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DHT must be blamed BC it is like key which unlock the lock ,which after unlocking can rarely be locked again.
Genes Regulating Inflammation, Stress, And Fibrosis Were Massively Overexpressed In All Androgenetic Alopecia Groups
- Thread starter Warmer82
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This may be the case only for those who aren’t prone.
But bodybuilders who take tons of steroids that are dht based some of them never lose their hair
Maybe dht doesn’t accumulate in their follicles. Or maybe it just doesn’t affect them.
Dht is def the Cause Of androgenic alopecia but it’s doesn’t wreak havoc by itself something else coupled with it pushes it
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Problem with this study, is that it wont look at what 5ar inhibits for example do to the gene expression/how much it changes the game and where we can supplement treatment.
T/DHT start cascade into PGD2/PGJ2, Dkk1... Also there seem to be different stages how Androgenetic Alopecia expresses itself. Once skin is bald it expresses pgd2 by itself. A recent study also implied that it would be better to looks at PTGDS inhibitors instead of crth2 inhibitors. Which are extremely difficults as they need to inhibit L-PGDS and H-PGDS with a long half life as the enzyme renews very quickly. There is HQL-79 which was back in the days already too expensive to produce and now in japan they trialed TAS-205 a HPGDS inhibitor.
Basically, this paper leaves tons of open questions. Sure we knew fgf5 would be upregulated, but we dont know how much seti or finasteride does change that (its induced as pgd2 downstream).
Ppl ask how to deal with fibrosis. There basically to key factors inducing it in Androgenetic Alopecia:
TGF-ß1: Taurine, ALK5 inhibitors, Zinc, NAC...
TGF-ß2: Sandalore, Carnitine
Deep woundings and peelings (with dmso for example) help with existing fibrosis. Some ppl believe here still in calcification. Sodium thiosulfate can deal with it and has also anti-fibrotic aspects. PGE2 and PGE1 also reduce collagen while inducing lots of growth factors downstream.
I am still waiting for one of the clown research to finally do a study with SW033291 and hair. It is so obv that it is a potent hair growth inducer.
T/DHT start cascade into PGD2/PGJ2, Dkk1... Also there seem to be different stages how Androgenetic Alopecia expresses itself. Once skin is bald it expresses pgd2 by itself. A recent study also implied that it would be better to looks at PTGDS inhibitors instead of crth2 inhibitors. Which are extremely difficults as they need to inhibit L-PGDS and H-PGDS with a long half life as the enzyme renews very quickly. There is HQL-79 which was back in the days already too expensive to produce and now in japan they trialed TAS-205 a HPGDS inhibitor.
Basically, this paper leaves tons of open questions. Sure we knew fgf5 would be upregulated, but we dont know how much seti or finasteride does change that (its induced as pgd2 downstream).
Ppl ask how to deal with fibrosis. There basically to key factors inducing it in Androgenetic Alopecia:
TGF-ß1: Taurine, ALK5 inhibitors, Zinc, NAC...
TGF-ß2: Sandalore, Carnitine
Deep woundings and peelings (with dmso for example) help with existing fibrosis. Some ppl believe here still in calcification. Sodium thiosulfate can deal with it and has also anti-fibrotic aspects. PGE2 and PGE1 also reduce collagen while inducing lots of growth factors downstream.
I am still waiting for one of the clown research to finally do a study with SW033291 and hair. It is so obv that it is a potent hair growth inducer.
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What that "something else " could be? I am always hearing something else is at play,but what is that?
DHT is sole cause of alopecia. It could be hairs sensitivity or could be dht induces skull bone growth or anything ,but dht is responsible, it is upstream the cascade ,if it were not then then enuchs would go bald also.
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yesterday I saw a presentation where there was a pie chart like this:
Causes of hair loss (men and women):
Androgenetic Alopecia : 96%
non-Androgenetic Alopecia: 4%
We need to look into TGF-b inhibitors.????
https://www.sigmaaldrich.com/catalog/product/sigma/s4317?lang=en®ion=GB
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Rancid sebum in scalp can develop chronic microinflammation.
More sebum, more DHT
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I’ve taken taurine. Curcumin and ginkgo but not consistent enough and I am only on finasteride 3 months and 2 days today
What dose for taurine?
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1 gram
Try sticking with those and try 1g in morning and 1g at night for taurine. Im sure you have to have something else with curcumin to be effective, Cant think what it is.
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Black pepper?
piperine extract from black pepper
dht is not the cause of hair loss . the way finadteride works is by ihnhibiting dht to stop the inflamation and the regrowth is due to the new elevated free estrogen levels (more estrogen with dutasteride so more regrowth and sides) .i think the way swisstemples regrew his hairline buy using a pgd2 inhibitor to stop inflamation(sulfasalazine) with huge sucess is a good proof .even with equol we can inhibit much more dht but we dont get regrowth due to the same estrogen levels ,regrowth is much harder to achieve , even maintenace requares at least some minoxidil pge1 or other pge2
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Do you have proof that estrogen is the Cause of the growth. I am actually 100% sure estrogen can cause hairloss due to estrogen dominance which isn’t fully u derstood and often when people have bad results with finasteride or duta their estrogen levels are high.
The way transsexuals achieve their results is mainly cause their entire hormonal profile changes its not just high estrogen
androgenic alopecia didn’t get its name from a child. PhDs concluded this.
The way transsexuals achieve their results is mainly cause their entire hormonal profile changes its not just high estrogen
androgenic alopecia didn’t get its name from a child. PhDs concluded this.