Finasteride’s Effect on Prostate Cancer. Part 2
A major limitation of this sero-epidemiological study is based on the fact that fatal prostate cancer takes many years from formation until death occurs. The question is whether the fatty acid content of a man’s blood on two days out of the thousands of days over those years is a reliable measure of his average fatty acid status. Another limitation is that the researchers did not take into account the impact of vitamin E, selenium, lycopene, cruciferous vegetables, meat and dairy intake.
EPA and DHA are hypothesized to reduce cancer risk in general through their anti-inflammatory and immunomodulatory properties, and by affected cell permeability, gene expression, and signal transduction. The effects of omega-3s on these pathways in prostate carcinogenesis are not fully understood. There is no known mechanism by which EPA or DHA would be procarcinogenic, nor is there any evidence suggesting anticancer properties of trans-fats.
Genetic and molecular studies of high-grade prostate intraepithelial neoplasia have indicated that loss of heterozygosity is prominent and that certain oncogenes are expressed. What causes the expression of these oncogenes? What downregulates their expression?
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Androgenic hormones are necessary for prostate growth and development. It is not surprising that polymorphic variants of genes involved in androgen action may affect PCa risk. African Americans, who have higher PCa risks than Asians, have androgen-receptor polymorphisms that result in their increased predisposition. 5-alpha reductase variants also may respond differently to inhibition by finasteride.
The key lifestyle factor in the United States most likely responsible for high PCa incidence is the diet, generally rich in animal fats and meats and poor in fruits and vegetables.
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Accumulated epidemiologic evidence implicates the environment as the major contributor to the development of most prostate cancers. PCa incidence has wide geographic variation, with high rates in the US and Western Europe and low rates in Asia. African Americans have very high PCa risks. The geographic variation can be explained best by lifestyle, as Asian immigrants to North America have higher PCa risks. The key lifestyle factor in the United States most likely responsible for high PCa incidence is the diet, generally rich in animal fats and meats and poor in fruits and vegetables. Total fat intake, animal fat intake, and consumption of red meats are associated with increased PCa risk.3 Ingestion of 2-amino-1-methyl-6-phenylimidazopyridine, one of the hererocyclic amine carcinogens that appear in “well-done” red meats, leads to PCa in rats. Consumption of dairy products also increases PCa risk.
Consumption of lycopene, cruciferous vegetables, vitamin E and selenium reduce PCa risk.
The role of genetics in identifying individuals at high risk for prostate cancer are in their infancy, but epidemiologic studies support the concept that genetic risk plays a role, and clinical studies support the observation that early prostate cancer in some individuals is highly aggressive, while in the majority it is indolent. Linking these two factors should identify a population of men in whom screening, early detection, and chemoprevention agents can be intensively directed. In the meantime, the take-home message of this study was expressed by the chief author: “Overall, the beneficial effects of eating fish to prevent heart disease outweigh any harm related to prostate cancer risk.”