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The colon is the third most common site of cancer, after the lung and breast. The American Cancer Society estimates that there will be 107,300 new cases of colon cancer and 48,100 deaths from this disease in 2002. The Harvard Report on Cancer concluded that physical inactivity was the environmental risk factor most consistently shown to be associated with an increased risk of colon cancer. Remarkably, observations across numerous studies have shown that individuals at the highest level of physical activity have a 50% reduction in the incidence of colon cancer, and those who are sedentary have twice the incidence of colon cancer as compared to these individuals.

Physical activity is more powerful than any drug (there being none) to primarily preventive third most prevalent cancer. We estimate that 18,935 premature colon cancer cases and 8488 deaths are already prevented in those 30% of individuals who are more physically active than the U.S. Surgeon General's recommended 30 minutes of moderate activity each day. An additional 44,182 premature cases and 19,806 premature deaths from colon cancer could be prevented each year if the remaining 70% of sedentary individuals undertook high levels of physical activity each day.

The American Cancer Society (ACS) states that one-third of the more than 500,000 cancer deaths that occur in the United States each year can be attributed to diet and physical activity habits, with another third due to cigarette smoking. Our conservative calculations indicate that at least 34,000 premature cancer deaths occur each year in the U.S. due to physical inactivity. The ACS has issued guidelines on nutrition and physical activity for cancer prevention.

Biochemical/Cellular Mechanisms

Men at low levels of physical activity were more likely than women at the same low levels to have a tumor with a Kirsten-ras (K-ras) mutation. On the other hand, women with a higher BMI were more likely to have a K-ras mutation in their tumor. Mutations in the K-ras gene are associated with 30-50% of colon tumors and are thought to follow the initiation of the neoplastic process by an earlier mutation in the adenomatous polyposis coli (APC) gene.