Abstract

Abstract Population-based observational studies have shown remarkably strong and consistent evidence that there is higher risk for many cancer sites among those who carry more body fat and among those who are more sedentary. Obesity is associated with increased risk for cancers of the colorectum, endometrium, esophagus, liver, kidney, pancreas, and gall bladder, and for cancer of the breast among postmenopausal women. Physical activity is associated with reduced risk for cancers of the lung, pancreas, colorectum, endometrium, and both pre-menopausal and post-menopausal breast cancer. The well documented adverse trends in obesity over the past 15 years have occurred in the same era in which both incidence and mortality rates have been declining for breast and colorectal cancer, two of the cancer sites most strongly related to obesity. This apparent contradiction points to the multifactoral causation of these cancers, and suggests that without the headwind of obesity trends, these cancer trends would have been even more favorable. Clearly, physical activity and adiposity are causally linked together. Importantly, however, the relationship between physical activity and cancer does not appear to be due entirely to its relationship with obesity, and the relationship between obesity and cancer does not seem to be due entirely to its relationship with physical activity. The independent and covarying mechanisms that account for the relationships between obesity, physical activity, and cancer risk are not entirely known, but there is ample evidence that these relationships involve multiple pathways, including sex hormones, insulin, insulin-like growth factors, cytokines, and others. Cancer risk seems to be related to energy balance across a wide gradient of levels of adiposity and physical activity that are common in the population. Important for policy and guideline development are the observations that there may be substantial benefits to cancer risk from even small reductions in body fatness and from only small changes in physical activity. Current body weight guidelines and guidelines to increase physical activity to moderate levels, if translated into population-wide changes in behavior, would therefore have substantial impact on cancer risk as well as on risk for diabetes and cardiovascular disease. The needs for research in energy balance are clear: to better understand mechanisms linking adiposity and physical activity to cancer risk by conducting well controlled clinical trials that are powered to assess biomarker relevance directly tied to cancer endpoints. Trials among cancer survivors aimed at elucidating energy balance relationships with recurrence and survival may be more feasible than trials aimed at reducing a first occurrence of cancer incidence. A better understanding of biomarker relationships to energy balance could provide sufficient evidence to negate the need for large scale prevention trials only if those mechanisms paint a picture that is both coherent and compelling. To date, that a picture is unclear. In the meantime, current evidence about the many benefits to quality of life derived from weight control and physical activity and the coherence of evidence relating energy balance to the prevention of cancer, diabetes, and cardiovascular diseases, is already sufficient to more widely institute energy balance interventions as a routine standard for quality clinical care in the population. Citation Information: Cancer Prev Res 2010;3(1 Suppl):CN05-04.

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