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Why follicles minitaurize? Bryan, benji, haraldo, anyone?


Before you say ‘Duh! DHT’…what I wanna know is why hairs minitaurize, if DHT attacks follicles then why don’t they just stop making hair, why do they have to minitaurize?

I’ve lost my hair quickly (NW6 @ 26) and I remember when my hair use to fall out and I could see the tip being much thicker than the root area. So they were minitaurizing rather quickly during a single anagen phase.

Is it because DHT affects certain signaling (WNT?), and as the signaling required for hair growth decreases the follicle becomes less active and hair diameter decreases? If this indeed is the case, then do you guys think it would be possible to increase that particular signaling so that the follicle starts producing terminal hair right way, without having to go through several cycles during which hair gets thicker - as is the case with finas/minox.

I read somewhere (don’t remember where though) that hair minitaurize because DHT is essentialy destroying the follicles and area around it is filled up with collagen. However, that theory fails to explain many success stories of people getting a lot of their hair back when going on finas/minox. And also that if the follicle has been killed/minitaurized permanently then how anti-inflammatory drugs can reverse baldness.


Duh, DHT!

:stuck_out_tongue: :stuck_out_tongue: :stuck_out_tongue:


Sorry, I couldn’t help it.

How about this article?

J Am Acad Dermatol. 2004 May;50(5):777-9. Related Articles, Links

Pathogenesis of androgenetic alopecia.

Rebora A.

Although it is universally accepted that dihydrotestosterone causes baldness, how it does so is not well understood. I propose that 3 mechanisms are at work: miniaturization by a dihydrotestosterone-induced acceleration of the mitotic rate of the matrix that leaves less and less time for differentiation; an increased telogen shedding as a result of the shortening of the hair cycles that increases the telogen number per unit of time; and the increased number and duration of the lag phase or kenogen. That this last mechanism is related to dihydrotestosterone is unclear.

PMID: 15097964


» Sorry, I couldn’t help it.


» How about this article?
» PMID: 15097964

I don’t have access to these online pay sites. Can you copy/paste portion of the study that talks about mitosis and such?

Also, This still leaves my question unanswered. Which was that if we increase the WNT signaling which, according to Elaine Fuchs’ video, increases hair regeneration. Would we be able to get follicles straight into producing terminal hair? or would the follicle still need to go through the thickening phase?

I understand that the science isn’t clear yet…but what do you guys think? any hypothesis?


My “theory” of baldness… (Topicals)Post reply
For any of you who may be newbies wondering about baldness-------------you inherit a variant of the androgen receptor gene that can express itself more or less strongly depending on genetic chance. If it expresses itself strongly with CAG-repeates on the AR-receptor polymorphism, the hair outside your hippocratic wreath’s androgen receptor’s are much more adept at uptaking male hormone, especially dihydrotestosterone. Having alot of DHT in the scalp (balding scalp has more DHT prevalent in it, despite the fact that no difference in the genes that are associated with alpha five reductase have ever been found) has been shown to be able to invigorate androgen receptors even MORE. One too much androgen is uptaken…eventually something happens to the hair follicle and a different set of genetic instructions are obeyed within it. The dermal papilla starts cranking out more negative growth factors like DKK-1, thromobospondin, FGF-5, PKC, TGF-beta 1, TGF beta 2, etc. In particular, DKK_1, which leads to the cell death of the keratincoyetes in the root sheath, is probably very important…these dead cells in turn hanging around the infidulum (the small opening in the dermis where the hair shaft emerges from the body) is probably why the immune system begins attacking the hair follicle and TGF beta overexpression which is associated with excessive collagenous deposition in other autoimmune disorders, is downstream from it. According to researchers, common baldness looks like organ-rejection. Cyclosporin, an immunosuppressant, is the best regrowth agent we have still, but it would kill you. I think there is a good chance that these dead keratinocyte cells in the infidula, downstream of DKK-1 expression, just might be what gets the immune system interested in the hair follicle and gets it to begin a slow attack upon it. Immuno cells gather around the follicle in larger than normal numbers, and the inflammatory cytokines start to inflame the INFIDULUM FIRST, the associated oxides, Reactive Oxygen Species, killer cells, etc. begin to prematurely age and degrade the follicle-damaging cells and harming various cell’s DNA (damaged DNA is something else the immune system might begin to attack as it would also look like a foreign body). Like in other autoimmune disorders, excessive collagen gets deposited around the offending organ as a consequence of too much TGF-beta expression—which also happens to be a negative growth factor in the dermal papilla released to other follicle cells in the hair cycle after androgenic uptake at the androgen receptors, but I digress. Ass the collagen fibers in the connective tissue sheath around the follicle get crosslinked and harden, its hard for necessary blood vessels to grow through them, and the now-weakened follicel to re-enlarge in its next anagen phase. But then again, if the follicle was in good condition, as Ralf Paus has suggested, the necessary cytokines to eat through that collagen would probably be secreted. Anyway, over time, a certain CD200 type of molecules that usually are at the base of the follicle stop being present, and this molecule is an immuno-marker that tells the immune system not to attack a certain organ. So even if you stop androgenic uptake (castration), the immune system is probably still doing some meager suppression of the now miniaturized follicle that keeps it from re-enlarging. Vellus hairs from MPB men have been moved to immuno-deficient mice and were noted to regrow as well as donor hairs on their backs, but these mice dont have immune systems and probably extremely low androges…but it does show that the ability to grow and thrive is still present in the follicles. That is probably “baldness”, as the immune system is going to try to eliminate dead cells and anything around the area is going to be effected by all the infllammatory subtstances the immune system will use. Baldness looks like organ rejection microscopically. Its been shown that wreath area hairs can succumb to testosterone and DHT if experiments give enough of them to the hairs…so I dont believe their is some magic difference in the hair’s basic characteristics but a difference in the amount of DHT the hair can make via its alpha five reductase enzyme in their root sheaths and a big difference in how well the hairs androgen receptors work and how chemcially stable they are. In a way male baldness is probably because you have too-well-working-androgen-receptors and too-well-working-alpha-five-reductase-enzymes in your hair. You are “too manly” in a place you dont want to be.

Obviously, “my theory” places the blame at DKK-1’s doorstep, but its all because of cag-repeat mutations on the androgen receptor gene and how these mutations get more prevalent as you age. Its the one gene that has been nailed down as being associated with androgenic alopecia thusfar. Over 98 percent of men with baldness have this variant of the androgen-receptor gene and how many mutations of the gene you have would make its manifestation within you even more intense, while only 76 percent of men without baldness have it. A large German study with over 1500 men determined that, so its a solid fact. Experiments have shown that occipital hair, when given a high androgen stimulis, will react negatively to male hormone. This is your hippocratic wreath hair going bald when scientists simply give it MORE male hormone. Your hippocratic wreath’s hair doesn’t have as much androgen receptors or as much alpha five reductase activity, so it seldom would ever entertain nearly the amount of androgenic stimulis as frontal hair does, but when it does have it…it will bald. So much for their being some kind of “difference” in the “hair’s response”. I think frontal and vertex area hair simply gets too much DHT, and at some point it starts expressing different androgenic marker genes post-recptor uptake and different DNA instructions are obeyed within it. Then the negative growth factors and catagen-inducing growth factors are secreted by the dermal papilla to the other cells of the hair follicle. It may be a chemopreventative mechanism, or whatever, but when too much male hormone is uptaken, the dna in the hair starts to react negatively to it, and baldness ensues. That this can happen in wreath hair as a response to high androgens speaks volumes and in my opinon lays the blame on too-well-working androgen receptors on the hairs themselves. I honestly think if you could get Brad Pitts hair to uptake the amount of androgen our follicles uptake…he’d be going bald too, by the same mechanisms we are for the most part dependent on the intesitity of his immune systems response. Its known that the variant of the androgen receptor gene is located on the x-chromosome and comes from your mother, but the other genes in baldness are autologous (or are thought to be) and aren’t parent specific. Too many androgens duing fetal development may play a role. We will know if someone ever does a study on digit ratios and baldness in a large population. Im guessing at least a small correlation will be found myself.

There are marker genes that get expressed after androgenic uptake before the dermal papilla releases any mitogens or anti-gens. I wonder if these marker genes change over time as more and more androgen is uptaken and repeat mutations manifest themselves as you age. It could be as easy as one or two of them increase or decrease and stopping them from doing so would keep you from going bald-------------------Anything that could seriously decrease receptor expression in your scalp in my opinion would have been a good preventative way to stop baldness before it began. Once the hair’s become “sensitive” to male hormone, then you need to keep as much male hormone away from the receptors as possible. We dont know if DHT is the only male hormone that can keep carrying out baldness after the hair’s response to androgen changes. It could be that after you begin to go bald, just Testosterone, or androstenidione is “enough” to keep you slowly balding over the decades----but dutasteride seems to slow it to damn near a halt in experiments…but then again androgen receptor expression reportedly gets a bit more intense with alpha-five inhibitors so who knows if the effect would last for four or five decades, etc.

The damage is primarily immunological in humans, but macaques that bald dont exhibit inflammation (Uno) so maybe your hair would eventually go without the immuno response over a long amount of time (senesence).