Morgentaler, A, “Testosterone and prostate cancer: an historical perspective on a modern myth,” Eur Urol, 2006 Nov;50(5):935-9.
Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, Massachusetts
Back in 2003 Dr. John Lee published his booklet, “Hormone Balance for Men.” The basic premise was Dr. Lee’s seemingly revolutionary stance that it’s not testosterone that causes prostate cancer, it’s estrogen dominance. Yes, men can also be estrogen dominant. Of course this stance was greeted with scorn by his colleagues because it’s been commonly accepted in conventional medicine that testosterone causes prostate cancer. Of course the tide is now turning and this review from Harvard of the “testosterone causes prostate cancer” literature is the first wave.
According to an article in the Harvard University Gazette, the author of the study, Abraham Morgentaler, a urologist at Beth Israel Deaconess Medical Center and associate clinical professor at Harvard Medical School said, “We reviewed decades of research and found no compelling evidence that testosterone replacement therapy increases the incidence of prostate cancer or cardiovascular disease.”
In the review, Morgentaler reports that, “Multiple subsequent reports revealed no pCA [prostate cancer growth] progression with T [testosterone] administration, and some men even experienced subjective improvement, such as resolution of bone pain. More recent data have shown no apparent increase in pCA rates in clinical trials of T supplementation in normal men or men at increased risk for pCA, no relationship of pCA risk with serum T levels in multiple longitudinal studies, and no reduced risk of pCA in men with low T. The apparent paradox in which castration causes pCA to regress yet higher T fails to cause pCA to grow is resolved by a saturation model, in which maximal stimulation of pCA is reached at relatively low levels of T.”
Morgentaler concludes, “This historical perspective reveals that there is not now—nor has there ever been—a scientific basis for the belief that T causes pCA to grow. Discarding this modern myth will allow exploration of alternative hypotheses regarding the relationship of T and pCA that may be clinically and scientifically rewarding.”