There is a large body of evidence on the role of dietary lipids in cancer. It is based on epidemiolo-gical studies of various sorts in humans, and on feeding studies in animals. It should be stressed that the evidence is in all cases somewhat conflicting. In 1997-1998, two major reports on diet and cancer were published in which all existing evidence was reviewed (see Further Reading). The expert groups who compiled these reports assessed the literature and graded the evidence for associations between dietary components and specific cancers on a scale from 'convincing' to 'insufficient'. For dietary fat, no association was found to be convincing, and a few 'possible'. There was considered to be strong evidence, however, for a relationship between obesity (particularly central fat deposition) and risk of both endometrial cancer and breast cancer in post-menopausal women.
Ken Carroll, a Canadian biochemist who studied this subject extensively, wrote two thorough review articles shortly before his death in 1998, ironically from stomach cancer. In those reviews, Carroll distinguished indirect from direct effects. Indirect effects are mainly related to dietary fat as a form of energy, leading to overweight or obesity.
As reviewed above, the evidence is strong for a link between adiposity and breast cancer and for endometrial cancer, both in post-menopausal women. The most consistent theory implicates the production of oestrogens by the excess adipose tissue. Adipose tissue is an important site for the conversion of androgens (particularly androstene-dione, secreted from the adrenal cortex) to oestrogens, oestradiol and oestrone. The development of some forms of breast and endometrial cancer is stimulated by oestrogens, and hence the association with dietary fat or obesity. The intake of some antioxidants, including tocopherols and lycopene (the red carotenoid pigment of tomatoes), has been linked to protection against certain cancers, including prostate. Even if these findings should be confirmed, it should be emphasized that cancer prevention may not be as simple as supplementation with the antioxidant vitamins at high doses. A number of supplementation studies has been carried out, none so far with positive results, and in one study of P-carotene supplementation, there was an excess of mortality from lung cancer (in those already at high risk).
Cancer of the colon is common, but its incidence varies widely between countries. In comparisons between countries, colon cancer incidence is correlated with meat and fat consumption. However, the interpretation of such studies needs caution as many other factors may be different between countries. The evidence from other types of study, such as case-control studies (where each 'case', or person suffering from the disease, is matched with a similar non-sufferer), for the link between meat consumption and colon cancer is very conflicting, with some studies showing clear positive links and others the opposite. There is moderately consistent evidence, however, for a protective effect of dietary fibre intake against colon cancer. Whilst dietary fibre (or non-starch polysaccharides) is not a dietary lipid, this association is relevant to this book. The mechanism responsible is believed by most to be that fermentation of non-starch polysaccharides by bacteria in the colon produces the short-chain fatty acids, acetic, propionic and butyric. Butyric acid is an important and preferred fuel for the colonic mucosa, but there is now also strong evidence that butyric acid exerts anti-proliferative effects on the mucosal cells.
Evidence for direct effects of dietary fat on cancer is based mainly on animal studies. Ken Carroll and other workers have consistently found that n-6 PUFA in the diet act as mammary tumour promoters when tumours are induced by a carcinogen such as 7,12-dimethylbenz(a)anthracene. Saturated fatty acids in the diet had no such effect, and n-3 PUFA have been found to inhibit tumorigenesis. However, the relevance to human cancer remains unclear. Likewise, the therapeutic usefulness of CLA (Section 22.214.171.124) for human cancer patients remains to be demonstrated.
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