Hey guys,
While this might seem almost too straightforward, this has been on my mind since receiving my Pelvic MRI a few weeks back. The purpose of the MRI was to see if there was any vessel blockage preventing semen from coming through, but they found none. What they did find was “Prostate atrophy with diffuse low T2 signal in the peripheral zone. No suspicious findings for intermediate or high-grade neoplasia.”
Not sure how much this has been discussed on the forum, but what if all our persistent side-effects are coming from a shrunken or atrophied prostate? Of course there are many other things that Finasteride effects, but I’d like to open a discussion around how an atrophied prostate affects us. As we know, Proscar/Finasteride was designed first-and-foremost as a drug to reduce Benign Prostatic Hyperplasia (BPH), or an enlarged prostate. Through reduction of DHT, the prostate is shrunken, robbed of it’s function.
Would it not seem plausible that if a prostate has taken a reduction in size (ie. it has less operable cells than before), that it would also have a reduction in function? Some of the roles of the prostate and the ultimate cause for our symptoms:
- weak ejaculation: This is probably the most common and easily seen physical symptoms of PFS - An atrophied prostate definitely explains the reduced and non-forceful ejaculate as the prostate muscle is simply not as strong as it once was, thus, it’s weakend pumping mechanism is only capable of shooting out little dribbles.
- Poor, weakened erections: The prostate erection nerves are responsible for erections. These nerves trigger the penis to swell and harden with extra blood flow into it, producing an erection. A atrophied prostate MAY have an effect on the maintenence of these nerves, leading to an erection that is <50% of what it once was.
- Reduction of 5a-reductace - The prostate gland is an area of the body where the crucial enzyme, 5-alpha-reductase, is acutely gathered. As we all know, this enzyme converts the hormone testosterone in the body to DHT (dihydrotestosterone), which is at least ten times more powerful than simple testosterone. The prostate being a central location of where this enzyme is hosted would lead one to assume that an atrophied prostate would no longer be able to support the 5a enzyme, leading us to forever be able to produce testosterone, but always have a reduction in the conversion to DHT. This reduction in enzyme also leads to countless downstream effects that can also have an effect on neurosteroid levels, gut flora, and a host of mental sides. It would be interesting to see how these are all mapped out.
My questions are:
- Would increasing our prostate size have an impact on improving it’s role in sexual function and enzyme production?
- Why does the prostate not go back to its original size pre-fin?
- How would we be able to increase our prostate size? De-atrophy prostate.
Happy to share the rest of my results of the MRI. But I’m wondering if so much of our problems have to do with a prostate that has remained atrophied from FIN use.
