Skull expansion: Alternative model for primary mech. of Androgenetic Alopecia

bornthisway

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Big head? Bald head! skull expansion: Alternative model for the primary mechanism of Androgenetic Alopecia.

Med Hypotheses. 2008 Sep 10.
Taylor PJ.

Currently, the predominant hypothesis explains androgenetic alopecia (Androgenetic Alopecia) as a process reliant upon affected follicles being individually programmed to accumulate dihydrotestosterone (DHT), which then causes progressive follicular miniaturisation. The goal of this paper is to suggest that such miniaturisation may result from an exaggeration of the bone remodelling process causing a reduction in blood supply to the capillary network within the affected region. The bones of the human skull continue to grow during adulthood and observations made of those with Androgenetic Alopecia suggest that such growth may be responsible for the development of this condition. Studies of human cranial anatomy indicate that frontal and parietal bone growth can account for the development of the male pattern baldness (male pattern baldness) profile and the variations that can occur in the rate and location of hair loss. Steroid hormones such as DHT promote facial and body hair growth. Logically, this suggests that DHT should stimulate hair growth within the male pattern baldness region and not hair loss. However, DHT also has an anabolic effect on bone formation, and it is hypothesised that this stimulation of bone growth that will overwhelm the hair growth promoting effects of DHT. Androgen receptor sites, 5-alpha-reductase (5alpha-R) and DHT have all been associated with Androgenetic Alopecia, but they also exist within numerous types of bone cells. DHT will stimulate the proliferation of osteoblast cells and the formation of new bone. Verification of this hypothesis would imply that DHT is primarily involved with Androgenetic Alopecia through its stimulation of the skull expansion process rather than through interaction with individual follicles. Also, increased androgen receptor gene expression, 5alpha-R activity and subsequent production of DHT within the male pattern baldness region of balding individuals, may simply represent the body's attempt to compensate for the skull expansion expression of hair follicle miniaturisation. Furthermore, it suggests that male pattern baldness region follicles are not individually programmed for hair loss. A redirection of genetic research towards the identification of those genes responsible for skull shape and development would be appropriate, and may reveal the genetic connection to Androgenetic Alopecia including its paternal link.

PMID: 18789604
 

squeegee

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Good find Born!
 

bobs

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hmmm... then why don't transplanted hairs shrink? If is NOT up to the hair but rather the skull-environment then transplanted hairs should suffer the same fate right?

Otherwise an interesting theory. It is a fact that we don't know for sure what causes male pattern baldness. We know androgens play a role but we don't know how exactly.
 

elguapo

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I think there is some truth to this. Just looking at the pattern of baldness in men, especially men that are completely bald, with hair growing in the sides of their heads (the horse shoe pattern), makes me think that there is something "funky" about the skin on the very top of the head (the balding scalp). And the skin on the sides and back of the head is so plush compared to the top of the head. When you look in the mirror, and you raise your eye brows, you can see that the skin on the forehead is much more plush, thicker, than the skin just above it where the hairline is receding. And the skin on the temples is especially thin, which makes me think that this is why the hair on the temples is usually the first to go.

Also, I believe I read somewhere that there is a type of hair restoration procedure in which the sides of the scalp are pulled up and joined at the top of the head. In other words, the idea is to cover the balding scalp - the top of the head - by "spreading" the sides of the head upward so that they meet in the middle of the head. And I heard that when this procedure is performed, the hairs that were at the top of the sides of the head also fall out. So again, this makes me think that there is something about the top of the head and the stretching of the skin that causes, or at least influences is some way, hair loss.

But the fact that you can transplant hairs from the back of the scalp to the top of the head in a common hair transplant procedure, and those hairs do survive, does punch a hole in this theory.

I don't know. But I'm glad they are looking into it. I can't cite details off hand at the moment, but so often in science has mankind thought they had a working model of some scientific phenomenon, only to realize that the model was wrong later on. The atom is a good example, I suppose.

I agree, good find!
 

goata007

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At least this theory explains the reason why some of us (including me) experience new bony growth in the middle of our crown.
 

xcvq

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goata007 said:
At least this theory explains the reason why some of us (including me) experience new bony growth in the middle of our crown.

New bone growth or just loss of subcutaneous fat that makes the scalp feel bony?
 

goata007

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xcvq said:
goata007 said:
At least this theory explains the reason why some of us (including me) experience new bony growth in the middle of our crown.

New bone growth or just loss of subcutaneous fat that makes the scalp feel bony?

That's another theory, but then the transplated hairs grow too right?? It would be good if they figure out how to restore scalp to it's original state.
 

elguapo

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I still wish that they (whoever "they" might be=) would take the hair follicle dermal papilla cells from the back of the head, cultivate and multiply them, but instead of transplanting the cultivated cells to the balding scalp, transplant them to another part of the body, like the top of the foot or the thigh or something, where the skin is more plush, to see if the cells result in thicker, more terminal hairs than what they are seeing so far in the Phase II trials of ICX-TRC. I just think that the skin on the top of the bald scalp is so inhospitable to the growth of transplanted dp cells, much like dry dirt on a corn field, that we would learn more by first trying to grow hairs in skin that is more supple.

Perhaps this is a lame idea, but I don't see any harm in trying it. 6 billion people in the world, and we can't try this on ONE?
 

Bryan

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Move over, Stephen Foote and Armando Jose! Time for another new goof-ball theory of balding! :)
 

elguapo

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My girlfriend recently broke up with me, and I lost 15 lbs in 2 months, and my hairline receded at the temples about a half inch since then, I swear it. So as crazy as it sounds, I really believe that the thinner the scalp skin is, the quicker the hair loss. Yes, it's just a theory, and it sounds crazy. But until they find a no-kidding cure/solution to hair loss, I think it's fair to allow such theories to stand until proven wrong.

I just don't think that the hair follicle alone and its susceptibility to DHT is the sole culprit of hair loss. I think the skin has something to do with it, too. Or maybe the lymphatic system, or something. But something more than just the follicle. But that's just my opinion, based on my own observations of how when I lose weight, I also lose quite a bit more hair than usual.
 

Armando Jose

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Bryan said:
Move over, Stephen Foote and Armando Jose! Time for another new goof-ball theory of balding! :)

dear Bryan;

The current androgenetic theory is not very clever due one of its foundations is the genetic "lottery". You know very well that important androgens in hair are synthesized in the pilosebaceous unit, and very important, years before puberty. The same with neurosteroids in brain. It is called intracrinology. Are you agree?

OTOH, any theory must explain, at least, the special pattern and the different impact on both sexes. This last one theory don't talks about it.

Armando
 

debris

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this theory is complete BS, it does not fit and the simplest known facts like the donor dominance pretty much invalidate this theory completely.

in other words there are proofs all this skull expansion model is BS.
 

Bryan

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Armando Jose said:
The current androgenetic theory is not very clever due one of its foundations is the genetic "lottery". You know very well that important androgens in hair are synthesized in the pilosebaceous unit, and very important, years before puberty. The same with neurosteroids in brain. It is called intracrinology. Are you agree?

While the pilosebaceous unit does seem to have the metabolic machinery to produce androgens on their own, it seems clear that the level of androgens it produces is insufficient either to initiate, or maintain balding. The obvious evidence for that is the much-discussed finding that castration prevents the future occurrence of balding entirely if done before it starts, or stops the further progression of balding if done after balding has already started.
 

CCS

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Bryan said:
Armando Jose said:
The current androgenetic theory is not very clever due one of its foundations is the genetic "lottery". You know very well that important androgens in hair are synthesized in the pilosebaceous unit, and very important, years before puberty. The same with neurosteroids in brain. It is called intracrinology. Are you agree?

While the pilosebaceous unit does seem to have the metabolic machinery to produce androgens on their own, it seems clear that the level of androgens it produces is insufficient either to initiate, or maintain balding. The obvious evidence for that is the much-discussed finding that castration prevents the future occurrence of balding entirely if done before it starts, or stops the further progression of balding if done after balding has already started.

I don't understand what you are getting at Bryan. We need testosterone to make DHT. Castration greatly reduces testosterone production. How does that say anything about how much of the balding is caused by locally produced DHT?
 

Bryan

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CCS said:
I don't understand what you are getting at Bryan. We need testosterone to make DHT. Castration greatly reduces testosterone production. How does that say anything about how much of the balding is caused by locally produced DHT?

Armando was referring to more recent evidence suggesting that hair follicles have the metabolic ability to produce all androgens, including (apparently) even testosterone. He wasn't referring specifically to DHT.

My response to Armando is simply how can locally-produced androgens within the hair follicle be very significant, since castration has such a profound effect on balding?
 

Armando Jose

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Bryan said:
Armando Jose said:
The current androgenetic theory is not very clever due one of its foundations is the genetic "lottery". You know very well that important androgens in hair are synthesized in the pilosebaceous unit, and very important, years before puberty. The same with neurosteroids in brain. It is called intracrinology. Are you agree?

While the pilosebaceous unit does seem to have the metabolic machinery to produce androgens on their own, it seems clear that the level of androgens it produces is insufficient either to initiate, or maintain balding. The obvious evidence for that is the much-discussed finding that castration prevents the future occurrence of balding entirely if done before it starts, or stops the further progression of balding if done after balding has already started.

Thank you Bryan for your response;

I thought you are angry with me ;)

But there is any reference about "castration prevents the future occurrence of balding" apart the obscure citation of Hamilton???

Yours sincerely

Armando
 

Bryan

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Armando Jose said:
But there is any reference about "castration prevents the future occurrence of balding" apart the obscure citation of Hamilton???

I certainly wouldn't call that an "obscure citation"! :) Hamilton's studies are still referenced to this very day by all the top doctors studying androgenetic alopecia. Have you read them yourself, Armando?
 
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