moxsom said:
Lord_Justin13 wrote:
Dang, I've been noticing all these pros lately, who just know the metabolic clearance like the back of their hand, so moxsom, what causes hair loss exactly then?
It would takes pages of text to explain every single biological pathway responsible for male pattern baldness and most of these processes are not fully understood. I'll try to break it down easy for you.
Androgens like DHT can enter the cell. The cell in question here are the dermal papilla cells on your scalp, at the base of the hair follicles. Once bound to the androgen receptor, the androgen receptor will bind to a promoter site in the nucleus on the DNA of that cell. The DNA will then transcribe mRNA that will move to the cytoplasm of the cell and be translated to Polypeptides.
The polypeptides will be proteins like growth factors that will have negative effects of the dermal papilla or not allow the dermal papilla to transcribe proteins that are necessary for proper hair cycling. The dermal papilla will not return to it's original state once damaged and become smaller and the anagen phase shortens. This will give the appearance of a shorter, thinner hair, and the accumulation of the damage may not allow for the DP to produce hairs at all eventually.
Hope that helps.
This is all very interesting, I always appreciate to hear different points of view, to try and understand male pattern baldness as much as possible.
First it's important to understand why the DHT was created in the first place, if any kind of events in the persons life has a relevance the increase of DHT, whether that be from food, lifestyle choices, what have you etc...
So in regards to the idea you've driven up, it seems not only are there multiple pathways lead to hair loss/male pattern baldness, but a few keys things we could focus on, that prevent male pattern baldness, one being to stop the formation of DHT, either through inhibiting the 5-alpha reductase, or through finding a way to down regulate the conversion of T to DHT, (whether that be by redirecting the T, or lowering it, ((yet I don't know if that's healthy for men)).
Then we see, if DHT enters the cell, perhaps strengthen the cell, or finding a way of the cell evading DHT from entering it, etc...Anything to prevent the passing through, (as long as it's safe), and maybe find a way to target the resistance of the dermal papilla as well, (if that's possible).
We see that this androgen receptor containing DHT, binds to the nucleus of cell, where it is ultimately translated into polypeptides, perhaps other hormones would then provide a different transcription for RNA, unless the transcription is solely in charge by the DNA, and not affected by the androgen receptor bound DHT, thus, a different hormone or structure could be translated into some other form of poly, or something else.
However, there must be a way of reversing this damage done to the dermal papilla, and what of inducing other structures, that promote the dermal papilla to transcribe proteins that are necessary for proper hair cycling?
), it does tie in all these ideas of high DHT/testosterone, estrogen, inflammation, sebum etc etc. Whatever theory is true, it does seem that ALL these things play a role in the big picture. Those who claim with great confidence that sebum or inflammation or whatever makes little difference are often proven wrong when an anti-sebum or anti-inflammatory treatment seems to ease male pattern baldness (hence my enthusiastic inclusion of them in my regimen!).
