Ulter said:Posted by Primordial Performance:
Since ATD resembles testosterone’s structure, it competes for the aromatase enzyme, only it cannot be converted to estrogen like testosterone can. However, all steroidal based inhibitors tend to mimic the action of there parent compound, which means they can inhibit steroidogenesis from the hypothalamus and testis by directly interacting with the androgen receptor (AR) and lowering LH & FSH release.
Yes, I still believe steroidal based inhibitors can eventually limit pituitary release of LH & FSH, and eventually down-regulate the estrogen receptors needed for healthy HTPA function. You don’t see a negative effect like this with the AI’s we’ve chosen for dermacrine, which have been shown to enhance fertility across the whole endocrine axis. (references provided earlier)
Ulter said:You're already in way over your head making a product that has so many flaws we aren't even going to list them all. We'll just let the marketplace decide.
Dermacrine has so many flaws? Please enlighten us.
Ulter said:Neither product is any more than a component of PCT. There may be some value to your product. We examined the clinical research on your ingredients in 2003 and found it lacking. This is why we asked you to post it. There simply isn't any and we know that already. But just because no one has laid out the cash for clinical research doesn't mean a product is no good or doesn't do what it says. So until I see a couple hundred men posting it's the end all to PCT, I'll reserve judgment.
Fair enough, keep your eye on the Dermacrine threads.
-Pp