The reason for use of aromatase inhibitors in the treatment of BPH has nothing to do with their effect on DHT, both estrogens and androgens have been shown to induce BPH.
Testosterone converts directly into DHT via 5alpha-reductase.
Aromatase inhibitors (when used off cycle) would actually increase your DHT, since they increase LH/Test.
That's the main reason why aromatase inhibitors like atamestane have little effect on BPH, since they also increase androgens which promote prostatic growth.
Use an aromatase inhibitor +1- 5 mg of Finasteride ED.
Some herbal meds like saw palmetto & nettles are also effective.
Endocrine treatment of benign prostatic hypertrophy: current concepts.
Matzkin H, Braf Z.
...Recently, the role of estrogens has been emphasized with the finding that stromal hyperplasia is the main change occurring in BPH. Lately, research has been initiated to examine the clinical effect aromatase inhibitors would have in the treatment of human BPH. Since there is enough evidence that both the epithelial and stromal components of the human prostate undergo hyperplasia in BPH, and individuals vary with respect to their relative epithelial/stromal components, both structures would have to be reduced for therapy to be successful. Therefore, the combination of an antiandrogenic and antiestrogenic effect is theoretically promising...
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J Urol (Paris) 1995;101(1):22-5 Related Articles, Links
Endocrine therapy for benign prostatic hyperplasia in the 90's.
Ekman P.
Department of Urology, Karolinska Hospital, Stockholm, Sweden.
Endocrine therapy by means of castration for benign prostatic hyperplasia was introduced already in the middle of the 19th century. The technique was never popularized and was abandoned following the introduction of safe surgical techniques. In the second half of this century, small series of various endocrine treatments have been reported, mainly using progestational agents. The hormone dependency of the prostate is unique, since testosterone itself is not very active on the prostate cells but has to be converted to 5 alpha-dihydrotestosterone, which is almost ten times as effective an androgen in the prostate cell. By blocking this conversion, highly specific antiandrogenic effect will be obtained in the prostate but not in other organs of the body. The first 5 alpha-reductase inhibitor, finasteride, has proven effective in reducing prostate DHT. In large clinical trials, it has shown to reduce prostate size, improve urinary flow and reduce symptom score, statistically significantly better than placebo. The effect is sustained over at least 3 years. In a double-blind, randomized, placebo-controlled study over 2 years, patients were similarly improved in the finasteride group, whereas they deteriorated in the placebo group. This indicates that finasteride is able to halt the progression of the natural course of benign prostatic hyperplasia. Benign prostatic hyperplasia, generally believed to be a stromal disease, is potentially dependent on estrogens for its development. By blocking aromatization of testosterone to estrogen in the prostate cells, a hypothetical beneficial effect on the disease process should be gained...
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Estrogen reduction by aromatase inhibition for benign prostatic hyperplasia: results of a double-blind, placebo-controlled, randomized clinical trial using two doses of the aromatase-inhibitor atamestane. Atamestane Study Group.
Radlmaier A, Eickenberg HU, Fletcher MS, Fourcade RO, Reis Santos JM, van Aubel OG, Bono AV.
Department of Clinical Development Oncology, Schering AG, Berlin, Germany.
BACKGROUND: The concept of estrogen withdrawal by an aromatase inhibitor in the treatment of benign prostatic hyperplasia (BPH) was assessed in a prospective, randomized, double-blind, placebo-controlled multicenter trial. METHODS: Two hundred and ninety-two patients with clinical symptoms of BPH were randomly allocated to one of the following treatments for 48 weeks: placebo or the selective aromatase inhibitor, atamestane, at a daily dose of 100 mg or 300 mg. Both doses of atamestane significantly reduced serum concentrations of estradiol and estrone, and produced a slight, dose-dependent, counter-regulatory increase in peripheral androgen concentration. RESULTS: Clinical symptoms improved during treatment in all three groups. Even after 48 weeks, the effect of active treatment did not exceed the effect seen with placebo. Overall tolerance of 100 mg atamestane was excellent, but 300 mg showed a slightly increased incidence of side effects compared with placebo. CONCLUSIONS: The conclusion from this study is that the reduction in estrogen concentration using the selective aromatase inhibitor atamestane has no effect on clinically established BPH.
