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Yes Tsuji did mention APM reconnection is his trials without explaining why, maybe he struggled for that only for goosebumps....yeah right
Mythbusters : Follicles Permanent Death In Androgenetic Alopecia ?
- Thread starter BaldyBalderBald
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Yes Tsuji did mention APM reconnection is his trials without explaining why, maybe he struggled for that only for goosebumps....yeah right
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Dude, it was just an observation they made, they didn't start off with the goal of reconnection, it just sort of clicked after they mimicked the cells' natural early stage environment successfully. It happened on its own.
Now I'm not saying the apm doesn't play a role in baldness for sure... It just makes more sense for a correlation like this to be an effect rather than a cause of baldness because as you move along the cascade of events the effects multiply, like a river. There are more effects than causes so by probability alone...
As for the part you cited about nephronectin being a potential link for hair loss between bulge and apm... Here's my thought process and I'm sorry if this doesn't make sense cause I've been in front of a screen all day and my brain is fried rn.
There's this little bit from the article: " In α8 integrin knockout mice, the APM attaches to both the nephronectin and EGFL6-positive regions. These mice have normal nephronectin expression in the bulge, but the APM lacks nephronectin. "
Now a8 integrin was the receptor for nephronectin. We have 3 cases of mice. 1, mice with no nephronectin, in which the normal connection region doesn't exist and a "false" one exists in another region (egfl6). 2, normal mice with connections at nephronectin region. 3, mice with integrin knocked out, so nephronectin can't bind to the receptors, which show BOTH connections.
In the 3rd case we have nephronectin in the bulge but not in the apm. Yet we see a connection at the nephronectin site. This means nephro in the apm is NOT necessary for right connection. We also see in case 1 that mice without nephro in the bulge (or anywhere else) don't have right connections, so nephro in the bulge IS necessary for right connection. This means right connection of apm to the follicular unit is mediated through nephronectin by the BULGE, not by the apm. Boom. Effect, not cause. At least as far as nephronectin is concerned.
Also there's a nice little comment about muscle degeneration and fat infiltration: "It has been suggested that fatty infiltration in damaged muscles, such as after tendon tear, is not a degenerative process, but a necessary rearrangement of the tissue after macroarchitectural changes caused by musculo-tendinous retraction." Again, just a suggestion, but like I said before shrinkage may cause separation, which in turn may cause muscle degeneration as implied here. Use it or lose it right?
Ok enough Asperger's for today. It's late here anyway. If you can shred my points to bits don't hesitate to do so. Goodnight everybody.
Waiting for Hellouser to update like
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Good article for the transgenders hypers, a bit of broscience on some aspects but still interesting theories based on studies
Trans Hormone Replacement Therapy Hair Regrowth: The Science
https://perfecthairhealth.com/trans-hormone-replacement-therapy-hair-regrowth/
Theory involving structural tension on sclap, inflammation response to DHT, why products like finasteride don't regrow a good amount of hair on most responders, and also why even most of transgenders don't have a full recovery.
A good read
Trans Hormone Replacement Therapy Hair Regrowth: The Science
https://perfecthairhealth.com/trans-hormone-replacement-therapy-hair-regrowth/
Theory involving structural tension on sclap, inflammation response to DHT, why products like finasteride don't regrow a good amount of hair on most responders, and also why even most of transgenders don't have a full recovery.
A good read
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Nice find bro !
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It maybe implies that you need other things than anti-androgens to really grow out new hairs like CD200 and things like this.
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Sure, Androgenetic Alopecia is multi-factorial anyway, always have been, if the cure was only about anti-androgens, this sh*t will be already cured since 20 years
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This artical is pretty silly in its assertion that we don't know why anti-androgens only stop and not reverse hair loss. We do know, the number of dermal papilla (DP) cells are depleted over time. Stopping the depletion wont cause those lost cells to come back and also wont reverse the changes in gene expression (such as VDR). Also your skull does n't change shape once you stop growing, as you age changes are due to bone loss. If there is an increase in bloodflow from estrogen it is probably due to it increasing VEGF. Finasteride causes ~10% increase in estrogen which is why you get some minimal regrowth.
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Told you, lots of broscience, but still interesting theory on dermal pressure and mechanical involvements on scalp skin.
Actually some parts of the skull do not fuse on adults and will keep changing (in a reasonable way) during lifetime.Of course bone loss will affect the skull at old age, but this is at "old" age, not middle age or young age.
The most convincing example is the long term effect HGH (Human Growth Hormone) on adults, i don't know if DHT and estrogen can affect as much skull, but the influence of HGH is undeniable
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Bone loss pretty much starts (slowly) as soon as you become an adult, HGH probably allievates that loss however biological aging is pretty much baked in to all living things. Also note that a thickening of the skull bone from HGH usage is not the same as changing shape outside of non fused regeons. Hormones definitely effect Testosterone/Estrogen bone growth, however after you have matured your bone structure cant be reversed, ie hands don't get smaller when you have male-to-female so why would your skull change shape?
As I mentioned if there is any link to blood supply it is due to an increase in VEGF, which is by the way linked to breast cancer in women who take hormone replacement therapy.
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Actually, most aspects of tooth development are highly conserved between sharks and mammals, so for the most part our teeth are like shark teeth. Sharks reuse the same pathways involved in tooth morphogenesis for regeneration (just like hair follicles do), while we've lost that ability (Rasch et al.). And yes, anyone who's well-read in hair biology will also know that the core pathways involved in hair morphogenesis and cycling are conserved between mammals. Granted, most of those are done in mice, and we're a bit more closely related to mice than we are to sea otters. But the point is: Since core functions in HFs are conserved between mammals, and since some species of mammals have terminal hair but no APMs, and since there's zero evidence that APMs are required for terminal hair growth, the onus is on the person claiming APMs are critical for terminal hair growth to provide evidence and not the other way around.
Exactly.
By the way, the "bit of broscience" on scalp tension was tested (and failed) decades ago.
Source: RE Nordstrom
Also, estrogen affects hair follicles directly. It potently enhances frontotemporal hair growth.
Source: Conrad et al.
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Since you seems quite qualified in hair biology, maybe you could answer to the topic (no irony here, i'm genuinely interested by your answer), you just debunked theories, what's yours ? Follicle permanent death is real ? Some damage done to HFs are irreversible or not ?
Subject is getting complex and that's why i made this thread, sorry if i don't express myself clearly, English is not my first language
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I'm not qualified in hair biology - I'm just an amateur like just about everyone else on this forum.
Anyway, I've attached a paper by El-Domyati et al. They show that follicles are sometimes destroyed in A.G.A, but this is rare and only seen in old people with advanced balding.
But A.G.A becomes hard to reverse very early.
Now, if you compare genes for different traits related to hair growth -- beard thickness, unibrow, male pattern baldness, eyebrow thickness, and alopecia areata -- the genes associated with each are very similar, except for alopecia areata which is a clear outlier (involving mostly immunity-related genes). Of the 50 genetic loci associated with unibrows, 21 are also associated with A.G.A (42 percent). Eyebrow thickness shares 6 out of 10 (60 percent) with A.G.A. Beard thickness shares 3 out of 8 (37.5 percent). These genes are mostly members of major HF developmental pathways (Wnt, EDA, Shh, BMP, etc.) or transcription factors that control members of those pathways (Sox2, Runx1, Trps1, Blimp1, etc.). The outlier, alopecia areata, shares 0 out of 14 with A.G.A.
In other words, the genes determining whether you have short unpigmented vellus hair or long dark terminal hair between your eyes overlap heavily with the genes that determine whether you have short unpigmented vellus hair or long dark terminal hair on your temples. Or the same over a wider or narrower region of skin above your eyes, and so on. Given the tremendous overlap, sex hormones might influence hair growth by modulating the key developmental pathways (Wnt, EDA, Shh, BMP, etc.) and the transcription factors that control these pathways.
So I suspect the answer to "Why are androgens required for progression of A.G.A but not for maintaining miniaturization of affected hairs?" is probably similar to the answer to "Why are androgens required for development of terminal facial hair but not their maintenance?" And the answer to "Why is it so hard to turn A.G.A-affected vellus hairs terminal again?" is probably similar to "Why is it so hard to grow terminal hair all over my forehead?" I don't know the answers to these questions.
Note: Genetic loci with p < 1e-5 counted for A.G.A.
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I'm not qualified in hair biology - I'm just an amateur like just about everyone else on this forum.
Anyway, I've attached a paper by El-Domyati et al. They show that follicles are sometimes destroyed in A.G.A, but this is rare and only seen in old people with advanced balding.
But A.G.A becomes hard to reverse very early.
Now, if you compare genes for different traits related to hair growth -- beard thickness, unibrow, male pattern baldness, eyebrow thickness, and alopecia areata -- the genes associated with each are very similar, except for alopecia areata which is a clear outlier (involving mostly immunity-related genes). Of the 50 genetic loci associated with unibrows, 21 are also associated with A.G.A (42 percent). Eyebrow thickness shares 6 out of 10 (60 percent) with A.G.A. Beard thickness shares 3 out of 8 (37.5 percent). These genes are mostly members of major HF developmental pathways (Wnt, EDA, Shh, BMP, etc.) or transcription factors that control members of those pathways (Sox2, Runx1, Trps1, Blimp1, etc.). The outlier, alopecia areata, shares 0 out of 14 with A.G.A.
In other words, the genes determining whether you have short unpigmented vellus hair or long dark terminal hair between your eyes overlap heavily with the genes that determine whether you have short unpigmented vellus hair or long dark terminal hair on your temples. Or the same over a wider or narrower region of skin above your eyes, and so on. Given the tremendous overlap, sex hormones might influence hair growth by modulating the key developmental pathways (Wnt, EDA, Shh, BMP, etc.) and the transcription factors that control these pathways.
So I suspect the answer to "Why are androgens required for progression of A.G.A but not for maintaining miniaturization of affected hairs?" is probably similar to the answer to "Why are androgens required for development of terminal facial hair but not their maintenance?" And the answer to "Why is it so hard to turn A.G.A-affected vellus hairs terminal again?" is probably similar to "Why is it so hard to grow terminal hair all over my forehead?" I don't know the answers to these questions.
Note: Genetic loci with p < 1e-5 counted for A.G.A.
Interesting, whether follicles are completely destroyed or not, fibrosis is still a bad thing and not reversible as of today.Maybe all of this skin regeneration research ongoing today can help baldness after all (PolarityTE, Cots and Tsuji aswell)
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There may never be a definitive answer because the process of hairloss is personalised or at least differs between individuals to varying degrees. What can be said is that a reversal of miniaturisation is possible in some cases - even if that reversal is not permanent.
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I think it should go without saying there are multiple factors:
- How long the follicles are "bald" for. Ie. Guys that go from NW1 to NW3 in the span of 3-5 years are often the ones that get mega regrowth when they get on a good regimen. Probably anything gone >10 years will be gone for most men.
- How old you are. Again, guys in their early 20s often get the best regrowths, partly because they've been "bald" for less time but partly I'm sure also because their skin is more supple and full of stem cells.
- Individual genetics. Just like anything, I think it should be expected everyone will have a different regenerative capacity and different time frame before permanent damage.
What about the guys that go from a nw1 to a 3 in 1 year?
I can say you one f*****g thing as someone who had an extremely fast hair loss, going from NW1 to NW3 relatively quick.
I can still see some dark pores / almost microscopic dark hairs which I assume are not yet dead follicles on a scalp area which looks bald, they are everywhere where my original hairline was.
Mind you, if they were vellus, those hairs would have lighter colour. True, I'm ussing Minoxidil to keep these trash hairs alive as long as I can.
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I used to experience the same, now they are just gone, and replaced by a nice slick skin
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Yeah i think that's sort of valid but in my opinion the only way to know if your hair is truly gone is:
1) Take 600 mg darolutamide and 5 mg minoxidil orally twice daily for 6-12 months.
2) See what happens.
Of course it's not practical to do. But i think that's the only way to know for sure.
Even dutasteride only reduces scalp dht like 50-60% as someone posted. There's still loads of dht and test then to inhib your hair follicles and prevent them from de-miniaturizing.