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Co-carcinogenic effects of dietary cholesterol in experimental colon cancer

Nature volume 276, pages 822–825 (1978)Cite this article

Abstract

COLORECTAL CANCER is now the most common internal malignancy in the US (ref. 1), but its aetiology is unknown. Western dietary factors are likely to be implicated2,3, and high fat diets correlate well with the geographical incidence of colon cancer4–6. Patients with colon cancer have high levels of faecal bile acids and cholesterol7 as do patients with diseases known to be associated with colon cancer, for example, familial polyposis8 and ulcerative colitis9, and also other high-risk populations10. It is thought that faecal bile acid and cholesterol metabolites may act as promoters, co-carcinogens or carcinogens in large bowel tumorigenesis11–13. As cholesterol is the obligatory precursor of the bile acids14, we have tested the ability of dietary cholesterol to promote the induction of colon cancer by dimethylhydrazine (DMH) in the rat. We report here evidence from an animal study that cholesterol is a potent dietary co-carcinogen.

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Authors and Affiliations

  1. Surgical Unit, University College Hospital Medical School, University Street, London, WC1, UK

    J. P. CRUSE, M. R. LEWIN, G. P. FERULANO & C. G. CLARK

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  1. J. P. CRUSE
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  2. M. R. LEWIN
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  3. G. P. FERULANO
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  4. C. G. CLARK
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CRUSE, J., LEWIN, M., FERULANO, G. et al. Co-carcinogenic effects of dietary cholesterol in experimental colon cancer. Nature 276, 822–825 (1978). https://doi.org/10.1038/276822a0

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