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International Journal of Toxicology
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Dietary and other Modulators of Carcinogenesis

Adrianne E. Rogers, M.D.

Massachusetts Institute of Technology

Nutritional or dietary status and interactions between carcinogens and nutrient absorption, storage or metabolism influence carcinogenesis in many experimental animal models and probably in people. Use of dose-response data to indicate a threshold exposure for carcinogenesis must include consideration of dietary and nutritional factors that may alter the dose response. Two models in rats in which there is clear evidence of dietary or nutritional modulation of chemical carcinogenesis are mammary tumors induced by 7, 12-dimethylbenzanthracene (DMBA) or N-nitrosomethyl-urea (NMU) and hepatocarcinomas induced by many compounds. Mammary tumorigenesis is increased by increasing dietary content of some, but not all, fats. The time in tumor development at which fats act varies. Their mechanisms of action are not known but appear to include effects on the hormonal mileu and possibly mammary gland cell turnover and response to hormones.

Hepatocarcinogenesis by chemicals is increased by dietary deficiency of the lipotropes methionine, choline and folate, possibly through alteration of carcinogen metabolism and increased hepatocyte DNA synthesis. The same deficiency induces cirrhosis. In humans, cirrhosis induced by alcoholism, viral hepatitis or unknown factors increases the risk for hepatocarcinoma. Alcohol-induced folate or other deficiency can be a contributory factor in the alcoholics. Infection with hepatitis B virus is increased in alcoholics and in patients with hepatocarcinoma and may be an initiating or modulating factor for tumors.

International Journal of Toxicology, Vol. 2, No. 3, 307-319 (1983)
DOI: 10.3109/10915818309140709
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