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I think we may be focusing on wrong things


#1

I’d say the main reason why its so hard to regrow any hair is not DHT, but the periofollicular fibrosis that is caused by the balding process.

Anyone ever heard about anything that could reverse hardening of the collagen?


#2

» I’d say the main reason why its so hard to regrow any hair is not DHT, but
» the periofollicular fibrosis that is caused by the balding process.
»
» Anyone ever heard about anything that could reverse hardening of the
» collagen?

http://www.androgeneticalopecia.com/hair-loss-biology/hair-loss-histology-men-women.shtml

When the hair miniaturizes, it ascends upward from the reticular dermis to the papillary dermis with a long streamer behind it and cycles up and down through anagen and telogen in the papillary dermis as a small vellus-like hair. If this hair is re-stimulated by treatment to transform again into a terminal hair, it travels back down that streamer or tract to the reticular dermis and generates a terminal hair again. In fact it is the presence of arrector pili muscle and angiofibrotic streamers which helps to differentiate miniaturized hairs of androgenetic alopecia from true vellus hairs.In the vast majority of cases, there is no genuine reduction in the number of follicles, and follicular fibrosis is only seen in about 10% of cases. . However, fibrosis is seen in a small number of normal scalp biopsies as well.

So fibrosis is not an issue at young age, unless obviously you’ve been bald for ages then your scalp probably has lot of follicular fibrosis.


#3

» » I’d say the main reason why its so hard to regrow any hair is not DHT,
» but
» » the periofollicular fibrosis that is caused by the balding process.
» »
» » Anyone ever heard about anything that could reverse hardening of the
» » collagen?
»
» http://www.androgeneticalopecia.com/hair-loss-biology/hair-loss-histology-men-women.shtml
»
» When the hair miniaturizes, it ascends upward from the reticular dermis to
» the papillary dermis with a long streamer behind it and cycles up and down
» through anagen and telogen in the papillary dermis as a small vellus-like
» hair. If this hair is re-stimulated by treatment to transform again into a
» terminal hair, it travels back down that streamer or tract to the reticular
» dermis and generates a terminal hair again. In fact it is the presence of
» arrector pili muscle and angiofibrotic streamers which helps to
» differentiate miniaturized hairs of androgenetic alopecia from true vellus
» hairs.In the vast majority of cases, there is no genuine reduction in
» the number of follicles, and follicular fibrosis is only seen in about 10%
» of cases. . However, fibrosis is seen in a small number of normal scalp
» biopsies as well.

»
»
» So fibrosis is not an issue at young age, unless obviously you’ve been
» bald for ages then your scalp probably has lot of follicular fibrosis.

I’ve heard that it takes 5 years and than the process happens. But this article suggests the fibrosis is much more rare then I thought.


#4

There must be something going on there. I mean if even 100% dht reduction does not reverse the process… there must be some reason.


#5

» There must be something going on there. I mean if even 100% dht reduction
» does not reverse the process… there must be some reason.

Immune system anyone?


#6

I’m just pulling stuff out of my a** here that I can’t remember the source.

But I think I read once that when hair growth gets restarted with extreme means (serious amounts of Cyclosporine, etc), the new hairs just shove any collagen fibrosis aside and come right up.


#7

» I’m just pulling stuff out of my a** here that I can’t remember the source.
»
»
» But I think I read once that when hair growth gets restarted with extreme
» means (serious amounts of Cyclosporine, etc), the new hairs just shove any
» collagen fibrosis aside and come right up.

so its the growth inhibitory factors

But still I dont understand what suddenly happens that the follicle just gives up forever.


#8

I think it’s basically just the ongoing immune system attack to the follicle’s cells, nothing more glorious than that.