Dietary epidemiology of colon cancer.

Epidemiologic studies of the relationship of diet to cancer etiology are hampered by methodologic difficulties which can be overcome by careful trial design. The use of appropriate dietary assessment instruments is necessary to minimize bias and improve accuracy of diet assessment. Population studies implicate dietary fat intake in the etiology of colorectal carcinogenesis, and the incidence of colorectal malignancies around the world is positively correlated with meat and fat consumption and total calorie intake. Retrospective studies of fat intake yield equivocal results, whereas prospective studies have failed to show a relationship between fat intake and colon cancer risk. An inverse relationship exists between fiber consumption and colorectal cancer incidence and mortality rates. The positive observational studies are supported by laboratory studies of experimental carcinogenesis which show a greater number of tumors in animals fed high-fat or high-calorie diets. Increased fiber intake appears to offer some protection against colorectal cancer. Plausible mechanisms have been proposed in animals for the role of fat and fiber in colorectal carcinogenesis; the mechanisms in human populations await further description. The interrelationships between fat consumption and consumption of dietary fiber and micronutrients have made it difficult to assess the roles of these substances in the etiology of colorectal cancer. Calcium offers protection in animal systems, and the data in humans are suggestive but not yet conclusive. Data on the role of alcohol in colorectal carcinogenesis remain inconclusive. Little evidence exists for a protective effect of retinoids and carotenoids; the evidence for selenium and vitamin C is limited and evolving.