Could Scalp Thickness A Cause Or Effect Of Androgenetic Alopecia

Gone

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I was reading in a different thread that kerastem is meant to increase scalp thickness. However it seems the consensus is that kerastem doesn't regrow hair. The question is then, does kerastem fail to regrow hair because it doesn't thicken the scalp? Or is its success in thickening the scalp not relevant to hair growth.

Transplanted hairs are not quite as thick as normally growing DHT unaffected hairs, but the figure is like 97% thickness or something like that.

http://drcarloswesley.com/T/06082014.pdf

Anyway, we know that transplanted hairs can grow in areas of thinned scalp. Maybe this means that the scalp thinning is responsible for the 3% decrease, or simply isn't relevant at all.

But is there any causal link between scalp dermis/fat thickness and hair loss?

This article seems really biased and didn't dismiss the counterarguments to this point, but I learned from it that testosterone decreases subcutaneous fat, which might explain the fat thinning in bald scalp, however the dermal thinning remains unexplained. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4174066/#!po=45.0000
 
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Gone

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The title makes it sound like I was drunk, why can't I change it lol
 

InBeforeTheCure

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Much more likely the other way around (i.e. hair loss causes the fat thinning). Hairs which are in telogen are already known to be surrounded by a much thinner layer of fat, and once they go into anagen this layer of fat expands.

adipoe.png


Hair follicles’ transit-amplifying cells govern concurrent dermal adipocyte production through Sonic Hedgehog

Growth and regeneration of one tissue within an organ compels accommodative changes in the surrounding tissues. However, the molecular nature and operating logic governing these concurrent changes remain poorly defined. The dermal adipose layer expands concomitantly with hair follicle downgrowth, providing a paradigm for studying coordinated changes of surrounding lineages with a regenerating tissue. Here, we discover that hair follicle transit-amplifying cells (HF-TACs) play an essential role in orchestrating dermal adipogenesis through secreting Sonic Hedgehog (SHH). Depletion of Shh from HF-TACs abrogates both dermal adipogenesis and hair follicle growth. Using cell type-specific deletion of Smo, a gene required in SHH-receiving cells, we found that SHH does not act on hair follicles, adipocytes, endothelial cells, and hematopoietic cells for adipogenesis. Instead, SHH acts directly on adipocyte precursors, promoting their proliferation and their expression of a key adipogenic gene, peroxisome proliferator-activated receptor γ (Pparg), to induce dermal adipogenesis. Our study therefore uncovers a critical role for TACs in orchestrating the generation of both their own progeny and a neighboring lineage to achieve concomitant tissue production across lineages.

Given that balding hair follicles have been shown to lack progenitor cells (Garza et al.) which give rise to transit amplifying cells, and the telogen-to-anagen ratio is higher in A.G.A., it's no surprise then that bald scalp is thin.
 

Captain Rex

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I was reading in a different thread that kerastem is meant to increase scalp thickness. However it seems the consensus is that kerastem doesn't regrow hair. The question is then, does kerastem fail to regrow hair because it doesn't thicken the scalp? Or is its success in thickening the scalp not relevant to hair growth.

Transplanted hairs are not quite as thick as normally growing DHT unaffected hairs, but the figure is like 97% thickness or something like that.

http://drcarloswesley.com/T/06082014.pdf

Anyway, we know that transplanted hairs can grow in areas of thinned scalp. Maybe this means that the scalp thinning is respinsible for the 3% decrease, or simply isn't relevant at all.

But is there any causal link between scalp dermis/fat thickness and hair loss?

This article seems really biased and didn't dismiss the counterarguments to this point, but I learned from it that testosterone decreases subcutaneous fat, which might explain the fat thinning in bald scalp, however the dermal thinning remains unexplained. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4174066/#!po=45.0000
u got one thing wrong - kerastem failed because they failed to keep the adipose tissues in the scalp, they migrated away to the different parts, so the scalp didn't thicken up and eventually led to a failure

and about transplantation- the hair follicles taken from back have not miniaturized so when they are transplanted they look good but with time they get affected by Dht and its a long process(takes years) and it finally wears off. If transplantation was the solution then it wud have been a cure but its not the case.

skull expansion has a direct link to male pattern baldness and i think its the main culprit, dht is the driving factor.
from my experience, i noticed skull expansion from the beginning but didn't notice hairline receding at first
it was only after the itches at hairline (the attack of Dht) followed by receding hairline which made me realize i had male pattern baldness
now i have itches at crown too!! but all thanx to finasteride it stopped it or rather reduced it but when i sweat a lot i still get those itches badly.

so in brief, skull expands or so called remodeling and scalp thins a bit and this goes on up to a point where DHT starts binding up around hair follicles but not Testosterone (why? two extra hydrogen in DHT than testosterone so more bulky). The process goes on and u end up bald after certain time based on the rate of skull expansion ( a little later if u take anti androgen drugs)
pls excuse me i am not a scientist just sharing what i feel.( i hate details which i don't understand)

that's y when i hear stem cell treatment on hair loss i see a possible cure other than that its a waste of time
 

Gone

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Much more likely the other way around (i.e. hair loss causes the fat thinning). Hairs which are in telogen are already known to be surrounded by a much thinner layer of fat, and once they go into anagen this layer of fat expands.

adipoe.png


Hair follicles’ transit-amplifying cells govern concurrent dermal adipocyte production through Sonic Hedgehog



Given that balding hair follicles have been shown to lack progenitor cells (Garza et al.) which give rise to transit amplifying cells, and the telogen-to-anagen ratio is higher in A.G.A., it's no surprise then that bald scalp is thin.

So dermal and adipose thinning are essentially the same issue? If you're correct then kerastem wouldn't regrow hair even if it stayed in the scalp and thickened it.

The second article I linked makes the claim that DHT actually does not have a paradoxical effect on hair growth. It claims that DHT is actually beneficial to scalp hair growth, but that it thins the dermis, dht is upregulated to offset the change and regrow hair. It doesn't really make sense to me but it was helpful for showing a possible reason why the scalp is thinner, though I think InBeforeTheCure's explanation makes perfect sense.
 
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InBeforeTheCure

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So dermal and adipose thinning are essentially the same issue? If you're correct then kerastem wouldn't regrow hair even if it stayed in the scalp and thickened it.

Well, preadipocytes are also known to drive anagen entry through secretion of PDGF (see here) -- this is what Kerastem is based on, I think. Obviously though it's nothing spectacular.

The second article I linked makes the claim that DHT actually does not have a paradoxical effect on hair growth. It claims that DHT is actually beneficial to scalp hair growth, but that it thins the dermis, dht is upregulated to offset the change and regrow hair. It doesn't really make sense to me but it was helpful for showing a possible reason why the scalp is thinner, though I think InBeforeTheCure's explanation makes perfect sense.

Right, that article makes zero sense, and contains so many errors and absurdities that I wouldn't even know where to begin. That guy's idea is just another one of those entertaining crackpot theories of baldness, along with Stephen Foote's, Armando's sebum theory, the skull expansion theory that Rex just alluded to, and Ernie Primeau's baldness-is-a-result-of-body-hair-stealing-nutrients theory (which is the funniest of all).
 

WMQ

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Much more likely the other way around (i.e. hair loss causes the fat thinning). Hairs which are in telogen are already known to be surrounded by a much thinner layer of fat, and once they go into anagen this layer of fat expands.

adipoe.png


Hair follicles’ transit-amplifying cells govern concurrent dermal adipocyte production through Sonic Hedgehog



Given that balding hair follicles have been shown to lack progenitor cells (Garza et al.) which give rise to transit amplifying cells, and the telogen-to-anagen ratio is higher in A.G.A., it's no surprise then that bald scalp is thin.
If we follow the reasoning here, does that mean transplanted hairs would actually transform the scalp surrounding them, and over time make the recipient scalp thick and healthy again?
 

Folliman

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Isn't kerastem applying fat to the scalp to grow hair? Man, it's so hard to keep up with the science behind all these treatments...
 

wilfred

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Isn't kerastem applying fat to the scalp to grow hair? Man, it's so hard to keep up with the science behind all these treatments...
Yes they extract sub cutaneous fat and then enrich it with stem cells from the fat then reinject it.

So you get 4 or 5 injections of fat all over your scalp in "zones". Then about 100 stem cell injections after that. Btw I had it and it did nothing for me (4 months in).
 

Swoop

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If we follow the reasoning here, does that mean transplanted hairs would actually transform the scalp surrounding them, and over time make the recipient scalp thick and healthy again?

Yes they do alter their environment. When a graft is cut off from the blood supply and implanted into the recipient area it takes approximately 3 days before re-vascularization occurs.

Often, but not always they go into catagen followed by the telogen phase. That's why most people shed almost all of their hair after having a hair transplant.

Put it this way.

Anagen hair follicle - high vascularization, high amount adipose tissue

Telogen hair follicle - low to non-existent vascularization, low amount adipose tissue.

The hair follicle cycle is dynamic.

Right, that article makes zero sense, and contains so many errors and absurdities that I wouldn't even know where to begin.

I stopped reading at "DHT receptors". :p
 

Gone

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Not only does kerastem seem to be ineffective, if the kerastem injection is fat itself, it could potentially cause blindness if it travels to the eye, as some fillers are known to do. Of course they wouldn't tell people about that though. If you know anyone considering cosmetic fillers, tell them to never have them injected above the eyes.
 
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