I really find it hard to believe how no doctors can point the pin on this.
We are all from different countries, seen different doctors. Still have no conclusion?
The only factors making us completely different is we don’t know all of our previous medical history. We all suffer from “Post Finasteride Syndrome”, We all want to know why? We all spend hours thinking about how?
Why are we different? Did we all have low T at the time of consumption or was our T lowered throughout? Was the crash due to supression of DHT? we simply don’t know.
These questions need to be answered. We as a group need to figure out why…The information is in front of us, we are the answer.
I think it would be great to have a consensus on similiarites of blood/siliva results of hormonal levels, age, weight, underlying issues, past medications etc.
Why did finasteride alter our GNRH production?
I benefited greatly from my treatment, though there is still other abnormalitys in my levels. I have so many un-answered questions, Where these other symptoms previous discrepencies, did finasterides actions alter other levels. Why?
We know now that 5AR2 has other actions other than Testosterone —> DHT.
While we are waiting on the studies, we can do other things.
It’s almost 2013. Let’s beat this shit.
en.wikipedia.org/wiki/Finasteride
[Size=4]Mechanism of actionTestosterone in males is produced primarily in the testicles, but also in the adrenal glands. The majority of testosterone in the body is bound to sex hormone-binding globulin (SHBG), a protein produced in the liver that transports testosterone through the bloodstream, prevents its metabolism, and prolongs its half-life. Once it becomes unbound from SHBG, free testosterone can enter cells throughout the body. In certain tissues, notably the scalp, skin, and prostate, testosterone is converted into 5α-dihydrotestosterone (DHT) by the enzyme 5α-reductase. DHT is a more powerful androgen than testosterone (as it has approximately 3-10x the potency at the androgen receptor, the site of action of the androgen hormones), so 5α-reductase can be thought to amplify the androgenic effect of testosterone in the tissues in which it’s found.
Finasteride, a 4-azasteroid and analogue of testosterone, works by acting as a potent and specific, competitive inhibitor of one of the two subtypes of 5α-reductase, specifically the type II isoenzyme.[32] In other words, it binds to the enzyme and prevents endogenous substrates such as testosterone from being metabolized. 5α-reductase type I and type II are responsible for approximately one-third and two-thirds of DHT production in the body, respectively.[33] Accordingly, finasteride selectively prevents the conversion of testosterone into DHT by the type II isoenzyme, resulting in a decrease in serum DHT levels by about 65-70% and in prostate DHT levels by up to 85-90%,[34] where expression of the type II isoenzyme dominates. Unlike dual inhibitors of both isoenzymes of 5α-reductase which can reduce DHT levels in the entire body by more than 99%, finasteride cannot completely suppress DHT production because it lacks significant inhibitory effects on the 5α-reductase type I isoenzyme, possessing approximately 100-fold less affinity for it compared to type II.[33] In addition to blocking the 5α-reductase type II isoenzyme, finasteride is a competitive inhibitor of the 5β-reductase type II isoenzyme,[35] though this is not believed to play any role in its effects on androgen metabolism.
By blocking DHT production, finasteride reduces androgenic activity in the scalp, treating hair loss at its hormonal source. In the prostate, inhibition of 5α-reductase leads to a reduction of prostate volume, which improves the symptoms of benign prostatic hyperplasia (BPH) and reduces the risk of prostate cancer. Inhibition of 5α-reductase also leads to a reduction in the weight of the epididymis and a decrease in the percentage of motile and morphologically normal spermatozoa found in the epididymis.[36]
Cause of mood-related and sexual side effectsDHT, and neuroactive steroids (NAs) such as allopregnanolone (ALLO) and tetrahydrodeoxycorticosterone (THDOC), potent positive allosteric modulators of the GABAA receptor—which is the same site of action of euphoriant and anxiolytic drugs like benzodiazepines and alcohol), are important endogenous neuroregulators that have been shown to possess powerful antidepressant and anxiolytic effects as well as to play a positive role in sexual function.[24][23][37] Their biosynthesis is dependent on both isoforms of 5α-reductase, and accordingly, finasteride has been shown to reduce their formation in the body.[38][39][40] As such, this effect of finasteride is a likely cause of the emotional and sexual side effects associated with the drug.[23][24] Additionally, due to the fact that the NAs and not just DHT are involved, the fact that the mood and anxiety-related side effects occur not only in men but in women as well[25] can also potentially be explained.[/size]