One of my hair follicles is the key for male pattern baldness cure

[S&L]

The title is both serious and humourous , here's why .

My agressive hairloss started 2 years ago , before I knew it my hairline was gone , I barely had the time to realise it , but since then there is ONE hair in a bald frontal zone that just keeps going !
I cut it with scissors regularly ( not too short I don't want to mix it up with another eventual hair , even if there are none around )and I'm absolutely positive it's been the SAME HAIR for more than 1 year now .

So this can seem really anecdotal but IMO raises some questions :

- How can it survive when all the others are gone ? it's way on the front , an area that was rapidly decimated , that area is clearly bald , there are not even miniaturized hair remaining . It has the thickness of my original hair and the same of what I have left mostly ( as strange as this is for me the majority of my hair do not miniaturize , they just fall , everything for me started with a ginourmous effluvium )

- How does one follicle eludes the 3 phases of the hair cycle ? it should have fallen out and regrown like 4 times now .

I'm gonna ask a surgeon to take it ou with the follicle , keep it in the freezer and sell it to a big company :mrgreen:

 

[Rutt]

yeah i have 3 of these

it's no more a cure to male pattern baldness then donor area hair [back of your head] is.

 

[S&L]

And you have thoroughly followed the progression of these 3 hairs for a long time ? like a year or more ?
Hairs in donor area cycle like all the other hairs in the body , they just don't miniaturize , hair that doesn't cycle seems kinda weird to me

 

[freakout]

The title is both serious and humourous , here's why .

...there is ONE hair in a bald frontal zone that just keeps going !
I cut it with scissors regularly ( not too short I don't want to mix it up with another eventual hair , even if there are none around )and I'm absolutely positive it's been the SAME HAIR for more than 1 year now .

It's possible that it's similar to other follcles but rather than being fed by an arterioles, the follicle is connected directly to an artery.

Have you tried massaging your scalp? Fast occuring baldness could be sebum related.

 

[anxious1]

It's possible that it's similar to other follcles but rather than being fed by an arterioles, the follicle is connected directly to an artery.

i dont know how u came about that idea, sounds like something u just made up.

I dont see how this would make the hair immune to miniurization. It would just get more blood, and more dht to the receptors in the follicle.

Theres no way a better blood supply would stop it from miniturizing. More than likley it just is a non male pattern baldness hair growing in the male pattern baldness area for some reason. I have a few of those myself.

 

[freakout]

Read these:

http://www.ncbi.nlm.nih.gov/pubmed/12734505

http://www2.massgeneral.org/pubaffairs/ ... 01hair.htm

I don't just make things up. I think and study outside the androgenetics theory (Androgenetic Alopecia). Androgenetic Alopecia is exactly what Merck (Propecia) wants us to believe. I don't subscribe to mainstream medicine specialy when pronouncements come from people who work for pharmaceutical companies.

If you don't have access to the full text of the first link, I can send you a pdf. That study was repeated twice. It involves 28 men and 11 women. All regrew hair follicles samples into terminal hair.

 

[S&L]

I had , mostly at the beginning huge buildups of sebum around the hair follicles , I really thought it wasn't Androgenetic Alopecia untill the corners of my hairline went way up and started fo feel the difference of density when touching my head .
I still don't know what to think and do about it , I basically shed tons of hair ,

I don't know about that artery thing but more blood supply actually improves things , like you can see from the clinical study of botox for Androgenetic Alopecia :

http://journals.lww.com/plasreconsu..._Male_Pattern_Baldness_with_Botulinum.79.aspx

Botox seems to work to some extent and the reason is , like they cite from another article :
Hypoxia favorises conversion of testosterone to DHT , whereas with more O2 , conversion to estradiol is favored

 

[freakout]

I see. You still in school or do you already work?

 

[cyberprimate]

IMO the presence of the galea aponeurotica has to be considered here. The galea is a tendon like structure that covers the balding area exactly and is pulled down around the skull by surrounding muscles that tighten it like a drumskin. I've posted the following text on hairlosshelp but I'll repost it here.

My hypothesis combines both androgen and galea/blood flow theories. I'll base my understanding of the role of galea and blood flow on two recent studies that have been pretty much ignored as far as i know. The whole idea is not that the galea aponeurotica is the sole cause of male pattern baldness, but that it is the one substantial contribucting factor, in the sense that its presence multiplies the levels of dht production in the follicles.

We all know that all scalp hair have a negative reaction to dht, including on the horseshoe area (as opposed to body hair that up to a certain level have stimulated growth when in presence of dht). Horse shoe hair are also affected by male pattern baldness but not to the point of causing a substantial esthetic problem. So why are galea follicles more affected by dht than off galea follicles on the scalp? The dominant hypothesis is that there's a genetic difference between galea follicles and off galea ones. I've never found that idea convincing as it fails to explain why the development of hair thinning on the galea tends generally to be faster on regions of the galea where the galea tightness is mechanically highest because of skull angles, namely the vertex and the frontalis. The idea that there is a fundamental genetic difference between horseshoe follicles and galea follicles is pretty acceptable in thoery. After all there seems to be a genetic difference between scalp follicles and body follicles, so why not a second follicular difference, on the scalp this time? But I reckon the idea that there may be a third genetic difference between vertex/frontalis follicles and the rest of the galea follicles, seems a bit much to not invite us to further questioning...

Based on two studies that I'll post at the bottom of this post, here's my current hypothesis concerning these various differences of follicular reactions we see on all regions of the scalp. The quotes are taken from the two studies I've mentioned.

1. The scalp has 5 layers and the 3 top layers are like "glued" together (although one can separate them in surgery). This is not my opinion but an objective observation. So when the surrounding muscles are pulling on the galea, they tighten the galea and the dermis above it, that layer that contains the follicles and the blood vessels.
"Mechanistically, the scalp behaves like a drum skin with tensioning muscles around the periphery. These muscle groups - the frontalis, occipitalis, and periauricular muscles and to a minor degree the temporalis - can create a "tight" scalp when chronically active." (second study)

2. Because it's tightened, the dermis is thinner than normal (just like a stretched rubber piece gets thinner and longer than when not stretched), and this thinner dermis gives less space for blood vessels to flow blood and the oxygen it contains, hence the hypoxia in the region.
"There is a relative microvascular insufficiency to regions of the scalp that lose hair in male pattern baldness. Because the blood supply to the scalp enters through the periphery, a reduction in blood flow would be most apparent at the distal ends of the vessels, specifically, the vertex and frontal peaks". (first study)

3. This hypoxia then causes a greater dht conversion in the follicles on the galea
"The enzymatic conversion of testosterone to dihydrotestosterone is oxygen dependent. In low-oxygen environments, the conversion of testosterone to dihydrotestosterone is favored; whereas in high-oxygen environments, more testosterone is converted to estradiol. We have identified a previously unreported tissue hypoxia (condition in which a region is deprived of adequate oxygen supply) in bald scalp compared with hair-bearing scalp." (first study)

4. This higher production of dht by the follicles on the galea damages the follicles' structure (by the release of growth-suppressing chemicals in the dermal papillae and other possible changes), and follicles miniaturize over time. We get bald...
"Areas of the scalp with sparse hair growth have been shown to be relatively hypoxic, have slow capillary refill, and to have high levels of dihydrotestosterone". (second study)

To sum it up:

Tight galea >> reduced blow flow >> hypoxia (lack of oxygen) >> higher dht conversion by follicles >> gradual and long term follicle damage >> thinning hair


Now just a word on the 1979 Nordström study. One can think that the conclusions of it are adamant and that the galea case is closed. But I'm questioning the absoluteness of the conclusion of that study. Why? Imagine that living many years in one environment "A" causes a long lasting alteration of an organism and damages it gradually. If you transfer this organism in a safe environment "B", the long lasting effect of the environment "A" could well cause the damage to last further despite the change of environment. No? (also if this alteration by the environment "A" takes a decade to be observable, you may put another similar organism in it and not see any damage to it for months or years). What I'm suggesting is the possibility of inertia in follicle damage that was not considered by Nordström, all the more since it wasn't conducted over a decade or more, if follicles could ever regain their original unaltered structure with time and without external intervention.

As for the absence of problems with transplanted follicles on the galea, one has to remember that follicle damage happens in most cases over many years, and transplanted follicles don't have to face the high levels of testosterone production happening in early adult years.

http://journals.lww.com/plasre...n_Male_Pattern.3.aspx

http://journals.lww.com/plasre...with_Botulinum.79.aspx

 

[armandein]

Interesting theory, but how do you explain the diferent incidence of common baldness between women and men?

 

[cyberprimate]

The links that you posted do not work, can you please repost them?

http://journals.lww.com/plasreconsurg/A ... ern.3.aspx
http://journals.lww.com/plasreconsurg/F ... um.79.aspx

I notice it's the same link that S&L posted earlier.

how do you explain the diferent incidence of common baldness between women and men?

Different Testosterone levels in the system I guess, hence different DHT production on the scalp. On average men produce FAR more testosterone than women, but interinstingly men with super low production and women with super high production, have very similar testosterone levels apparently. The skull expansion, if it really happens, could also be a factor by a greater tightening of the galea and therefore a greater DHT production. Interestingly when women experience baldness due to hormonal changes, their hair loss is also mostly located on the galea.

 

[anxious1]

someone was saying (i think it was bryan), that a bunch of people decades ago got their galea removed, to try and cure male pattern baldness, and no difference was observed, therefore the galeas relationship to male pattern baldness was disproved.

perhaps bryan (if it was u) can chime in and tell us more about it.

in any case, youve just taken the Androgenetic Alopecia theory and added a few contributing factors. So this doesnt disprove the Androgenetic Alopecia theory, it just expands it.

i'd like to believe what ur saying though. I guess the next step for u is to prove it somehow by fixing it. Good luck.

 

[freakout]

Interesting theory, but how do you explain the diferent incidence of common baldness between women and men?

There is no doubt that male hormones are involved BUT NOT in a manner that scalp hair follicles are DIRECTLY influenced by androgens but rather in a INDIRECT manner:

androgens + genes + x + x + x = male pattern baldness

The galea is a naturally susceptible area because of the blood supply factor. A purely androgenic standpoint simply cannot explain this.

The additional factors should account for CVDs or even prostate cancer.

There are more factors than mainstream is focusing on BUT they want to focus on these two factors because they are driven by biomedical 'science' (pharmacological science). In other words, no ROIs by looking at lifestyles.

Even while genes are also involved, why would we, as laymen, want to drop it from the equation? Because there is absolutely nothing we can do about it. The other is, our genome (genes) contain the records of our ancestors' life's events. Our genes GENERALLY protect us from adverse environmental conditions that our ancestors were exposed to.

In male pattern baldness, the other side of the picture can be painted: we don't have the genes that protect us from male pattern baldness. If this is the first time you're hearing this is because mainstream medical research community sucks.

Even while male hormones are indisputably involved, why would we want to drop it from the equation? Because it is part of our system as advanced organisms.

So we focus on something that we can do something about.

 

[cyberprimate]

if your theory was correct Vasoldilators combined with antiandrogens would be a cure for hair loss

Well first, just like with the Nordström study one has to consider the inertia in follicle structure once it's altered by years and years of dht production. The other thing is I'm not sure that in the context of the galea region vasodilators would be enough to improve capillary deficiency. If the dermis is really stretched there may not be enough space for capillary development anyway. In other words there can only be substantial capillary change when there's enough space available for it in the scalp. Touch your galea, see how tight and thin it is? Do you think you can dramatically change blood supply there with vasodilators? Also if i may say, the advocates of the sole Androgenetic Alopecia theory have to provide an explanation as to why hair loss is generally faster on the vertex and the front hairline…

I guess the next step for u is to prove it somehow by fixing it. Good luck.

I'm experimenting a method that may artificially improve oxygen supply to follicles without touching blood circulation itself. I'll report about it in 4-5 months.

 

[armandein]

Interesting theory, but how do you explain the diferent incidence of common baldness between women and men?

http://www.nature.com/jidsp/journal/v10 ... 0214a.html

Thank you for the study regarding estrogen in vitro frontoparietal hairs of women and men, not really Androgenetic Alopecia.

 

[armandein]

The links that you posted do not work, can you please repost them?

http://journals.lww.com/plasreconsurg/A ... ern.3.aspx
http://journals.lww.com/plasreconsurg/F ... um.79.aspx

I notice it's the same link that S&L posted earlier.

how do you explain the diferent incidence of common baldness between women and men?

Different Testosterone levels in the system I guess, hence different DHT production on the scalp. On average men produce FAR more testosterone than women, but interinstingly men with super low production and women with super high production, have very similar testosterone levels apparently. The skull expansion, if it really happens, could also be a factor by a greater tightening of the galea and therefore a greater DHT production. Interestingly when women experience baldness due to hormonal changes, their hair loss is also mostly located on the galea.

Hormones really important in Androgenetic Alopecia are produced in the pilosebaceous unit, exist differences among women and men in scalp hairs?

 

[cyberprimate]

The fact that the galea feels ''tight'' is irrelevant, do you not realise how small capillaries are?

Do you know the quantity of capillaries that are necessary to give the same blood supply as on the other areas of the scalp? if not we're just debating in the absence of necessary data here. If capillaries are so small then the non balding areas can have even more capillaries than galea follicles, right? If there's largely enough space on the galea region for capillaries, then what's the point of experimenting with increasing vascularity with vasodilators for a start?

And what's your explanation for the microvascular insufficiency observed in the study I posted? And hypoxia? How do you explain the interesting results had in the botoxin study i mentioned? And how do you explain the earlier hairloss of the most angular regions of the galea (vertex and hairline)? You just can't use the argument of genetic follicular difference for every regional singularity observed on the scalp, and also on the galea itself.

Also how long were the vasodilators applied on the scalp in those studies?

 

[cyberprimate]

Nobody denies there are capillaries reaching follicles… You seem to have a binary notion of vascularity and think there's either blood flow or not. We're talking about "relative microvascular insufficiency", not radical absence of blood supply which may explain why follicles get altered over several decades. For scalp cell apoptosis there would need radical insufficiency and it's not what I've suggested.

As for the failure of the botoxin experiment, first it seems to be relative since some subjects did show improvement of their hair as pictures show, but it may confirm the fact that the sole increase of blood flow is not enough to revive follicular activity after years of dht alteration, just like in the 1979 Nordström study.

I don't feel like playing Q&A right now.

There's a need for explanation as to why there's hypoxia, why there's this regional variation of hair loss pace over the galea (vertex and hairline vs the rest of it) and more generally why baldness happens mostly on the galea.

btw if the sole explanation for all these observations is genetic difference amongst scalp follicles before puberty, i'm surprised there's no DNA study showing these differences.

 

[S&L]

The Clinical Botox Androgenetic Alopecia trials ended in 2009 and they have decided not to pursue approval which suggests that the botox was found ineffective, in the phase II trials. http://www.clinicaltrials.gov/ct2/show/ ... ia&rank=17

I do not see where they say it failed , actually it worked to some extent , the result of the study shows it .
You don't agree with the fact that galea is involved / worsens the condition ? fine , but please don't make stuff up like saying it was found ineffective , because it ain't true .
Now is it effective enough to fund more research ? and go against the big players that are finasteride and minoxidil on the field ? that's another story .

 

[cyberprimate]

Finfighter, that's not what I was referring to. I'm speaking of a genetically caused difference amongst follicles that cmakes galea follicles far more sensitive to androgens than horseshoe follicles.