In my recent Ironman magazine feature about testosterone and prostate cancer, I suggested that testosterone is not the major player in either causing or promoting prostate cancer, as is the belief of many medical professionals. Instead, I pointed an accusatory finger at dihydrotestosterone (DHT), a metabolite of testosterone that is far more active in the prostate gland compared to testosterone (DHT causes prostate gland enlargement), and estrogen. While estrogen is thought of as more of a "female hormone," men also synthesize estrogen, primarily by way of the ubiquitous aromatase enzyme found in many tissues, particularly fat. Estrogen does have some positive functions in the male body, such as being involved in sperm development, and in helping to maintain beneficial high density lipoprotein (HDL) levels, which help protect against the onset of cardiovascular disease (CVD). But as men age, muscle mass often declines, which is related to low testosterone levels, while estrogen levels rise. The latter effect has to do with increased body fat levels, which harbor the aromatase enzyme that converts testosterone into estrogen.
In my Ironman feature, I discussed how one type of estrogen receptor, type-B, provides protection against prostate cancer, while the other type of estrogen receptor, type-A, actively promotes tumor development in the prostate gland. Various foods, such as soy, which are touted to offer protection against PC onset, work by interacting and promoting the activity of the estrogen B receptor.A new study confirms that the effects of estrogen in relation to PC depend on the type of estrogen involved. While there are three primary types of estrogen, the most active by far is 17-beta estradiol. This form of estrogen, unlike testosterone, is offically classified as a carcinogen, or a substance capable of promoting cancer. But there are also numerous metabolites of estrogen that also play a role in various types of cancer, including prostate cancer.
In the new study, researchers measured estrogens and their metabolites in the urine collected from 77 men with prostate cancer;77 healthy controls;and 37 men who underwent prostate biopsies, but were diagnosed as cancer-free. The results showed that the amounts of 15 estrogens and their metabolites in the PC men were similar to that of those without cancer, with the exception of one metabolite: 4-OH1.Men with PC showed significantly higher levels of this particular estrogen metabolite. Interestingly, other estrogen metabolites known to stimulate breast cancer, namely 16-KE2 and 17-epiE3, were higher in men without PC and lower in those with PC. As such, these particular estrogens may be protective against the onset of PC,most likely by either interfering with the activity of estrogen A receptors in the prostate, or boosting the activity of estrogen receptor B, which blocks estrogen A receptor promotion of PC.
