Why do anti-androgens cause "regrowth"?

BitchBoy

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It's known that anti-androgens cause regrowth in the sense of thickening existing hairs, meaning they must cause follicular enlargement. But how do they do this?

Is it that DHT in the follicle eventually dies but there's such an ever increasing onslaught of DHT that there is always enough in the follicle to replace what ever dies plus extra to cause a build up. And, when the this onslaught is reduced the follice enlarges because there's now more DHT dieing than is being replaced?

I have no idea is this is even close to what happens, it's pure guess work. Surely DHT is not an imortal cell so it must have a life span. Is it the actual presence of DHT in the hair follicle that inhibits hair growth or does it damage the hair follicle is some way that continues to effect the follicle even after the cell has died?

Any info, studies, data would be appreciated.
 

moxsom

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bboy said:
Is it the actual presence of DHT in the hair follicle that inhibits hair growth or does it damage the hair follicle is some way that continues to effect the follicle even after the cell has died?

Any info, studies, data would be appreciated.

You basically hit it on the head with these two sentences here. When DHT interacts with your DP, they turn into transcription factors for your DP cells. They usually code for inflammatory proteins, or growth factors that negatively effect hair growth. Once DHT is suppressed by whatever means, the hair cell may produce positive growth factors and have longer shaft length and width. Although it should be noted that significant hair growth is rare. One study found that those who had significant regrowth on finasteride also had significantly higher levels of scalp IGF-1, a known hair growth promoting enzyme. The correlation seemed significant, but may not be the causative factor.

The confusing part is the usual permanent changes on dermal papilla cells after DHT effects it. Like other sensitive follicles (think armpit, facial, or pubic hair), once activated by androgens they seem to be permanently effected. While it is the opposite of scalp hairs, and not exactly the same mechanism it may be similar.

Androgen metabolism by cells is an extremely confusing science, but I encourage you to read on.
 

Hoppi

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If you strip the DHT from a follicle you just give it the room to heal basically, as it no longer has the trigger which is forcing it to die. The role of inflammation and stuff seems huge too but I'm still learning about all that myself :)

Oh yeah, and wow don't go increasing insulin or IGF-1, you want your liver in tip top shape, plus that stuff messes up your T and E balance, and that's the last thing you want. Hormonal balance and good health is very important ^_^
 

moxsom

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Hoppi said:
Oh yeah, and wow don't go increasing insulin or IGF-1, you want your liver in tip top shape, plus that stuff messes up your T and E balance, and that's the last thing you want. Hormonal balance and good health is very important ^_^


Have any proof that IGF-1 would harm a hair follicle or cause inflammation. Products like raspberry ketone, and ascorbic 2-acid phosphate have shown evidence of hair growth through indirect induction of increased IGF-1.
 

Hoppi

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moxsom said:
Hoppi said:
Oh yeah, and wow don't go increasing insulin or IGF-1, you want your liver in tip top shape, plus that stuff messes up your T and E balance, and that's the last thing you want. Hormonal balance and good health is very important ^_^


Have any proof that IGF-1 would harm a hair follicle or cause inflammation. Products like raspberry ketone, and ascorbic 2-acid phosphate have shown evidence of hair growth through indirect induction of increased IGF-1.

I dunno I just reckon it's not healthy, it will lower your SHBG and probably overwork the liver. I dunno, drink a load of milk and soya if you want, see what happens O.O heh

Plus I dunno what effect it has on T production, as too much insulin apparently lowers it. But yeah erm, unless your IGF-1 is actually LOW, I see no reason to go increasing it.
 
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