The development of the normal prostate, like other male sexual organs, depends on male hormones, primarily testosterone from the testicles. Testosterone must be converted into another form, called dihydrotestosterone (DHT), for prostate development to take place. An enzyme called 5AR is responsible for this conversion. The DHT form of testosterone plays a key role in the development of a benign enlargement of the prostate, and is also believed to be involved in the development of prostate cancer.
Men born with a deficiency of the 5AR enzyme have underdeveloped prostates because not enough DHT is available, but they also never develop benign prostatic hyperplasia (BPH) or prostate cancer. Similarly, men who were castrated prior to puberty (e.g., testicular cancer, trauma or sexual reassignment) do not develop BPH or prostate cancer.
Further evidence supporting the role of male hormones in the development of prostate cancer is the relationship between prostate cancer risk and testosterone levels in various populations. A number of studies have shown that testosterone levels, especially DHT levels, are highest in African-Americans, followed by Caucasians, and are lowest in native Japanese. The risks for prostate cancer follow the same pattern.
This evidence, although certainly not conclusive, suggests that a greater lifetime exposure to male hormones, particularly DHT, appears to be related to an increased risk of prostate cancer. Therefore, if DHT levels could be reduced, the risk for prostate cancer also may be reduced.
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Important: This content reflects information from various individuals and organizations and may offer alternative or opposing points of view. It should not be used for medical advice, diagnosis or treatment. As always, you should consult with your healthcare provider about your specific health needs.