Question for Dr. Houser

  1. Question for Dr. Houser

    We're discussing issues related to the prostrate on the "35 and over" section and one of the posters cited your comments on DHT and E2 as it relates to the prostrate. I wanted to ask clarification if I may.

    Last August I suffered from prostatitis. Bad enough to where urine flow was totally stopped and a catheter tube inserted. I had just finished a heavy cycle which included 1 gram of tren (suspension, A and E), 1 gram of test and HCG per week. I didn't use any AI/SERMs, because I didn't notice any sides. I immediately got a full blood panel when I was discharged and found my E2 to be 35 (Lab Corp) but my DHT was over the top. I concluded, as did the physicians, that it was DHT that caused the enlarged prostrate, not E2. Since then, I've been concerned about my DHT levels and not overly concerned about the E2, although the E2 is well within limits. Then again, I'm only on a TRT dose of 200 mgs per week.

    Is it your belief that DHT has little or no bearing on an enlarged prostrate? My understanding is that the prostrate has receptors with equal affinity for both E2 and DHT, but since I seem to be more DHT sensitive, it's DHT that I worry about and not E2.

  2. Well, a key we are missing here is delineating ERalpha and ERbeta.

    Androgens and estrogens exert similar, yet different, effects in the prostate, and it is becoming clear that a finely tuned balance between the effects mediated by AR, ER-A, and ER-B is required for the maintenance of prostate health.

    When talking about estrogens in particular, the action is complex having both adverse and beneficial roles via ER-A and ER-B respectively (I believe we have talked about this somewhere on this forum in the past). The adverse effects, specifically aberrant proliferation, inflammation, and malignancy all require the presence and activity of ER-A and establishes a rationale for the use of ER-A-specific antagonists in the chemoprevention of prostate pathology. ER-B, however, appears to mediate beneficial effects through preventing hyperplasia and potentially preventing inflammation and carcinogenesis, thus establishing the rationale for using ER-B agonists for the treatment of benign prostatic hyperplasia and, potentially, PCa.

    In other words, if you are trying to mediate BPH or PCa, your best bet would be to completely eliminate E2 all in all, merely because we don't have great ER-A and ER-B specific agents at this time. That said; my prostate protection option is very simple:

    1) AI (although 2nd and 3rd generation have produced mixed results)

    2) Nettle (bathe in it; sounds unfortunate, but the reality is that it blocks the inherent binding of IGF-1 and E2 in prostatic and hair follicular membranes preventing very cumbersome sides).

    3) Phytosterols - prevent inflammation to the prostate better than any pharmaceutical agent I could offer you.

    4) Pumpkin Seed Oil...again, this is one to keep an eye on; if you're lucky - you can get one that tastes pretty good; use it 2-3 times per day.

    D_ Featured Author

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