Dietary cholesterol is co-carcinogenic for human colon cancer
1979
Cruse, Peter | Lewin, Michael | Clark, Charles G.
Co-carcinogens facilitate the development, growth and spread of cancer, but do not initiate it. Dietary cholesterol may be a co-carcinogen in human colon cancer. Patients with colon cancer have raised levels of faecal cholesterol and cholesterol metabolites. Serum-cholesterol concentrations do not correlate with incidence of colon cancer; a reciprocal relation may exist between serum and faecal levels. Dietary cholesterol is co-carcinogenic in animals with experimental colon cancer. Possible mechanisms are: 1) cholesterol exerts a preparative action on the colonic epithelium; 2) it may be a permissive agent, affecting the solubility, metabolism, or excretion of a cancer-initiating factor; 3) it may promote action of an already initiated carcinogenic process; or 4) it may exert a systemic, conditional influence via hormonal or immunological mechanisms. Western man consumes excess cholesterol which is excreted in the faeces, possibly aiding the growth of any tumors already present in the colon. High levels of colon cancer in populations indicate the presence of both the mutagenic initiator and the dietary promoter (cholesterol). A low- or cholesterol-free diet is recommended to prevent or retard the growth of colon cancer.
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