Finasteride
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 also is 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 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 relation 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, next highest in Caucasians, and lowest in native Japanese. The risks for prostate cancer follow the same pattern. All this evidence, although certainly not conclusive, suggests that a greater lifetime exposure to male hormones, particularly DHT testosterone, 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.
