Evaluation and Treatment of Childhood Obesity



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Am Fam Physician. 1999 Feb 15;59(4):861-868.

  See related patient information handouts on helping your child keep a healthy weight and helping your child lose weight, written by the authors of this article.

  Related Editorial

The prevalence of childhood obesity in the United States has risen dramatically in the past several decades. Although 25 to 30 percent of children are affected, this condition is underdiagnosed and undertreated. Hormonal and genetic factors are rarely the cause of childhood obesity; unnecessary diagnostic evaluations can be avoided with a careful history and physical examination. Because obese children may suffer life-long physical and emotional consequences, it is imperative to discuss prevention with parents during well-child examinations. All obese children should be screened for cardiac risk factors, as well as for possible orthopedic, dermatologic and psychiatric sequelae. Treatment should be initiated when the trend in increasing weight obviously surpasses the trend in increasing height. Treatment plans should include reasonable weight-loss goals, dietary and physical activity management, behavior modification and family involvement, which may include weight loss in the parents. Anorexiant medications are not approved by the U.S. Food and Drug Administration for use in pediatric populations.

Adult obesity is associated with significant morbidity, including hypertension, type 2 diabetes mellitus (formerly known as non–insulin-dependent diabetes), hyperlipidemia, hyperuricemia, some forms of cancer (especially colon cancer) and lower socioeconomic status in women.13 It is also directly related to all-cause mortality.4 Treatment of obesity in adults is notoriously frustrating for patients and physicians alike, and it rarely meets with long-term success. Thus, prevention is the best hope for decreasing the prevalence of this condition. In many obese people, the roots of their disorder can be traced back to childhood. Obesity tends to “track” throughout life, meaning that its presence at any age will increase the risk of persistence at subsequent ages.3,5 While most obese infants will not remain so, they are at increased risk of becoming obese children. These children are in turn more likely to become obese adolescents, who are then very likely to remain obese as adults.

Evaluation of obesity in childhood is important for several reasons. First, it offers the best hope for preventing disease progression with its associated morbidities into adulthood. Second, while genetic and hormonal causes of obesity are rare, they do warrant consideration in obese children. In addition, obesity has a negative impact on the self-esteem of children and adolescents, which may have significant implications for long-term happiness and success in life. Finally, directed sessions that emphasize healthy eating and exercise habits for children and their families may have lasting effects on the lifestyle of these patients.

Epidemiology

Various definitions of obesity and severe obesity are listed in Table 1.6 Since the 1960s, several large, nationally representative surveys have assessed the prevalence of obesity in children. These include the National Health Examination Survey Cycles I to III and the National Health and Nutrition Examination Surveys I to III. From these surveys, the prevalence of childhood obesity is estimated to be 25 to 30 percent.7 Furthermore, over the years encompassed by these surveys, the prevalence of obesity has increased by 54 percent in children six to 11 years of age and by 39 percent in adolescents 12 to 17 years of age. The prevalence of severe obesity jumped 98 percent and 64 percent within these groups, respectively. Hispanic, Native American and black patients tend to be more affected than other populations.8

TABLE 1

Definitions of Obesity and Severe Obesity

Index Obesity Severe obesity Relevant information

Mean weight for height

> 120 percent

> 140 percent

Actual weight is 20 percent or more above the mean weight for children of this height.

Weight for height

> 85 percentile

> 95 percentile

Readily available reference charts. Easy to use but do not differentiate lean body mass from fat.

Triceps skin fold

> 85 percentile

> 95 percentile

Direct measurement of subcutaneous fat. More accurate measurement of obesity but more intra-observer variability.

Body mass index (kg per m2)

≥ 85 percentile

≥ 95 percentile

Percentiles are age- and gender-specific. Better correlates excess weight to fat in younger children and adolescents.

Ponderal index (kg per m3)

> 85 percentile

> 95 percentile

Percentiles are age- and gender-specific. Better correlates excess weight to fat in older children.


Adapted with permission from Williams CL, Campanaro LA, Squillace M, Bollella M. Management of childhood obesity in pediatric practice. Ann N Y Acad Sci 1997;817:225–40.

TABLE 1   Definitions of Obesity and Severe Obesity

View Table

TABLE 1

Definitions of Obesity and Severe Obesity

Index Obesity Severe obesity Relevant information

Mean weight for height

> 120 percent

> 140 percent

Actual weight is 20 percent or more above the mean weight for children of this height.

Weight for height

> 85 percentile

> 95 percentile

Readily available reference charts. Easy to use but do not differentiate lean body mass from fat.

Triceps skin fold

> 85 percentile

> 95 percentile

Direct measurement of subcutaneous fat. More accurate measurement of obesity but more intra-observer variability.

Body mass index (kg per m2)

≥ 85 percentile

≥ 95 percentile

Percentiles are age- and gender-specific. Better correlates excess weight to fat in younger children and adolescents.

Ponderal index (kg per m3)

> 85 percentile

> 95 percentile

Percentiles are age- and gender-specific. Better correlates excess weight to fat in older children.


Adapted with permission from Williams CL, Campanaro LA, Squillace M, Bollella M. Management of childhood obesity in pediatric practice. Ann N Y Acad Sci 1997;817:225–40.

The persistence of obesity into adulthood depends on several factors, including the age at which the child becomes obese, the severity of the disease and the presence of obesity in at least one parent. Overweight in a child under three years of age does not predict future obesity, unless at least one parent is also obese.5 After age three, however, the likelihood that obesity will persist into adulthood increases with the advancing age of the child and is higher in children with severe obesity in all age groups.5 After an obese child reaches six years of age, the probability that obesity will persist exceeds 50 percent,5 and 70 to 80 percent of obese adolescents will remain so as adults.9,10 The presence of obesity in at least one parent increases the risk of persistence in children at every age.5

Pathophysiology

A person gains weight when energy input exceeds energy output. Energy input is food. Several studies have shown that, on average, obese children do not consume significantly more calories than their thin peers.1114 Energy output comprises the basal metabolic rate, the thermal effect of food and activity. The thermal effect of food is the energy required to absorb and digest meals. Of these variables, activity is the one least influenced by genetic inheritance and is therefore the one most susceptible to change.15 By measure, 3,500 calories is equivalent to 1 lb; thus, an excess intake of only 50 to 100 calories per day will lead to a five- to 10-lb weight gain over one year. As a result, a relatively small imbalance between energy input and output can lead to significant weight gain over time. In fact, most obese children demonstrate a slow but consistent weight gain over several years.15

Evaluation of Obese Children

Only a small percentage of childhood obesity is associated with a hormonal or genetic defect, with the remainder being idiopathic in nature. The most common of the endogenous causes of childhood obesity and their associated characteristics are listed in Table 2. An endogenous cause for obesity can be either suspected or eliminated from the differential diagnosis in virtually all children based on a careful history and physical examination. In most cases, this should negate the need for expensive and unnecessary laboratory evaluations.16

TABLE 2

Endogenous Causes of Childhood Obesity

Hormonal causes Diagnostic clues

Hypothyroidism

Increased TSH, decreased thyroxine (T4) levels

Hypercortisolism

Abnormal dexamethasone suppression test; increased 24-hour free urinary cortisol level

Primary hyperinsulinism

Increased plasma insulin, increased C-peptide levels

Pseudohypoparathyroidism

Hypocalcemia, hyperphosphatemia, increased PTH level

Acquired hypothalamic

Presence of hypothalamic tumor, infection, syndrome trauma, vascular lesion

Genetic syndromes

Associated characteristics


Prader-Willi

Obesity, unsatiable appetite, mental retardation, hypogonadism, strabismus

Laurence-Moon/Bardet-Biedl

Obesity, mental retardation, pigmentary retinopathy, hypogonadism, spastic paraplegia

Alström

Obesity, retinitis pigmentosa, deafness, diabetes mellitus

Börjeson-Forssman-Lehmann

Obesity, mental retardation, hypogonadism, hypometabolism, epilepsy

Cohen

Truncal obesity, mental retardation, hypotonia, hypogonadism

Turner's

Short stature, undifferentiated gonads, cardiac abnormalities, webbed neck, obesity, 45, X genotype

Familial lipodystrophy

Muscular hypertrophy, acromegalic appearance, liver enlargement, acanthosis nigricans, insulin resistance, hypertriglyceridemia, mental retardation

Beckwith-Wiedemann

Gigantism, exomphalos, macroglossia, visceromegaly

Sotos'

Cerebral gigantism, physical overgrowth, hypotonia, delayed motor and cognitive development

Weaver

Infant overgrowth syndrome, accelerated skeletal maturation, unusual facies

Ruvalcaba

Mental retardation, microcephaly, skeletal abnormalities, hypogonadism, brachymetapody

Gene associations


Leptin

Beta3-adrenergic receptor


TSH = thyroid-stimulating hormone; PTH = parathyroid hormone.

TABLE 2   Endogenous Causes of Childhood Obesity

View Table

TABLE 2

Endogenous Causes of Childhood Obesity

Hormonal causes Diagnostic clues

Hypothyroidism

Increased TSH, decreased thyroxine (T4) levels

Hypercortisolism

Abnormal dexamethasone suppression test; increased 24-hour free urinary cortisol level

Primary hyperinsulinism

Increased plasma insulin, increased C-peptide levels

Pseudohypoparathyroidism

Hypocalcemia, hyperphosphatemia, increased PTH level

Acquired hypothalamic

Presence of hypothalamic tumor, infection, syndrome trauma, vascular lesion

Genetic syndromes

Associated characteristics


Prader-Willi

Obesity, unsatiable appetite, mental retardation, hypogonadism, strabismus

Laurence-Moon/Bardet-Biedl

Obesity, mental retardation, pigmentary retinopathy, hypogonadism, spastic paraplegia

Alström

Obesity, retinitis pigmentosa, deafness, diabetes mellitus

Börjeson-Forssman-Lehmann

Obesity, mental retardation, hypogonadism, hypometabolism, epilepsy

Cohen

Truncal obesity, mental retardation, hypotonia, hypogonadism

Turner's

Short stature, undifferentiated gonads, cardiac abnormalities, webbed neck, obesity, 45, X genotype

Familial lipodystrophy

Muscular hypertrophy, acromegalic appearance, liver enlargement, acanthosis nigricans, insulin resistance, hypertriglyceridemia, mental retardation

Beckwith-Wiedemann

Gigantism, exomphalos, macroglossia, visceromegaly

Sotos'

Cerebral gigantism, physical overgrowth, hypotonia, delayed motor and cognitive development

Weaver

Infant overgrowth syndrome, accelerated skeletal maturation, unusual facies

Ruvalcaba

Mental retardation, microcephaly, skeletal abnormalities, hypogonadism, brachymetapody

Gene associations


Leptin

Beta3-adrenergic receptor


TSH = thyroid-stimulating hormone; PTH = parathyroid hormone.

Growth failure characterizes endogenous obesity. Children with an associated genetic or hormonal syndrome are short, usually at or under the 5th percentile of height for age. Conversely, children with idiopathic obesity are taller, usually above the 50th percentile. Even the onset of a hormonal abnormality in a previously tall child will be marked by a significantly slower rate of growth compared with the child's previous growth curve.16  Table 36 compares the important differences in the history and physical examination of patients with endogenous and idiopathic obesity.

TABLE 3

Characteristics of Idiopathic and Endogenous Obesity

Idiopathic obesity Endogenous obesity

> 90 percent of cases

< 10 percent of cases

Tall stature (usually > 50th percentile)

Short stature (usually < 5th percentile)

Family history of obesity common

Family history of obesity uncommon

Mental function normal

Often mentally impaired

Normal or advanced bone age

Delayed bone age

Physical examination otherwise normal

Associated stigmata on physical examination


Adapted with permission from Williams CL, Campanaro LA, Squillace M, Bollella M. Management of childhood obesity in pediatric practice. Ann N Y Acad Sci 1997; 817:225–40.

TABLE 3   Characteristics of Idiopathic and Endogenous Obesity

View Table

TABLE 3

Characteristics of Idiopathic and Endogenous Obesity

Idiopathic obesity Endogenous obesity

> 90 percent of cases

< 10 percent of cases

Tall stature (usually > 50th percentile)

Short stature (usually < 5th percentile)

Family history of obesity common

Family history of obesity uncommon

Mental function normal

Often mentally impaired

Normal or advanced bone age

Delayed bone age

Physical examination otherwise normal

Associated stigmata on physical examination


Adapted with permission from Williams CL, Campanaro LA, Squillace M, Bollella M. Management of childhood obesity in pediatric practice. Ann N Y Acad Sci 1997; 817:225–40.

Although rarely encountered, hypothyroidism is the most frequently considered endogenous abnormality in obese children. By itself, hypothyroidism seldom causes massive weight gain, and its prevalence in obese patients does not significantly differ from its prevalence in the rest of the population.14,16 When present, hypothyroidism is usually associated with other signs and symptoms of the disease, such as constipation, cold intolerance and dry skin. If this disorder is suspected, a thyroid-stimulating hormone (TSH) level should be determined.

Hypercortisolism (Cushing's syndrome) is another frequently suspected cause of endogenous obesity. Although it is usually iatrogenic in nature, it can also be secondary to adrenal tumors or primary pituitary over-production of adrenocorticotropic hormone (ACTH). Pediatric hypercortisolism is characterized by linear growth failure and generalized weight gain. If this condition is suspected, the patient can be evaluated with a 24-hour urine cortisol collection or a dexamethasone-suppression test.16

OFFICE EVALUATION

Obese children must be evaluated for associated morbidity. This includes an assessment of cardiac risk factors, weight-related orthopedic problems, skin disorders and potential psychiatric sequelae.6

Cardiac risk factors include a family history of early cardiovascular disease, high cholesterol and blood pressure levels, cigarette smoking, the presence of diabetes mellitus and decreased physical activity. Obesity in childhood is known to be associated with abnormal indices of lipolysis, including high cholesterol levels (greater than 170 mg per dL [4.40 mmol per L]), high triglyceride levels and low levels of high-density lipoprotein.1719 The National Cholesterol Education Program Expert Panel on Blood Cholesterol Levels in Children and Adolescents20 therefore recommends that physicians consider screening all obese children over two years of age for elevated cholesterol levels.

Obese children also have increased average blood pressure, heart rate and cardiac output when compared to non-obese peers.18,19,21 When evaluating blood pressure in obese children, use of an appropriately sized blood pressure cuff is essential, because one that is too small may yield falsely elevated readings. Tobacco use should be ascertained in all adolescents, as this represents an independent risk for cardiovascular disease. Finally, the presence of diabetes should be considered in all morbidly obese children. While overt type 2 diabetes mellitus is rare in childhood, hyperinsulinemia and glucose intolerance are nearly universal in morbidly obese children.21

The child's level of physical activity must also be assessed. This is important not only for cardiac risk evaluation but also to help guide future treatment. As a corollary to this, television viewing patterns should be reviewed, as television viewing has been shown to be associated with obesity in childhood.2224

Because they carry excess weight, obese children are at increased risk for orthopedic problems. These include tibial torsion and bowed legs, slipped capital femoral epiphysis (especially in boys) and symptoms of weight stress in the joints of the lower extremities.6,16

Obese children are much more prone to skin disorders than are non-obese children, especially if deep skin folds are present. These disorders include heat rash, intertrigo, monilial dermatitis and acanthosis nigricans (a condition that may be a marker for type 2 diabetes).6,16 In addition, acne should be treated when present, as this may help improve the child's self-image.

It is essential to address any existing psychiatric problems, including depression, poor self-esteem, negative self-image and withdrawal from peers. From an early age, society stigmatizes obese people as lazy, stupid, slow and self-indulgent. Studies25,26 have shown that children express negative attitudes toward their obese peers as early as kindergarten, and that they prefer a playmate who is bound to a wheelchair or disabled by a major physical handicap to one who is obese. There is a clear association between obesity and low self-esteem, especially in adolescents.27,28 During the office visit, it is imperative that physicians be sensitive to and accepting of these patients, focusing on positive aspects and ensuring that treatment plans will not further damage an already fragile sense of self-esteem.

Treatment

The best way to significantly affect the prevalence of obesity is to prevent it. Therefore, the issue of obesity should be addressed during every well-child examination. Parents should know that both bottle- and breast-fed infants can be overfed, although overfeeding is more common in infants fed by bottle. Parents should be taught to respect their child's appetite and to understand that it is not necessary for an infant to finish every bottle. Breast feeding and delaying the introduction of solid foods may decrease the risk of future weight problems.29

Skim milk can safely replace whole milk after two years of age.29 Food should not be used for non-nutritive purposes such as comfort or reward. Children should not be offered sweets as a reward for finishing a meal, as this teaches them to place a higher value on dessert foods and may make desserts more desirable to them.30 Family meals should be oriented toward a healthy diet with 30 percent or less of calories derived from fat. Finally, parents should limit the amount of television that the child is allowed to watch and should encourage active play in its place.29  Table 4 lists tips for parents that can be provided during routine well-child visits.

TABLE 4

Preventing Obesity: Tips for Parents

Respect your child's appetite: children do not need to finish every bottle or meal.

Avoid pre-prepared and sugared foods when possible.

Limit the amount of high-calorie foods kept in the home.

Provide a healthy diet, with 30 percent or fewer calories derived from fat.

Provide ample fiber in the child's diet.

Skim milk may safely replace whole milk at 2 years of age.

Do not provide food for comfort or as a reward.

Do not offer sweets in exchange for a finished meal.

Limit amount of television viewing.

Encourage active play.

Establish regular family activities such as walks, ball games and other outdoor activities.

TABLE 4   Preventing Obesity: Tips for Parents

View Table

TABLE 4

Preventing Obesity: Tips for Parents

Respect your child's appetite: children do not need to finish every bottle or meal.

Avoid pre-prepared and sugared foods when possible.

Limit the amount of high-calorie foods kept in the home.

Provide a healthy diet, with 30 percent or fewer calories derived from fat.

Provide ample fiber in the child's diet.

Skim milk may safely replace whole milk at 2 years of age.

Do not provide food for comfort or as a reward.

Do not offer sweets in exchange for a finished meal.

Limit amount of television viewing.

Encourage active play.

Establish regular family activities such as walks, ball games and other outdoor activities.

When a child does develop obesity, a serious attempt to treat it should be undertaken. Table 5 lists the components of a successful treatment plan.

TABLE 5

Components of a Successful Weight Loss Plan

Component Comment

Reasonable weight-loss goal

Initially, 5 to 10 lb, or a rate of 1 to 4 lb per month.

Dietary management

Provide dietary prescription specifying total number of calories per day and recommended percentage of calories from fat, protein and carbohydrates.

Physical activity

Begin according to child's fitness level, with ultimate goal of 20 to 30 minutes per day (in addition to any school activity).

Behavior modification

Self-monitoring, nutritional education, stimulus control, modification of eating habits, physical activity, attitude change, reinforcements and rewards.

Family involvement

Review family activity and television viewing patterns; involve parents in nutrition counseling.

TABLE 5   Components of a Successful Weight Loss Plan

View Table

TABLE 5

Components of a Successful Weight Loss Plan

Component Comment

Reasonable weight-loss goal

Initially, 5 to 10 lb, or a rate of 1 to 4 lb per month.

Dietary management

Provide dietary prescription specifying total number of calories per day and recommended percentage of calories from fat, protein and carbohydrates.

Physical activity

Begin according to child's fitness level, with ultimate goal of 20 to 30 minutes per day (in addition to any school activity).

Behavior modification

Self-monitoring, nutritional education, stimulus control, modification of eating habits, physical activity, attitude change, reinforcements and rewards.

Family involvement

Review family activity and television viewing patterns; involve parents in nutrition counseling.

SETTING GOALS FOR WEIGHT LOSS

Weight loss goals should be obtainable and should allow for normal growth. Goals should initially be small, so that the child doesn't become overwhelmed or discouraged. Five to 10 lb is a reasonable first goal or, if preferred, a rate of 1 to 4 lb per month can be established.6

DIETARY MANAGEMENT

The child should maintain a food record to aid in dietary assessment. The food diary should include not only the type and quantity of food eaten, but also where it was eaten, the time of day and who else was present. In most cases, the diary will be inaccurate in figuring total calories consumed but will be useful in reviewing problem foods and eating patterns. A straightforward dietary prescription should be offered, keeping in mind that 3,500 calories must be eliminated by diet and exercise to lose 1 lb. It is necessary to provide parents with a specific calorie-per-day recommendation that follows guidelines for percentages of fat, protein and carbohydrates.6,29 Dietary fiber is also important, as it increases satiety and displaces fat in the diet.6,29 The patient and family should be referred to books that describe the nutritional contents of foods and food exchange lists such as Exchange Lists for Weight Management.31 Finally, the patient and his family should be referred to a nutritional consultant, if this service is available in the community.

PHYSICAL ACTIVITY

Exercise is necessary to maintain weight loss and to redistribute body fat into muscle. It is, therefore, an essential part of any weight management program. Initial exercise recommendations should be small and exercise levels should be increased slowly, to avoid possible discouragement. A reasonable goal is 20 to 30 minutes of moderate activity per day, in addition to whatever exercise the child gets during the school day.6,29

BEHAVIOR MODIFICATION

Table 5 lists areas of behavior modification that should be addressed.6 Self-monitoring is accomplished by food and activity logs, which force the child to become more aware of his or her eating and exercise patterns. Nutritional education should be aimed at both the child and the family. It should include the components of a healthy diet and an understanding of food labels and the importance of dietary fiber. The patient should be taught that 3,500 calories equals 1 lb; there are nine calories per gram of fat and only four calories per gram of carbohydrate or protein. Furthermore, 25 percent of the energy from carbohydrates will be used in its conversion and storage as fat in the body.6

Stimulus control includes limiting the amount of fattening foods in the house, eating all meals at the dinner table and at designated times, and serving food only once before putting it away (no second helpings). Parents should not verbally encourage the child to eat, and the child should not be forced to finish the entire meal. Examples of modifying eating behavior include taking smaller bites, chewing food longer, putting the fork down between bites and leaving some food on the plate.6

Activity patterns are an important target for behavior modification. The child should help set a weekly activity goal, sign a contract to perform the activity and help determine the reward for reaching the goal.6,16 Family television-viewing patterns should be reviewed and modified accordingly. Attitude change involves teaching the child to turn negative self-statements into positive ones, and helping him or her cope with the negative remarks of others. Finally, reinforcements and rewards include verbal praise from the physician and family members, as well as tangible rewards for achieving dietary, activity and weight-loss goals.6 Rewards should be determined with input from the child, and they should encourage further physical activity, such as sporting equipment or a trip to the skating rink.16

FAMILY INVOLVEMENT

It is important to involve the entire family when treating obesity in children. Many studies have demonstrated a familial aggregation of risk factors for obesity,32,33 and the family provides the child's major social learning environment. It has been demonstrated that the long-term (10-year) effectiveness of a weight control program is significantly improved when the intervention is directed at the parents as well as the child, rather than aimed at the child alone.34,35

ALTERNATIVE THERAPIES

At this time no anorexiant medications are approved by the U.S. Food and Drug Administration for use in children. Surgical procedures such as gastric bypass have not been studied sufficiently in children to advise their use. Structured weight loss programs such as Weight Watchers and Jenny Craig Weight Loss Centres will accept older children with permission from their parents and physician. The Shapedown Pediatric Obesity Program (telephone: 415-453-8886; Website: www.shapedown.com) is a structured weight loss and weight management program for children between the ages of six and 20 years. It has offices in 600 cities and in all 50 states.

Final Comment

If a child fails to lose weight despite what appears to be adequate treatment, it is important to refrain from accusing the child of cheating on the diet or misreporting physical activity. Rather, a “face-saving” way out of the weight loss program should be offered. Many of these children have already experienced several perceived failures in their lives, and an unsuccessful attempt to lose weight should not be added to their emotional burden.

The Author

REBECCA MORAN, M.D., is in private practice in Gilbert, Ariz. She received her medical degree at the University of Pennsylvania School of Medicine, Philadelphia, and completed a residency in the Department of Family Medicine at the University of Michigan Medical School, Ann Arbor.

Address correspondence to Rebecca Moran, M.D., Dinsdale Medical Group, 7 E. Paloverde St., #9, Gilbert, AZ 85296. Reprints are not available from the author.

The author thanks Barbara Apgar, M.D., M.S., and Colm Moran for assistance in the preparation of the manuscript.

REFERENCES

1. Harlan WR. Epidemiology of childhood obesity. A national perspective. Ann N Y Acad Sci. 1993;699:1–5.

2. Gortmaker SL, Must A, Perrin JM, Sobol AM, Dietz WH. Social and economic consequences of overweight in adolescence and young adulthood. N Engl J Med. 1993;329:1008–12.

3. Power C, Lake JK, Cole TJ. Measurement and long-term health risks of child and adolescent fatness. Int J Obes Relat Metab Disord. 1997;21:507–26.

4. Manson JE, Willett WC, Stampfer MJ, Colditz GA, Hunter DJ, Hankinson SE, et al. Body weight and mortality among women. N Engl J Med. 1995;333:677–85.

5. Whitaker RC, Wright JA, Pepe MS, Seidel KD, Dietz WH. Predicting obesity in young adulthood from childhood and parental obesity. N Engl J Med. 1997;337:869–73.

6. Williams CL, Campanaro LA, Squillace M, Bollella M. Management of childhood obesity in pediatric practice. Ann N Y Acad Sci. 1997;817:225–40.

7. Gortmaker SL, Dietz WH Jr, Sobol AM, Wehler CA. Increasing pediatric obesity in the United States. Am J Dis Child. 1987;141:535–40.

8. Kumanyika S. Ethnicity and obesity development in children. Ann N Y Acad Sci. 1993;699:81–92.

9. Epstein LH, Wing RR, Valoski A. Childhood obesity. Pediatr Clin North Am. 1985;32:363–79.

10. Malina RM. Ethnic variation in the prevalence of obesity in North American children and youth. Crit Rev Food Sci Nutr. 1993;33:389–96.

11. Schlicker SA, Borra ST, Regan C. The weight and fitness status of United States children. Nutr Rev. 1994;52:11–7.

12. Webber LS, Wattigney WA, Srinivasan SR, Berenson GS. Obesity studies in Bogalusa. Am J Med Sci. 1995;310(suppl 1):S53–61.

13. Nicklas TA, Webber LS, Srinivasan SR, Berenson GS. Secular trends in dietary intakes and cardiovascular risk factors of 10-year-old children: the Bogalusa Heart Study (1973–1988). Am J Clin Nutr. 1993;57:930–7.

14. Dietz WH. Childhood obesity. Prevention and Treatment of Childhood Obesity. Conference proceedings. Bethesda, Md., March 9–11, 1993. Ann N Y Acad Sci. 1993;699:47–54.

15. Dietz WH, Bandini LG, Gortmaker S. Epidemiologic and metabolic risk factors for childhood obesity. Prepared for the Fourth Congress on Obesity Research, Vienna, Austria, December 1988. Klin Padiatr. 1990;202:69–72.

16. Golden MP. An approach to the management of obesity in childhood. Pediatr Clin North Am. 1979;26:187–97.

17. Williams DP, Going SB, Lohman TG, Harsha DW, Srinivasan SR, Webber LS, et al. Body fatness and risk for elevated blood pressure, total cholesterol, and serum lipoprotein ratios in children and adolescents. Am J Public Health. 1992;82:358–63[Published erratum in Am J Public Health 1992; 82:527]

18. Wattigney WA, Harsha DW, Srinivasan SR, Webber LS, Berenson GS. Increasing impact of obesity on serum lipids and lipoproteins in young adults. The Bogalusa Heart Study. Arch Intern Med. 1991;151:2017–22.

19. McMurray RG, Harrel JS, Levine AA, Gansky SA. Childhood obesity elevates blood pressure and total cholesterol independent of physical activity. Int J Obes Relat Metab Disord. 1995;19:881–6.

20. U.S. Dept. of Health and Human Services, Public Health Service, National Institutes of Health, National Heart, Lung, and Blood Institute, National Cholesterol Education Program. Report of the Expert Panel on Blood Cholesterol Levels in Children and Adolescents. Bethesda, Md.: 1991. NIH publication no. 91-2732.

21. Berenson GS, Srinivasan SR, Wattigney WA, Harsha DW. Obesity and cardiovascular risk in children. Ann N Y Acad Sci. 1993;699:93–103.

22. Klesges RC, Shelton ML, Klesges LM. Effects of television on metabolic rate: potential implications for childhood obesity. Pediatrics. 1993;91:281–6.

23. Tucker LA, Friedman GM. Television viewing and obesity in adult males. Am J Public Health. 1989;79:516–8.

24. Dietz WH Jr, Gortmaker SL. Do we fatten our children at the television set? Obesity and television viewing in children and adolescents. Pediatrics. 1985;75:807–12.

25. Lerner RM, Gellert E. Body build identification, preference, and aversion in children. Dev Psychol. 1969;1:456–62.

26. Richardson SA, Boodman N, Hastorf AH, Dornbush SM. Cultural uniformity in reaction to physical disabilities. Sociol Rev. 1961;26:241–7.

27. French SA, Story M, Perry CL. Self-esteem and obesity in children and adolescents: a literature review. Obes Res. 1995;3:479–90.

28. Braet C, Mervielde I, Vandereycken W. Psychological aspects of childhood obesity: a controlled study in a clinical and nonclinical sample. J Pediatr Psychol. 1997;22:59–71.

29. Barness L, ed. Pediatric nutrition handbook. 3d ed. Elk Grove Village, Ill.: American Academy of Pediatrics, 1993.

30. Ray JW, Klesges RC. Influences on the eating behavior of children. Ann N Y Acad Sci. 1993;699:57–69.

31. American Dietetic Association and American Diabetes Association. Exchange lists for weight management. Rev. ed. Chicago and Alexandria, Va.: The Associations, 1995.

32. Patterson TL, Rupp JW, Sallis JF, Atkins CJ, Nader PR. Aggregation of dietary calories, fats, and sodium in Mexican-American and Anglo families. Am J Prev Med. 1988;4:75–82.

33. Sallis JF, Patterson TL, Buono MJ, Atkins CJ, Nader PR. Aggregation of physical activity habits in Mexican-American and Anglo families. J Behav Med. 1988;11:31–41.

34. Epstein LH, Valoski A, Wing RR, McCurley J. Ten-year follow-up of behavioral, family-based treatment for obese children. JAMA. 1990;264:2519–23.

35. Epstein LH. Family-based behavioural intervention for obese children. Int J Obes Relat Metab Disord. 1996;20(suppl 1):S14–21.



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