Childhood obesity: Medical Consequences

Because of the dangers associated with childhood obesity, early intervention and family support is critical.

Childhood obesity is associated with a variety of adverse effects on psychosocial function, skeletal growth, and cardiovascular risk factors. Although several periods in childhood appear critical for the development of obesity, it is not yet clear whether these periods are also associated with an increased risk for the complications of obesity in either childhood or adulthood.

PSYCHOLOGICAL CONSEQUENCES
The psychosocial consequences of obesity are among the most widespread adverse effects of the disease. Children in kindergarten have already learned to associate obesity with a variety of less desirable traits, and rank obese children as those they like the least.
College acceptance rates for obese adolescent girls are lower than those for nonoverweight girls of comparable academic background. Adult women who are obese as adolescents or young adults earn less, more frequently remain unmarried, complete fewer years of school, and have higher rates of poverty than their nonobese peers.
Few of these effects occur among obese men. These results persist when controlled for the income and educational level of the young women’s parents, their IQ, or their self-esteem at baseline. The social effects of obesity in young adult women therefore appear related to an extension of the discrimination that begins in early childhood

SKELETAL GROWTH AND MATURATION
Obesity has multiple effects on growth and function in children and adolescents. For example, obese children tend to be taller, their bone ages are advanced, their fat-free mass is increased, and menarche in girls occurs earlier than in the non obese.
The origin of these effects is unclear. Increased height, advanced bone age, and earlier menarche may reflect the auxotrophic effects of increased food intake, whereas the increase in fat-free mass may result from both the increased muscle mass to support the increased weight and the nuclear mass of adipocytes. Because of their larger size, overweight children are frequently perceived and treated as older than they are, much to their confusion.
Furthermore, the increased stress of weight may cause bowing of the tibia (Blount’s disease) or femur and predispose young children to slipped capital femoral epiphysis.

CARDIOVASCULAR RISK FACTORS
As in adults, obesity affects blood pressure, lipid levels, and glucose tolerance in children and adolescents. Sixty percent of overweight children as young as 5–10 years of age have at least one of these cardiovascular disease risk factors, and more than 20% have two or more.
Obesity appears to be the leading cause of hypertension in children. Lipid profiles are similar to those in adults: low density lipoprotein levels are increased, and high density lipoprotein levels are low.
Increased rates of type 2 diabetes have followed the rapid increases in the prevalence of childhood and adolescent obesity. In some settings, type 2 diabetes now accounts for 30–40% of all new cases of diabetes. Although the prevalence of type 2 diabetes in the general population is low (0.5%), among some Native American groups the prevalence is close to 5%. Pediatric cases of type 2 diabetes generally occur among those 10–19 years of age, with a positive family history of type 2 diabetes, and more frequently among obese females or individuals with acanthosis nigricans.
At presentation, cases of type 2 diabetes in children and adolescents may resemble type 1 diabetes, suggesting that the actual prevalence of type 2 diabetes may be somewhat higher than it currently appears.
The most important factor related to the likelihood of obesity-associated hypertension, hyperlipidemia, and glucose intolerance in adults appears to be visceral fat. The few studies of adolescents that have controlled for total body fat have demonstrated an independent association of visceral fat, with unfavorable levels of systolic blood pressure and low- and high-density lipoprotein cholesterol.

PSEUDOTUMOR CEREBRI, SLEEP APNEA,
HEPATIC STEATOSIS, AND POLYCYSTIC OVARY DISEASE
Two of the most malignant consequences of childhood onset obesity are pseudotumor cerebri and sleep apnea. Obesity accounts for a significant proportion of pseudotumor cerebri, although the mechanism remains unclear.
The diagnosis is established by a history of headaches and the presence of papilledema. The most important sign of sleep apnea is daytime somnolence. Apnea is rarely mentioned spontaneously by parents, despite their apprehension and clear recognition of the difficulty that their child has breathing at night. If the tonsils are enlarged, a tonsillectomy may cure sleep apnea.
However, either unremitting sleep apnea or pseudotumor warrant the aggressive use of a restrictive hypocaloric diet in conjunction with vigorous family therapy.
Recent data from several studies indicate that 5–10% of overweight children and adolescents have modestly elevated liver enzymes. Ultrasound studies of these patients demonstrate increased hepatic fat deposition. Liver biopsies in severe cases have demonstrated steatohepatitis. Alcohol use appears to increase the likelihood of these changes.
Liver enzymes normalize with weight reduction. As in adults, polycystic ovary disease (PCOD) in adolescents is associated with obesity. The pathophysiology of PCOD is complicated; hyperinsulinemia is frequently associated with the syndrome, and hyperandrogenemia may contribute to increased fat-free mass and a male distribution of body fat.

EFFECTS OF CHILDHOOD OBESITY
ON PERSISTENCE INTO ADULTHOOD
The likelihood that obesity present during childhood will persist into adulthood rises with the age of the child, independent of the effect of parental obesity. Several studies have indicated that approximately 70% of overweight adolescents become obese adults. Age-of-onset effects of obesity in childhood or adolescence on either the severity or complications of adult obesity remain uncertain.
Obesity in adolescence appears to entrain a variety of morbid consequences. For example, in a cohort of adults originally studied from the time of their enrollment in elementary school through high school, all-cause and cardiovascular mortality rates were higher among men who were obese in high school, but not among women. The risk of diabetes and subsequent atherosclerosis was greater among both men and women who were obese during high school. Except for diabetes, the risk of death or subsequent morbidity was only modestly attenuated when controlled for the effect of adolescent obesity on adult weight. These results suggested that the effect of adolescent obesity on adult morbidity and mortality was not mediated by the effect of adolescent obesity on adult obesity. Either adolescent obesity had a direct impact on adult morbidity and mortality,or a third factor predisposed individuals to both adolescent obesity and adult disease.
Body fat distribution may represent the mechanism whereby obesity present in adolescence affects morbidity and mortality. Body fat distribution is more strongly centralized in adolescent males than in adolescent females. Therefore, one possibility is that the regionalization of fatness that occurs in obese adolescent males may increase the risk of later complications of obesity.


Based on book : EATING DISORDERS AND OBESITY Edited by Christopher G. Fairburn and Kelly D. Brownell