Fibrosis (in the follicle) correlates with the time when the follicle is so far gone that it's very difficult to revive.
I understand why people suspect it's part of the problem. That timeframe is a suspicious correlation.
But that's all it is - correlation, not causation. Follicles don't need fibrosis in order to be fully shut down. If the follicle is reactivated then the new terminal hair shaft will push through the fibrosis just fine. The closest thing we have to a method of clearing the fibrosis would be deep scalp needling, and the results don't show a big improvement over shallow needling.
So... The hairs miniaturize because of the "specific dna" ... Nothing to do to save them then?
You gotta work with me on this one. I'm not trying to defend this particular theory, I'm just trying to raise and answer pertinent questions about hairloss.
For me the simple answer that many people defend "scalp hair is simply genetically predisposed to miniaturize" is a cheap way out and simply hasn't been proven to be the case.
On the article they counterargue this point and give an explanation (that was kinda weak but still)
"One study comparing characteristics of transplanted hairs to and from legs and balding scalps found that “the recipient site influences the growth characteristics of transplanted hairs” [87], with “the thickness of the epidermis, dermis, or subcutaneous tissue, blood supply, or other factors play[ing] a role in survival and growth rate differences.”
" , ie: if hair was genetically predisposed to die, it would die anywhere.
They talk about transplanted "non-Androgenetic Alopecia-prone scalp hair" into the balding scalp... their explanation is kinda weak too. "
Explaining donor hair transplant survival rates"
"
hair transplant hair count survival rates can exceed 90% one year after surgery [84]. If calcification and fibrosis are the rate-limiting factors to Androgenetic Alopecia recovery, then why do hair transplant donor hairs not miniaturize? This is answered with the model. hair transplant surgeries transplant more than just the hair follicle itself. Follicular unit grafts (FUG) procedures transplant “1–4 terminal hair follicles, one (or rarely two) vellus follicles, associated sebaceous lobules, insertion of erector pili muscle, [and the] perifollicular neurovascular network” [85]. Follicular unit extraction (FUE) procedures target singular follicles more specifically, typically with a 1 mm punch [86]. In either case, tissues surrounding each donor hair follicle are also transplanted. hair transplant donor tissue sites are not above the GA, and are therefore not under the same chronic tension before their transplantation – implying an absence of perifollicular fibrosis or dermal sheath thickening present in Androgenetic Alopecia-affected tissues. Androgenetic Alopecia progression is a decades-long process. If most transplanted donor hair follicles survive one year after hair transplantation, it’s likely these hair transplant follicles have not yet had enough time under tension exposure for fibrosis or dermal sheath thickening onset, and thereby hair follicle miniaturization."
ie: (TLDR); transplanted hairs weren't subjected to the "stress" that the scalp hairs were and Hairloss is a long process that takes ages.
their explanations are weak but at least it's something. There are some people out there that claim their only regiment is scalp massage
https://www.jdmoyer.com/2015/04/13/hair/
Either this JDmoyer guy is one big shill that uses minoxidil and finasteride OR he is into something real about hairloss.
The closest thing we have to a method of clearing the fibrosis would be deep scalp needling, and the results don't show a big improvement over shallow needling.
We don't know to what degree does dermarolling actually cleans all fibrosis but it's a fact that it does help a lot.
I want to know WHY estrogen "revives" hair follicles.. thats my main quest now
