Prostate Health
Benign enlargment of the prostate gland effects most men over the age of 60. Those afflicted with benign prostate hyperplasia (BPH) have trouble urinating and voiding and are overly sensitive to any residual urine left in the bladder resulting in a feeling that they have not completely emptied their bladder. Men with BPH are also at a higher risk of developing prostate cancer.
According to conventional views BPH/prostate cancer develops due to the presence of a metabolite of testosterone known as dihydrotestosterone (DHT). Testosterone is converted into DHT by an enzyme known as 5-alpha-reductase. When DHT binds to receptors in the prostate gland it activates growth factors that stimulate cell proliferation. Although this is the most widely accepted theory there is insufficient scientific evidence to support it. If indeed this was the case we would expect the highest incidence of prostate problems to occur when either testosterone levels were at their peak (ages 18 to 25) which is obviously not the case, or alternatively when DHT levels rise. There is no evidence which suggests an increase in 5-alpha-reductase activity occurs with the aging process as DHT levels remain fairly constant throughout life for most men. In addition it has been shown that there is no accumulation of DHT in the prostate gland with the aging process. This theory therefore does not adeqately account for an increase in prostate problems with age.
Recent evidence and a new emerging theory suggests estrogen dominance may be responsible for BPH/prostate cancer, not DHT as previously believed. It is accepted fact that as men age their testosterone levels decline reducing their testosterone/estrogen ratio thus allowing estrogens to adhere to receptors on the prostate due to a lack of competition with testosterone causing prostate growth. In addition German researchers have clearly documented a dramatic, age-related accumulation of estrogen in human prostate glands. This work correlated age, estrogen accumulation, and the presence of benign prostatic hypertrophy. This finding highlights the role of estrogen as a growth promoting hormone in prostate. Recent work also shows that estradiol provokes increases in prostate specific antigen (PSA) production in human prostate tissue. This increase in PSA is as great as that seen with testosterone. In addition it was found that PSA production was specifically inhibited by 2-methoxyestradiol, the beneficial estrogen metabolite whose production is promoted by DIM (see below).
In addition recent research findings also suggests that prostate cancer may be caused not by the estrogens themselves but by one of their metabolites. Research on the minor metabolites of estrogens, specifically the metabolites 2-hydroxyestrone and 16-alpha-hydroxyestrone has revealed the 2-hydroxyestrone metabolite is a “good” estrogen, while the 16-alpha-hydroxyestrone metabolite is a “bad” estrogen because it tends to damage DNA and cause abnormal cellular proliferation. In a variety of animal models, it is definitely associated with a higher risk of cancer and with the progression of that cancer. In these same animal models, if the proportion of 16-alpha-hydroxyestrone can be made to go down and that of 2-hydroxyestrone to go up, the incidence of cancer is reduced.
At this stage until more research is done to determine a definite cause BPH/prostate cancer should be considered to be the result of possibly a combination of increasing DHT levels, estrogen dominance and unfavourable estrogen metabolism. In addition an age related decline in progesterone levels may cause an increase in DHT in some men as progesterone is a potent 5-alpha-reductase inhibitor.
Diagnosis Testing
Obviously a lot more research is needed before a definite physical cause can be identified. However if you suffer increased frequency of urination, hesitation before urination or increased dribbling make sure you have the following tests:
(1) A prostate exam – you should also have your urologist evaluate the size of your prostate gland.
(2) PSA test – Prostate-Specific Antigen (PSA) testing, although not totally reliable, still remains the primary screening test to differentiate between BPH and prostate cancer.
(3) Hormone tests – in addition you should have your estradiol, estrone,free testosterone, dihydrotestosterone, DHEA and progesterone levels checked by either urine/serum or saliva tests to determine if any imbalances exist.
(4) Urinary estrogen metabolite tests are also available to measure the levels of the 2- and 16- hydroxyestrone to determine if there is an unfavorable balance between the two which may be feeding the prostate proliferation.
Treatment
The treatment of BPH should include optimising hormone levels and balance including estrogen metabolism in conjunction with ceratin beneficial supplements.
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