children between the 95th and 97th BMI percentiles.17 Preventing more children from becoming overweight, therefore, is crucial. Our results for youth who were overweight at ages 12 to 17 in the NHANES 1999–2002 indicate that they had accumulated an average of 26.5 kg in excess to normal growth, 5 to 6 times higher than the population average. The corresponding energy gap mounted to 678 to 1017 kcal/day. It is likely that focusing on single risk factors will not be enough; eliminating the consistent energy imbalance responsible for this level of excess weight will clearly require changes in multiple environmental and behavioral factors that contribute to sedentary lifestyles and excess dietary intake.

To date, population-based prevention approaches are believed to hold the key for reversing the forecast of this "epidemic."42 Substantiating these initiatives requires an evidenced-based framework to ensure that goals and recommendations are consistent with biological, psychosocial, and environmental knowledge. A comprehensive strategy, possibly similar to or even more extensive than the concerted interventions in tobacco control, is a critical need. Pediatricians stand at a pivotal position in fostering such effort.58 In addition to their close watch on the etiology and complications associated with already-overweight children, pediatricians and pediatric nurse practitioners are expected to play important roles in assisting families and communities initiate environmental and individual changes to halt the overweight epidemic.


    APPENDIX 1: STATISTICAL REVERSAL OF CDC GROWTH-CHART MACROS
 TOP
 ABSTRACT
 METHODS
 RESULTS
 DISCUSSION
 APPENDIX 1: STATISTICAL REVERSAL...
 APPENDIX 2: ADJUSTMENT FOR...
 APPENDIX 3: MEAN-DIFFERENCE...
 REFERENCES
 
The purpose of reversing the statistical program ("macro") provided by the CDC in their construction of growth charts is to automate the process of looking up gender- and age-specific values of BMI, weight, or height for a given percentile.

The Original SAS Macro
The original SAS program provided on the CDC Web site allows researchers to generate indices of anthropometric status (in percentiles) for his or her own target population from birth to 20 years of age on the basis of their subjects’ gender, age (in months), and body measures. For example, with a 5-year-old boy who weighs 41.5 lb and is 43 in tall, the program calculates that he is at the 50th BMI-for-age percentile. This procedure follows the mathematical algorithm based on the modified LMS method.28,29 The program can be downloaded at www.cdc.gov/nccdphp/dnpa/growthcharts/sas.htm.

The development of 2000 growth charts involves estimating 3 parameters from nationally representative data using the LMS technique: the median (M), the generalized coefficient of variation (S), and the power in the Box-Cox transformation (L). The L reflects the degree of skewness. The detail of this procedure and the subsequent smoothing process is outside the scope of this article; however, detailed information can be obtained from the CDC at www.cdc.gov/nchs/data/series/sr_11/sr11_246.pdf.

For a given body measure (eg, BMI), the process can be summarized as follows:

  1. Identify outlier values and assign "missing" to the percentile output.
  2. Look up L, M, and S values specific to the subject’s age (in months) from the standard distributions that the CDC constructed (let’s call them L*, M*, and S* to denote them specific to the subject’s age and gender).
  3. Find his or her z score (z*) and corresponding percentile (PCT*) by mapping it on the standard distribution (defined by L*, M*, and S*). Mathematically, the "mapping" entails the following:

    Formula 1(1)

    Formula 2(2)

    Formula 3(3)

The statistical relation between percentile and z score is:

Formula 4(4)
where PROBNORM(z*) is a function that returns the probability that an observation from the standard normal distribution is ≤z*. In other words,

Formula 5(5)

Reversed Macro
In constructing our counterfactual projection of distributions, we need to repetitively calculate the corresponding BMI, weight, and height values for the hypothetical future for each NHANES III child. For example, for a sampled child in NHANES III who is a 3-year-old girl who is at the 50th weight-for-age percentile, we calculate the corresponding weight (in kg) for the 50th weight-for-age percentile for 13-year-old girls. In other words, we need a statistical algorithm that serves the opposite of the function provided by the original macro on the CDC Web site. A straightforward reverse of the original mathematical algorithm is:

Formula 6(6)

Formula 7(7)

Formula 8(8)


    APPENDIX 2: ADJUSTMENT FOR INCREASE IN TOTAL ENERGY EXPENDITURE AFTER WEIGHT GAIN
 TOP
 ABSTRACT
 METHODS
 RESULTS
 DISCUSSION
 APPENDIX 1: STATISTICAL REVERSAL...
 APPENDIX 2: ADJUSTMENT FOR...
 APPENDIX 3: MEAN-DIFFERENCE...
 REFERENCES
 
We assume the excess weight gain is linearly accumulated over 10 years (eg, an average child gains 0.43 kg/year for a total of 4.3 kg in excess weight). Thus,

Formula 9(9)
where total excess = 4.3 kg in the above example. Excess weight accumulated up to any given time point t can be estimated as:

Formula 10(10)

Assuming no change in PAL, this excess weight leads to an elevated rate of energy expenditure. The energy surplus (on day t) to sustain a continuing weight gain is the sum of (1) joules required to offset excess energy expenditure from already-gained weight up to time t, and (2) energy stored to further gain weight (by the amount of daily weight gain.) We used a differential equation as follows to estimate this time-varying quantity, the daily gap (daily energy surplus):

Formula 11(11)

The parameter f reflects our assumption that the efficiency of energy storage is 63%. Multiplier c represents the conversion factor of excess energy to weight gain. We assume the same value as did Hill et al24 (ie, 3500 kcal stored equals 1 lb of weight gain as fat; hence, in standard units, c = 3500 x 2.205 = 7717.5 kcal/kg). Multiplier k represents the average additional daily energy expenditure associated with carrying each extra kilogram of excess body weight (as opposed to carrying no excess weight as the counterfactual normal growth cohort). We adopted the most widely used Schofield equations59 that assume a linear relationship; however, other sources have suggested a nonlinear relationship between body weight and total energy expenditure or BMR.26,32,41

We derive 2 values of k assuming different PALs. We assume that total energy expenditure is proportional to body weight, and there is no change in PAL associated with gains in excess weight, although at least 1 study has found a small difference (eg, 5% lower) in PAL among overweight youth.60 We calculate age- and gender-specific products of (1) the incremental BMR (kcal/day) per kg higher body weight and (2) PAL.

Quantity (1) is estimated from the BMR prediction equations developed by Schofield59 (FAO/WHO report, Tables 4.2 and 4.3).26 The slope coefficients of these equations (eg, 22.706 for boys between 3 and 10 years of age) represent this incremental increase; for example, a 20-kg boy expends 22.706 kcal/day more on basal metabolism than a 19-kg boy of the same age. As for PAL, the FAO/WHO report provided age- and gender-specific estimates for both average and light activity levels. We impute a number of light PAL estimates in some younger age groups using the same average-to-light PAL ratios in other ages. Finally, we average these age- and gender-specific products of quantities 1 and 2 to derive our overall k = 34.14, assuming an average level of PAL. Assuming the lighter PAL value leads to k = 29.11. Fig A2 shows the resulting time course of daily gap(t). The main text reports the average value of daily gap(t) over the entire 10-year period for different subpopulations.

Intensity and implications on energy expenditure of various physical activities (measured as multiples of BMR, equivalent to PAL) are taken from Annex 5 of the WHO/FAO report.26


    APPENDIX 3: MEAN-DIFFERENCE PLOTS AND THEIR INTERPRETATIONS
 TOP
 ABSTRACT
 METHODS
 RESULTS
 DISCUSSION
 APPENDIX 1: STATISTICAL REVERSAL...
 APPENDIX 2: ADJUSTMENT FOR...
 APPENDIX 3: MEAN-DIFFERENCE...
 REFERENCES
 
Let x represent a continuous random variable and f(x) represent the probability density function of x; then,

Formula 12(12)
and the cumulative distribution function (or distribution function)

Formula 13(13)

One way of quantifying the shift of a cumulative distribution is by the area enclosed by the "before" and "after" curves. To conceptually link the graphical presentations of distribution shifts, the Fig A3 contains 3 generic cases, each presented in 3 different ways. The left panels illustrate the frequency distribution of the population in 2 time periods, for example. The middle panels show the corresponding cumulative density distribution. Finally, the right panels show the mean-difference plots.57 Each point on the mean-difference plot represents the difference against the mean for the corresponding percentile of the 2 distributions.


Figure 4
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[in this window]
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FIGURE A3 Case 1, Equal-distance shift to the right. All points from the first distribution move an equal distance to the right. Case 2, Widening distribution without change in mean. Without change in the mean/median, the second distribution simply has a wider distribution (larger variance). Case 3, mixed case. The distribution overall shifts to the right but is characterized by an elongating right tail.

 
For example, if the 20th percentile of distribution A is 18.5 and the 20th percentile of distribution B is 22.5, then one will plot 4.0 (22.5 – 18.5) on the y-axis against 20.5 [(22.5 + 18.5)/2] on the x-axis.

The mean-difference plot is informative in identifying a shift that is by a greater amount at one end of the distribution (case 3), such as in the case of weight shift in children. The plot will show a pattern of bigger differences at higher percentiles.


    ACKNOWLEDGMENTS
 
This study was supported by Robert Wood Johnson Foundation grant 052194. The sponsor reviewed the manuscript but had no role in the design and conduct of the study, interpretation of the data, or preparation of the manuscript.

We thank Drs William Dietz, Claude Bouchard, and Boyd Swinburn for valuable comments. We are also in debt to Drs Gerald Berenson and David Freedman for providing access and analytical assistance with the Bogalusa Heart Study data.


    FOOTNOTES
 
Accepted Jun 23, 2006.

Address correspondence to Y. Claire Wang, MD, ScD, Department of Health Policy and Management, Harvard School of Public Health, 718 Huntington Ave, 2nd Floor, Boston, MA 02115. E-mail: ywang{at}hsph.harvard.edu

The authors have indicated they have no financial relationships relevant to this article to disclose.

Earlier versions of this manuscript were presented at the Pennington Scientific Symposium; December 4–6, 2005; Baton Rouge, LA; and the 27th annual meeting of the Society for Medical Decision Making; October 21–24, 2005; San Francisco, CA.


    REFERENCES
 TOP
 ABSTRACT
 METHODS
 RESULTS
 DISCUSSION
 APPENDIX 1: STATISTICAL REVERSAL...
 APPENDIX 2: ADJUSTMENT FOR...
 APPENDIX 3: MEAN-DIFFERENCE...
 REFERENCES
 

  1. Troiano RP, Flegal KM, Kuczmarski RJ, Campbell SM, Johnson CL. Overweight prevalence and trends for children and adolescents. The National Health and Nutrition Examination Surveys, 1963 to 1991. Arch Pediatr Adolesc Med. 1995;149 :1085 –1091[Abstract]
  2. Ogden CL, Flegal KM, Carroll MD, Johnson CL. Prevalence and trends in overweight among US children and adolescents, 1999–2000. JAMA. 2002;288 :1728 –1732[Abstract/Free Full Text]
  3. Ebbeling CB, Pawlak DB, Ludwig DS. Childhood obesity: public-health crisis, common sense cure. Lancet. 2002;360 :473 –482[CrossRef][ISI][Medline]
  4. World Health Organization. Obesity: Preventing and Managing the Global Epidemic. Geneva, Switzerland: World Health Organization; 2000. WHO technical report series, No. 894
  5. Centers for Disease Control and Prevention, National Center for Health Statistics. CDC growth charts: United States. Available at: www.cdc.gov/growthcharts. Accessed January 12, 2005
  6. Strauss RS, Pollack HA. Epidemic increase in childhood overweight, 1986–1998. JAMA. 2001;286 :2845 –2848[Abstract/Free Full Text]
  7. Kimm SY, Barton BA, Obarzanek E, et al. Obesity development during adolescence in a biracial cohort: the NHLBI Growth and Health Study. Pediatrics. 2002;110 (5). Available at: www.pediatrics.org/cgi/content/full/110/5/e54
  8. US Department of Health and Human Services. Healthy People 2010: Understanding and Improving Health and Objectives for Improving Health. 2nd ed. Vol 1 and 2. Washington, DC: US Government Printing Office; 2000
  9. Manson JE, Stampfer MJ, Hennekens CH, Willett WC. Body weight and longevity: a reassessment. JAMA. 1987;257 :353 –358[Abstract]
  10. Field AE, Coakley EH, Must A, et al. Impact of overweight on the risk of developing common chronic diseases during a 10-year period. Arch Intern Med. 2001;161 :1581 –1586[Abstract/Free Full Text]
  11. Must A, Spadano J, Coakley EH, Field AE, Colditz G, Dietz WH. The disease burden associated with overweight and obesity. JAMA. 1999;282 :1523 –1529[Abstract/Free Full Text]
  12. Allison DB, Fontaine KR, Manson JE, Stevens J, Van Itallie TB. Annual deaths attributable to obesity in the United States. JAMA. 1999;282 :1530 –1538[Abstract/Free Full Text]
  13. Rosenbaum M, Leibel RL, Hirsch J. Obesity [published correction appears in N Engl J Med. 1998;338:555]. N Engl J Med. 1997;337 :396 –407[Free Full Text]
  14. Lew EA, Garfinkel L. Variations in mortality by weight among 750,000 men and women. J Chronic Dis. 1979;32 :563 –576[CrossRef][ISI][Medline]
  15. Calle EE, Rodriguez C, Walker-Thurmond K, Thun MJ. Overweight, obesity, and mortality from cancer in a prospectively studied cohort of U.S. adults. N Engl J Med. 2003;348 :1625 –1638[Abstract/Free Full Text]
  16. 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 :1350 –1355[Abstract]
  17. Freedman DS, Dietz WH, Srinivasan SR, Berenson GS. The relation of overweight to cardiovascular risk factors among children and adolescents: the Bogalusa Heart Study. Pediatrics. 1999;103 :1175 –1182[Abstract/Free Full Text]
  18. Fagot-Campagna A, Pettitt DJ, Engelgau MM, et al. Type 2 diabetes among North American children and adolescents: an epidemiologic review and a public health perspective. J Pediatr. 2000;136 :664 –672[CrossRef][ISI][Medline]
  19. Rosenbloom AL, Joe JR, Young RS, Winter WE. Emerging epidemic of type 2 diabetes in youth. Diabetes Care. 1999;22 :345 –354[Abstract/Free Full Text]
  20. Mendelson BK, White DR. Relation between body-esteem and self-esteem of obese and normal children. Percept Mot Skills. 1982;54 :899 –905[ISI][Medline]
  21. Wallace WJ, Sheslow D, Hassink S. Obesity in children: a risk for depression. Ann NY Acad Sci. 1993;699 :301 –303
  22. US Department of Health and Human Services. The Surgeon General’s Call to Action to Prevent and Decrease Overweight and Obesity. Rockville, MD: US Department of Health and Human Services, Public Health Service, Office of the Surgeon General; 2001
  23. 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 :1008 –1012[Abstract/Free Full Text]
  24. Hill JO, Wyatt HR, Reed GW, Peters JC. Obesity and the environment: where do we go from here? Science. 2003;299 :853 –855[Abstract/Free Full Text]
  25. Swinburn B, Ravussin E. Energy balance or fat balance? Am J Clin Nutr. 1993;57 (5 suppl):766S–770S; discussion 770S–771S
  26. United Nations, Food and Agriculture Organization. Human Energy Requirements: Report of a Joint FAO/WHO/UNU Expert Consultation. Rome, Italy: Food and Agriculture Organization; 17–24 October, 2001. Food and nutrition technical report series 1
  27. Kuczmarski RJ, Ogden CL, Grummer-Strawn LM, et al. CDC growth charts: United States. Adv Data. 2000;(314) :1 –27[Medline]
  28. Kuczmarski RJ, Ogden CL, Guo SS, et al. CDC growth charts for the United States: methods and development. Vital Health Stat 11. 2000;(246) :1 –190
  29. Cole TJ. The LMS method for constructing normalized growth standards. Eur J Clin Nutr. 1990;44 :45 –60[ISI][Medline]
  30. Horton TJ, Drougas H, Brachey A, Reed GW, Peters JC, Hill JO. Fat and carbohydrate overfeeding in humans: different effects on energy storage. Am J Clin Nutr. 1995;62 :9 –29
  31. Tremblay A, Despres JP, Theriault G, Fournier G, Bouchard C. Overfeeding and energy expenditure in humans. Am J Clin Nutr. 1992;56 :857 –862[Abstract/Free Full Text]
  32. Deriaz O, Tremblay A, Bouchard C. Non linear weight gain with long term overfeeding in man. Obes Res. 1993;1 :179 –185[Medline]
  33. Salbe AD, Fontvieille AM, Harper IT, Ravussin E. Low levels of physical activity in 5-year-old children. J Pediatr. 1997;131 :423 –429[ISI][Medline]
  34. Baker PC, Keck CK, Mott FL, Quinlan SV. NLSY Child Handbook: A Guide to the 1986–90 National Longitudinal Survey of Youth Child Data. Revised ed. Columbus, OH: Center for Human Resource Research, Ohio State University; 1993
  35. Center for Human Resource Research. 1998 Child and Young Adult Data: User’s Guide. Columbus, OH: Center for Human Resource Research, Ohio State University; 1993
  36. Berenson GS, McMahon CA, Voors AW, et al. Cardiovascular Risk Factors in Children: The Early Natural History of Atherosclerosis and Essential Hypertension. New York, NY: Oxford University Press; 1980
  37. Siegal JS, Swanson DA. The Methods and Materials of Demography. 2nd ed. San Diego, CA: Elsevier Academic Press; 2004
  38. Lane PW, Nelder JA. Analysis of covariance and standardization as instances of prediction. Biometrics. 1982;38 :613 –621[CrossRef][ISI][Medline]
  39. Lohr SL. Sampling: Design and Analysis. Pacific Grove, CA: Duxbury Press; 1999
  40. 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 :2847 –2850[Abstract/Free Full Text]
  41. White CR, Seymour RS. Mammalian basal metabolic rate is proportional to body mass2/3. Proc Natl Acad Sci USA. 2003;100 :4046 –4049[Abstract/Free Full Text]
  42. Koplan JP, Liverman CT, Kraak VI, eds. Preventing Childhood Obesity: Health in the Balance. Washington, DC: National Academies Press; 2005
  43. Forbes GB. Do obese individuals gain weight more easily than nonobese individuals? Am J Clin Nutr. 1990;52 :224 –227[Abstract/Free Full Text]
  44. Bouchard C, Tremblay A, Despres JP, et al. The response to long-term overfeeding in identical twins. N Engl J Med. 1990;322 :1477 –1482[Abstract]
  45. Ludwig DS, Peterson KE, Gortmaker SL. Relation between consumption of sugar-sweetened drinks and childhood obesity: a prospective, observational analysis. Lancet. 2001;357 :505 –508[CrossRef][ISI][Medline]
  46. James J, Thomas P, Cavan D, Kerr D. Preventing childhood obesity by reducing consumption of carbonated drinks: cluster randomised controlled trial. BMJ. 2004;328 :1237[Abstract/Free Full Text]
  47. Mattes RD. Dietary compensation by humans for supplemental energy provided as ethanol or carbohydrate in fluids. Physiol Behav. 1996;59 :179 –187[CrossRef][Medline]
  48. Bellisle F, Rolland-Cachera MF. How sugar-containing drinks might increase adiposity in children. Lancet. 2001;357 :490 –491[CrossRef][ISI][Medline]
  49. Bowman SA, Gortmaker SL, Ebbeling CB, Pereira MA, Ludwig DS. Effects of fast-food consumption on energy intake and diet quality among children in a national household survey. Pediatrics. 2004;113 :112 –118[Abstract/Free Full Text]
  50. Andersen RE, Crespo CJ, Bartlett SJ, Cheskin LJ, Pratt M. Relationship of physical activity and television watching with body weight and level of fatness among children: results from the Third National Health and Nutrition Examination Survey. JAMA. 1998;279 :938 –942[Abstract/Free Full Text]
  51. Crespo CJ, Smit E, Troiano RP, Bartlett SJ, Macera CA, Andersen RE. Television watching, energy intake, and obesity in US children: results from the third National Health and Nutrition Examination Survey, 1988–1994. Arch Pediatr Adolesc Med. 2001;155 :360 –365[Abstract/Free Full Text]
  52. Dietz WH Jr, Gortmaker SL. Do we fatten our children at the television set? Obesity and television viewing in children and adolescents. Pediatrics. 1985;75 :807 –812[Abstract/Free Full Text]
  53. Robinson TN. Reducing children’s television viewing to prevent obesity: a randomized controlled trial. JAMA. 1999;282 :1561 –1567[Abstract/Free Full Text]
  54. Epstein LH, Paluch RA, Consalvi A, Riordan K, Scholl T. Effects of manipulating sedentary behavior on physical activity and food intake. J Pediatr. 2002;140 :334 –339[CrossRef][ISI][Medline]
  55. Epstein LH, Roemmich JN, Paluch RA, Raynor HA. Influence of changes in sedentary behavior on energy and macronutrient intake in youth. Am J Clin Nutr. 2005;81 :361 –366[Abstract/Free Full Text]
  56. Wiecha JL, Peterson KE, Ludwig DS, Kim J, Sobol AM, Gortmaker SL. When children eat what they watch: impact of television viewing on dietary intake in youth. Arch Pediatr Adolesc Med. 2006;160 :436 –442[Abstract/Free Full Text]
  57. Flegal KM, Troiano RP. Changes in the distribution of body mass index of adults and children in the US population. Int J Obes Relat Metab Disord. 2000;24 :807 –818[CrossRef][ISI][Medline]
  58. Teutsch SM, Briss PA. Spanning the boundary between clinics and communities to address overweight and obesity in children. Pediatrics. 2005;116 :240 –241[Free Full Text]
  59. Schofield WN. Predicting basal metabolic rate, new standards and review of previous work. Hum Nutr Clin Nutr. 1985;39 (suppl 1):5–41
  60. Ekelund U, Aman J, Yngve A, Renman C, Westerterp K, Sjostrom M. Physical activity but not energy expenditure is reduced in obese adolescents: a case-control study. Am J Clin Nutr. 2002;76 :935 –941[Abstract/Free Full Text]

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