Obesity now affects one in five children in the United States. Discrimination against overweight children begins early in childhood and becomes progressively institutionalized. Because obese children tend to be taller than their nonoverweight peers, they are apt to be viewed as more mature. The inappropriate expectations that result may have an adverse effect on their socialization. Many of the cardiovascular consequences that characterize adult-onset obesity are preceded by abnormalities that begin in childhood. Hyperlipidemia, hypertension, and abnormal glucose tolerance occur with increased frequency in obese children and adolescents. The relationship of cardiovascular risk factors to visceral fat independent of total body fat remains unclear. Sleep apnea, pseudotumor cerebri, and Blount's disease represent major sources of morbidity for which rapid and sustained weight reduction is essential. Although several periods of increased risk appear in childhood, it is not clear whether obesity with onset early in childhood carries a greater risk of adult morbidity and mortality. Obesity is now the most prevalent nutritional disease of children and adolescents in the United States. Although obesity-associated morbidities occur more frequently in adults, significant consequences of obesity as well as the antecedents of adult disease occur in obese children and adolescents. In this review, I consider the adverse effects of obesity in children and adolescents and attempt to outline areas for future research. I refer to obesity as a body mass index greater than the 95th percentile for children of the same age and gender.

Health Consequences of Obesity in Youth: Childhood Predictors of Adult Disease

Effects of weight reduction on blood lipids and lipoproteins: a meta-analysis.

Cholesterol gallstone disease is initiated in a liver which produces abnormal bile with excess cholesterol relative to bile salts and phospholipid. To define the responsible secretory mechanism(s), the rate of biliary lipid secretion was measured by a duodenal marker perfusion technique, while the bile salt pool was simultaneously estimated by isotope dilution. Two groups of control patients expected to have normal biliary lipid composition--14 subjects without hepatobiliary disease and 6 patients with pigment gallstones, were compared to two experimental groups expected to have abnormal bile--10 nonobese patients with cholesterol gallstones and 7 obese subjects without gallstones. Both control groups had nearly identical biliary lipid secretion rates, and a corresponding low relative molar concentration of cholesterol. Two different secretory mechanisms were found to be responsible for the abnormal bile in the experimental groups. In the nonobese patients with cholesterol gallstones, bile salt and phospholipid secretion rates were both significantly reduced. Conversely, the grossly obese subjects had an increased cholesterol secretion. To determine how cholecystectomy improves biliary lipid composition, three groups of gallstone patients --6 with pigment stones, 4 grossly obese with cholesterol stones, and 13 nonobese with cholesterol stones --were all examined after full recovery from surgery. In the nonobese patients with cholesterol gallstones, both bile salt and phospholipid secretion significantly increased, causing a definite improvement in bile composition. Cholecystectomy produced a similar but less marked trend in the obese patients with cholesterol stones, and in the patients with pigment stones. Cholesterol secretion, however, was unaffected by surgery. The bile salt pool was definitely small in the nonobese patients with cholesterol gallstones and became slightly smaller after cholecystectomy. The pool was significantly reduced by cholecystectomyin the patients with cholesterol gallstones. Removal of the gallbladder in all three groups caused a greater fraction of the pool to cycle around the enterohepatic circulation each hour. This more rapid cycling produced the increase in bile salt and phospolipid secretion, and was responsible for the improved composition found after cholecystectomy.

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Biliary lipid secretion in cholesterol gallstone disease. The effect of cholecystectomy and obesity.

Retinoids and retinoid-binding protein expression in rat adipocytes.

Cholesterol, a Cell Size-dependent Signal That Regulates Glucose Metabolism and Gene Expression in Adipocytes

By analysis of 124 specimens in 16 different patients, isolated human adipocyte cholesterol concentration is highly correlated with fat cell size but not with plasma cholesterol concentration. Less than 6 percent of total cholesterol is esterified; after subcellular fractionation, 88 percent of the cholesterol is recovered in the triglyceride-rich supernatant oil. This latter finding supports the observation that fat cell cholesterol is determined by triglyceride content, and hence by fat cell size. After intravenous administrtion of radioactive cholesterol, the sum of a three-exponential equation was fit simultaneously to both the plasma and adipocyte specific activity time curves in six patients. In five of the six, a slowly turning over pool (pool 3) closely fit the adipocyte data. Two model structures, mammillary and catenary, were fitted to the data. There was no synthesis in pool 3 using a mammillary model but a mean 5.3 percent of the total body production rate was found in compartment 3 if a catenary model was assumed. Although a catenary model is biologically unlikely, it could not be excluded. Obesity is associated with an increased cholesterol synthetic rate equal to 20 mg/day for each kilogram of body fat. To test (by an independent method) if this synthesis might be occurring in adipose tissue, human fat cells were obtained under a wide variety of dietary conditions and incubated in vitro with radioactive glucose or acetate. Incorportation of these precursors into sterol could account for no more than 1 mg cholesterol synthesis/kg fat per day. These in vitro data taken together with the in vivo mammillary compartmental analysis data are compatible with the possiblity that the excess cholesterol synthesis of obesity occurs in pool 1, most likely from hepatic or intestinal sites.

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P H Schreibman

Papers

Human adipocyte cholesterol. Concentration, localization, synthesis, and turnover.