Red Clover Has Some Preventive Effect Against Prostate Cancer,
Preventing Prostate Cancer - Herbal
Red Clover Has Some Preventive Effect Against Prostate Cancer,
By Monday, January 12 2009 00:00
The effect on the prostate of dietary isoflavones including those in red clover is believed to involve tamping down of the steroidal hormone DHEA, which is metabolized in the body to produces androgens and/or estrogens. DHEA is a natural circulating hormone and the body’s production of it decreases with age. Some men take DHEA as an over-the-counter supplement in hope that it will reverse or slow effects of aging.
As part of a series of studies of effects of DHEA on the prostate and effects of dietary supplements on DHEA, NIH researchers report on manipulation of DHEA levels in prostate cells by means of red clover in the laboratory. Julia Arnold, Ph.D., a staff scientist at the National Center for Complementary and Alternative Medicine (NCCAM) at NIH, believes more data may be obtainable from settings in which men and women concerned about health problems tend to self-prescribe based on information they find on the Internet.Meanwhile the NCCAM laboratory is studying signaling between human prostate cancer cells and their supporting stromal cells as they grow together in laboratory culture.
"DHEA effects in the prostate tissues may depend on how these two cells types 'talk to each other' and further, it may be potentially harmful in tissues containing inflammation or with early cancer lesions because the cells can induce DHEA to become more androgenic," Arnold said.
Combining DHEA with transforming growth factor beta-1 increased testosterone production in the stromal cells, raised PSA secretion two to four-fold and increased gene expression up to 50-fold in the cancer cells. When these cell cultures were treated with red clover isoflavones, the androgenic effects of DHEA were reversed.
"Something is happening in the prostate tissue microenvironment that is illustrating a potential cancer prevention effect from this supplement," Arnold said.
Red clover isoflavones may modify androgenic effects in the prostate but much more work in the laboratory and clinic is needed to validate these effects.
This sort of laboratory manipulation will allow scientists to understand more about basic prostate biology as well as to learn cellular and molecular mechanisms of over-the-counter supplements and other botanical or herbal agents. Arnold said NCCAM will continue to study DHEA with other supplements to determine any cancer preventive effects.
Arnold's findings are published in Cancer Prevention Research, a journal of the American Association for Cancer Research.
RELATED:
DHEA metabolism in prostate: For better or worse? Mol Cell Endocrinol. 2008 Nov 1. [Epub ahead of print]
Abstract: Dehydroepiandrosterone (DHEA) is commonly used in the USA as a nutritional supplement for antiaging, metabolic support or other uses. Investigations into understanding the effects of DHEA on human prostate cancer progression have posed more questions than answers and highlight the importance of communications between stromal and epithelial elements within the prostate that contribute to the regulation of DHEA metabolism. Intracrine metabolism of DHEA to androgens (A) and/or estrogens (E) may occur in one cell compartment (stromal) which may release paracrine hormones or growth/inhibitory factors to the epithelial cells. Alternatively no metabolism of DHEA may occur, resulting in no harmful consequences of high levels of DHEA in prostate tissues. We herein review the tissue components involved and interactions with the prohormone, DHEA and/or resulting metabolites, including dihydrotestosterone (DHT) or 17beta-estradiol (E(2)) in an in vitro model of endocrine-immune-paracrine interactions within the prostate. This work raises questions and hypotheses concerning the role of DHEA in prostate in normal tissues, vs. preneoplastic tissues.
Human prostate stromal cells stimulate increased PSA production in DHEA-treated prostate cancer epithelial cells. J Steroid Biochem Mol Biol. 2008 Sep;111(3-5):240-6. Arnold JT, Gray NE, Jacobowitz K, Viswanathan L, Cheung PW, McFann KK, Le H, Blackman MR.
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