(Circulation. 1996;94:3383-3387.)
© 1996 American Heart Association, Inc.
Articles |
Understanding Obesity in Youth
A Statement for Healthcare Professionals From the Committee on Atherosclerosis and Hypertension in the Young of the Council on Cardiovascular Disease in the Young and the Nutrition Committee, American Heart Association
Key Words: AHA Medical/Scientific Statements • obesity • cardiovascular diseases • diabetes mellitus • risk factors
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Introduction |
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Obesity is strongly linked to cardiovascular disease and non–insulin-dependent diabetes mellitus through the promotion of insulin resistance and other associated physiological abnormalities, including dyslipidemia, elevated blood pressure, and increased left ventricular mass.1 2 3 4 Overweight and insulin resistance have been linked to the early development of atheromata in young adults independent of other cardiovascular risk factors.5 Pulmonary, skeletal, dermatologic, immunologic, and endocrinologic systems display obesity-related morbidities (Table 1
).6 Adverse social and psychological effects of obesity have also been demonstrated.6 7 8
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Obesity is a major public health problem with both genetic and environmental causes.9 10 Longitudinal studies of children followed into young adulthood suggest that overweight children may become overweight adults, particularly if obesity is present in adolescence.11 12 13 There is substantial evidence that obesity in childhood lays the metabolic groundwork for adult cardiovascular disease.14 Studies of families and twins have clearly demonstrated a strong genetic component in the etiology of obesity.15 16 17 Just as persuasively, a recent study of secular trends in anthropometry has shown an increase in the prevalence of overweight in children and young adults over the last 10 to 20 years, indicating a potent interaction between environment and genetics.18 This secular trend is associated with worsening cardiovascular risk.19
This statement reviews the medical consequences of obesity in youth. Epidemiology, morbidity (especially cardiovascular), and etiology are considered and approaches to prevention and treatment presented. Areas for additional research are highlighted.
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Definition |
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Obesity is defined as the presence of excess adipose tissue. In normal individuals the percentage of body tissue that is adipose tissue varies by gender (greater in postpubertal females than males) and age (about 12% at birth, increasing to 25% at 5 months, then decreasing to 15% to 18% during puberty).20 Clinical standards for defining obesity in children are not well established. In general, any child with weight for height above the 75th percentile for age and sex or who has significantly increased his weight for height percentile and who suffers from a morbidity that would be worsened by obesity (eg, dyslipidemia, diabetes mellitus, or hypertension) should be considered obese. For diagnostic and therapeutic purposes, obese persons must be distinguished from those who are overweight because of increased lean body mass.
Attempts to standardize a definition of obesity have relied on calculations of weight significantly above that expected for height or measurements exceeding an anthropometric standard such as triceps or subscapular skinfold thickness.18 21 22 Measurements that adjust weight for height, such as body mass index (weight in kg÷height in meters squared), ponderal index (kg/m3), or percent ideal body weight for height (from published weight tables for adults or normal growth curves for children) do not differentiate between excess adiposity and increased lean body mass. Height, weight, and other anthropometric measures are advantageous for directly measuring body fat; in particular, subscapular skinfold measurements and waist-to-hip ratio help define the regional deposition of fat and differentiate the more medically significant central obesity from peripheral obesity in adults. For adults and adolescents, significant obesity in adults has been defined as a body mass index 
30 kg/m2 or 130% ideal body weight for height.22a22A Waist-to-hip ratio is difficult to standardize in children because of changes in body habitus with normal development. Subscapular skinfold measures correlate well with morbidity associated with obesity and measures of adiposity made by hydrodensitometry.22 23 For this reason, consideration should be given to incorporating skinfold measurements into clinical practice.
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Epidemiology |
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Estimates of the prevalence of obesity in children and adolescents in the United States are difficult to make because of the lack of a consensus definition and the existence of only a few data sets that mirror the ethnic and socioeconomic composition of the population. Recent analyses from the third National Health and Nutrition Examination Survey (NHANES III) show a continuing increase in prevalence. Based on age-specific calculations of triceps skinfold referenced to the 85th percentile of the earliest survey in 1963, prevalence increased to 25% in the 1976-1980 survey. Comparisons using the 85th percentile for body mass index in the 1976-1980 survey showed a further increase from 15% to 22% in the 1990 survey.18
The Bogalusa Heart Study24 has shown that measures of weight for height but not height have increased over the first 15 years of the study. This increase appears to be concentrated among those at the higher end of the weight for height percentiles. Weight has increased by 2% to 3% in children at the lowest quartiles for height and 7% to 10% in the uppermost height quartile.25 This trend is associated with worsening cardiovascular risk.19
Data on obesity for different racial groups are more sparse. In both the Bogalusa and Coronary Artery Risk Development in Young Adults (CARDIA) cohorts, however, obesity appears to be more prevalent in African-Americans, particularly females.24 26 Native Americans and Hispanics may also have relatively high rates of obesity.27 28 There are important regional and seasonal differences in the prevalence of obesity. Prevalence is increased when weight is measured during winter rather than summer. Obesity is much more common in the Northeast and the Midwest than in the South and the West, a phenomenon independent of race, population density, and season.9
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Morbidity |
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The relation of obesity to diabetes mellitus and cardiovascular risk is thought to be mediated partially by insulin, although it is unclear whether increased circulating levels of insulin or the presence of a physiological milieu counterregulatory to insulin (insulin resistance) is the primary problem.29 30 31 In cross-sectional population studies, higher fasting serum insulin levels are directly related to increases in body fatness, particularly in those with central adiposity.32 The combination of increased insulin and insulin resistance is the mechanism responsible for non–insulin-dependent or type II diabetes mellitus, a disease whose increase in frequency may parallel the increased prevalence of obesity.33
Elevated insulin levels have been associated with cardiovascular risk factors other than diabetes mellitus. Mechanisms for the association of elevated blood pressure with insulin levels include the increased presence of counterregulatory hormones such as norepinephrine and increased renal sodium and fluid retention.34 35 An association between insulin resistance and the combined dyslipidemia of hypertriglyceridemia as well as low levels of HDL cholesterol has also been found.36 Modest weight reduction results in correction of these abnormalities.34 35 Finally, the clustering of these risk factors identified in cross-sectional epidemiological studies can be explained by the association of elevated insulin with obesity.37 38
Obesity is important in the evolution of cardiovascular risk. As children progress with relatively low risk from childhood into adulthood with higher blood pressure, higher levels of LDL cholesterol, lower levels of HDL cholesterol, and increased risk for non–insulin-dependent diabetes, the major predictor of acquiring risk other than risk factor levels measured in childhood is the acquisition of excess weight.39 40 41 These trends may be independent of physical activity levels.42 Increased left ventricular mass, another independent cardiovascular risk factor, is associated with overweight and development of increased blood pressure.43 44 45 46 Coronary atherosclerosis is more likely to be present in young adults with excess adipose tissue independent of other risk factors.5
There are significant noncardiovascular morbidities of obesity, particularly central obesity, as well as orthopedic abnormalities, premature onset of puberty, hypoventilation, endocrinopathies, and skin problems. Being overweight in adolescence may be associated with premature morbidity and mortality not only from cardiovascular disease but colorectal cancer, gout, and arthritis.47 Social stigmatization and poor self-image have both been associated with significant obesity.7 8 Popular culture has clearly associated positive social rewards with leanness and negative social rewards with obesity. Body fat distribution in central (abdominal, male pattern) versus peripheral (gluteal, female pattern) adipose tissue depots is more predictive of many adipose-related morbidities than absolute body fatness.32 48 49
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Etiology |
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In studies comparing identical with fraternal twins and adopted children with their adoptive and their biological parents, the heritability of body fatness and body fat distribution has been estimated to be 65% to 75%.15 16 17 Twin studies have demonstrated genetic influences on resting metabolic rate, feeding behavior, changes in energy expenditures in response to overfeeding, lipoprotein lipase activity, and basal rate of lipolysis.50-5550 51 52 53 54 55 A recent population-based study suggests that 35% of the adjusted variation in body mass index was accounted for by a single recessive locus while polygenetic loci accounted for 42% of the variation. This study has also shown that obese family members of obese children have excess mortality from cardiovascular disease and other obesity-related causes.56 56A
Environmental factors associated with obesity include socioeconomic status, race, region of residence, season, urban living, and being part of a smaller family.9 Numerous studies have addressed the relation between energy expenditure and obesity. Although some studies suggest that obesity is associated with increased sedentary activity, particularly watching television, or with a lower resting metabolic rate, these differences have been inconsistently demonstrated.57 58 59 60 61 Several studies indicate that energy expenditure per kilogram is lower in obese children but similar to nonobese children when indexed to lean body mass. Obese persons may be socially stigmatized by their leaner peers; this may lead to less participation in athletic activities but may not translate into dramatic differences in daily energy expenditure.
Studies of diet composition in children also do not identify the cause of obesity in youth. Current dietary fat and saturated-fat intakes of American children are lower than in the past.62 Sequential cross-sectional studies of total caloric intake suggest little change in the total caloric intake of children over many years.63 Children appear to regulate their food intake over time when allowed to select their own food.64 Although meal-to-meal energy intake varies significantly, there is little day-to-day variation in energy intake at a given age.64
Inevitably, obesity must result from an imbalance between energy intake and energy expenditure. Obesity in a child or adult may reflect small excesses of energy intake over expenditure over a long period of time. Maintenance of a certain level of adiposity may be centrally regulated. Studies of people who have gained or lost weight suggest that there is metabolic resistance to alterations in body weight.65 66 67
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Prevention and Treatment |
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Because long-term studies of weight reduction in children have shown that 80%-90% return to their original weight percentile, efforts at primary prevention should be made.68 During health maintenance visits, measuring and recording height and weight on both standard charts and height and weight velocity charts is critical to detect the onset of relative excess weight gain. Body mass index can be calculated in adolescents. Subscapular skinfolds may also be measured. Values greater than the 75th percentile for skinfolds and weight for height measures should be considered at risk.18 This is particularly important when there is a family history of obesity, diabetes mellitus, dyslipidemia, or hypertension.
In the significantly overweight child, more aggressive medical intervention and treatment are warranted (Table 2). Evaluation of a child at 130% of ideal body weight for height or greater than the 95th percentile for subscapular skinfolds should include testing for obesity-related morbidities, including lipoprotein analysis, blood pressure assessment, fasting glucose and/or glucose tolerance test, assessment for nocturnal hypoventilation by history (and sleep study if severe involvement is suspected), and physical examination to exclude orthopedic abnormalities. Infants should undergo thyroid function testing.
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For individual therapy of most obese children, the primary emphasis of treatment should be prevention of weight gain above that appropriate for expected increases in height (ie, prevention of increased weight gain velocity). For many children this may mean limited or no weight gain while linear growth proceeds normally. Recommendations for weight maintenance should include regular physical activity and careful attention to diet to avoid excessive caloric intake. Interventions that have been most successful in promoting long-term weight maintenance have been implemented in children between the ages of 6 and 12 years.69 70 Factors predicting success are frequent intervention visits, inclusion of parents in the dietary treatment program, strong social support for the dietary intervention from others involved in food preparation, and regular exercise prescription. Achieving ideal weight for height should be considered an unrealistic goal. The importance of continuing these lifestyle modifications well past the initial treatment period should be emphasized to the entire family. The healthiest way to change weight for height is slowly.
The risks and difficulties of weight reduction may exceed the benefits in an older and otherwise healthy overweight child without a family history of cardiovascular morbidity related to adiposity. Caloric intake should not be restricted in infants; rather, prevention of overfeeding should be emphasized.
Conditions for which weight loss is recommended include hypertension, diabetes mellitus, cor pulmonale, sleep apnea, orthopedic abnormalities, and severe psychosocial stress secondary to obesity. Treatment should be continued until the medical or psychological condition has improved. Physician monitoring of weight reduction in children is essential because caloric restriction has been associated with problems, including precipitation of eating disorders, stigmatization of the child, and systemic complaints such as fatigue, headaches, dysmenorrhea, and syncope.71 Pharmacological or surgical therapy is indicated only with life-threatening complications of obesity and after conventional therapy has failed. Weight loss is not recommended for infants because of potential deleterious effects on somatic and brain growth.
Public health interventions for primary prevention should be directed toward the promotion of healthful behaviors. These include accumulation of at least 30 minutes of endurance-type physical activity of at least moderate intensity on most—preferably all—days of the week72 and consumption of the prudent diet recommended by the American Academy of Pediatrics and the American Heart Association.73 High-fat diets in parents are associated with their children's eating patterns and obesity. Therefore, the entire family should be targeted in recommendations.74 75 To improve compliance with recommendations, the entire family should be involved in treatment recommendations to improve family health and avoid stigmatizing the overweight child. The goal of prevention should be maintenance of normal growth patterns rather than weight loss.
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Future Directions |
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Further research on obesity in children should be directed toward understanding the critical periods for its development, devising successful family-oriented interventions, establishing clinical and genetic markers that identify individuals and populations at risk, improving standards for the diagnosis of obesity, and developing effective public health measures to increase participation in active rather than sedentary lifestyles. Current research leaves the hope that the trend toward increased obesity can be reversed through a public health policy that encourages regular physical activity and prudent diet combined with new insights into pathophysiology for specific therapy of severely affected individuals.
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Footnotes |
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A single reprint is available by calling 800-242-8721 (US only) or writing the American Heart Association, Public Information, 7272 Greenville Ave, Dallas, TX 75231-4596. Ask for reprint No. 71-0099. To purchase additional reprints: up to 999 copies, call 800-611-6083 (US only) or fax 413-665-2671; 1000 or more copies, call 214-706-1466, fax 214-691-6342, or E-mail pubauth@amhrt.org. To make photocopies for personal or educational use, call the Copyright Clearance Center, 508-750-8400.
"Understanding Obesity in Youth" was approved by the American Heart Association Science Advisory and Coordinating Committee in June 1996.
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References |
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1. Medalie JH, Papier CM, Goldbourt U, Herman JB. Major factors in the development of diabetes mellitus in 10,000 men. Arch Intern Med. 1975;135:811-817.
2. Mann GV. The influence of obesity on health. N Engl J Med. 1974;291:178-185, 226-232.
3. Barrett-Connor EL. Obesity, atherosclerosis, and coronary artery disease. Ann Intern Med. 1985;103:1010-1019.
4.
Pi-Sunyer FX. Medical hazards of obesity. Ann Intern Med. 1993;119:655-660.
5.
McGill HC Jr, McMahan A, Malcolm GT, Oalmann MC, Strong JP. Relation of glycohemoglobin and adiposity to atherosclerosis in youth. Arterioscler Thromb Vasc Biol. 1995;15:431-440.
6. Dietz WH Jr. Nutrition and obesity. In: Grand RJ, Sutphen JL, Dietz WH, eds. Pediatric Nutrition: Theory and Practice. Boston, Mass: Butterworths; 1987:525-538.
7.
Stunkard A, Mendelson M. Obesity and the body image, I: characteristics of disturbances in the body image of some obese persons. Am J Psychiatry.. 1967;123:1296-1300.
8.
Stunkard A, Burt V. Obesity and the body image, II: age at onset of disturbances in the body image. Am J Psychiatry.. 1967;123:1443-1447.
9.
Dietz WH Jr, Gortmaker SL. Factors within the physical environment associated with childhood obesity. Am J Clin Nutr. 1984;39:619-624.
10. Leibel RL, Behary N, Friedman JF. Strategies for the molecular genetic analysis of obesity in humans. Crit Rev Food Sci Nutr. 1993;33:351-358.[Medline] [Order article via Infotrieve]
11. Braddon F, Rodgers B, Wadsworth M, Davies J. Onset of obesity in a 36 year birth cohort study. Br Med J. 1986;293:299-303.
12. Serdula MK, Ivery D, Coates RJ, Freedman DS, Williamson DF, Byers T. Do obese children become obese adults? A review of the literature. Prev Med. 1993;22:167-177.[Medline] [Order article via Infotrieve]
13.
Guo SS, Roche AF, Chumlea WC, Gardner JC, Siervogel RM. The predictive value of childhood body mass index values for overweight at age 35. Am J Clin Nutr. 1994;59:810-819.
14. Gidding SS. A perspective on obesity. Am J Med Sci. 1995;310(suppl 1):S68-71.
15. Stunkard A, Sorenson T, Hanis C, Teasdale T, Chakraborty R, Schull W, Schulsinger F. An adoption study of human obesity. N Engl J Med. 1986;314:193-198.[Abstract]
16.
Stunkard A, Foch T, Hrubec Z. A twin study of human obesity. JAMA. 1986;256:51-54.
17. Borjeson M. The aetiology of obesity in children. Acta Paediatr. 1976;65:279-287.
18.
Troiano RP, Flegal KM, Kuczmarski RJ, Campbell SM, Johnson CL. Overweight prevalence and trends for children and adolescents: the National Health and Examination Surveys, 1963 to 1991. Arch Pediatr Adolesc Med. 1995;149:1085-1091.
19. Gidding SS, Bao W, Srinivasan SR, Berenson GS. Effects of secular trends in obesity on coronary risk factors in children: the Bogalusa Heart Study. J Pediatr.. 1995;127:868-874.[Medline] [Order article via Infotrieve]
20.
Roche AF, Siervogel FM, Chumlea WB, Webb P. Grading body fatness from limited anthropometric data. Am J Clin Nutr. 1981;34:2831-2838.
21.
Marshall JD, Hazlett CB, Spady DW, Quinney HA. Comparison of convenient indicators of obesity. Am J Clin Nutr. 1990;51:22-28.
22. Dietz WH. Childhood obesity: susceptibility, cause, and management. J Pediatr. 1983;103:676-686.[Medline] [Order article via Infotrieve]
22.
Report of the National Cholesterol Education Program Expert Panel on Detection, Evaluation, and Treatment of High Blood Cholesterol in Adults. The Expert Panel. Arch Intern Med.. 1988;148:36-39.
23. Deurenberg P, Pieters JJ, Hautvast JG. The assessment of the body fat percentage by skinfold thickness measurements in childhood and young adolescence. Br J Nutr.. 1990;63:293-303.[Medline] [Order article via Infotrieve]
24. Webber LS, Harsha DW, Nicklas TA, Berenson GW. Secular trends in obesity in children. In: Filer LJ, Lauer RM, Luepker RV, eds. Prevention of Atherosclerosis and Hypertension Beginning in Youth. Philadelphia, Pa: Lea & Febiger; 1994:194-203.
25. Webber LS, Wattigney WA, Srinivasan AR, Berenson GS. Obesity studies in Bogalusa. Am J Med Sci. 1995;310(suppl):S53-S61.
26. Lewis CE, Smith DE, Williams OD, Bild DE, Coan B, Jacobs DR Jr. Seven year trends in weight and weight gain in black and white young adults: the CARDIA study. Circulation.. 1994;89:939. Abstract.
27.
Brussard BA, Johnson A, Himes JH, Story M, Fichtner R, Hauck F, Bachman-Carter K, Hayes J, Frohlich K, Gray N, Valway S, Gohdes D. Prevalence of obesity in American Indians and Alaska natives. Am J Clin Nutr. 1991;53:1535S-1542S.
28.
Pawson IG, Martorell R, Mendoza FE. Prevalence of overweight and obesity in U.S. Hispanic populations. Am J Clin Nutr. 1991;53:1522S-1528S.
29. Resnick LM. Cellular calcium and magnesium metabolism in the pathophysiology and treatment of hypertension and related metabolic disorders. Am J Med. 1992;93(suppl 2A):11S-20S.
30. Modan M, Halkin H, Almog S, Lusky A, Eshkol A, Shefi M, Shitrit A, Fuchs Z. Hyperinsulinemia: a link between hypertension, obesity, and glucose intolerance. J Clin Invest. 1985;75:809-817.
31. Gidding SS. Relationships between blood pressure and lipids in childhood. Pediatr Clin North Am. 1993;40:41-49.[Medline] [Order article via Infotrieve]
32.
Freedman D, Srinivasan S, Burke G, Shear C, Smoak D, Harsha D, Webber L, Berenson G. Relationship of body fat distribution to hyperinsulinemia in children and adolescents: the Bogalusa Heart Study. Am J Clin Nutr. 1987;46:403-410.
33. Pinhas-Hamiel O, Standiford D, Daniels SR, Zeitler P, Dolan LM. Non-insulin dependent diabetes mellitus is increasing among adolescents. Pediatr Res. 1995;37:7A. Abstract.
34. Rocchini AP. Adolescent obesity and hypertension. Pediatr Clin North Am. 1993;60:81-92.
35.
Rocchini AP, Katch V, Kveselis D, Moorehead C, Martin M, Lampman R, Gregory M. Insulin and renal sodium retention in obese adolescents. Hypertension. 1989;14:367-374.
36.
Knip M, Nuutinen O. Long term effects of weight reduction on serum lipids and plasma insulin on obese children. Am J Clin Nutr. 1993;57:490-493.
37.
Smoak CG, Burke GL, Webber LS, Harsha DW, Srinivasan SR, Berenson GS. Relation of obesity to clustering of cardiovascular disease risk factors in children and young adults: the Bogalusa Heart Study. Am J Epidemiol. 1987;125:364-372.
38.
Manolio TA, Savage PJ, Burke GL, et al. Association of fasting insulin with blood pressure and lipids in young adults: the CARDIA Study. Arteriosclerosis. 1990;10:430-436.
39. Lauer RM, Clarke WR. Childhood risk factors for high adult blood pressure: the Muscatine Study. Pediatrics. 1984;74:633-641.
40. Lauer RM, Lee J, Clarke WR. Factors affecting the relationship between childhood and adult cholesterol levels: the Muscatine Study. Pediatrics. 1988;82:577-582.
41.
Wattigney WA, Harsha DW, Srinivasan SR, et al. Increasing impact of obesity on serum lipids and lipoproteins in young adults. Arch Intern Med. 1991;151:2017-2022.
42. McMurray RG, Harrell JS, Levine AA, Gansky SA. Childhood obesity elevates blood pressure and total cholesterol independent of physical activity. Int J Obes Relat Metab Disord. 1995;19:881-886.[Medline] [Order article via Infotrieve]
43.
Urbina EM, Gidding SS, Bao W, Pickoff A, Berdusis K, Berenson GS. Effect of body size, ponderosity, and blood pressure on left ventricular growth in children and young adults in the Bogalusa Heart Study. Circulation. 1995;91:2400-2406.
44.
Mahoney LT, Schieken RM, Clarke WR, Lauer RM. Left ventricular mass and exercise responses predict future blood pressure: the Muscatine Study. Hypertension. 1988;12:206-213.
45. De Simone G, Daniels SR, Devereux RB, Meyer RA, Roman MJ, de Divitiis O, Alderman MH. Left ventricular mass and body size in normotensive children and adults: assessment of allometric relations and impact of overweight. J Am Coll Cardiol. 1992:20:1251-1260.
46.
Daniels SR, Kimball TR, Morrison JA, Khoury P, Witt S, Meyer RA. Effect of lean body mass, fat mass, blood pressure, and sexual maturation on left ventricular mass in children and adolescents: statistical, biological, and clinical significance. Circulation. 1995;92:3249-3254.
47. Must A, Jacques P, Dallai G, Bajema D, Dietz W. Long term morbidity and mortality of overweight adolescents. N Engl J Med. 1992;327:1350-1355.[Abstract]
48. DuRant R, Baranowski T, Rhodes T, Gutin B, Thompson WO, Carroll R, Puhl J, Greaves KA. Association among serum lipid and lipoprotein concentrations and physical activity, physical fitness, and body composition in young children. J Pediatr.. 1993;123:185-192.[Medline] [Order article via Infotrieve]
49. Rosenbaum M, Leibel R. Pathophysiology of childhood obesity. Adv Pediatr. 1988;35:73-137.[Medline] [Order article via Infotrieve]
50. Bouchard C, Tremblay A, Despres JP, Nadeau A, Lupien PJ, Theriault G, Dussault J, Moorjani S, Pinault S, Fournier G. The response to long-term overfeeding in identical twins. N Engl J Med. 1990;322:1477-1482.[Abstract]
51. Bogardus C, Lillioja S, Ravussin E, Abbot W, Zawadski J, Young A, Knowler W, Jacobwitz R, Moll P. Familial dependence of the resting metabolic rate. N Engl J Med. 1986;315:96-100.[Abstract]
52.
Brook C. Genetic aspects of obesity. Postgrad Med J. 1977;53:93-99.
53.
Poehlman E, Despres J, Marcotte M, Tremblay A, Theriault G, Bouchard C. Genotype dependency of adaptation in adipose tissue metabolism after short term overfeeding. Am J Physiol. 1986;250:E480-E485.
54. Bouchard C. Inheritance of fat distribution and adipose tissue metabolism. In: Vague J, Bjorntorp P, Guy-Grand B, Rebuffe-Scrive M, Vague P, eds. Metabolic Complications of Human Obesity. Amsterdam, the Netherlands: Excerpta Medica; 1985
55.
Mitchell BD, Kammerer CM, Mahaney MC, Blangero J, Comuzzie AG, Atwood LD, Haffner SM, Stern MP, MacCluer JW. Genetic analysis of the IRS: pleiotropic effects of genes influencing insulin levels on lipoprotein and obesity measures. Arterioscler Thromb Vasc Biol.. 1996;16:281-288.
56.
Burns TL, Moll PP, Lauer RM. The relationship between ponderosity and coronary risk factors in children and their relatives: the Muscatine Ponderosity Family Study. Am J Epidemiol.. 1989;129:973-987.
56. Moll PP, Burns TL, Lauer RM. The genetic and environmental sources of body mass index variability: the Muscatine Ponderosity Family Study. Am J Hum Genet.. 1991;49:1243-1255.[Medline] [Order article via Infotrieve]
57. Bandini LG, Schoeller DA, Dietz WH. Energy expenditure in obese and nonobese adolescents. Pediatr Res. 1990;27:198-202.[Medline] [Order article via Infotrieve]
58.
Dietz WH, Gortmaker SL. Do we fatten our children at the television set? Obesity and television viewing in children and adolescents. Pediatrics. 1985;75:807-811.
59.
Gortmaker SL, Must A, Sobol AM, Peterson K, Colditz GA, Dietz WH. Television viewing as a cause of increasing obesity among children in the United States, 1986-1990. Arch Pediatr Adolesc Med.. 1996;150:356-362.
60. Tucker LA. The relationship of television viewing to physical fitness and obesity. Adolescence. 1986;21:797-806.[Medline] [Order article via Infotrieve]
61. Reybrouck T, Weymans M, Vinckx J, Stijns H, Vanderschueren-Lodeweyckx M. Cardiorespiratory function during exercise in obese children. Acta Paediatr Scand. 1987;76:342-348.[Medline] [Order article via Infotrieve]
62. Centers for Disease Control. Energy and macronutrient intakes of persons ages 2 months and over in the United States: third national health and nutrition examination survey, Phase I, 1988-1991. MMWR Morb Mortal Wkly Rep. 1994;43:116-125.[Medline] [Order article via Infotrieve]
63.
Nicklas TA, Webber LS, Srinivasan SR, Berenson GS. Secular trends in dietary intakes and cardiovascular risk factors of 10 year old children (1973-1988). Am J Clin Nutr. 1993;57:930-937.
64. Birch L, Johnson S, Andresen G, Peters J, Schultz M. The variability of young children's energy intake. N Engl J Med. 1991;324:232-235.[Abstract]
65.
Leibel R, Rosenbaum M, Hirsch J. Changes in energy expenditure resulting from altered body weight. N Engl J Med.. 1995;332:621-628.
66. Weigle D, Brunzell J. Assessment of energy expenditure in ambulatory reduced obese subjects by techniques of weight stabilization and exogenous weight replacement. Int J Obes Relat Metab Disord.. 1990;14:69-77.
67. Leibel R, Hirsch J. Diminished energy requirements in reduced obese patients. Metabolism.. 1984;33:164-170.[Medline] [Order article via Infotrieve]
68. Lloyd J, Wolff O, Whelan W. Childhood obesity: a long term study of height and weight. Br Med J. 1961;2:145-148.
69. Epstein LH, Valoski A, Wing RR, McCurley J. Ten-year outcomes of behavioral family-based treatment for childhood obesity. Health Psychol.. 1994;13:373-383.[Medline] [Order article via Infotrieve]
70. Wilson GT. Behavioral treatment of childhood obesity: theoretical and practical implications. Health Psychol.. 1994;13:371-372. Editorial.[Medline] [Order article via Infotrieve]
71.
Mallick H. Health hazards of obesity and weight control in children: a review of the literature. Am J Public Health. 1983;73:78-87.
72. US Dept of Health and Human Services. Physical Activity and Health: A Report of the Surgeon General. Atlanta, Ga: US Department of Health and Human Services, Centers for Disease Control and Prevention, National Center for Chronic Disease Prevention and Health Promotion, 1996.
73.
National Cholesterol Education Program. Report of the Expert Panel on Blood Cholesterol Levels in Children and Adolescents. Pediatrics. 1992;89:525-584.
74.
Klesges RC, Klesges LM, Haddock CK, Eck LH. A longitudinal analysis of the impact of dietary intake and physical activity on weight change in adults. Am J Clin Nutr. 1992;55:818-822.
75. Orlet-Fisher J, Birch L. Fat preferences and fat consumption of 3-5 year old children are related to parental adiposity. J Am Diet Assoc. 1995;95:759-764.[Medline] [Order article via Infotrieve]
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 American Heart Association, S. S. Gidding, B. A. Dennison, L. L. Birch, S. R. Daniels, M. W. Gilman, A. H. Lichtenstein, K. T. Rattay, J. Steinberger, N. Stettler, et al. Dietary Recommendations for Children and Adolescents: A Guide for Practitioners Pediatrics, February 1, 2006; 117(2): 544 - 559. [Abstract] [Full Text] [PDF]
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 Endorsed by the American Academy of Pediatrics, S. S. Gidding, B. A. Dennison, L. L. Birch, S. R. Daniels, M. W. Gilman, A. H. Lichtenstein, K. T. Rattay, J. Steinberger, N. Stettler, et al. Dietary Recommendations for Children and Adolescents: A Guide for Practitioners: Consensus Statement From the American Heart Association Circulation, September 27, 2005; 112(13): 2061 - 2075. [Abstract] [Full Text] [PDF]
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G. S. Boyd, J. Koenigsberg, B. Falkner, S. Gidding, and S. Hassink Effect of Obesity and High Blood Pressure on Plasma Lipid Levels in Children and Adolescents Pediatrics, August 1, 2005; 116(2): 442 - 446. [Abstract] [Full Text] [PDF]
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S. R. Daniels, D. K. Arnett, R. H. Eckel, S. S. Gidding, L. L. Hayman, S. Kumanyika, T. N. Robinson, B. J. Scott, S. St. Jeor, and C. L. Williams Overweight in Children and Adolescents: Pathophysiology, Consequences, Prevention, and Treatment Circulation, April 19, 2005; 111(15): 1999 - 2012. [Abstract] [Full Text] [PDF]
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 J. A. Nelson, M. A. Chiasson, and V. Ford Childhood Overweight in a New York City WIC Population Am J Public Health, March 1, 2004; 94(3): 458 - 462. [Abstract] [Full Text] [PDF]
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 J J Reilly, E Methven, Z C McDowell, B Hacking, D Alexander, L Stewart, and C J H Kelnar Health consequences of obesity Arch. Dis. Child., September 1, 2003; 88(9): 748 - 752. [Abstract] [Full Text] [PDF]
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Committee on Nutrition Prevention of Pediatric Overweight and Obesity Pediatrics, August 1, 2003; 112(2): 424 - 430. [Abstract] [Full Text] [PDF]
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 American Diabetes Association Management of Dyslipidemia in Children and Adolescents With Diabetes Diabetes Care, July 1, 2003; 26(7): 2194 - 2197. [Full Text] [PDF]
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M. S. Faith, A. Pietrobelli, C. Nuñez, M. Heo, S. B. Heymsfield, and D. B. Allison Evidence for Independent Genetic Influences on Fat Mass and Body Mass Index in a Pediatric Twin Sample Pediatrics, July 1, 1999; 104(1): 61 - 67. [Abstract] [Full Text]
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S. R. Daniels, J. A. Morrison, D. L. Sprecher, P. Khoury, and T. R. Kimball Association of Body Fat Distribution and Cardiovascular Risk Factors in Children and Adolescents Circulation, February 2, 1999; 99(4): 541 - 545. [Abstract] [Full Text] [PDF]
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S. S. Gidding, L. C. Bookstein, and E. V. Chomka Usefulness of Electron Beam Tomography in Adolescents and Young Adults With Heterozygous Familial Hypercholesterolemia Circulation, December 8, 1998; 98(23): 2580 - 2583. [Abstract] [Full Text] [PDF]
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 L. V. Horn Prevention of Coronary Artery Disease Is a Pediatric Problem JAMA, December 3, 1997; 278(21): 1779 - 1780. [Abstract] [PDF]
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