Understanding Obesity in Youth
A Statement for Healthcare Professionals From the Committee on Atherosclerosis and Hypertension in the Young of the Council on Cardiovascular Disease in the Young and the Nutrition Committee, American Heart Association
Obesity is strongly linked to cardiovascular disease and non–insulin-dependent diabetes mellitus through the promotion of insulin resistance and other associated physiological abnormalities, including dyslipidemia, elevated blood pressure, and increased left ventricular mass.1 2 3 4 Overweight and insulin resistance have been linked to the early development of atheromata in young adults independent of other cardiovascular risk factors.5 Pulmonary, skeletal, dermatologic, immunologic, and endocrinologic systems display obesity-related morbidities (Table 1⇓).6 Adverse social and psychological effects of obesity have also been demonstrated.6 7 8
Obesity is a major public health problem with both genetic and environmental causes.9 10 Longitudinal studies of children followed into young adulthood suggest that overweight children may become overweight adults, particularly if obesity is present in adolescence.11 12 13 There is substantial evidence that obesity in childhood lays the metabolic groundwork for adult cardiovascular disease.14 Studies of families and twins have clearly demonstrated a strong genetic component in the etiology of obesity.15 16 17 Just as persuasively, a recent study of secular trends in anthropometry has shown an increase in the prevalence of overweight in children and young adults over the last 10 to 20 years, indicating a potent interaction between environment and genetics.18 This secular trend is associated with worsening cardiovascular risk.19
This statement reviews the medical consequences of obesity in youth. Epidemiology, morbidity (especially cardiovascular), and etiology are considered and approaches to prevention and treatment presented. Areas for additional research are highlighted.
Obesity is defined as the presence of excess adipose tissue. In normal individuals the percentage of body tissue that is adipose tissue varies by gender (greater in postpubertal females than males) and age (about 12% at birth, increasing to 25% at 5 months, then decreasing to 15% to 18% during puberty).20 Clinical standards for defining obesity in children are not well established. In general, any child with weight for height above the 75th percentile for age and sex or who has significantly increased his weight for height percentile and who suffers from a morbidity that would be worsened by obesity (eg, dyslipidemia, diabetes mellitus, or hypertension) should be considered obese. For diagnostic and therapeutic purposes, obese persons must be distinguished from those who are overweight because of increased lean body mass.
Attempts to standardize a definition of obesity have relied on calculations of weight significantly above that expected for height or measurements exceeding an anthropometric standard such as triceps or subscapular skinfold thickness.18 21 22 Measurements that adjust weight for height, such as body mass index (weight in kg÷height in meters squared), ponderal index (kg/m3), or percent ideal body weight for height (from published weight tables for adults or normal growth curves for children) do not differentiate between excess adiposity and increased lean body mass. Height, weight, and other anthropometric measures are advantageous for directly measuring body fat; in particular, subscapular skinfold measurements and waist-to-hip ratio help define the regional deposition of fat and differentiate the more medically significant central obesity from peripheral obesity in adults. For adults and adolescents, significant obesity in adults has been defined as a body mass index ≥30 kg/m2 or ≥130% ideal body weight for height.22a22A Waist-to-hip ratio is difficult to standardize in children because of changes in body habitus with normal development. Subscapular skinfold measures correlate well with morbidity associated with obesity and measures of adiposity made by hydrodensitometry.22 23 For this reason, consideration should be given to incorporating skinfold measurements into clinical practice.
Estimates of the prevalence of obesity in children and adolescents in the United States are difficult to make because of the lack of a consensus definition and the existence of only a few data sets that mirror the ethnic and socioeconomic composition of the population. Recent analyses from the third National Health and Nutrition Examination Survey (NHANES III) show a continuing increase in prevalence. Based on age-specific calculations of triceps skinfold referenced to the 85th percentile of the earliest survey in 1963, prevalence increased to 25% in the 1976-1980 survey. Comparisons using the 85th percentile for body mass index in the 1976-1980 survey showed a further increase from 15% to 22% in the 1990 survey.18
The Bogalusa Heart Study24 has shown that measures of weight for height but not height have increased over the first 15 years of the study. This increase appears to be concentrated among those at the higher end of the weight for height percentiles. Weight has increased by 2% to 3% in children at the lowest quartiles for height and 7% to 10% in the uppermost height quartile.25 This trend is associated with worsening cardiovascular risk.19
Data on obesity for different racial groups are more sparse. In both the Bogalusa and Coronary Artery Risk Development in Young Adults (CARDIA) cohorts, however, obesity appears to be more prevalent in African-Americans, particularly females.24 26 Native Americans and Hispanics may also have relatively high rates of obesity.27 28 There are important regional and seasonal differences in the prevalence of obesity. Prevalence is increased when weight is measured during winter rather than summer. Obesity is much more common in the Northeast and the Midwest than in the South and the West, a phenomenon independent of race, population density, and season.9
The relation of obesity to diabetes mellitus and cardiovascular risk is thought to be mediated partially by insulin, although it is unclear whether increased circulating levels of insulin or the presence of a physiological milieu counterregulatory to insulin (insulin resistance) is the primary problem.29 30 31 In cross-sectional population studies, higher fasting serum insulin levels are directly related to increases in body fatness, particularly in those with central adiposity.32 The combination of increased insulin and insulin resistance is the mechanism responsible for non–insulin-dependent or type II diabetes mellitus, a disease whose increase in frequency may parallel the increased prevalence of obesity.33
Elevated insulin levels have been associated with cardiovascular risk factors other than diabetes mellitus. Mechanisms for the association of elevated blood pressure with insulin levels include the increased presence of counterregulatory hormones such as norepinephrine and increased renal sodium and fluid retention.34 35 An association between insulin resistance and the combined dyslipidemia of hypertriglyceridemia as well as low levels of HDL cholesterol has also been found.36 Modest weight reduction results in correction of these abnormalities.34 35 Finally, the clustering of these risk factors identified in cross-sectional epidemiological studies can be explained by the association of elevated insulin with obesity.37 38
Obesity is important in the evolution of cardiovascular risk. As children progress with relatively low risk from childhood into adulthood with higher blood pressure, higher levels of LDL cholesterol, lower levels of HDL cholesterol, and increased risk for non–insulin-dependent diabetes, the major predictor of acquiring risk other than risk factor levels measured in childhood is the acquisition of excess weight.39 40 41 These trends may be independent of physical activity levels.42 Increased left ventricular mass, another independent cardiovascular risk factor, is associated with overweight and development of increased blood pressure.43 44 45 46 Coronary atherosclerosis is more likely to be present in young adults with excess adipose tissue independent of other risk factors.5
There are significant noncardiovascular morbidities of obesity, particularly central obesity, as well as orthopedic abnormalities, premature onset of puberty, hypoventilation, endocrinopathies, and skin problems. Being overweight in adolescence may be associated with premature morbidity and mortality not only from cardiovascular disease but colorectal cancer, gout, and arthritis.47 Social stigmatization and poor self-image have both been associated with significant obesity.7 8 Popular culture has clearly associated positive social rewards with leanness and negative social rewards with obesity. Body fat distribution in central (abdominal, male pattern) versus peripheral (gluteal, female pattern) adipose tissue depots is more predictive of many adipose-related morbidities than absolute body fatness.32 48 49
In studies comparing identical with fraternal twins and adopted children with their adoptive and their biological parents, the heritability of body fatness and body fat distribution has been estimated to be 65% to 75%.15 16 17 Twin studies have demonstrated genetic influences on resting metabolic rate, feeding behavior, changes in energy expenditures in response to overfeeding, lipoprotein lipase activity, and basal rate of lipolysis.50-5550 51 52 53 54 55 A recent population-based study suggests that 35% of the adjusted variation in body mass index was accounted for by a single recessive locus while polygenetic loci accounted for 42% of the variation. This study has also shown that obese family members of obese children have excess mortality from cardiovascular disease and other obesity-related causes.56 56A
Environmental factors associated with obesity include socioeconomic status, race, region of residence, season, urban living, and being part of a smaller family.9 Numerous studies have addressed the relation between energy expenditure and obesity. Although some studies suggest that obesity is associated with increased sedentary activity, particularly watching television, or with a lower resting metabolic rate, these differences have been inconsistently demonstrated.57 58 59 60 61 Several studies indicate that energy expenditure per kilogram is lower in obese children but similar to nonobese children when indexed to lean body mass. Obese persons may be socially stigmatized by their leaner peers; this may lead to less participation in athletic activities but may not translate into dramatic differences in daily energy expenditure.
Studies of diet composition in children also do not identify the cause of obesity in youth. Current dietary fat and saturated-fat intakes of American children are lower than in the past.62 Sequential cross-sectional studies of total caloric intake suggest little change in the total caloric intake of children over many years.63 Children appear to regulate their food intake over time when allowed to select their own food.64 Although meal-to-meal energy intake varies significantly, there is little day-to-day variation in energy intake at a given age.64
Inevitably, obesity must result from an imbalance between energy intake and energy expenditure. Obesity in a child or adult may reflect small excesses of energy intake over expenditure over a long period of time. Maintenance of a certain level of adiposity may be centrally regulated. Studies of people who have gained or lost weight suggest that there is metabolic resistance to alterations in body weight.65 66 67
Prevention and Treatment
Because long-term studies of weight reduction in children have shown that 80%-90% return to their original weight percentile, efforts at primary prevention should be made.68 During health maintenance visits, measuring and recording height and weight on both standard charts and height and weight velocity charts is critical to detect the onset of relative excess weight gain. Body mass index can be calculated in adolescents. Subscapular skinfolds may also be measured. Values greater than the 75th percentile for skinfolds and weight for height measures should be considered at risk.18 This is particularly important when there is a family history of obesity, diabetes mellitus, dyslipidemia, or hypertension.
In the significantly overweight child, more aggressive medical intervention and treatment are warranted (Table 2⇓). Evaluation of a child at ≥130% of ideal body weight for height or greater than the 95th percentile for subscapular skinfolds should include testing for obesity-related morbidities, including lipoprotein analysis, blood pressure assessment, fasting glucose and/or glucose tolerance test, assessment for nocturnal hypoventilation by history (and sleep study if severe involvement is suspected), and physical examination to exclude orthopedic abnormalities. Infants should undergo thyroid function testing.
For individual therapy of most obese children, the primary emphasis of treatment should be prevention of weight gain above that appropriate for expected increases in height (ie, prevention of increased weight gain velocity). For many children this may mean limited or no weight gain while linear growth proceeds normally. Recommendations for weight maintenance should include regular physical activity and careful attention to diet to avoid excessive caloric intake. Interventions that have been most successful in promoting long-term weight maintenance have been implemented in children between the ages of 6 and 12 years.69 70 Factors predicting success are frequent intervention visits, inclusion of parents in the dietary treatment program, strong social support for the dietary intervention from others involved in food preparation, and regular exercise prescription. Achieving ideal weight for height should be considered an unrealistic goal. The importance of continuing these lifestyle modifications well past the initial treatment period should be emphasized to the entire family. The healthiest way to change weight for height is slowly.
The risks and difficulties of weight reduction may exceed the benefits in an older and otherwise healthy overweight child without a family history of cardiovascular morbidity related to adiposity. Caloric intake should not be restricted in infants; rather, prevention of overfeeding should be emphasized.
Conditions for which weight loss is recommended include hypertension, diabetes mellitus, cor pulmonale, sleep apnea, orthopedic abnormalities, and severe psychosocial stress secondary to obesity. Treatment should be continued until the medical or psychological condition has improved. Physician monitoring of weight reduction in children is essential because caloric restriction has been associated with problems, including precipitation of eating disorders, stigmatization of the child, and systemic complaints such as fatigue, headaches, dysmenorrhea, and syncope.71 Pharmacological or surgical therapy is indicated only with life-threatening complications of obesity and after conventional therapy has failed. Weight loss is not recommended for infants because of potential deleterious effects on somatic and brain growth.
Public health interventions for primary prevention should be directed toward the promotion of healthful behaviors. These include accumulation of at least 30 minutes of endurance-type physical activity of at least moderate intensity on most—preferably all—days of the week72 and consumption of the prudent diet recommended by the American Academy of Pediatrics and the American Heart Association.73 High-fat diets in parents are associated with their children's eating patterns and obesity. Therefore, the entire family should be targeted in recommendations.74 75 To improve compliance with recommendations, the entire family should be involved in treatment recommendations to improve family health and avoid stigmatizing the overweight child. The goal of prevention should be maintenance of normal growth patterns rather than weight loss.
Further research on obesity in children should be directed toward understanding the critical periods for its development, devising successful family-oriented interventions, establishing clinical and genetic markers that identify individuals and populations at risk, improving standards for the diagnosis of obesity, and developing effective public health measures to increase participation in active rather than sedentary lifestyles. Current research leaves the hope that the trend toward increased obesity can be reversed through a public health policy that encourages regular physical activity and prudent diet combined with new insights into pathophysiology for specific therapy of severely affected individuals.
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“Understanding Obesity in Youth” was approved by the American Heart Association Science Advisory and Coordinating Committee in June 1996.
- Copyright © 1996 by American Heart Association
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