We examined the relations between obesity in parents and fat intake in their children, and the effect of fat intake on fat mass in these children. Our heterogenous sample (-x+/-SD: 20.2+/-3.4 kg; 3.2+/-1.3kg fat mass) consisted of 56 white and 15 Mohawk children 4-7 y of age (35 girls and 36 boys). Dietary intake was assessed with the Willett food-frequency questionnaire revised for children. Body composition was measured by bioelectrical resistance and subscapular and triceps skinfold thicknesses. Physical-activity energy expenditure was estimated by the difference between total energy expenditure (measured over 14 d by the doubly labeled water method) and postprandial resting energy expenditure (measured by indirect calorimetry). Before statistical analysis, fat mass was adjusted for fat-free mass, and fat intake was adjusted for nonfat intake. There was no effect of sex or ethnicity on fat intake and no effect of ethnicity on the relation between fat intake and fat mass. Adjusted mean (+/-SE) fat intakes for the groups of children, based on parental obesity status, were as follows: 1.65+/-0.09 MJ/d (nonobese mother and father), 2.58+/-0.10 MJ/d (obese father, nonobese mother), and 2.79+/-0.10 MJ/d (obese mother and father). We found an influence of maternal obesity on dietary fat intake in children (P=0.052) and a significant correlation between fat mass and fat intake in boys (r=0.48, P<0.01) but not in girls after adjustment for physical-activity energy expenditure. Our data suggest that 1)mothers may contribute to the development of obesity in children by influencing their dietary fat intake, and 2) dietary fat intake contributes to obesity in boys, independent of physical-activity energy expenditure.

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Rates of overweight and obesity have been on a steady rise for decades, and the problems society faces from this and associated metabolic diseases are many. As a result, the need to understand the contributing factors is great. A very compelling case can be made that excess sugar consumption has played a significant role. In addition, fructose, as a component of the vast majority of caloric sweeteners, is seen to be particularly insidious. Evidence shows that fructose bypasses many of the body's satiating signals, thus potentially promoting overconsumption of energy, weight gain, and the development on insulin resistance. It has also been shown to increase uric acid levels, which in turn promotes many of the abnormalities seen in the metabolic syndrome including hypertriglyceridemia. However, the main source of fructose in the diet is high-fructose corn syrup (HFCS), an artificially manufactured disaccharide that is only 55% fructose. This review highlights the fact that limited data are available about the metabolic effects of HFCS compared with other caloric sweeteners. The data suggest that HFCS yields similar metabolic responses to other caloric sweeteners such as sucrose.

High-fructose corn syrup (HFCS) has been implicated in excess weight gain through mechanisms seen in some acute feeding studies and by virtue of its abundance in the food supply during years of increasing obesity. Compared with pure glucose, fructose is thought to be associated with insufficient secretion of insulin and leptin and suppression of ghrelin. However, when HFCS is compared with sucrose, the more commonly consumed sweetener, such differences are not apparent, and appetite and energy intake do not differ in the short-term. Longer-term studies on connections between HFCS, potential mechanisms, and body weight have not been conducted. The main objective of this review was to examine collective data on associations between consumption of HFCS and energy balance, with particular focus on energy intake and its regulation.