Friday, December 24, 2010


Dihydrotestosterone or DHT is a metabolite of testosterone. The body produces DHT from testosterone by the actions of the enzyme, 5-alpha reductase. In most tissues of the body, DHT is the predominant androgen, since it binds to the androgen cell receptor 5-times greater than does testosterone. In muscle, however, DHT is rapidly degraded by enzymes, making testosterone the predominant androgen in muscle tissue. DHT, among other effects, plays a major role in the development of male sex organs. On the negative side, DHT is associated with male pattern baldness, acne onset, and prostate gland enlargement.
    In the prostate gland, DHT is the major androgen, not testosterone. Many studies have suggested that DHT stimulation of prostatic glandular tissue may be a root cause of prostate cancer. Most doctors are averse to providing supplemental testosterone treatment, even to men with a clear clinical deficiency of the hormone, because of fears of initiating prostate cancer onset. This fear is unfounded, since the prostate is receptive to normal blood levels of testosterone, and taking anything above this amount doesn't have any effect on the prostate. Conversely, having a chronic low testosterone level can induce subtle changes in the gland that may result in prostate cancer.
    Some doctors think that even if testosterone itself won't adversely affect the prostate gland, the fact that testosterone is converted into DHT by way of 5-alpha reductase makes testosterone therapy a hazardous choice. They are assuming that using any type of testosterone drug will lead to higher levels of DHT, and thereby increase the chances of prostate cancer. This notion was examined in a new study that involved 31 healthy men, ages 35 to 55. These men received either a DHT gel preparation or a placebo for one month. After four weeks, 27 men completed the study. In those who used the DHT gel, blood levels of DHT rose sevenfold, while testosterone levels decreased, presumably due to a negative feedback effect to the brain. In the placebo group, testosterone (T) levels remained unchanged. But the levels of DHT inside the prostate gland didn't differ between those who used the DHT drug and those who did not. In addition, other measures of prostate growth and function, including PSA, epithelial cell proliferation (an indicator of cancer), and androgen-related gene expression were not different between groups.
     Thus, this study shows that DHT activity mimics that of supplemental testosterone, in that although blood levels may increase when you use these hormones, the levels inside of the prostate gland don't change. This is further proof of the notion that testosterone causes prostate cancer is rubbish.

Page, S, et al. Dihydrotestosterone administration does not increase intraprostatic androgen concentrations or alter prostate androgen action in healthy men: A randomized-controlled trial. J Clin Endocrin Metabol 2010: in press.

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