Studies in metabolic epidemiology have shown a strong association between dietary fat intake, level of fecal anaerobic bacteria, fecal acid, and neutral sterols and the risk of colon cancer among different populations. Current concepts visualize that colonic bile acids and cholesterol metabolites play a modifying role in large bowel carcinogenesis, that these compounds are derived from dietary factors (directly or indirectly), and that they subsequently are modified by the intestinal bacteria. In the animal model, 2 bile acids (lithocholic and taurodeoxycholic) acted as colon tumor promoters.

Rats fed a high-fat diet were more susceptible to colon tumor induction by 1,2-dimethylhydrazine compared to animals fed a normal-fat diet. The intestinal microflora also played a modifying role in enhancing colon tumor production by 1.2-dimethylhydrazine.

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Presented at the Conference on Nutrition in the Causation of Cancer, May 19 to 22, 1975, Key biscayne, Fla. Supported by USPHS contract CP-33208, Carcinogenesis Programs, National Cancer Institute and Grants CA 16382 and CA 15400 from the National Cancer Institute through The National Large Bowel Project.

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©1975 American Association for Cancer Research.
1975
Cancer Research, Inc.