Author: Steven M Schwarz, Professor of Pediatrics, Children's Hospital at Downstate, SUNY-Downstate Medical Center
Coauthor(s): Michael Freemark, MD, Professor of Pediatrics, Duke University;
Updated: Apr 13, 2010
Obesity is the most prevalent nutritional disorder among children and adolescents in the United States. Currently available data report that approximately 21-24% of American children and adolescents are overweight and that another 16-18% are obese; the prevalence of obesity is highest among specific ethnic groups.
Childhood obesity predisposes to insulin resistance and type 2 diabetes, hypertension, hyperlipidemia, liver and renal disease, and reproductive dysfunction. It also increases the risk of adult-onset obesity and cardiovascular disease.
Operational definitions of obesity in adults are derived from statistical data analyzing the association between body mass and the risk of acute and long-term morbidity and mortality. Because acute medical complications of obesity are less common in children and adolescents than in adults, and because longitudinal data on the relation between childhood weight and adult morbidity and mortality are more difficult to interpret, no single definition of obesity in childhood and adolescence has gained universal approval.
Some investigators have used the terms overweight, obese, and morbidly obese to refer to children and adolescents whose weights exceed those expected for heights by 20%, 50%, and 80-100%, respectively.
The body mass index (BMI) has not been consistently used or validated in children younger than 2 years. Because weight varies in a continuous rather than a stepwise fashion, the use of these arbitrary criteria is problematic and may be misleading. Nevertheless, children and adolescents defined as overweight or obese according to published criteria are highly likely to maintain this ponderal status as adults.
The BMI is a continuous, although imperfect, measure of body fatness. Calculated as weight (kg) divided by height (m2), BMI corrects for body size and can be readily and reliably quantified in clinical settings.
The BMI correlates closely with total body fat (TBF), which is estimated using dual-energy x-ray absorptiometry (DEXA) scanning in children who are overweight and obese.
Normal values for BMI vary with age, sex, and pubertal status, and standard curves representing the 5th through the 95th percentiles for BMI in childhood and adolescence have been generated using data from the National Health and Nutrition Examination Surveys of 1988-1994.1
Consensus committees have recommended that children and adolescents be considered overweight or obese if the BMI exceeds the 85th or 95th percentiles, on curves generated from the 1963-1965 and 1966-1970 surveys, or exceeds 30 kg/m2 at any age.2
McGavock et al demonstrated that low cardiorespiratory fitness and reductions in fitness over time are significantly associated with weight gain and the risk of being overweight in children aged 6-15 years. Analysis on a cohort of 902 schoolchildren showed higher waist circumference and disproportionate weight gain over a 12-month follow-up period in those children with low cardiorespiratory fitness (P < 0.05). The 12-month risk of overweight classification was 3.5-fold (95% confidence interval [CI], 2.0-6.0; P < 0.001) higher in youth with low cardiorespiratory fitness, relative to fit peers. Reductions in cardiorespiratory fitness were significantly and independently associated with increasing body mass index (P < 0.05). Pathophysiology During childhood and adolescence, excess fat accumulates when total energy intake exceeds total energy expenditure. This energy imbalance can result from excessive energy intake and/or reduced energy expenditure, the latter is usually a consequence of a sedentary lifestyle. This is particularly associated with excessive television viewing, excessive computer use, and insufficient physical activity. In infancy, excess fat deposition occurs when excess energy is provided, especially when protein-to-energy ratio is altered. This is often seen when feedings are supplemented with additives such as carbohydrates or fat and protein content remains the same. In individuals who are obese, dysfunction in the gut-brain-hypothalamic axis via the ghrelin/leptin hormonal pathway has been suggested to have a role in abnormal appetite control and excess energy intake. See the image below. Studies indicate that dysfunction in this hormonal axis may be the causative factor in as many as 10% of obese subjects, with emphasis particularly on those individuals who appear to manifest familial morbid obesity. In these families, several reports have shown a dramatic, weight loss response to hormone replacement therapy in patients with leptin deficiency. Reductions in energy expenditure characterize other hormonal deficiency states, including hypothyroidism and growth hormone deficiency. Increases in energy intake are observed in genetic syndromes, such as Prader-Willi syndrome, Cushing syndrome, and drug-induced obesity. Despite observations of an etiologic role for genetic and hormonal disorders, these factors alone do not explain the excess weight gain observed in most patients who have obesity and are referred to physicians for evaluation and treatment. Although most overweight children have a familial form of obesity, with 1 or 2 obese parents, excess weight gain in obese children clearly depends on both genetic and environmental factors. Correlations between parent and child habitus likely reflect, at least in part, the familial patterns of food intake, exercise, and selection of leisure activity (including amount of television watching), as well as familial and cultural patterns of food selection. Nevertheless, evidence from twin, adoption, and family studies suggests that genetic factors also play a considerable role in the development of childhood obesity. Concordance rates for obesity and type 2 diabetes mellitus are higher in monozygotic twins than in dizygotic twins, and measures of TBF correlate nearly as strongly in monozygotic twins reared apart (r = 0.61) as in monozygotic twins reared together (r = 0.75). Still, genetic factors cannot explain the increased prevalence of obesity observed among American adolescents over the past generation. The accumulation of body fat, particularly in a visceral distribution, reduces the sensitivity to insulin in skeletal muscle, liver tissue, and adipose tissue; this "insulin resistance" predisposes to glucose intolerance and hypertriglyceridemia. Low levels of high-density lipoprotein (HDL), observed both genetically and in association with a sedentary lifestyle, likely contribute to the increase of premature coronary artery disease observed in adults with obesity. Increases in circulating levels of insulin and insulin-like growth factor I may increase blood pressure (BP) and may stimulate the production of androgens from ovarian and adrenocortical cells, with consequent dysmenorrhea and virilization in females. Aromatization of adrenal androgens to estrone leads to gynecomastia in males. The insulin resistance, dyslipidemia, and hypertension predispose to type 2 diabetes and cardiovascular disease, reducing life expectancy. Frequency United States Using BMI criteria, the most recent national surveys demonstrate that 21-24% of American children and adolescents are overweight and that another 16-18% are obese. These findings indicate that the prevalence of overweight (BMI = ³ 85th percentile) children and adolescents in the United States has increased by 50-60% in a single generation, and the prevalence of obesity has doubled. The prevalence of obesity in American Indians, Hawaiians, Hispanics, and blacks is 10-40% higher than in whites. Mortality/Morbidity For many years, complications arising from obesity were considered unusual in childhood. However, a plethora of minor and major problems may arise in children and adolescents with obesity; most of these problems have considerable impact on quality of life, and some may reduce life expectancy. Acute complications o Acute complications of childhood obesity include type 2 diabetes, hypertension, hyperlipidemia, accelerated growth and bone maturation, ovarian hyperandrogenism and gynecomastia, cholecystitis, pancreatitis, and pseudotumor cerebri. Fatty liver is common; rarely, patients develop cirrhosis and renal disease (focal glomerulosclerosis). Sleep apnea and sleep-disordered breathing are common in children and adolescents with obesity; in some cases, the apnea is accompanied by neurocognitive dysfunction. Tonsillectomy and adenoidectomy and/or bilevel positive airway pressure/continuous positive airway pressure (BIPAP/CPAP) may be beneficial in patients with reduced oxygenation or carbon dioxide retention. o Numerous orthopedic disorders, including genu valgum, slipped capital femoral epiphysis, and tibia vara, are observed more commonly in children with obesity. Excess weight in young children can cause bowing of the tibia and femurs; the resulting overgrowth of the proximal tibial metaphysis is called Blount disease. o Evidence of liver dysfunction, with elevated plasma concentrations of transaminases, is observed in 20% of children with obesity; the liver dysfunction most commonly reflects hepatic steatosis, but cirrhosis may develop in rare instances. Vitamin E supplements may be effective in reversing this so-called steatohepatitis, suggesting that the disorder reflects a relative state of vitamin E deficiency.4 Cholelithiasis is more common in adults with obesity than in adults with normal weight. Although gallstones are unusual in childhood, nearly one half of all cases of cholecystitis in adolescents are associated with obesity. Cholecystitis may be even more common during rapid weight loss, particularly with very controlled–energy diets. o Emotional and psychosocial sequelae are widespread. Anecdotal evidence suggests that depression and eating disorders are common in children and adolescents referred to obesity clinics. Prejudice and discrimination against individuals with obesity are ubiquitous within US culture; even young children have been found to regard their peers who have obesity in negative ways. Social isolation, peer problems, and lower self-esteem are frequently observed. o Obesity during childhood and adolescence is associated with numerous cardiovascular risk factors, including hyperinsulinism and insulin resistance, hypercholesterolemia, hypertriglyceridemia, reduced levels of HDL, and hypertension. A hallmark of insulin resistance is acanthosis nigricans, the presence of which indicates an increased risk of type 2 diabetes. Adolescent girls with obesity also demonstrate a hyperandrogenic profile, consisting of elevated serum concentrations of androstenedione, dehydroepiandrosterone-sulfate (DHEA-S), and testosterone, as well as reduced levels of sex hormone–binding globulin. The clinical picture resembles that of polycystic ovary syndrome (PCOS). The excess androgens are of adrenal and ovarian origin and may be related, at least in part, to increased serum concentrations of insulin and insulin growth factor 1 (IGF-I). o Among sexually mature adolescents, changes in serum lipids and androgens seem to correlate more strongly with body fat distribution than with absolute weight. Thus, adolescents with central obesity (ie, android or abdominal fat pattern) are more likely to manifest these cardiovascular risk factors than individuals with peripheral obesity (ie, gynoid or gluteal pattern). In prepubertal children, however, the cardiovascular risk factors correlate better with body weight than with body fat distribution. The increasing prevalence of obesity in childhood and adolescence, accompanied by insulin resistance, appears to explain the increasing incidence of type 2 diabetes in adolescents, particularly in minority populations. * Long-term complications o Obesity during childhood and adolescence is associated with an increased risk of obesity during adulthood, with its attendant long-term health risks. This increased risk appears most pronounced for adolescent males with moderate-to-severe obesity. The long-term implications of obesity during infancy and early childhood on subsequent health are less clear. In general, the proportion of children with obesity who have obesity as adults increases with increased age at onset of obesity, such that 26-41% of preschoolers with obesity have obesity as adults, compared with 42-63% of school-aged children. Additionally, the higher the degree of obesity during childhood, the higher the risk of adult obesity. Individuals aged 18 years individuals with a BMI at or above the 95th percentile have a 66-78% risk of being overweight at age 35 years. o The dramatic increase in the prevalence of type 2 diabetes among adolescents with obesity is likely to be accompanied by a host of diabetic-related complications in adulthood and a reduction in life span. The epidemiological data, although limited, indicate that adolescent obesity is associated with increased morbidity and mortality in later life. o An increased risk of death from all causes and from coronary artery disease (CAD) has been consistently observed in males, but not in females, who had obesity during adolescence. In a follow-up of the Harvard Growth Study, the risk of morbidity from CAD and atherosclerosis was increased among men and women who had been overweight (BMI >75th percentile) as teenagers. Gout and colorectal cancer increased among men who had obesity as adolescents, and arthritis increased among women who had obesity as adolescents. Many of these adverse health outcomes appear to be independent of adult weight, suggesting a direct effect of adolescent obesity on adult health and mortality.
o Psychosocial dysfunction in individuals who have obesity in childhood and adolescence is a serious concern. Among teens and young adults who were tracked after 7 years, overweight females were found to have completed less schooling, were less likely to have married, and had higher rates of household poverty compared to their nonoverweight peers. For overweight males, the only adverse outcome was a decreased likelihood of being married.