docj077 said:
Bryan said:
docj077 said:
http://endo.endojournals.org/cgi/content/full/138/1/356[/url]
Quote:
"Testosterone-induced inhibition of outer root sheath cell proliferation occurred only in coculture with dermal papilla cells derived from the bald scalps of adult macaques but not with dermal papilla cells from the hairy occipital scalps of adult macaques or the prebald frontal scalps of juvenile macaques"
S Foote.
Foote,
Again, you fail to read your own studies. Androgens do not work directly on the keratinocytes that grow hair. The androgen receptor is found on the dermal papillae cells and molecular mediators are released from the dermal papillae cells that cause both inhibition of growth and the necessary molecules needed for perifollicular fibrosis and collagen deposition.
Doctor, Stephen is well-aware of all that, now. His specific point in that quote above is about what causes PRE-BALDING hair follicles to eventually become sensitive to androgens after puberty in the way that you described in your paragraph above. He tries to make as much hay as possible out of the simple fact that medical science doesn't yet understand exactly how that process works. He has his own theory, which is that fluid pressure and contact inhibition CAUSE them to become sensitive to androgens in that way, although he is unable to cite any other biological evidence of contact inhibition causing such a change in any kind of tissue at all.
Bryan
It's rather frustrating to attempt a logical debate with someone when they don't even read the studies that they post. I'm trying to figure out if he made it past the title and neglected to even read the abstract, because what he's saying is completely different from what that study is saying.
This is bulls**t.
Both you and Bryan are deliberately trying to avoid the simple point here :roll:
The "changed" response to androgens of pre-existing male pattern baldness follicles against non male pattern baldness follicles, can be logically explained by indirect actions in-vivo.
It is you two that make a wild assumption that androgens are "directly causing" this change!
The in-vitro studies prove you wrong, end of story!
Pre-male pattern baldness follicles are "NOT" turned into male pattern baldness follicles by direct exposure to androgens for God's sake can't you read??? :roll:
You have to try to play this down Bryan because you cannot explain it without making up fantasy mechanisms that get more and more ridiculous.
That is not science, and if you two think the people here are stupid enough to just take your word for all this, you are arrogant beyond belief :wink:
So just provide some "REAL" science to prove your claim that follicles are inherently "different"????
If you can't, your idea's fail, simple. You can both try to distract from the evidence that proves you both wrong, but you are not fooling anyone. 8)
S Foote.[/quote:82600]
Why are you turning this on us? For the longest time you said that androgens directly caused striated muscle hypertrophy, which led to lymphedema and contact inhibition. It's you that assumes that androgens are the only molecules needed for this to take place. You turn coat far too easily and it's quite annoying how you consistantly try to cover your ***.
My theory dictates that androgens bind the androgen receptor, this complex is internalized where it moves to the nucleus as a nuclear receptor, and finally this complex initiates the transcription of TGF-beta genes within the dermal papillae cells.
TGF-beta II is the regulatory molecule in my theory, not androgens. In fact, I don't even think that androgen inhibition is the only target that a hair loss regimen should embrace.
TGF-beta II causes fibroblast activation with subsequent in vivo collagen deposition and fibrosis. Not only that, but TGF-beta II also causes keratinocyte apoptosis. The previously mentioned process has been proven to be inhibited in vitro by minoxidil. TGF-beta II has also been shown to cause this same fibrosis in studies involving retinoids.
That's my theory and androgens are only required to begin the process. However, they are not required to finish the process as completely different molecules take over.
Inhibition of androgens, androgen receptors, androgen metabolism and formation, and inhibition of TGF-betaII molecules and receptors are all very real avenues of treatment and all of them are also available to the public in the form of 5AR type II inhibitors, androgen receptor blockers, apple poly or minoxidil, immunosuppressants, and topical macrolides. All these drugs target the processes and molecules in my theory.
Androgens do not directly cause apoptosis, fibrosis, or any other process. They bind to nuclear receptors, which means they must be internalized and initiate transcription of genes to serve their function.
Stop changing your theory just to make yourself look better. It's getting old
Also, stop using in vitro studies using cultured hair follicles as any sort of foundation for your argument. Cultured follicles lack the appropriate extracellular matrix and tissues necessary for the minaturization process to even occur. The molecular mediators may be produced (which they are in vitro), but you will not necessarily see a change unless all factors are in place including the required surrounding cells such as fibroblasts.
Again, the most pressing concern is to finally get to the bottom of why androgens produce those substances in an opposite fashion in scalp hair follicles versus body hair follicles. Of course, I fully acknowledge that identifying all those growth factors and growth inhibitors in the first place will probably be a prerequisite for that.
