Glad to see you're reducing your T dose. It will help. I have always done copious amounts of BW and my dht runs just above range even on 120-140 mgs of T per week.
A few years ago my psa jumped up from its norm of .07-.08 to 1.2. This got me curious so I checked it again two weeks later and it was a 2.0. Went and got a 3T MRI (non invasive thank god) and all was well.
Ended up starting on Finasteride and it came back down to around 1.2 I believe. I then went off the Fina for a few months to experiment and pulled BW for psa again. Came back at 7.0 with 4.0 being the top of the range. Sooo, back on Fina. It's quite effective and keeps my dht sub-normal even on elevated mgs of test pw. I've had no issues while being on it. Obviously if you can avoid it, do so. I could not.
Consider 5-10 mgs per day of Cialis. It's approved by the FDA for BPH. Mix that with 1-2 mgs of Doxazosin per day and it will help even more. Doxa is an alpha blocker / smooth muscle relaxer (your weiner is smooth muscle) thus they work synergistically and will help your prostate. Your doc should have written you for Cialis a long time ago actually.
ps: There are even some studies on the effectiveness for serms in controlling BPH:
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3179830/
An important area of study that is lacking in BPH research is prevention. Since the manifestation of BPH takes decades, preventatives, especially those that target ARs and/or ERs can be utilized over time to determine their efficacy for a particular individual or type of BPH. In this regard, the androgen pathway has been the most studied and clinically used. However use of SERMs in the prevention and/or treatment of BPH [129] has merit. For example, Ellem and Risbridger argued in 2007 that potential therapies based on anti-estrogen action in the prostate will depend critically on understanding the “differential effects of ER-α versus ER-β activation” [129]. A potential strategy to inhibit proliferation in the prostate would be to block ER-α but promote ER-β activation. Perhaps the greatest promise in future anti-estrogen strategies for BPH lies in therapy with SERMs. Tamoxifen, 4-hydroxy-Tamoxifen, Toremifene, and Raloxifene inhibit proliferation of both prostatic epithelial and stromal cells in vitro [195, 196]. In another study, Raloxifene and Tamoxifen did not affect proliferation induced by E2 of a stromal cell line (WPMY-1) or BPH epithelial cell line (BPH-1), but both SERMs inhibited proliferation of prostate stromal cells in a rat model of prostatic hyperplasia induced by estrogen and androgen treatment [197]. In a study of seven beagles with spontaneous BPH, treatment with the SERM Tamoxifen resulted in decreased prostate volume [165]. A randomized trial of Tamoxifen in dogs with BPH showed an average 28.5% decrease in prostate volume compared to placebo [198]. SERMs are well-tolerated in men, and have been shown to ameliorate side effects of androgen ablation therapy in men with metastatic prostate cancer, reduce fracture risk and improve lipid profiles [199, 200]. The added prostate cancer chemopreventive benefit of SERMs furthers the attractiveness of these compounds as potential adjuvant or alternative therapies for men with BPH and LUTS [124].
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