Viox and phen phen, WERE REMOVED FROM THE MARKET! If Finasteride is so dangerous why has it not also been removed from the market?
In time, that's a question only the FDA and lawyers can answer, not me. Maybe it won't be removed from the market; maybe labelling changes about undisclosed mechanisms of action and potential irreversible side effects are all that is required. But plenty of drugs HAVE BEEN APPROVED, only to be removed from the market down the road -- and Finasteride is not exempt from such possibilities.
Why are the millions of finasteride users worldwide not demanding and petioning for finasterides removal?
You and I wouldn't know even if they were, because its an embarrassing problem to be left impotent by a drug and to drum up media frenzy around such a thing, putting your face out there with such a humiliating condition... so many men choose to suffer in silence, or do not go public about things. In addition, most likely men whose lives have been damaged by the medication seek out guidance and "petitioning" via their own doctors and FDA adverse reaction reports -- not through the media, so you and I wouldn't know any different unless there was a specific, published report done on this "problem". Granted, some media attention has been developing on the issue (ie, Swedish TV reports), and as more men take this drug and have problems from it, there will likely be more.
"Hard wired differently at the genetic level"? HUH?? Yeah, they're definitely hard wired differently, all right: they don't make 5a-reductase type II. That's their ONLY genetic difference.
You and I both know that's what I was referring to, Bryan! That may be their "only" genetic difference, but as I explained, its a major one. 5AR2 is a critical enzyme responsible for a variety of hormonal/neurosteroid pathways, not just T to DHT... and if people actually did their research, they'd realize this. Not having a functional 5AR2 enzyme is not some "trivial" matter.
That's a far cry from taking a normal male and then transforming his hormonal profile to match that of a 5AR2 deficient pseudohermaphrodite.
I don't think it's a "far cry" at all.
When 99.9% of the world's population has a functional 5AR2 enzyme, you cannot say that transforming such people's hormonal profile to match that of a genetically 5AR2-deficient pseudohermaphrodite is normal -- it's anything but. If we weren't meant to have functional 5AR2 enzymes, we wouldn't -- the pseudohermaphrodites are the EXCEPTION to the rule -- "freaks" of nature, mutations -- not THE rule.
The medical community has a complete understanding of A5R2
The medical community is still trying to figure out how MANY processes in the body works, to say they have a "complete" understanding of 5AR2 is asinine. They do not have a "complete" understanding of 5AR2 at all and are in fact discovering new things they never knew about the enzyme and its various functions as time goes on.
I believe that the DHT levels during/post finasteride are safe, this is the consensus among the vast majority of medical profesionals and the FDA, if it were not Finasteride would have been pulled off the market by now.
Just because you believe something doesn't make it true. As for being pulled from the market, see previous comments.
there are tens of millions of men worldwide who take finasteride without side effects
Tens of millions eh? Where'd you pull that stat from?
Straight from Merck:
http://www.propecia.co.nz/safety.asp
"Worldwide, more than 2 million men have taken PROPECIA".
Granted it says "more than 2 million", but it certainly doesn't say "tens of millions", either.
Finally, as for comments that DHT has no use in the human male after puberty:
http://www.biolreprod.org/content/72/4/851.full
"Testosterone, the most abundantly produced androgen, is reduced by 5?-reductase to
the more potent dihydrotestosterone (DHT). DHT mediates many of the actions ascribed to androgens, including the differentiation of the male external genitalia and prostate during fetal development, virilization at puberty, and
male sexual and aggressive behavior [1–3]. "
http://www.ncbi.nlm.nih.gov/sites/entre ... s=19090946
"Sexual AEs are reported in clinical trials at rates of 2.1% to 38%. The most common sexual AE is ED, followed by EjD and decreased libido. These effects occur early in therapy and attenuate over time. A
proposed mechanism for sexual dysfunction involves decreased nitric oxide synthase activity due to decreased dihydrotestosterone. "