Co-carcinogenic effects of dietary cholesterol in experimental colon cancer

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 implicated 2,3 , and high fat diets correlate well with the geographical incidence of colon cancer 4–6 . Patients with colon cancer have high levels of faecal bile acids and cholesterol 7 as do patients with diseases known to be associated with colon cancer, for example, familial polyposis 8 and ulcerative colitis 9 , and also other high-risk populations 10 . It is thought that faecal bile acid and cholesterol metabolites may act as promoters, co-carcinogens or carcinogens in large bowel tumorigenesis 11–13 . As cholesterol is the obligatory precursor of the bile acids 14 , 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.