extent to which increased physical activity or decreased dietary intake might improve the body’s own ability to regulate energy balance.

Furthermore, greater understanding is needed regarding the relative contribution of energy intake and energy expenditure to the energy imbalance that is driving the obesity epidemic. The increasing prevalence of obesity among children and youth in the United States could be the result of an upward shift in energy intake, a downward shift in energy expenditure, or the occurrence of both trends concurrently (Hill and Peters, 1998; Harnack et al., 2000; Hill et al., 2003). Some researchers have suggested that most of the effect is attributable to excessive energy intake (Sturm, 2005), while others have focused on the decline in regular physical activity and the increase in sedentary behaviors (Cutler et al., 2003).

It has been hypothesized that obesity can result from very small excesses in energy intake relative to expenditure and that the average weight gain in U.S. adults could be prevented if chronic energy expenditure exceeded intake by only 100 calories per day (Hill and Peters, 1998; Hill et al., 2003). However, estimates in a population of Hispanic children have shown greater potential energy gaps, ranging from approximately 200 to 500 calories per day (Butte and Ellis, 2003). This is an area requiring further research.

The following sections provide a brief overview of the context for energy balance and the complexities that researchers and policy makers face in these areas.

Genetic Variation and Biological Considerations

Obesity has long been recognized to occur in families, and having overweight or obese parents increases a child’s risk of being obese. After age 3, parental obesity is a stronger predictor of a child’s future obesity as an adult than is the child’s current weight (Whitaker et al., 1997).

Nonetheless, the familial clustering of obese individuals does not alone predict an individual’s weight characteristics, which reflect the combined effects of genetic variations, the common or shared environmental variations within family (which may include both intrauterine and infant feeding factors), and the environmental variations external to the family (Bouchard et al., 2003).

Quantifying with any precision the specific contributions of each of these factors to the development of obesity has been difficult, despite a variety of studies in nuclear families, in families with identical twins reared together or reared apart, and in families with adopted children. Bouchard and colleagues (2003) reviewed approximately 50 such studies and concluded that heritability accounts for about 25 to 40 percent of an individual’s expressed variation in weight and body fat mass. Specific ma-

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