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Accutane and hair changes
A friend did the hair transplants and I think he was happy about it. I'd give things a bit more time, you know? This is a lengthy process.
When I compare pics, I do feel like the hair I have is smoother and each hair is stronger and thicker. That can add up. I'm happier with my hair changes than my face changes, LOL.
@tim-2 Same here, hair shedding continues at the same rate as before going low VA. But just thinking, if VA really affected hair, why are female protected from it. Maybe it is the higher T converting too much to E in males, and VA makes this happen quicker...
I have only ever seen regrowth reported in males transitioning to female(downing E, so this negates the above theory...), even then the photos are not great. Fingers are crossed for luck, but i think regrowth is impossible, it just doesn't happen in males...
I was just thinking of one more little tidbit I'd like to say and that is that hair might not just be for looks! But I guess we do have it other places and not just on the head.
My grandfather didn't have much hair any time that I knew him. He was adorable. He always wore a french sailor hat, it was the perfect thing for his style.
It's well established that Hypervitaminosis A causes hairloss though?
The mechanism is a real puzzle, I've been thinking about it for a long time. Retinoic acid actually inhibits DHT production, it has been used with minoxidil to promote hair growth. So if it inhibits DHT why does it cause hair loss when taken systemically? Well there could be lots of reason including inducing deficiencies of K2, D, zinc and riboflavin, inducing insulin resistance and also by affecting hormonal balance.
Whatever the reason, vA is intimately connected with sex hormones in the skin:
Abstract
Retinol dehydrogenase-4 (RoDH-4) converts retinol and 13-cis-retinol to corresponding aldehydes in human liver and skin in the presence of NAD+. RoDH-4 also converts 3α-androstanediol and androsterone into dihydrotestosterone and androstanedione, which may stimulate sebum secretion. This oxidative 3α-hydroxysteroid dehydrogenase (3α-HSD) activity of RoDH-4 is competitively inhibited by retinol and 13-cis-retinol. Here, we further examine the substrate specificity of RoDH-4 and the inhibition of its 3α-HSD activity by retinoids. Recombinant RoDH-4 oxidized 3,4-didehydroretinol—a major form of vitamin A in the skin—to its corresponding aldehyde. 13-cis-retinoic acid (isotretinoin), 3,4-didehydroretinoic acid, and 3,4-didehydroretinol, but not all-trans-retinoic acid or the synthetic retinoids acitretin and adapalene, were potent competitive inhibitors of the oxidative 3α-HSD activity of RoDH-4, i.e., reduced the formation of dihydrotestosterone and androstandione in vitro. Extrapolated to the in vivo situation, this effect might explain the unique sebosuppressive effect of isotretinoin when treating acne.
When you say regrowth is impossible what about drugs that cause it? It definitely can happen but whether it will happen drug free is another question...
Now I see here that they say the follicles in MPB are *more sensitive* to testosterone. Sensitive...
It sure does seem to me that high VA and sex hormones are a match made in hell. Perhaps a way of saying it is that the inflammation magnifies.
My face is "more sensitive" to loads of things and so apt to become red. My gums too. I'm definitely not detoxed and healed yet.
It is interesting that MPB runs in family lines, perhaps it has to do with where genes decide to put VA Hubs seems to be very good at storing VA around the liver. Is that why his hair has been spared?
Will the scalp go back to normal sensitivity when the detox is in the rear view mirror?
@tim-2 yes definitely a real puzzle. My hopes are that you and I see regrowth, we could be the only two hair shedders in 7.8 billion people that are trying low VA, if it eventually works I will post regrowth pictures 🙂
I have been following all the health forums on hair growth for a decade now, there has never been proof posted. Only from drugs, like Fin which is a progestin, and it comes with huge risks. I think that progesterone is the key somehow
Count me in, although I don't think I've taken retinal drugs (although it is possible, memory doesn't serve). And I'm not a guy. But I do have thin patches. Hey skin doesn't look too crap today.
Uploaded files:
The longer hair (not in the patch) is so much smoother and non-frizzy. Although I still think of my hair as "textured". I think the smoother hair says something about the inflammation of my follicles improving. And if those baby hairs in that triangular zone can get happier and happier... it could fill in.
Conclusions
AGA is the result of chronic GA-transmitted scalp tension mediated
by pubertal and post-pubertal skull bone growth and/or the overdevelopment
and chronic contraction of muscles connected to the GA.
This tension induces a pro-inflammatory cascade (increased ROS, COX-
2 signaling, IL-1, TNF-α, etc.) which induces TGF-β1 alongside increased
androgen activity (5-αR2, DHT, and AR), which furthers TGF-
β1 expression in already-inflamed AGA-prone tissues. The concomitant
presence of DHT and TGF-β1 mediates perifollicular fibrosis, dermal
sheath thickening, and calcification of the capillary networks supporting
AGA-prone hair follicles. These chronic, progressive conditions
are the rate-limiting factors in AGA recovery. They restrict follicle
growth space and decrease oxygen and nutrient supply to AGA-prone
tissues – leading to tissue degradation, hair follicle miniaturization, and
eventually pattern baldness.
This model allows for genetic influence during any step-process, but
refutes the belief that AGA-prone follicles are genetically programmed
to become sensitive to DHT. Rather, the model implies that AGA-prone
tissues are predisposed to respond to chronic tension-mediated inflammation
by inducing DHT and androgen-mediated TGF-β1, which
restructure tissue – of which a symptom is hair loss. The model also
provides a rationale for unexplained phenomena in AGA pathology,
such as:
• Why DHT increases in AGA-prone scalp tissues (i.e., DHT is a response
to tension-mediated inflammation)
• The mechanisms by which DHT is involved in AGA progression (i.e.,
DHT is involved in the onset of fibrosis and calcification)
• The pattern of AGA (i.e., AGA progression matches that of where
GA-transmitted scalp tension is highest, and progresses as peak
tension points change during fibrosis onset)
• Why AGA is observed more often in elderly populations versus
young adults (i.e., calcification and fibrosis have had more time to
accumulate)
• Why DHT is associated with body and facial hair growth and also
AGA-related hair loss (i.e., tension-mediated inflammation induces
TGF-β1 and DHT, and remodels tissue in AGA sites – a phenomenon
not observed in body and facial hair growth sites)
• Why androgen suppression stops AGA, but does not regrow all hair
(i.e.; DHT inhibitors may reduce fibrosis progression in AGA, but do
not reverse fibrosis already present)
Future AGA research should focus on utilizing mechanotransduction
to potentially reverse AGA-related tissue remodeling. If the model holds
true, then reversing AGA tissue remodeling – rather than attenuating it
– may pave the pathway to full AGA recoveries.
This paper gives the best explanation I've seen for the cause of mpb.
Note both TGF-β1 and calcification are influenced by elevated levels of retinoic acid.
@tim-2 have you tried the Detumescence Therapy? I did it for 2yrs experiment, this was before low VA, and it did nothing, wonder it if would be helpful now. Do you think that just low VA would do the trick, or other therapies applied as well.
Only thing I am trying now is ice cold showering(~5mins), after having a normal shower. Supposed to help rush blood away from head and extremities, and strengthen those tiny little muscle in the blood pathway, helping overall blood flow to extremities. I also wonder from an evolutionary standpoint, that true ice cold exposure would trigger some type of hair growth response to keep the head warm 🙂
Click to access detumescence-therapy-of-human-scalp-for-natural-hair-regrowth-2155-9554.1000138.pdf