An Extremely Interesting And Well Researched Thread About Hair Loss

baba_yaga

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you clear have no idea how much more important it is.
I know what you're talking about. Perhaps I've not had the sides that bad, but finasteride gave me sides. My sex drive was non-existent (it is now much better, but still lower than pre-finasteride). I can force myself though. Also my orgasms are all over the place. The sides did bother me but not by much. Now, having a dead dick is another beast lol and I dont know how I would react if I ever had this problem.
Yes I agree, sexual life is VERY important, however hair is also VERY important to me as I know loosing it will turn me back to my old, depressing, introverted days. So, I am willing to push things a bit harder than others.
 

Derelict

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HRT/castration is not even a route. Believe me, Have a working dick, have good orgasm , dont have ED , it much, much, much importan that all the hair in the world. You are young, and you clear have no idea how much more important it is.
I use during many , many , many years dutasteride . My orgasm and libido , and not just that, the feeling well ( cause I am producing neursteroids like allopregnolone ) again, it is irreplaceable . I should pay a millon dollar to have, this same information that I am giving now back 1996 when I first started to get balding hairline.

Good information can change people life, not get a bad hair transplant ( or not get one at all ) , or not using certain drugs, it make a whole different life.

And we are not even talking about " well, I am young now, who care in the future " . Cause , with that kind of regimen , you don't get a good quality life ( that include a life with good sex and without anxiety cause you are not producing neurosteroids or you are blocking them ) . So, we are not even talking about long term side effects.

Yeah, sexual well being is important no doubt, unless you are asexual or something, but i can handle weaker orgasms on dutasteride for my hair, it's each individuals choice to make in the end, prioritize and find out for yourself what you can handle.
 

jamesbooker1975

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That guy is extremly wrong, First at all, estrogen are really important too. If you use Letrozole like this guy tell, that is simple insane. First anti aromatase are well know to cause ligament and muscle tears , ask to any bodybuildind, powerlifting or people that use it during teenager years ( you can use it instead of growth hormone , cause the levels of estrogen is what make the epiphysis get " solid " so bones done get larger ) and they all have tears .
Then, again, is not " well I can live without testosterone if I kill estrogen too " both things are extremly important in short and long term .
Yeah, sexual well being is important no doubt, unless you are asexual or something, but i can handle weaker orgasms on dutasteride for my hair, it's each individuals choice to make in the end, prioritize and find out for yourself what you can handle.

For a while, may be . But if you want to get an steady girlfriend, will not work . Lack of libido and weaker orgasm to produce even more lack of libido. And that is you are lucky and don't get ED . I never got ED, from dutasteride. It also reduce fertility , so you might need to get other drugs like clomiphen if you want to get a child.

Plus, is not just the problem that you are killing DHT, you are killing an enzyme that it is use it in many other reactions. Check for example neurosteroids , for example, the conversion of pregnolone into allopregnolone need this enzyme. Allopregnolone give you a sense of calm and wellness . As long as many other neurosteroids that use this enzyme.
Again, Dutasteride, Isotretinoin an finasteride, all 3 are link it, for this reason , with depression and anxiety. there is a reason why Glaxo never did phase 3 in USA for Androgenetic Alopecia, even after the great results that phase 2 got in stopping and regrowing hair.
 

jamesbooker1975

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I wish I could get ED. It doesn't matter what I'm on I wake up horny, I'm horny all day, and I go to bed horny, no matter how much sexual release I have. How the heck people get ED from these drugs I don't understand because they haven't done anything to me.
Masturbation is not the same a sex. It don't have the same effect on the brain neither.
 

Michael1986

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The HRT route has the best chance of regrowing hair of all routes available, but at the expense of losing your masculinity. It is not a viable treatment route for normal men. And I personally doubt that even HRT would be able to regrow long lost hair. It has been shown in studies that irreversible changes take place in the hair follicles once the miniaturization process progresses past a certain point. Once a hair follicle has undergone these irreversible changes and is past the point of no return, there's no bringing that follicle back, even with the most hardcore treatment options available.
 

Michael1986

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This does not apply to neogenesis. Wounding can create new hairs no matter how long your hair has been gone.
That is a good point, but I'm still not sure how wounding would be able to undo the irreversible changes that take place. Research shows that over time, miniaturized hairs lose contact with the Arrector Pili muscle, and once this contact has been lost, hair loss is irreversible. Also, bald scalps in men with Androgenetic Alopecia retain hair follicle stem cells, but have lost the progenitor cells that are believed to be necessary for hair growth.

Here are a few studies:

This one from 2012:

Miniaturized Hairs Maintain Contact with the Arrector Pili Muscle in Alopecia Areata but not in Androgenetic Alopecia: A Model for Reversible Miniaturization and Potential for Hair Regrowth
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3500053/


"Contact between the APM and the bulge in AA may be required for reversal of hair follicle miniaturization. Maintenance of contact between miniaturized follicles in AA could explain the complete hair regrowth while loss of contact between the APM and the bulge in MPHL and FPHL may explain why the hair loss is largely irreversible. This loss of contact may reflect changes in stem cell biology that also underlie irreversible miniaturization."

ijt-4-154-g003-jpg.jpg


Three-dimensional reconstructions of AA (a) and FPHL (b) demonstrating the loss of contact of the APM with the ORS of the vellus hair follicle in FPHL which is largely irreversible compared with maintenance of this contact of the APM with ORS in AA which is potentially completely reversible

And a second study from 2014:

Destruction of the arrector pili muscle and fat infiltration in androgenic alopecia.
https://www.ncbi.nlm.nih.gov/pubmed/24579818


"Hair loss is caused by follicle miniaturization, which is largely irreversible beyond a certain degree of follicular regression."

"APM degeneration and replacement with fat in Androgenetic Alopecia has not previously been described. The underlying mechanism remains to be determined. However, we speculate that this phenomenon might be related to depletion of stem or progenitor cells from the follicle mesenchyme, explaining why Androgenetic Alopecia is treatment resistant."

And another study from 2011:

Bald Scalp in Men With Androgenetic Alopecia Retains Hair Follicle Stem Cells but Lacks CD200-rich and CD34-positive Hair Follicle Progenitor Cells
https://pubmed.ncbi.nlm.nih.gov/21206086/

Abstract:
"Androgenetic alopecia (Androgenetic Alopecia), also known as common baldness, is characterized by a marked decrease in hair follicle size, which could be related to the loss of hair follicle stem or progenitor cells. To test this hypothesis, we analyzed bald and non-bald scalp from Androgenetic Alopecia individuals for the presence of hair follicle stem and progenitor cells. Cells expressing cytokeratin15 (KRT15), CD200, CD34, and integrin, α6 (ITGA6) were quantitated via flow cytometry. High levels of KRT15 expression correlated with stem cell properties of small cell size and quiescence. These KRT15(hi) stem cells were maintained in bald scalp samples. However, CD200(hi)ITGA6(hi) and CD34(hi) cell populations--which both possessed a progenitor phenotype, in that they localized closely to the stem cell-rich bulge area but were larger and more proliferative than the KRT15(hi) stem cells--were markedly diminished. In functional assays, analogous CD200(hi)Itga6(hi) cells from murine hair follicles were multipotent and generated new hair follicles in skin reconstitution assays. These findings support the notion that a defect in conversion of hair follicle stem cells to progenitor cells plays a role in the pathogenesis of Androgenetic Alopecia."
 

polishkickbuttowski

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That is a good point, but I'm still not sure how wounding would be able to undo the irreversible changes that take place. Research shows that over time, miniaturized hairs lose contact with the Arrector Pili muscle, and once this contact has been lost, hair loss is irreversible. Also, bald scalps in men with Androgenetic Alopecia retain hair follicle stem cells, but have lost the progenitor cells that are believed to be necessary for hair growth.

Here are a few studies:

This one from 2012:

Miniaturized Hairs Maintain Contact with the Arrector Pili Muscle in Alopecia Areata but not in Androgenetic Alopecia: A Model for Reversible Miniaturization and Potential for Hair Regrowth
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3500053/


"Contact between the APM and the bulge in AA may be required for reversal of hair follicle miniaturization. Maintenance of contact between miniaturized follicles in AA could explain the complete hair regrowth while loss of contact between the APM and the bulge in MPHL and FPHL may explain why the hair loss is largely irreversible. This loss of contact may reflect changes in stem cell biology that also underlie irreversible miniaturization."

View attachment 143428

Three-dimensional reconstructions of AA (a) and FPHL (b) demonstrating the loss of contact of the APM with the ORS of the vellus hair follicle in FPHL which is largely irreversible compared with maintenance of this contact of the APM with ORS in AA which is potentially completely reversible

And a second study from 2014:

Destruction of the arrector pili muscle and fat infiltration in androgenic alopecia.
https://www.ncbi.nlm.nih.gov/pubmed/24579818


"Hair loss is caused by follicle miniaturization, which is largely irreversible beyond a certain degree of follicular regression."

"APM degeneration and replacement with fat in Androgenetic Alopecia has not previously been described. The underlying mechanism remains to be determined. However, we speculate that this phenomenon might be related to depletion of stem or progenitor cells from the follicle mesenchyme, explaining why Androgenetic Alopecia is treatment resistant."

And another study from 2011:

Bald Scalp in Men With Androgenetic Alopecia Retains Hair Follicle Stem Cells but Lacks CD200-rich and CD34-positive Hair Follicle Progenitor Cells
https://pubmed.ncbi.nlm.nih.gov/21206086/

Abstract:
"Androgenetic alopecia (Androgenetic Alopecia), also known as common baldness, is characterized by a marked decrease in hair follicle size, which could be related to the loss of hair follicle stem or progenitor cells. To test this hypothesis, we analyzed bald and non-bald scalp from Androgenetic Alopecia individuals for the presence of hair follicle stem and progenitor cells. Cells expressing cytokeratin15 (KRT15), CD200, CD34, and integrin, α6 (ITGA6) were quantitated via flow cytometry. High levels of KRT15 expression correlated with stem cell properties of small cell size and quiescence. These KRT15(hi) stem cells were maintained in bald scalp samples. However, CD200(hi)ITGA6(hi) and CD34(hi) cell populations--which both possessed a progenitor phenotype, in that they localized closely to the stem cell-rich bulge area but were larger and more proliferative than the KRT15(hi) stem cells--were markedly diminished. In functional assays, analogous CD200(hi)Itga6(hi) cells from murine hair follicles were multipotent and generated new hair follicles in skin reconstitution assays. These findings support the notion that a defect in conversion of hair follicle stem cells to progenitor cells plays a role in the pathogenesis of Androgenetic Alopecia."

This is good justification for getting on a growth stimulant like minoxidil even if your not using an antiandrogen. You delay your hair follicles getting to the point of no return in hopes that something better comes out, or if you want to let your body develop more before your nuke your hormones.
 

jared garnith

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i have tretinoin 0.1% for something else. can i use it every other day to get an average daily dose of 0.05%? or how do i turn tretinoin 0.1% to 0.05%? also is it okay to use tretinoin daily and microneedle every two weeks?
Yeah, I ordered tretinoin from alldaychemist but all the percentages are too high
 

Nsas

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You can buy a cream base , like dermovate . Do this :
0,1 . 100 grams = 0, 025 . x

Then x will be 400 grams and that will be the final value . So you use 100 grams that contain that tretinoin 0.1 grams of tretinoin and then you ad 300 grams of cream/ointment ( without any active ingredient ) . That will give you a 0,025 :/: tretinoin .
Can you use eucerin, aquaphor, or something that you can get at the store?
 

jamesbooker1975

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Can you use eucerin, aquaphor, or something that you can get at the store?
Well, yes , in theory , yes. If you have problems making the calculation, advice. Remember that, for example, you have 0.1% cream but you have a tube, of 30 grams, the math shoul be :
in 100 grams of cream------------------------ 0.1 grams of tretininoin
in 30 grams---------------------------------- X

So X = 30 . 0.1 / 100 = 0.03 grams of tretinoin

So 0.03 grams of tretinoin is what you have in that 30 grams of cream. If you want, for example, a 0,03 % tretinoin cream, you mix really well that 30 grams with 70 grams of the eucerin or whatever other cream , and you get a final cream of 0.03 % tretinoin.
May be is stupid, but, more fluid the cleam, more easily to mix it. And more similar the both creams you are mixing, even better. So you can read on your tretinoin cream , all the other none active ingredients it have, and find some cream with similar ingredients.
 

jamesbooker1975

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I know what you're talking about. Perhaps I've not had the sides that bad, but finasteride gave me sides. My sex drive was non-existent (it is now much better, but still lower than pre-finasteride). I can force myself though. Also my orgasms are all over the place. The sides did bother me but not by much. Now, having a dead dick is another beast lol and I dont know how I would react if I ever had this problem.
Yes I agree, sexual life is VERY important, however hair is also VERY important to me as I know loosing it will turn me back to my old, depressing, introverted days. So, I am willing to push things a bit harder than others.

You need to dosage your T levels, your DHT and Estrogen levels. Also progesterone if you can as well as LH . There are since that can be done.
 

_Ayae

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Wait what, I didn't read this thread but is tretinoin the new 'hype' now? How tf will quicker cell turnover result in hair growth?
Stop believing all pseudoscience. Hair loss is a result of hormonal susceptibility. No topicals can or will replace the results of a reduction in DHT.

And oh, make sure to use sunscreen if you use tretinoin on your scalp for whatever reason. Or you'll have more chance to develop skin cancer than to regrow hair with retinoids.
 

whatevr

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Wait what, I didn't read this thread but is tretinoin the new 'hype' now? How tf will quicker cell turnover result in hair growth?
Stop believing all pseudoscience. Hair loss is a result of hormonal susceptibility. No topicals can or will replace the results of a reduction in DHT.

And oh, make sure to use sunscreen if you use tretinoin on your scalp for whatever reason. Or you'll have more chance to develop skin cancer than to regrow hair with retinoids.

You should at the very least read into available literature before you make a grandiose (yet ignorant) entrance into a thread:

https://pubmed.ncbi.nlm.nih.gov/17202653/
https://pubmed.ncbi.nlm.nih.gov/30974011/
https://pubmed.ncbi.nlm.nih.gov/2328551/
 

_Ayae

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You should at the very least read into available literature before you make a grandiose (yet ignorant) entrance into a thread:

https://pubmed.ncbi.nlm.nih.gov/17202653/
https://pubmed.ncbi.nlm.nih.gov/30974011/
https://pubmed.ncbi.nlm.nih.gov/2328551/

So you need 3 small studies to know that something that increases cell turnover would make sure minoxidil is better penetrated?
Glycolic and salicylic and virtually any other exfoliant will do that too, without me even having to read studies about it.

Doesn't that take hair loss obsession a bit too far? Literally no dermatologist will ever prescribe tretinoin "so minoxidil will get absorbed better".

But the fact that u could even use tretinoin on ur scalp means it's already quite shrivelled, and minoxidil will not really help anymore in those cases. If minoxidil and dermarolling/-penning/-whatevering won't do the trick, nothing will.
 

TK421

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He explanes this with VDR to AR ratio.

His theory should be easy to confirm with the use of calcipotriole. But he has not been active with updates?


It needs a lot more than a testimonial from someone pumping themselves full of estrogen already to confirm this theory


So is anyone here going to experiment with calcipotriol? Do you need a prescription for this?
 

John Difool

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I was interested to try it but all I could find was an ointment with calcipotriol 0.005 % and betamethasone 0.05 %.


Betamethasome lists
  1. Hair loss
  2. thinning of the hair
as sides. So I am not sure if this is an extreme side like retinol since it's marked as less common.
 

furtbr

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You guys stopped talking about the guy's theory from half of 1st page, and entered a meaningless debate. The guy who originally thought it isn't even a trans, the reddit link OP posted was just replicating other guy's comment on r/tressless.

I found it amazing because that's exactly my thought on hairloss, having to do with VDR and ARs. It makes so much sense our bald scalp being a big solar panel for Vitamin D reception. But my take on treatment is different from this guy's..
 
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