books.google.ca/books?id=ODBLQc2 … #PPA162,M1
Note that Fin inhibits Type I & II equally in rat, but is predominantly a Type II inhibitor in humans. Also, confirmation that drug has castrate-like effect on human prostate.
WOW!! Looks like a very interesting book, and a GREAT find Mew!! This finally clarifies A LOT of this complicated mess. At least for me… I suppose we can hope for two things after this:
-That this explains more or less enough now to get cured, because we know whats going on better, we may all get some effective treatment options now, and
-Maybe this shit will soon get banned, and we can all jump on board together for some sort of a possible class action lawsuit against Merck soon.
Because this stuff is BULL - SHIT!!!
Does this shed some light on some better possible treatment options in your eyes? Doesn’t this sort of tie everything together, and clarify? Now what would you propose doing to get out of this mess?
Boston, this is simply a summary of what other studies on this forum have already documented, it is actually nothing new – just another way of saying the same things.
Beyond the castrate like effects to the Prostate, we also have to remember that while on the drug, we alter androgen/estrogen ratio in favor of Estrogen, change our hormonal profile to match that of a pseudohermaphrodite via creating a surrogate state of 5AR2 (and thus DHT) deficiency, and inhibit 5AR-derived neurosteroid production in the brain.
Quitting the drug should reverse these effects as 5AR2 regenerates 1.5-2 weeks later – and as many have experienced, we did briefly return to our pre-Finasteride state at that time – however, it was short-lived as within another week or two, Testosterone levels came crashing down along with all the symptoms we have been stuck with since – in some cases despite guys going on TRT even.
So in my opinion while the prostate definitely has a relation to the mechanical aspects of getting an erection (ie, guys that undergo radical prostatectomy often find they are impotent after removal of the prostate), it doesn’t explain the complete loss of libido, chronic fatigue, scrotal shrinkage, impaired memory and other ongoing issues many have – despite being able to get hard with Viagra or being on TRT.
What the above does provide is just another scientifically documented example that the drug does vs how Merck markets it, based on the soft language they use in their prescribing information/website – because I doubt many of us would have been so eager to hop on it knowing we were about to chemically castrate and involute (loss of function) our prostates via apoptosis (cell death), for one (whereas Merck states Fin “shrinks” the prostate – not nearly as bad sounding, is it?).
Anyway, the search continues for the reasons behind the Post-Fin endocrine system crash, and why some of us can’t seem to recover since.
“Finasteride has been clinically proved to reduce the median volume of the prostate in patients and is currently prescribed for the treatment of BPH. The compound also has demonstrated efficacy in the treatment of male pattern baldness and is prescribed for this indication as well. Subsequent to the discovery of finnasteride, it was found that there are two isoforms of steroid 5a-reductase in mammals, type 1 and type 2. The type 2 isoform is primarily active in reproductive tissue, while the type 1 isoform contributes to DHT formation in the skin, liver, and reproductive tissue. Finasteride inhibits both isozymes in rats, but selectively inhibits the type 2 isozyme only in humans.”
Copeland, Robert A. Evaluation of Enzyme Inhibitors in Drug Discovery : A Guide for Medicinal Chemists and Pharmacologists.
Hoboken, NJ, USA: John Wiley & Sons, Incorporated, 2005. p 242.
Copyright © 2005. John Wiley & Sons, Incorporated. All rights reserved.