Alpha-linolenic acid and the risk of prostate cancer.
Alpha-linolenic acid and the risk of prostate cancer.
Year: 2004
Authors: Letter to the editor
Publication Name: Lipids.
Publication Details: Volume 39; Number 9; Page 929.
Abstract:
A number of recent prospective epidemiological and case-control studies have demonstrated a positive relationship between ALA in the diet or blood and prostate cancer. In contrast, other studies have found no relationship between ALA in diet, blood, or adipose tissue and prostate cancer. Overall, the role of individual fatty acids in cancer has been poorly investigated. In this letter to the editor, several issues are raised regarding studies investigating the association between ALA intake and risk of prostate cancer. First, the author questions the reliability of dietary assessment methods, such as food frequency questionnaires, in accurately capturing the intake of certain nutrients, including ALA. One difficulty with dietary ALA is that food databases are unlikely to be up to date, or contain sufficient detail, to accurately reflect ALA levels in different foods. Secondly, major food sources of ALA differ considerably among countries. For example, fats and oils in the US provide 59% of dietary ALA, whereas fats and oils provide only 16% of total ALA intake in Australia. Thirdly, do dietary and/or plasma levels of ALA accurately reflect ALA levels in prostate tissue? To date, no known studies have examined whether a relationship exists between plasma ALA levels and levels of ALA in the prostate gland. Fourth, does the prostate accumulate ALA? In reviewing the research, the author(s) found only three reports discussing human prostate fatty acid levels. Of these, only two reported ALA levels in prostate tissue, with values ranging from 0.5 – 2.7% of total fatty acids. One of these studies demonstrated that levels of ALA in the prostate tissue were significantly lower in patients with advanced cases of prostate cancer than in control subjects. This finding appears to be opposite of that predicted by findings in the epidemiological studies in question. Fifth, is there a plausible biological mechanism by which ALA promotes prostate, and possibly other cancers? To date, there is no evidence that ALA metabolites other than EPA and DHA are formed in humans. The majority of in vitro studies have shown that ALA and other n3 PUFAs inhibit the growth of prostate cancer cells, as well as other cancer cell lines such as human mammary tumor cells. Sixth, is it possible that ALA is a marker of another compound(s) associated with ALA in foods, which may ultimately be responsible for the associations observed in the epidemiological studies in question? For example, in the case of partial hydrogenation of ALA containing oils as commonly seen in the US, is it possible that a strong association exists between ALA and trans isomers of ALA and other fatty acids? It also may be possible that ALA is a marker for lipids from the non-saponifiable fraction of oils such as sterols, hydrocarbons, and tocopherols. This point has received no attention in the published literature. Overall, the author(s) states that more research is necessary before any conclusions can be drawn regarding the association between ALA and prostate and other cancers.
