BERKELEY, CA (UroToday.com) - My hypothesis presents a conceptual framework by which we can understand how certain drugs, like finasteride, may increase the risk for high-grade prostate cancer. As suggested and outlined in my manuscript, the mechanism behind male pattern baldness may prevent the proliferation and growth of prostate cancer. This protective effect is lost when medications are used to lower dihydrotestosterone (DHT) levels to treat androgenic alopecia. Interestingly, the protective effect is present for men experiencing frontal and vertex balding or frontal balding only. Unfortunately, men suffering from only vertex balding seem to have higher chances of developing prostate cancer. For this last group of men, I hypothesize that this is from the lack of DHT increasing the synthesis of prostaglandin D2 and less activation of estrogen receptor beta.
The hypothesis challenges the traditionally held belief that increasing amounts of DHT lead to increased prostate growth and cancer cell proliferation. In fact, recent studies have shown that increased levels of DHT do not lead to greater activity of the androgen receptor, since the point of maximum activation of androgen receptors through DHT binding is at a level far below normal physiological concentrations of DHT. For an in depth analysis of why this is relevant to my hypothesis and why increased levels of DHT do not activate more androgen receptors, I encourage the reader to peruse my manuscript.
Written by:
Shiva Bhargava as part of Beyond the Abstract on UroToday.com. This initiative offers a method of publishing for the professional urology community. Authors are given an opportunity to expand on the circumstances, limitations etc... of their research by referencing the published abstract.
Cornell University, Ithaca, NY USA
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