social environment, and to his/her likelihood of becoming obese given a particular level of energy intake and expenditure (Costanzo and Schiffman, 1989; Hill and Peters, 1998).
There is abundant evidence from animal and human models for genetic contributions to obesity, with 40 to 70 percent of the variability in susceptibility to human obesity attributable to heritable factors (Comuzzie and Allison, 1998). There are single gene disorders that include obesity as part of the syndrome, such as Prader-Willi and Bardet-Biedel; however, such major genetic effects are rare. Mutations studied in rodent models of obesity that are associated with leptin abnormalities also are rare in humans (Kopelman, 2000). For example, a single gene mutation in the melanocortin 4 receptor (MC4R) is thought to account for less than 5 percent of morbid obesity (Vaisse et al., 1998). Molecular genetic studies have identified a very large number of susceptibility genes for multiple obesity phenotypes, including BMI, feeding behavior, and satiety (Comuzzie and Allison, 1998); however, the attributable risks associated with these variants remain unclear. Candidate genes identified in these studies include those coding for agouti signaling proteins, leptin and leptin receptors, and cholecystokinin A receptor (reviewed in Comuzzie and Allison, 1998). Genetic variation in the dopamine transporter and dopamine 2 receptor also has been associated with obesity in some studies (Noble et al., 1994; Epstein et al., 2002). Despite the known complex etiology of obesity, studies of genetic modulation of social environmental exposures are rare. However, there is evidence that fetal nutrition may affect gene expression, possibly altering susceptibility to diet and environmental stressors that promote obesity in later life (Barker et al., 1989; Barker, 1995).
It is recommended that, to reduce health risks, healthy adults engage in at least 150 minutes of moderate intensity physical activity per week (Pate et al., 1995). Despite the positive effects of regular physical activity on breast and colon cancer (McTiernan et al., 1998) and on CVD risk factors (U.S. DHHS, 1996), approximately one-half of adult Americans do not engage in moderate physical activity for at least 30 minutes at least 3 times a week (Sullivan et al., 2005). Engaging in regular physical activity also has important benefits following a cancer diagnosis. A meta-analysis of randomized controlled trials of physical activity interventions concluded that such interventions have significant benefits for cardiovascular respiratory fitness and can reduce cancer treatment side effects (Schmitz et al., 2005b). Physical activity interventions