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Prevention of Childhood Obesity
Prevention in Primary Care
0031-3955/86 $0.00
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Prevention of Childhood Obesity William H. Dietz, Jr., M.D., Ph.D. *
Childhood obesity is among the most prevalent nutritional disorders affecting the pediatric population in the United States. The urgency of effective preventive programs is emphasized by three major arguments. First, the prevalence of obesity is increasing rapidly among children and adolescents in the United States. Second, obesity in childhood is accompanied by substantial morbidity. Third, few clinics in the United States are equipped to treat childhood obesity, treatment is based on traditional medical models, and existing approaches are ineffective given the magnitude of the problem in the pediatric population. In this article, we will consider the arguments that support the need for effective prevention of childhood obesity, the limitation of factors that identifY children and adolescents at risk for the development of childhood obesity, and practical suggestions for counseling families identified by these risk factors. Although the effectiveness of the preventive approaches proposed remains untested, these suggestions represent logical extensions of the current understanding of the disease. PREVALENCE Valid estimates of prevalence have been confounded by the lack of a standardized methodology to assess fatness and by the absence of representative studies of the pediatric population of the United States. Recently, we have examined data from four studies of children and adolescents representative of subjects of the same sex and age groups in the U.S. population. 12 Each study relied on a standardized measure of the triceps skinfold thickness to determine fatness. The studies included were the National Health Examination Survey (NHES) Cycle II, NHES Cycle III, the first National Health and Nutrition Examination Survey (NHANES I), and NHANES II. The NHES Cycle II examined approximately 7000 children aged 6 to 11 years between 1963 and 1965, the NHES Cycle III
*Assistant
Professor of Pediatrics, Tufts University School of Medicine; Director of Clinical Nutrition, New England Medical Center, Boston, Massachusetts
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Table 1. Morbid Aftereffects of Childhood Obesity Psychosocial dysfunction Orthopedic Blount"s disease Slipped capital femoral epiphysis Abnormal glucose tolerance Hypertension Abnormal cholesterol metabolism Elevated low-density lipoprotein Reduced high-density lipoprotein Persistence into adulthood Increased severity of adult disease Hypertension Diabetes mellitus Cholelithiasis Sudden death
examined approximately 7000 adolescents aged 12 to 17 years between 1966 and 1970, the NHANES I examined approximately 4000 children aged 6 to 17 years between 1971 and 1974, and the NHANES II examined approximately 4000 children aged 6 to 17 years between 1966 and 1980. Obesity was defined as a triceps skinfold thickness greater than or equal to the 85th percentile among children and adolescents studied in the NHES Cycle II and the NHES Cycle Hp6 The same skinfold definition of obesity then was used to determine the prevalence of obesity among children and adolescents of the same age and sex in the NHANES I and the NHANES
H. During the 15-year period encompassed by these surveys, the prevalence of obesity increased from approximately 18 per cent to 30 per cent in 6- to ll-year-old males and from approximately 17 per cent to 25 per cent in 6- to ll-year-old females. The prevalence in 12- to 17-year-old adolescent males increased from 15 per cent to 18 per cent, and in 12- and 17-year-old female adolescents from 16 per cent to 25 per cent. Although the prevalence of obesity is greater in whites, the increases in prevalence were substantially greater in black children and adolescents. These data indicate that obesity has become a major disease among children and adolescents in the United States. Clearly, a disease that affects 25 per cent to 30 per cent of the population requires effective prevention as well as comprehensive therapy. AFTEREFFECTS The principal aftereffects of obesity are shown in Table 1. The most prevalent of these is a psychosocial one. Preschoolers consistently rank obese children among those they least want to befriend,37 and the epithets directed at overweight children by their elementary school peers are well known. Although administration of the Piers-Harris questionnaire to elementary school failed to reveal differences in self-esteem among obese school children (W. H. Dietz, unpublished observations), by adolescence
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the cultural messages become internalized, and produce a distorted selfimage that persists into adulthood. 38 The cultural messages regarding obesity are reinforced by the portrayal of obesity on television. Few prime time stars are obese 27 despite a rising prevalence of the disease in the population. Furthermore, obese characters on television frequently are portrayed as humorous characters or buffoons. Despite an increased prevalence of obesity among whites, 90 per cent of the obese on television are black. The orthopedic complications of obesity are well recognized. Seventyfive per cent of patients affected by Blount's disease and slipped capital femoral epiphysis are obese. 5• 16 Obesity poses a significant cardiovascular risk factor for affected children and adolescents. The principal intervening complications are abnormal glucose tolerance, hypertension, and abnormal lipoprotein metabolism. Abnormal glucose tolerance appears to depend on the degree of obesity. Type II diabetes mellitus is rare in children and adolescents. In adults, however, obesity accounts for approximately 25 per cent of all cases of Type II diabetes.1O Obesity is the leading cause of sustained hypertension in children and adolescents. 28. 33 Approximately 25 per cent of obese hypertensive adolescents may suffer cerebrovascular or cardiovascular complications of hypertension within 7 years. 26 Approximately 30 per cent of adult hypertension is attributable to obesity.1O Obesity in children is associated with elevated low-density lipoprotein levels and reduced highdensity lipoprotein levels. 28. 40 In adults, increased cholesterol turnoVerl may be responsible for an increased frequency of cholelithiasis among the obese. 21 A final risk is that obesity in adolescents may persist into adulthood. This risk appears to be associated with the onset of obesity in late childhood or adolescence and is probably directly increased by the severity of the disease. 8 Adults that are obese as adolescents tend to be affected even more severely as adults. Fifty to seventy-five per cent of adults whose weight exceeds 160 per cent of ideal body weight were obese as children. 35 The prevalence of sudden death was approximately 25 per cent among young adult men whose weight was 200 per cent of ideal, most of whom were probably obese in adolescence. 17 Although the majority of aftereffects of childhood and adolescent obesity occur in adulthood, these data emphasize that obesity in childhood may be associated with significant disease. Furthermore, the effective prevention and treatment of obesity in children and adolescents may prevent severe adult obesity and its attendant morbidity and mortality. liMITATIONS OF THERAPY The therapy of childhood obesity has been notably unsuccessful. By 1983, data that examined therapeutic outcome were available from seven studies of a total of 162 children and adolescents treated with a variety of interventions. 9 The programs generally required a 3-month treatment period and utilized the services of two or more health professionals. A
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mean of 40 per cent of the subjects lost less than 2.4 kg, and a mean of 41 per cent lost more than 5 kg. These results probably overestimate shortterm weight losses because many of the interventions were comparative trials of one therapeutic modality and involved sample subjects biased by their willingness to participate. Fewer than 20 per cent of patients presenting to a weight reduction clinic lost more than 5 kg.9 Two observations suggest that family factors that affect the onset of obesity also may affect its course. Rates of weight loss in obese children between 7 and 13 years of age were independently affected by parental obesity and marital status. 9 Children who had one or both obese parents, and children whose parents were divorced or separated, lost weight at significantly lower rates than did children of normal weight or married parents. Additional data suggest that a weight reduction program that involves a mother and child is more successful than one that treats each member of the dyad separately. 4 These observations suggest that therapy for unselected patients is not only of limited value but is not likely to be cost effective. Second, the observation that family variables associated with onset also are associated with outcome suggests that causes of the onset of childhood obesity also may be associated with the response to therapy. Both observations emphasize that a focus on the family is the logical source of preventive efforts. RISK FACTORS
Multiple epidemiologic studies have demonstrated strong and consistent associations of childhood and adolescent obesity with variables in the physical, social, and family environment. Each of these will be considered in turn. Physical Environment Using NHES Cycle II data, we have recently shown that the prevalence of obesity is strongly influenced by season, region, and population density. 14 As shown in Figure 1, the prevalence of obesity is greatest in the northeast region of the United States, followed in descending order by the midwest, south, and west. Although the Northeast was not surveyed in winter, within each of the other regions, the prevalence of obesity was increased in the winter and spring, and was decreased in the summer and fall. The prevalence of obesity in densely populated urban areas was significantly greater than the prevalence observed in rural or suburban settings. Each variable within the physical environment caused twofold to threefold variations in prevalence when each of the other two variables was controlled. Despite the powerful effects of variables within the physical environment on the prevalence of childhood obesity, the intervening behavioral determinants remain unclear. Region, season, and population density all could affect the consumption of low caloric density foods such as fruit or vegetables by their effect on price or availability. Each also could affect activity patterns. Likewise, differences in ethnic distribution might alter the prevalence of obesity. For example, in adults, the prevalence of obesity
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30
Winter
DSpring ~Summer IlllllimFal1
o NORTHEAST
MIDWEST
SOUTH
WEST
REGION
Figure 1. Effect of region and season on the prevalence of obesity in 6- to ll-year-old children in the United States. Number under each bar represents number of children sampled in each region. (From Am. J. Clin. Nutr., 39:622, 1984; with permission.)
appears increased among recent immigrants, but decreases to the level present in the general population after three generations. 25 Social Environment Among children and adolescents, the effects of socioeconomic class and education consistently affect the prevalence of obesity. 130th level of education and income are directly related to obesity in black and white children of both sexes. 22 Women provide a notable exception: upper class women are leaner than those in lower socioeconomic categories. 24 Family Environment Variables within the family environment appear to be the most important determinants of childhood obesity. These are shown in Table 2. Parental obesity is a well-recognized risk factor for childhood obesity. Overall, the correlation of parental fatness with the fatness of offspring is r = 0.25. 24 The risk of obesity (defined by triceps skinfold thickness) has a direct relationship to the fatness category of the parent, however. The risk is lowest when both parents are lean, greater when one parent is obese (defined by skinfold thickness), and greatest when both parents are obese. 24 The resemblance in fatness between parents and children has been interpreted as evidence that obesity is inherited. The heritability of fatness has been demonstrated clearly by twin studies that show that the fatness Table 2. Family Variables Associated with Childhood Obesity Parental obesity Socioeconomic class Parental education Parental age Birth order Family size
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in monozygotic twins is more comparable than fatness in dizygotic twins. 2 Studies of adoptees have emphasized the importance of the family environment, however. For example, triceps skinfold measurements of biologic parent-child pairs were comparable to those observed in adoptive combinations. 23 In the most recent study of adoptees,39 a significant trend was observed in body mass index (used as a measure of fatness) between biologic parent-child pairs, whereas no significant trend existed among adoptive parent-child pairs. Careful inspection of the data presented in this study, however, indicates that the significance of the trends was based on the similarity in body mass index in the lean biologic parent-child pairs. No significant difference existed in the prevalence of obesity among biologic or adoptive parents when the examination was limited to the most obese adoptees. Furthermore, heritability does not explain the significant association of fatness in spouses,24 nor in most cases does heritability explain the resemblance in fatness between pets and their owners. 29 Most of the remaining family variables found in association with childhood obesity were derived from studies biased by small samples sizes, that failed to control for confounding variables, or studies that did not provide representative samples of the population of the United States. Use of the NHES and HANES surveys gave us the opportunity to examine these associations in a large population representative of the pediatric population of the United States, and one in which the effect of potentially confounding variables could be controlled. 14 Our studies clearly demonstrated that the prevalence of obesity was inversely proportional to family size. These data therefore confirm the previous observation that obesity is most prevalent among single children. 34 In addition, younger children are at greater risk of obesity than older children. Our findings also confirmed that education and socioeconomic class were related directly to the prevalence of obesity. Each of these effects remained significant after controlling for other variables. Television Viewing Next to the family; television is the most important determinant of child development. Recent Neilsen ratings indicate that children aged 6 to 11 years watch approximately 26 hours of television per week, and that children aged 12 to 17 years watch approximately 22 hours week. 30 We have shown that in both NHES Cycle II and Cycle III, time spent watching television was related directly to the risk of obesity. IS Among the 2000 children studied during Cycle II who were again studied during Cycle III, television viewing was the most important predictor of obesity in adolescence, after prior obesity was controlled. Furthermore, the association persisted after subsequent controls for region, season, population density, socioeconomic class, and time spent in other leisure activities were introduced. These observations suggest a causal relationship between television viewing and obesity. The observation was confirmed by the prospective and two cross-sectional studies that were performed. A dose-response effect was demonstrated: the more television that was Viewed, the greater the risk of obesity. The association between television viewing and obesity was
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statistically significant and persisted when potentially confounding variables were controlled. Finally, a logical mechanism exists to explain the observation. Obviously, children who view television are not involved in more energy-intensive activities. Children who view increased amounts of television are more likely to snack while watching television, and to consume those foods advertised on television. 6 • 18 Foods advertised on television have an increased caloric density. 1 Food consumption by televised characters during programs occurs with high frequency,27 and the absence of obese characters may convey the implicit message to children that it is possible to eat constantly without a risk of obesity. PREVENTION
The high and increasing prevalence of childhood obesity, the morbidity of its aftereffects, and the limited success of current therapy suggest that prevention may be the most cost-effective approach for dealing with this problem. The factors associated with obesity help to identify patients at risk. Unfortunately, the behaviors that link the recognized risk factors for childhood obesity to the disease remain unspecified. Nonetheless, we will consider logical interventions aimed at children in families at risk for the development of obesity, and at children in the United States. Interventions Within the Family Tolerance is the most important tenet in dealing with children in families in which one or both parents are obese. Obese adults already have been sensitized to the stigma of their weight and are hypersensitive to the attitudes of those who care for them and their children. Pediatricians and other physicians are not immune to the cultural biases of our society. Prevention therefore must begin with a sympathetic understanding of the problem faced by obese parents for effective counseling about obesity in their children. The two most important areas to consider are those of diet and activity patterns. Examination of growth charts of those children who become obese reveals that weight gains are rarely greater than 5 lbs anually in excess of that expected for age (W. H. Dietz, unpublished observations). Such gains can be accounted for by a caloric imbalance of approximately 50 kcal per day. These observations suggest that the image of the obese child consuming huge quantities of excess calories may be a stereotype used to categorize obese persons as socially deviant and to justify the widespread discrimination against them. These observations also justify the pediatric practitioner's attention to what otherwise might be considered trivial sources of energy imbalance, such as calorically dense snacks or time spent viewing television. In general, the most practical dietary advice is to reduce the quantity of fat in the diet to approximately 35 per cent of total calories. 7 Although the quantity of dietary fat has not yet been linked in a prospective fashion to the development of obesity in any age group, the justification for this approach is twofold. First, because the caloric equivalent of fat is 9 kcalJ gm, and that of carbohydrate is 4 kcal per gm, fat is more calorically dense
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than carbohydrate. The increased bulk accompanying carbohydrate ingestion therefore may produce greater satiety than an isocaloric quantity of fat. Second, the energy cost of converting dietary fat to adipose tissue stores is approximately 5 per cent of the energy contained in the ingested fat, whereas the cost of converson of dietary carbohydrate to adipose tissue is approximately 25 per cent of the energy contained in the carbohydrate. 19 This argument suggests that, gram for gram, the ingestion of fat may be more fattening than the ingestion of carbohydrate. Reductions in dietary fat can readily be achieved by consuming low-fat rather than whole milk, trimming fat from meat, serving low-fat meats such as lean roast beef, fish, or turkey, rather than bacon, pork, bologna, or ham, low-fat mayonnaise, and reducing butter or eliminating butter, margarine, and gravy. Seasonal variations in the intake of foods of low caloric density, such as fruits and vegetables, may help to explain the regional and seasonal variations in prevalence. Increased use of low caloric density foods as snacks therefore may be a relevant preventive measure. As outlined above, television viewing may represent one cause of childhood obesity. Parents should be counseled regarding the quantity of television viewed daily and the consumption of calorically dense foods advertised on television, such as sugared breakfast cereals. Although sugared and nonsugared breakfast cereals contain similar quantities of calories on an ounce-for-ounce basis, cereal rarely is consumed by the ounce. Because sugared breakfast cereals are more calorically dense, a bowl of sugared breakfast cereal will contain more calories than will a bowl of its nonsugared counterpart. 11 Reductions in television viewing have the potential not only to decrease the consumption of calorically dense foods, but also to increase the likelihood that time will be spent engaged in more energy-intensive activities. Parents should be counseled accordingly. Interventions Within the Community The power of community-based interventions to treat obesity has been demonstrated aptly by a school-based approach to weight reduction. 3 In this study, a program of behavior modification, nutrition education, and physical activity, introduced by a program involving parents, teachers, food service personnel, school administrators, the nurse's aide, and the physical education instructor, induced weight loss in 95 per cent of the children involved in the program. Interventions at the community level to prevent obesity have not been attempted. Two significant problems currently limit this approach. First, the mechanisms by which the environmental correlates affect onset and prevalence are not clear; however, a focus on food consumption and activity patterns during the winter months, when the prevalence of obesity rises, appears to be an appropriate area for counseling. Second, there exists a risk that a community or nationally based program of prevention could further stigmatize the already obese person. An increased awareness of the role of small caloric imbalances in the genesis of obesity, and refutation of the notion that obese persons become so by massive overeating may be a useful intervention at the community level. The widespread publicity given
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the recent report of the association of television viewing and obesity may itself represent an effctive intervention. Equally important are community-based programs aimed at increasing physical activity. In an era when budget cutbacks threaten extracurricular activities at all levels of the school system, the development of such programs will not be an easy task. Nonetheless, physical activity is inversely related to the prevalence of obesity. In fall and winter, activity decreases, whereas in the spring and summer activity increases. 32 Therefore, school programs to increase activity in the winter appear logical interventions to prevent the onset of obesity. Furthermore, less than 50 per cent of physical education classes in the schools are devoted to activities that can be continued into adulthood. 32 Increased exposure to lifetime physical activities in school-aged children may produce increased activity in later life, thereby preventing the onset of adult disease. A second community-based approach is to pass legislation that bans advertising directed at children. The market for sugared breakfast cereals would not exist without television advertising. Although prior attempts have been made to ban advertising directed at children, based on the difficulties children have distinguishing commercials from programming, such an approach is not likely to be successful in the current deregulatory climate. Nonetheless, foods advertised on television may provide the small increments in caloric imbalance necessary to produce obesity. A final aproach that may reduce the prevalence of obesity in the community but also promote dietary behaviors that reduce other cardiovascular risk factors is promotion of the dietary guidelines for the United States. 7 These guidelines include a reduction in dietary fat intake to 35 per cent of total calories. As discussed above, reduced fat intake may be a logical and easy means to prevent obesity.
SUMMARY The increasing prevalence of childhood obesity, its attendant morbidity, and the limited success of therapy mandate increased attention to preventive approaches. Environmental and family variables serve to identifY families with children at risk for the development of obesity. Although the behavioral correlates that link these risk factors to childhood obesity remain unclear, inactivity and increased dietary intake of fat appear at this time to be the most logical foci for preventive interventions. Television viewing, which promotes both increased food consumption and reduced activity, represents a major concern at which counseling should be directed.
REFERENCES 1. Barcus, E. F., and McLaughlin, L.: Food Advertising on Children's Television: An Analysis of Appeals and Nutritional Content. Newtonville, Massachusetts, Action for Children's Television, 1978.
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2. Borjeson, M.: The etiology of obesity in children: a study of 101 twin pairs. Acta Paediatr. Scand., 65:279-287, 1976. 3. Brownell, K. D., and Kaye, F. S.: A school-based behavior modification, nutrition education, and physical activity program for obese children. Am. J. Clin. Nutr., 35:277283, 1982. 4. Brownell, K. D., Kelman, J. H., and Stunkard, A. M.: Treatment of obese children with and without their mothers: changes in weight and blood pressure. Pediatrics, 71:515523, 1983. 5. Chung, S.: Diseases of the developing hip joint. Ped. Clin. North Am., 24:857-870, 1977. 6. Clancy-Hepburn, K., Hickey, A. A., and Nevill, G.: Children's behavior responses to TV food advertisements. J. Nutr. Ed., 6:93-96, 1974. 7. Committee on Dietary Allowances of the Food and Nutrition Board. Recommended Dietary Allowances. Washington, D.C., National Academy of Sciences, 1980, pp. 3537. 8. Dietz, W. H.: Childhood obesity: Susceptibility, cause and management. J. Pediatr., 103:676-686, 1983. 9. Dietz, W. H., Jr.: Family characteristics affect rates of weight loss in obese children. Nutr. Res., 3:43-50, 1983. 10. Dietz, W. H.: Obesity. In Chandra, R. (ed.): Precursors of Adult Disease in Pediatric Patients. Ross Laboratories, 1983, pp. 24-29. 11. Dietz, W. H., and Curatalo, P.: Energy per serving of sugared and unsugared cereals. J. N utr. Ed., 15:84, 1983. 12. Dietz, W. H., Gortmaker, S. L., Sobol, A. M., et al.: Trends in the prevalence of childhood and adolescent obesity in the United States. Pediatr. Res., 19:198A, 1985. 13. Dietz, W. H., and Gortmaker, S. L.: Factors within the physical environment associated with childhood obesity. Am. J. Clin. Nutr., 39:619-624, 1984. 14. Dietz, W. H., and Gortmaker, S. L.: Epidemiologic variables associated with childhood obesity. J. Am. Coli. Nutr., 3:267, 1984. 15. Dietz, W. H., and Gortmaker, S. L.: Do we fatten our children at the TV set? Television viewing and obesity in children and adolescents. Pediatrics, 75:807-812. 16. Dietz, W. H., Jr., Gross, W. L., and Kirkpatrick, J. A., Jr.: Blount disease (tibia vara): Another skeletal disorder associated with childhood obesity. J. Pediatr., 101:735-737, 1982. 17. Drenick, E. J., Bale, G. S., Seltzer, F., et al.: Excessive mortality and causes of death in morbidly obese men. J.A.M.A., 243:443-445, 1980. 18. Dussere, S. A.: The Effects of Television Advertising on Children's Eating Habits (Master's thesis). Amherst, Massachusetts, University of Massachusetts, 1976. 19. Flatt, J. P.: The biochemistry of energy expenditure. In Bray, G.: Recent advances in obesity research: II, London, Newman Publishing 1978, pp. 211-228. 20. Freedman, D. S., Burke, G. L., Harsha, D. W., et al.: Relationship of changes in obesity to serum lipid and lipoprotein changes in childhood and adolescence. J.A. M.A., 254:515-520, 1985. 21. Friedman, G. D., Kannel, W. B., and Dawber, T. R.: The epidemiology of gallbladder disease: Observations in the Framingham study. J. Chron. Dis., 19:273-292, 1966. 22. Gam, S. M., Bailey, S. M., Cole, P. E., et al.: Level of education, level of income, and level offatness in adults. Am. J. Clin. Nutr., 30:721-727, 1976. 23. Gam, S. M., Bailey, S. M., and Higgins, I. T.: Fatness similarities in adopted pairs. Am. J. Clin. Nutr., 29:1067, 1976. 24. Gam, S. M., and Clark, D. C.: Trends in fatness and the origins of obesity. Pediatrics, 57:443-456, 1976. 25. Goldblatt, P. B., Moore, M. E., and Stunkard, A. J.: Social factors in obesity. J.A.M.A., 192:97-100, 1965. 26. Heyden, S., Berte!, A. G., Hanes, C. G., et al.: Elevated blood pressure levels in adolescents, Evans County, Georgia. J.A.M.A., 209:1683-1689, 1969. 27. Kaufman, L.: Prime-time nutrition. J. Comm., 30:37-46, 1980. 28. Lauer, R. M., Connor, W. E., Reiter, M. A., et al.: Coronary heart disease risk factors in school children: The Muscatine study. J. Pediatr., 86:697-706, 1975. 29. Mason, E.: Obesity in pet dogs. Vet. Rec., 86:612-616, 1970. 30. Neilsen Company: 1985 Neilsen Report on Television. Chicago, A.C. Neilsen, 1985.
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31. Nestel, P. J., Schreibman, P. H., and Ahrens, E. J., Jr.: Cholesterol metabolism in human obesity. J. Clin. Invest., 52:2389-2397, 1973. 32. Office of Disease Prevention and Health Prevention: The National Children and Growth Fitness Study. Washington, U.S. Department of Health and Human Services, 1985, pp. 1-48. 33. Rames, L. K., Clarke, W. R., Connor, W. E., et al.: Normal blood pressures and the evaluation of sustained blood pressure elevation in childhood: The Muscatine stl1dy. Pediatrics, 61:245-251, 1978. 34. Ravelli, G. P., and Belmont, L.: Obesity in nineteen-year-old men: Family size and birth order associations. Am. J. Epidemio!', 109:66-70, 1979. 35. Rimm, 1. J., and Rimm, A. A.: Association between juvenile-onset obeSity and severe adult obesity in 73,532 women. Am. J. Public Health, 66:479:481, 1976. 36. Seltzer, C., and Mayer, J.: Simple criterion of obesity. Postgrad. Med. J., 38:A101-A108, 1965. . 37. Staffieri, J. R.: A study of social stereotype of body image in children. J. Pers. Soc. Psycho!., 7:101-104, 1967. 38. Stunkard, A., and Mendelson, M;: Obesity and the body image. 1. Characteristics of disturbances in the body image of some obese persons. Am. J. Psychiatr., 123:12961300, 1967. 39. Stunkard, A. J., Sorensen, T. 1. A., Hanes, C., et al.: An adoption study of human obesity. N. Eng!. J. Med., 314:193-198, 1986. 40. Voors, A. W., Harsha, D. W., Webber, L. S., et al.: Clustering of anthropometric parameters, glucose tolerance, and serum lipids in children with high and low B- and pre-B-lipoproteins. Arteriosclerosis, 2:346-355, 1982. New England Medical Center Box 213 171 Harrison Avenue Boston, Massachusetts 02111
0031-3955/86 $0.00
+ .20
Prevention of Childhood Obesity William H. Dietz, Jr., M.D., Ph.D. *
Childhood obesity is among the most prevalent nutritional disorders affecting the pediatric population in the United States. The urgency of effective preventive programs is emphasized by three major arguments. First, the prevalence of obesity is increasing rapidly among children and adolescents in the United States. Second, obesity in childhood is accompanied by substantial morbidity. Third, few clinics in the United States are equipped to treat childhood obesity, treatment is based on traditional medical models, and existing approaches are ineffective given the magnitude of the problem in the pediatric population. In this article, we will consider the arguments that support the need for effective prevention of childhood obesity, the limitation of factors that identifY children and adolescents at risk for the development of childhood obesity, and practical suggestions for counseling families identified by these risk factors. Although the effectiveness of the preventive approaches proposed remains untested, these suggestions represent logical extensions of the current understanding of the disease. PREVALENCE Valid estimates of prevalence have been confounded by the lack of a standardized methodology to assess fatness and by the absence of representative studies of the pediatric population of the United States. Recently, we have examined data from four studies of children and adolescents representative of subjects of the same sex and age groups in the U.S. population. 12 Each study relied on a standardized measure of the triceps skinfold thickness to determine fatness. The studies included were the National Health Examination Survey (NHES) Cycle II, NHES Cycle III, the first National Health and Nutrition Examination Survey (NHANES I), and NHANES II. The NHES Cycle II examined approximately 7000 children aged 6 to 11 years between 1963 and 1965, the NHES Cycle III
*Assistant
Professor of Pediatrics, Tufts University School of Medicine; Director of Clinical Nutrition, New England Medical Center, Boston, Massachusetts
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Table 1. Morbid Aftereffects of Childhood Obesity Psychosocial dysfunction Orthopedic Blount"s disease Slipped capital femoral epiphysis Abnormal glucose tolerance Hypertension Abnormal cholesterol metabolism Elevated low-density lipoprotein Reduced high-density lipoprotein Persistence into adulthood Increased severity of adult disease Hypertension Diabetes mellitus Cholelithiasis Sudden death
examined approximately 7000 adolescents aged 12 to 17 years between 1966 and 1970, the NHANES I examined approximately 4000 children aged 6 to 17 years between 1971 and 1974, and the NHANES II examined approximately 4000 children aged 6 to 17 years between 1966 and 1980. Obesity was defined as a triceps skinfold thickness greater than or equal to the 85th percentile among children and adolescents studied in the NHES Cycle II and the NHES Cycle Hp6 The same skinfold definition of obesity then was used to determine the prevalence of obesity among children and adolescents of the same age and sex in the NHANES I and the NHANES
H. During the 15-year period encompassed by these surveys, the prevalence of obesity increased from approximately 18 per cent to 30 per cent in 6- to ll-year-old males and from approximately 17 per cent to 25 per cent in 6- to ll-year-old females. The prevalence in 12- to 17-year-old adolescent males increased from 15 per cent to 18 per cent, and in 12- and 17-year-old female adolescents from 16 per cent to 25 per cent. Although the prevalence of obesity is greater in whites, the increases in prevalence were substantially greater in black children and adolescents. These data indicate that obesity has become a major disease among children and adolescents in the United States. Clearly, a disease that affects 25 per cent to 30 per cent of the population requires effective prevention as well as comprehensive therapy. AFTEREFFECTS The principal aftereffects of obesity are shown in Table 1. The most prevalent of these is a psychosocial one. Preschoolers consistently rank obese children among those they least want to befriend,37 and the epithets directed at overweight children by their elementary school peers are well known. Although administration of the Piers-Harris questionnaire to elementary school failed to reveal differences in self-esteem among obese school children (W. H. Dietz, unpublished observations), by adolescence
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the cultural messages become internalized, and produce a distorted selfimage that persists into adulthood. 38 The cultural messages regarding obesity are reinforced by the portrayal of obesity on television. Few prime time stars are obese 27 despite a rising prevalence of the disease in the population. Furthermore, obese characters on television frequently are portrayed as humorous characters or buffoons. Despite an increased prevalence of obesity among whites, 90 per cent of the obese on television are black. The orthopedic complications of obesity are well recognized. Seventyfive per cent of patients affected by Blount's disease and slipped capital femoral epiphysis are obese. 5• 16 Obesity poses a significant cardiovascular risk factor for affected children and adolescents. The principal intervening complications are abnormal glucose tolerance, hypertension, and abnormal lipoprotein metabolism. Abnormal glucose tolerance appears to depend on the degree of obesity. Type II diabetes mellitus is rare in children and adolescents. In adults, however, obesity accounts for approximately 25 per cent of all cases of Type II diabetes.1O Obesity is the leading cause of sustained hypertension in children and adolescents. 28. 33 Approximately 25 per cent of obese hypertensive adolescents may suffer cerebrovascular or cardiovascular complications of hypertension within 7 years. 26 Approximately 30 per cent of adult hypertension is attributable to obesity.1O Obesity in children is associated with elevated low-density lipoprotein levels and reduced highdensity lipoprotein levels. 28. 40 In adults, increased cholesterol turnoVerl may be responsible for an increased frequency of cholelithiasis among the obese. 21 A final risk is that obesity in adolescents may persist into adulthood. This risk appears to be associated with the onset of obesity in late childhood or adolescence and is probably directly increased by the severity of the disease. 8 Adults that are obese as adolescents tend to be affected even more severely as adults. Fifty to seventy-five per cent of adults whose weight exceeds 160 per cent of ideal body weight were obese as children. 35 The prevalence of sudden death was approximately 25 per cent among young adult men whose weight was 200 per cent of ideal, most of whom were probably obese in adolescence. 17 Although the majority of aftereffects of childhood and adolescent obesity occur in adulthood, these data emphasize that obesity in childhood may be associated with significant disease. Furthermore, the effective prevention and treatment of obesity in children and adolescents may prevent severe adult obesity and its attendant morbidity and mortality. liMITATIONS OF THERAPY The therapy of childhood obesity has been notably unsuccessful. By 1983, data that examined therapeutic outcome were available from seven studies of a total of 162 children and adolescents treated with a variety of interventions. 9 The programs generally required a 3-month treatment period and utilized the services of two or more health professionals. A
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mean of 40 per cent of the subjects lost less than 2.4 kg, and a mean of 41 per cent lost more than 5 kg. These results probably overestimate shortterm weight losses because many of the interventions were comparative trials of one therapeutic modality and involved sample subjects biased by their willingness to participate. Fewer than 20 per cent of patients presenting to a weight reduction clinic lost more than 5 kg.9 Two observations suggest that family factors that affect the onset of obesity also may affect its course. Rates of weight loss in obese children between 7 and 13 years of age were independently affected by parental obesity and marital status. 9 Children who had one or both obese parents, and children whose parents were divorced or separated, lost weight at significantly lower rates than did children of normal weight or married parents. Additional data suggest that a weight reduction program that involves a mother and child is more successful than one that treats each member of the dyad separately. 4 These observations suggest that therapy for unselected patients is not only of limited value but is not likely to be cost effective. Second, the observation that family variables associated with onset also are associated with outcome suggests that causes of the onset of childhood obesity also may be associated with the response to therapy. Both observations emphasize that a focus on the family is the logical source of preventive efforts. RISK FACTORS
Multiple epidemiologic studies have demonstrated strong and consistent associations of childhood and adolescent obesity with variables in the physical, social, and family environment. Each of these will be considered in turn. Physical Environment Using NHES Cycle II data, we have recently shown that the prevalence of obesity is strongly influenced by season, region, and population density. 14 As shown in Figure 1, the prevalence of obesity is greatest in the northeast region of the United States, followed in descending order by the midwest, south, and west. Although the Northeast was not surveyed in winter, within each of the other regions, the prevalence of obesity was increased in the winter and spring, and was decreased in the summer and fall. The prevalence of obesity in densely populated urban areas was significantly greater than the prevalence observed in rural or suburban settings. Each variable within the physical environment caused twofold to threefold variations in prevalence when each of the other two variables was controlled. Despite the powerful effects of variables within the physical environment on the prevalence of childhood obesity, the intervening behavioral determinants remain unclear. Region, season, and population density all could affect the consumption of low caloric density foods such as fruit or vegetables by their effect on price or availability. Each also could affect activity patterns. Likewise, differences in ethnic distribution might alter the prevalence of obesity. For example, in adults, the prevalence of obesity
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30
Winter
DSpring ~Summer IlllllimFal1
o NORTHEAST
MIDWEST
SOUTH
WEST
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Figure 1. Effect of region and season on the prevalence of obesity in 6- to ll-year-old children in the United States. Number under each bar represents number of children sampled in each region. (From Am. J. Clin. Nutr., 39:622, 1984; with permission.)
appears increased among recent immigrants, but decreases to the level present in the general population after three generations. 25 Social Environment Among children and adolescents, the effects of socioeconomic class and education consistently affect the prevalence of obesity. 130th level of education and income are directly related to obesity in black and white children of both sexes. 22 Women provide a notable exception: upper class women are leaner than those in lower socioeconomic categories. 24 Family Environment Variables within the family environment appear to be the most important determinants of childhood obesity. These are shown in Table 2. Parental obesity is a well-recognized risk factor for childhood obesity. Overall, the correlation of parental fatness with the fatness of offspring is r = 0.25. 24 The risk of obesity (defined by triceps skinfold thickness) has a direct relationship to the fatness category of the parent, however. The risk is lowest when both parents are lean, greater when one parent is obese (defined by skinfold thickness), and greatest when both parents are obese. 24 The resemblance in fatness between parents and children has been interpreted as evidence that obesity is inherited. The heritability of fatness has been demonstrated clearly by twin studies that show that the fatness Table 2. Family Variables Associated with Childhood Obesity Parental obesity Socioeconomic class Parental education Parental age Birth order Family size
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in monozygotic twins is more comparable than fatness in dizygotic twins. 2 Studies of adoptees have emphasized the importance of the family environment, however. For example, triceps skinfold measurements of biologic parent-child pairs were comparable to those observed in adoptive combinations. 23 In the most recent study of adoptees,39 a significant trend was observed in body mass index (used as a measure of fatness) between biologic parent-child pairs, whereas no significant trend existed among adoptive parent-child pairs. Careful inspection of the data presented in this study, however, indicates that the significance of the trends was based on the similarity in body mass index in the lean biologic parent-child pairs. No significant difference existed in the prevalence of obesity among biologic or adoptive parents when the examination was limited to the most obese adoptees. Furthermore, heritability does not explain the significant association of fatness in spouses,24 nor in most cases does heritability explain the resemblance in fatness between pets and their owners. 29 Most of the remaining family variables found in association with childhood obesity were derived from studies biased by small samples sizes, that failed to control for confounding variables, or studies that did not provide representative samples of the population of the United States. Use of the NHES and HANES surveys gave us the opportunity to examine these associations in a large population representative of the pediatric population of the United States, and one in which the effect of potentially confounding variables could be controlled. 14 Our studies clearly demonstrated that the prevalence of obesity was inversely proportional to family size. These data therefore confirm the previous observation that obesity is most prevalent among single children. 34 In addition, younger children are at greater risk of obesity than older children. Our findings also confirmed that education and socioeconomic class were related directly to the prevalence of obesity. Each of these effects remained significant after controlling for other variables. Television Viewing Next to the family; television is the most important determinant of child development. Recent Neilsen ratings indicate that children aged 6 to 11 years watch approximately 26 hours of television per week, and that children aged 12 to 17 years watch approximately 22 hours week. 30 We have shown that in both NHES Cycle II and Cycle III, time spent watching television was related directly to the risk of obesity. IS Among the 2000 children studied during Cycle II who were again studied during Cycle III, television viewing was the most important predictor of obesity in adolescence, after prior obesity was controlled. Furthermore, the association persisted after subsequent controls for region, season, population density, socioeconomic class, and time spent in other leisure activities were introduced. These observations suggest a causal relationship between television viewing and obesity. The observation was confirmed by the prospective and two cross-sectional studies that were performed. A dose-response effect was demonstrated: the more television that was Viewed, the greater the risk of obesity. The association between television viewing and obesity was
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statistically significant and persisted when potentially confounding variables were controlled. Finally, a logical mechanism exists to explain the observation. Obviously, children who view television are not involved in more energy-intensive activities. Children who view increased amounts of television are more likely to snack while watching television, and to consume those foods advertised on television. 6 • 18 Foods advertised on television have an increased caloric density. 1 Food consumption by televised characters during programs occurs with high frequency,27 and the absence of obese characters may convey the implicit message to children that it is possible to eat constantly without a risk of obesity. PREVENTION
The high and increasing prevalence of childhood obesity, the morbidity of its aftereffects, and the limited success of current therapy suggest that prevention may be the most cost-effective approach for dealing with this problem. The factors associated with obesity help to identify patients at risk. Unfortunately, the behaviors that link the recognized risk factors for childhood obesity to the disease remain unspecified. Nonetheless, we will consider logical interventions aimed at children in families at risk for the development of obesity, and at children in the United States. Interventions Within the Family Tolerance is the most important tenet in dealing with children in families in which one or both parents are obese. Obese adults already have been sensitized to the stigma of their weight and are hypersensitive to the attitudes of those who care for them and their children. Pediatricians and other physicians are not immune to the cultural biases of our society. Prevention therefore must begin with a sympathetic understanding of the problem faced by obese parents for effective counseling about obesity in their children. The two most important areas to consider are those of diet and activity patterns. Examination of growth charts of those children who become obese reveals that weight gains are rarely greater than 5 lbs anually in excess of that expected for age (W. H. Dietz, unpublished observations). Such gains can be accounted for by a caloric imbalance of approximately 50 kcal per day. These observations suggest that the image of the obese child consuming huge quantities of excess calories may be a stereotype used to categorize obese persons as socially deviant and to justify the widespread discrimination against them. These observations also justify the pediatric practitioner's attention to what otherwise might be considered trivial sources of energy imbalance, such as calorically dense snacks or time spent viewing television. In general, the most practical dietary advice is to reduce the quantity of fat in the diet to approximately 35 per cent of total calories. 7 Although the quantity of dietary fat has not yet been linked in a prospective fashion to the development of obesity in any age group, the justification for this approach is twofold. First, because the caloric equivalent of fat is 9 kcalJ gm, and that of carbohydrate is 4 kcal per gm, fat is more calorically dense
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than carbohydrate. The increased bulk accompanying carbohydrate ingestion therefore may produce greater satiety than an isocaloric quantity of fat. Second, the energy cost of converting dietary fat to adipose tissue stores is approximately 5 per cent of the energy contained in the ingested fat, whereas the cost of converson of dietary carbohydrate to adipose tissue is approximately 25 per cent of the energy contained in the carbohydrate. 19 This argument suggests that, gram for gram, the ingestion of fat may be more fattening than the ingestion of carbohydrate. Reductions in dietary fat can readily be achieved by consuming low-fat rather than whole milk, trimming fat from meat, serving low-fat meats such as lean roast beef, fish, or turkey, rather than bacon, pork, bologna, or ham, low-fat mayonnaise, and reducing butter or eliminating butter, margarine, and gravy. Seasonal variations in the intake of foods of low caloric density, such as fruits and vegetables, may help to explain the regional and seasonal variations in prevalence. Increased use of low caloric density foods as snacks therefore may be a relevant preventive measure. As outlined above, television viewing may represent one cause of childhood obesity. Parents should be counseled regarding the quantity of television viewed daily and the consumption of calorically dense foods advertised on television, such as sugared breakfast cereals. Although sugared and nonsugared breakfast cereals contain similar quantities of calories on an ounce-for-ounce basis, cereal rarely is consumed by the ounce. Because sugared breakfast cereals are more calorically dense, a bowl of sugared breakfast cereal will contain more calories than will a bowl of its nonsugared counterpart. 11 Reductions in television viewing have the potential not only to decrease the consumption of calorically dense foods, but also to increase the likelihood that time will be spent engaged in more energy-intensive activities. Parents should be counseled accordingly. Interventions Within the Community The power of community-based interventions to treat obesity has been demonstrated aptly by a school-based approach to weight reduction. 3 In this study, a program of behavior modification, nutrition education, and physical activity, introduced by a program involving parents, teachers, food service personnel, school administrators, the nurse's aide, and the physical education instructor, induced weight loss in 95 per cent of the children involved in the program. Interventions at the community level to prevent obesity have not been attempted. Two significant problems currently limit this approach. First, the mechanisms by which the environmental correlates affect onset and prevalence are not clear; however, a focus on food consumption and activity patterns during the winter months, when the prevalence of obesity rises, appears to be an appropriate area for counseling. Second, there exists a risk that a community or nationally based program of prevention could further stigmatize the already obese person. An increased awareness of the role of small caloric imbalances in the genesis of obesity, and refutation of the notion that obese persons become so by massive overeating may be a useful intervention at the community level. The widespread publicity given
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the recent report of the association of television viewing and obesity may itself represent an effctive intervention. Equally important are community-based programs aimed at increasing physical activity. In an era when budget cutbacks threaten extracurricular activities at all levels of the school system, the development of such programs will not be an easy task. Nonetheless, physical activity is inversely related to the prevalence of obesity. In fall and winter, activity decreases, whereas in the spring and summer activity increases. 32 Therefore, school programs to increase activity in the winter appear logical interventions to prevent the onset of obesity. Furthermore, less than 50 per cent of physical education classes in the schools are devoted to activities that can be continued into adulthood. 32 Increased exposure to lifetime physical activities in school-aged children may produce increased activity in later life, thereby preventing the onset of adult disease. A second community-based approach is to pass legislation that bans advertising directed at children. The market for sugared breakfast cereals would not exist without television advertising. Although prior attempts have been made to ban advertising directed at children, based on the difficulties children have distinguishing commercials from programming, such an approach is not likely to be successful in the current deregulatory climate. Nonetheless, foods advertised on television may provide the small increments in caloric imbalance necessary to produce obesity. A final aproach that may reduce the prevalence of obesity in the community but also promote dietary behaviors that reduce other cardiovascular risk factors is promotion of the dietary guidelines for the United States. 7 These guidelines include a reduction in dietary fat intake to 35 per cent of total calories. As discussed above, reduced fat intake may be a logical and easy means to prevent obesity.
SUMMARY The increasing prevalence of childhood obesity, its attendant morbidity, and the limited success of therapy mandate increased attention to preventive approaches. Environmental and family variables serve to identifY families with children at risk for the development of obesity. Although the behavioral correlates that link these risk factors to childhood obesity remain unclear, inactivity and increased dietary intake of fat appear at this time to be the most logical foci for preventive interventions. Television viewing, which promotes both increased food consumption and reduced activity, represents a major concern at which counseling should be directed.
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2. Borjeson, M.: The etiology of obesity in children: a study of 101 twin pairs. Acta Paediatr. Scand., 65:279-287, 1976. 3. Brownell, K. D., and Kaye, F. S.: A school-based behavior modification, nutrition education, and physical activity program for obese children. Am. J. Clin. Nutr., 35:277283, 1982. 4. Brownell, K. D., Kelman, J. H., and Stunkard, A. M.: Treatment of obese children with and without their mothers: changes in weight and blood pressure. Pediatrics, 71:515523, 1983. 5. Chung, S.: Diseases of the developing hip joint. Ped. Clin. North Am., 24:857-870, 1977. 6. Clancy-Hepburn, K., Hickey, A. A., and Nevill, G.: Children's behavior responses to TV food advertisements. J. Nutr. Ed., 6:93-96, 1974. 7. Committee on Dietary Allowances of the Food and Nutrition Board. Recommended Dietary Allowances. Washington, D.C., National Academy of Sciences, 1980, pp. 3537. 8. Dietz, W. H.: Childhood obesity: Susceptibility, cause and management. J. Pediatr., 103:676-686, 1983. 9. Dietz, W. H., Jr.: Family characteristics affect rates of weight loss in obese children. Nutr. Res., 3:43-50, 1983. 10. Dietz, W. H.: Obesity. In Chandra, R. (ed.): Precursors of Adult Disease in Pediatric Patients. Ross Laboratories, 1983, pp. 24-29. 11. Dietz, W. H., and Curatalo, P.: Energy per serving of sugared and unsugared cereals. J. N utr. Ed., 15:84, 1983. 12. Dietz, W. H., Gortmaker, S. L., Sobol, A. M., et al.: Trends in the prevalence of childhood and adolescent obesity in the United States. Pediatr. Res., 19:198A, 1985. 13. Dietz, W. H., and Gortmaker, S. L.: Factors within the physical environment associated with childhood obesity. Am. J. Clin. Nutr., 39:619-624, 1984. 14. Dietz, W. H., and Gortmaker, S. L.: Epidemiologic variables associated with childhood obesity. J. Am. Coli. Nutr., 3:267, 1984. 15. Dietz, W. H., and Gortmaker, S. L.: Do we fatten our children at the TV set? Television viewing and obesity in children and adolescents. Pediatrics, 75:807-812. 16. Dietz, W. H., Jr., Gross, W. L., and Kirkpatrick, J. A., Jr.: Blount disease (tibia vara): Another skeletal disorder associated with childhood obesity. J. Pediatr., 101:735-737, 1982. 17. Drenick, E. J., Bale, G. S., Seltzer, F., et al.: Excessive mortality and causes of death in morbidly obese men. J.A.M.A., 243:443-445, 1980. 18. Dussere, S. A.: The Effects of Television Advertising on Children's Eating Habits (Master's thesis). Amherst, Massachusetts, University of Massachusetts, 1976. 19. Flatt, J. P.: The biochemistry of energy expenditure. In Bray, G.: Recent advances in obesity research: II, London, Newman Publishing 1978, pp. 211-228. 20. Freedman, D. S., Burke, G. L., Harsha, D. W., et al.: Relationship of changes in obesity to serum lipid and lipoprotein changes in childhood and adolescence. J.A. M.A., 254:515-520, 1985. 21. Friedman, G. D., Kannel, W. B., and Dawber, T. R.: The epidemiology of gallbladder disease: Observations in the Framingham study. J. Chron. Dis., 19:273-292, 1966. 22. Gam, S. M., Bailey, S. M., Cole, P. E., et al.: Level of education, level of income, and level offatness in adults. Am. J. Clin. Nutr., 30:721-727, 1976. 23. Gam, S. M., Bailey, S. M., and Higgins, I. T.: Fatness similarities in adopted pairs. Am. J. Clin. Nutr., 29:1067, 1976. 24. Gam, S. M., and Clark, D. C.: Trends in fatness and the origins of obesity. Pediatrics, 57:443-456, 1976. 25. Goldblatt, P. B., Moore, M. E., and Stunkard, A. J.: Social factors in obesity. J.A.M.A., 192:97-100, 1965. 26. Heyden, S., Berte!, A. G., Hanes, C. G., et al.: Elevated blood pressure levels in adolescents, Evans County, Georgia. J.A.M.A., 209:1683-1689, 1969. 27. Kaufman, L.: Prime-time nutrition. J. Comm., 30:37-46, 1980. 28. Lauer, R. M., Connor, W. E., Reiter, M. A., et al.: Coronary heart disease risk factors in school children: The Muscatine study. J. Pediatr., 86:697-706, 1975. 29. Mason, E.: Obesity in pet dogs. Vet. Rec., 86:612-616, 1970. 30. Neilsen Company: 1985 Neilsen Report on Television. Chicago, A.C. Neilsen, 1985.
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31. Nestel, P. J., Schreibman, P. H., and Ahrens, E. J., Jr.: Cholesterol metabolism in human obesity. J. Clin. Invest., 52:2389-2397, 1973. 32. Office of Disease Prevention and Health Prevention: The National Children and Growth Fitness Study. Washington, U.S. Department of Health and Human Services, 1985, pp. 1-48. 33. Rames, L. K., Clarke, W. R., Connor, W. E., et al.: Normal blood pressures and the evaluation of sustained blood pressure elevation in childhood: The Muscatine stl1dy. Pediatrics, 61:245-251, 1978. 34. Ravelli, G. P., and Belmont, L.: Obesity in nineteen-year-old men: Family size and birth order associations. Am. J. Epidemio!', 109:66-70, 1979. 35. Rimm, 1. J., and Rimm, A. A.: Association between juvenile-onset obeSity and severe adult obesity in 73,532 women. Am. J. Public Health, 66:479:481, 1976. 36. Seltzer, C., and Mayer, J.: Simple criterion of obesity. Postgrad. Med. J., 38:A101-A108, 1965. . 37. Staffieri, J. R.: A study of social stereotype of body image in children. J. Pers. Soc. Psycho!., 7:101-104, 1967. 38. Stunkard, A., and Mendelson, M;: Obesity and the body image. 1. Characteristics of disturbances in the body image of some obese persons. Am. J. Psychiatr., 123:12961300, 1967. 39. Stunkard, A. J., Sorensen, T. 1. A., Hanes, C., et al.: An adoption study of human obesity. N. Eng!. J. Med., 314:193-198, 1986. 40. Voors, A. W., Harsha, D. W., Webber, L. S., et al.: Clustering of anthropometric parameters, glucose tolerance, and serum lipids in children with high and low B- and pre-B-lipoproteins. Arteriosclerosis, 2:346-355, 1982. New England Medical Center Box 213 171 Harrison Avenue Boston, Massachusetts 02111