Which Hairloss Theory Do You Believe?

[mryellowman]

And there we go, more proof!



Which means there must be a dna structure or some protein or even some Testosterone environment / characteristic that is behind alopecia. And it is the same for many people, tons of people lose ground while on strong medication that kills DHT. Which means antiandrogens are useless in the long run and it’s proof they target a secondary situation that isn’t the root cause which is why they stop working.

And like I said before, many people don’t bald. Many think they bald but they just lose some frontal ground because their hairline is maturing. So its not Finasteride that keeps heir hair, it’s the fact that there is nothing to make them fall. Examples are MANY of my friends and I’m sure you have PLENTY similar examples too! Fact! This is a damn fact, it’s no joke.

So for me as a NW5, sewing regrowth everywhere on medication clearly killed or blocked something but for how long? And was it really the root cause? No. Whatever it is, you need to block it entirely (MTF CASES) and permanently. There is a guy here I read about who explores the hormonal route he said. He did MTF drug use and he became full head of hair but no full temples as he wants BECAUSE that’s where his hairline has matured, it’s supposed to be there. So he has achieved 100% success, not 75 or 50. So we know whatever it is one does in MTF cases is making the trick. But like I said, it doesn’t cure. It just nuclear blocks. So when you come off the MTF drugs, book hair loss is back and alopecia is back.

Whatever the cure is, it lies on the DNA and it is the same for every living soul. Mark my words.

What about this guy's temple results ? https://www.hairlosstalk.com/interact/members/antydhtor.115041/

I think he was like nw2 but now you can see he has perfect hairline,temples than even any other women.

They talked about he had the most extreme hrt regimen but still it shows that you can grow those hairs back.

 

[Mandar kumthekar]

For me By reading above comments pattern baldness now becoming more mysterious than black holes . may be one day we will solve the mystery of what was there before the big bang ?but pattern bald will still remained a mystery.

 

[Mandar kumthekar]

Time for quantum theory to kicks in....

 

[MorningGlory]

As far as “environmental” factors go - and I know this is usually summarily laughed out of town - can we be sure masturbation doesn’t play a role?

 

[MorningGlory]

For me By reading above comments pattern baldness now becoming more mysterious than black holes . may be one day we will solve the mystery of what was there before the big bang ?but pattern bald will still remained a mystery.

There simply isn’t the same resource poured into male pattern baldness as there is pondering the universe. If Stephen Hawking had made androgenetic alopecia his life’s work he probably would have solved it, it just wasn’t his interest.

 

[Kagaho]

@Heinrich Harrer

You can chop a man's balls off and he won't regrow much hair. Those transgenders regrow that much because they also use estrogen.

@InBeforeTheCure whats your opinion about a possible relationship between minoxidil and the regulation of beta-catenin signaling

I ask this because im using it with dermaroller and the results im seeing are way beyond my expectations.

 

[Heinrich Harrer]

As far as “environmental” factors go - and I know this is usually summarily laughed out of town - can we be sure masturbation doesn’t play a role?

To put it simply, back when we were 12-14 we nut three ED, I lost my hair, bunch of my friends back then didn’t. Was it a sensitive-nonsensitive to DHT reason? Or masturbation doesn’t play a role at all? Yes it raises prolactin but so does higher levels of T. In my opinion, it plays no role at all. All this bs about zinc deficiency makes me laugh. For a guy to lose hair over zinc, he’s gotta be stranded on a deserted island eating cow sh*t for a year for his levels to go that low.

And that for me is the problem with hair loss scene in general. People will blame literally everything for their inevitable slow annoying loss of follicles. Maybe once the switch is turned on, everything does make it worse or maybe it’s a giant placebo BS that companies take advantage of to sell their snake oils.

@InBeforeTheCure you claim then that it is the combination that does the trick. I remember that there are cases of eunuchs who didn’t lose hair but it was dependent on when exactly you cut their testies off! Correct me if I’m wrong.

 

[Armando Jose]

To put it simply, back when we were 12-14 we nut three ED, I lost my hair, bunch of my friends back then didn’t. Was it a sensitive-nonsensitive to DHT reason? Or masturbation doesn’t play a role at all? Yes it raises prolactin but so does higher levels of T. In my opinion, it plays no role at all. All this bs about zinc deficiency makes me laugh. For a guy to lose hair over zinc, he’s gotta be stranded on a deserted island eating cow sh*t for a year for his levels to go that low.

And that for me is the problem with hair loss scene in general. People will blame literally everything for their inevitable slow annoying loss of follicles. Maybe once the switch is turned on, everything does make it worse or maybe it’s a giant placebo BS that companies take advantage of to sell their snake oils.

@InBeforeTheCure you claim then that it is the combination that does the trick. I remember that there are cases of eunuchs who didn’t lose hair but it was dependent on when exactly you cut their testies off! Correct me if I’m wrong.

Regarding eunuchs ...
https://academic.oup.com/jcem/article/84/12/4324/2864451
Most of them suffer from common baldness

Also in this video we can see that eunuchs have not scalp hair

 

[InBeforeTheCure]

@InBeforeTheCure whats your opinion about a possible relationship between minoxidil and the regulation of beta-catenin signaling

I ask this because im using it with dermaroller and the results im seeing are way beyond my expectations.

Minoxidil does activate beta-catenin in DPCs according to a couple studies. minoxidil's effects depend on AKT and ERK activation, and AKT can activate beta-catenin through GSK3 inhibition. But both AKT and ERK have many other downstream effectors besides beta-catenin that could also contribute.

@InBeforeTheCure you claim then that it is the combination that does the trick. I remember that there are cases of eunuchs who didn’t lose hair but it was dependent on when exactly you cut their testies off! Correct me if I’m wrong.

Their hair loss stops as soon as they're castrated, but doesn't regrow.

 

[Kagaho]

Regarding eunuchs ...
https://academic.oup.com/jcem/article/84/12/4324/2864451
Most of them suffer from common baldness

Also in this video we can see that eunuchs have not scalp hair

@Armando Jose you keep showing that video with eunuchs with their heads SHAVED as proof.

If you do not have a long-term study (15 years or more) with photos showing that an aesthetic deterioration happened in post castration eunuchs, dont bother with this crap anymore.

I give you a link to the study that laid the foundations of the current understanding of Androgenetic Alopecia:

https://academic.oup.com/jcem/article-abstract/20/10/1309/2719329?redirectedFrom=fulltext

BTW, Bryan destroyed you debating androgenetic alopecia causes. Those of us who have been reading this forum for some time have not forgotten it.

 

[TK421]

All the theories mentioned makes total sense on paper but each theory has cases that contradict that theory. I think inflammation plays a part, but isn't dht anti inflammatory? If so, why do so many people get results from reducing dht via finasteride and dutasteride? Wouldn't a reduction in dht lead to more inflammation? The more I try to research hair loss the more I've come to the conclusion that there is no one cause, but a few causes that lead to hair loss. Therefore, there probably won't ever be a single cure that will work for everyone. The key will be to try to diagnose the cause for each individual and tailor make a plan to address what's causing that individual's hair loss. From my experience, I think inflammation plays a part for me, which might explain why taking finasteride for 11 months not only didn't give me results, but it actually increased shedding throughout the whole 11 months. In my case, reducing dht might have led to more inflammation. I think the key for me will be to find what can successfully eliminate inflammation, although so far nothing I've tried worked (nizoral, salicylic acid, zinc, emu oil, coconut oil, olive oil). Scalp still irritated and itches throughout the day. I'm planning to experiment with 1% hydrocortisone.

 

[abcdefg]

Lets see do I believe random theories from bro scientists, or the theory that has tons of studies proving over 10 years that 85 percent of men start maintaining their hair vs placebo? Propecia has proven in the last 20 years that DHT is beyond any reasonable doubt significantly implicated in the pathology of male pattern baldness. Its like arguing smoking is not bad for you its just stupid.
Beyond DHT we say male pattern baldness is partly caused by inflammation, but the reality is we just dont know. We just flat out dont know anything beyond androgens trigger male pattern baldness for whatever reasons. Even things like PGD 2 are still more in the theory camp than fact for now. We just dont know enough yet to say how it all fits together, and how big each piece is. How important is PGD 2 or the WNT pathway, or any number of other pathways?

 

[Mandar kumthekar]

It would be reasonable to think that all above theories are correct to some extent but no single theory is 100% correct. If I ask to summarise I will summarise like this
Hairs above galea are dht sensitive. the skull bone and head muscles have varied dht sensitivity .
Dht sensitive hair starts to shrink moderately once puberty sets in.
Then skull bone expands due to dht sensitivity ,which put the hairloss problem into higher gear.
Head muscles grows in size and tension due to dht which exerts 24*7 pressure on galea which then transmitted to the scalp and puts entire hairloss vagon into TOP gear

 

[H]

I think the cure will be turning us into mice first...

 

[MorningGlory]

Can I get some considered opinion on PGD2’s role in hair loss please? Are any of you treating this aspect and if so using what?

 

[Armando Jose]

J Cutan Pathol. 2014 Apr;41(4):364-9. doi: 10.1111/cup.12286. Epub 2014 Jan 20.

A prostaglandin D-synthase-positive mast cell gradient characterizes scalp patterning.

Larson AR1, Zhan Q, Johnson E, Fragoso AC, Wan M, Murphy GF.

Author information

Abstract

BACKGROUND:

Pattern (androgenetic) alopecia is commonly encountered in scalp biopsies obtained for non-scarring hair loss. Prostaglandin D-synthase is known to be elevated in bald vs. non-alopetic scalp of patients with androgenetic alopecia. We hypothesized that this difference in pattern of prostaglandin D-synthase expression may constitute a developmental pattern inherent to normal as well as alopecic scalp skin, thus defining a 'field' vulnerable to acquired hair loss.

METHODS:

We immunohistochemically mapped prostaglandin D-synthase expression from supra-auricular to vertex scalp skin of 11 cadavers.

RESULTS:

We found significantly more dermal mast cells immunoreactive for prostaglandin D-synthase in the vertex compared to the lateral aspects of the scalp, with a decrement that spatially approximated the pattern of androgenetic alopecia. This difference was present in both balding and non-balding scalps and was independent of gender. Dual labeling established dermal cells expressing prostaglandin D-synthase as mast cells.

CONCLUSIONS:

These data indicate that scalp is spatially programmed via mast cell prostaglandin D-synthase distribution in a manner reminiscent of the pattern seen in androgenetic alopecia.

 

[Mandar kumthekar]

J Cutan Pathol. 2014 Apr;41(4):364-9. doi: 10.1111/cup.12286. Epub 2014 Jan 20.

A prostaglandin D-synthase-positive mast cell gradient characterizes scalp patterning.

Larson AR1, Zhan Q, Johnson E, Fragoso AC, Wan M, Murphy GF.

Author information

Abstract

BACKGROUND:

Pattern (androgenetic) alopecia is commonly encountered in scalp biopsies obtained for non-scarring hair loss. Prostaglandin D-synthase is known to be elevated in bald vs. non-alopetic scalp of patients with androgenetic alopecia. We hypothesized that this difference in pattern of prostaglandin D-synthase expression may constitute a developmental pattern inherent to normal as well as alopecic scalp skin, thus defining a 'field' vulnerable to acquired hair loss.

METHODS:

We immunohistochemically mapped prostaglandin D-synthase expression from supra-auricular to vertex scalp skin of 11 cadavers.

RESULTS:

We found significantly more dermal mast cells immunoreactive for prostaglandin D-synthase in the vertex compared to the lateral aspects of the scalp, with a decrement that spatially approximated the pattern of androgenetic alopecia. This difference was present in both balding and non-balding scalps and was independent of gender. Dual labeling established dermal cells expressing prostaglandin D-synthase as mast cells.

CONCLUSIONS:

These data indicate that scalp is spatially programmed via mast cell prostaglandin D-synthase distribution in a manner reminiscent of the pattern seen in androgenetic alopecia.

So according to this study male pattern baldness is preprogrammed phenomenon? Does this mean that pattern baldness has evolved for some unknown reason in men?
Most evolutionary theories couldn't explain high occurrence of balding in men and its pattern. If baldness had some advantage what that would be?

 

[Mandar kumthekar]

Why nobody is talking about androgen receptor gene?. AR gene has been coming into forefront in many studies with bigger sample sizes. Specific AR gene allele is cardinal prerequisite for baldness.

 

[Armando Jose]

It is not conclusive

In the study:
The results reported herein define a prostaglandin
and mast cell distribution within the scalp. It is
of interest that a difference did not exist between
subjects with hair loss and those without and
this suggests that other environmental factors are
probably at play impacting which people go on to
develop alopecia. In our study the absolute number
of mast cells varied between scalps and was not
a meaningful distinguishing factor between subjects
with alopecia and those without. More enlightening
was the finding of a relative difference, in all scalps,
between the vertex and the lateral edge. Scalp
heterogeneity is not limited to mast cells – types
of follicles are different including the lateral and
posterior scalp. The posterior scalp is a fertile area
for hair transplant donation and would also be
informative to study.

 

[abcdefg]

Why nobody is talking about androgen receptor gene?. AR gene has been coming into forefront in many studies with bigger sample sizes. Specific AR gene allele is cardinal prerequisite for baldness.

Is the AR encoded from just 1 gene or many genes? Even just 1 gene its not common or easy to adjust genes. So your right the AR is critical, but its not easy to fix. Its almost 30 years after invention of finasteride, and we still cant fix androgens interacting with hair. It sounds simple, but fixing it is not.
Its like saying building a road is easy without realizing the amount of work and planning involved with the details of doing it.