Why is the thinning area in male pattern baldness exactly the galea area ?

[Bryan]

We know through common observation that terminal hair growth continues in some follicles in bald areas. These can keep growing for years, before the area becomes slick bald. This wouldn't happen if the mechanism was as described above.

In my theory, all that is needed is for androgens, in particular DHT to increase the lymphatic pumping rate. This accounts for the hair growth and male pattern baldness in some by known physiology, and fluid dynamic principles. The survival of transplants how i proposed earlier, and the survival of some follicles for long periods because contact inhibition only happens to new enlarging anagen follicles.

Any valid theory must address these issues.

I agree that _some_ lone scalp hair follicles continue to grow relatively normally, even when surrounded by other balding hair follicles. In a study I've quoted several times in the past, Happle and Hoffmann found that the occasional scalp hair follicile (probably the same ones I just mentioned as growing normally) is relatively insensitive and unaffected by androgens, for some unknown reason(s).

However, I think it would be more difficult for YOU to try to explain why a single hair follicle like that in a mass of edema would not (supposedly) be affected by "contact inhibition", like all of its nearby neighbors. Can you explain that?

 

[freakout]

If the claim is that the pressure is reducing the blood supply and causing hair loss through "starvation" and hypoxia, there is a major flaw in it.

We know through common observation that terminal hair growth continues in some follicles in bald areas. These can keep growing for years, before the area becomes slick bald.

Starvation is can still be valid specialy if the focus is on the pattern rather than single hair follicles.

Arterioles diameter is not uniform throughout. Some are larger specially when they're connected to larger arteries. A follicle that survives could, by some freak of nature, connect directly to an artery, is a possibility.

Such a scenario would provide support to the scalp follicle hormone-independence assertion.

 

[cyberprimate]

Does anyone know whether blood vessels cross the galea from below and reach the follicles, or do blood vessels come to the follicles only from above the galea?

 

[freakout]

The galea is a separate layer. The scalp itself has five layers.
The galea and the scalp stuck or "glued" together but peelable.
No blood vessel goes through the galea.
Yon can actually peel off the scalp and turn it 180 degree and reattach.
That's how I understand the anatomy.

 

[dr_jekyll]

Here's a link to a study from NASA discussing cranial blood pressure and its causes/effects

http://www.ncbi.nlm.nih.gov/pubmed/8526836

 

[S Foote.]

We know through common observation that terminal hair growth continues in some follicles in bald areas. These can keep growing for years, before the area becomes slick bald. This wouldn't happen if the mechanism was as described above.

In my theory, all that is needed is for androgens, in particular DHT to increase the lymphatic pumping rate. This accounts for the hair growth and male pattern baldness in some by known physiology, and fluid dynamic principles. The survival of transplants how i proposed earlier, and the survival of some follicles for long periods because contact inhibition only happens to new enlarging anagen follicles.

Any valid theory must address these issues.

I agree that _some_ lone scalp hair follicles continue to grow relatively normally, even when surrounded by other balding hair follicles. In a study I've quoted several times in the past, Happle and Hoffmann found that the occasional scalp hair follicile (probably the same ones I just mentioned as growing normally) is relatively insensitive and unaffected by androgens, for some unknown reason(s).

However, I think it would be more difficult for YOU to try to explain why a single hair follicle like that in a mass of edema would not (supposedly) be affected by "contact inhibition", like all of its nearby neighbors. Can you explain that?

As i have said before Bryan, i suggest this is because of the normal human hair cycle. We know that the human scalp hair anagen period can be years. Contact inhibition will only effect enlarging follicles in early anagen. If the pressure increases around a follicle just after it has reached full anagen growth, it will take years before this follicle cycles again and "then" becomes effected.

Just to clarify a couple of points. it is not the fluid pressure "itself" that directly acts on follicles. The basic physics here is that enlarging anagen follicles have to push the surrounding dermal tissue away in order to enlarge. The anagen hair follicle is an enlarging pocket in dermal tissue.

The greater the tissue fluid pressure, the greater the force behind the dermal cells, that would naturaly try to fill any hollow space in the tissue. The greater this resistence to follicle expansion, the earlier normal contact inhibition will turn of anagen enlargement, and miniaturised follicles result.

The simple analogy here is a party baloon.

The air inside is the fluid pressure, and the skin of the baloon is the dermal tissue. You can "make" a follicle by pushing your finger into the baloon to form a pocket. How hard this is depends on the pressure in the baloon.

All normal non cancerous cells respond to the growth control of normal contact inhibition. This process must be related to a certain resistence level, that when reached stops further cell division and growth.

Apart from changes in fluid pressure, there is also the natural resistence or "toughness" of the tissue around follicles. I think this is already accepted in male pattern baldness as the fibrosis that developes has been called a barrier to follicle enlargement by Hideo Uno amongst others.

So why dont the follicles just force themselves though this barrier? Normal contact inhibition is why.

If i am right about this, then weak tissue should have the reverse effect. It should be easier for anagen follicles to push this out of the way and make a larger follicle and more hair growth?

I think we have a good example of this in humans.

Feel the tissue beneath your eyebrows. See how soft this is! Boxers know just how weak these strips of tissue are, that correspond to increased hair growth.

If you raise your eyebrows you can feel the weak "groove" of tissue here better.

S Foote.

 

[Bryan]

As i have said before Bryan, i suggest this is because of the normal human hair cycle. We know that the human scalp hair anagen period can be years. Contact inhibition will only effect enlarging follicles in early anagen. If the pressure increases around a follicle just after it has reached full anagen growth, it will take years before this follicle cycles again and "then" becomes effected.

Just to clarify a couple of points. it is not the fluid pressure "itself" that directly acts on follicles. The basic physics here is that enlarging anagen follicles have to push the surrounding dermal tissue away in order to enlarge. The anagen hair follicle is an enlarging pocket in dermal tissue.

The greater the tissue fluid pressure, the greater the force behind the dermal cells, that would naturaly try to fill any hollow space in the tissue. The greater this resistence to follicle expansion, the earlier normal contact inhibition will turn of anagen enlargement, and miniaturised follicles result.

I'm not sure here why you believe that miniaturized follicles would result. Wouldn't their size be limited to their original size (before contact inhibition began), with no further alteration in size, one way or the other?

 

[S Foote.]

As i have said before Bryan, i suggest this is because of the normal human hair cycle. We know that the human scalp hair anagen period can be years. Contact inhibition will only effect enlarging follicles in early anagen. If the pressure increases around a follicle just after it has reached full anagen growth, it will take years before this follicle cycles again and "then" becomes effected.

Just to clarify a couple of points. it is not the fluid pressure "itself" that directly acts on follicles. The basic physics here is that enlarging anagen follicles have to push the surrounding dermal tissue away in order to enlarge. The anagen hair follicle is an enlarging pocket in dermal tissue.

The greater the tissue fluid pressure, the greater the force behind the dermal cells, that would naturaly try to fill any hollow space in the tissue. The greater this resistence to follicle expansion, the earlier normal contact inhibition will turn of anagen enlargement, and miniaturised follicles result.

I'm not sure here why you believe that miniaturized follicles would result. Wouldn't their size be limited to their original size (before contact inhibition began), with no further alteration in size, one way or the other?

Not sure what you mean by original size in this context Bryan?


The original anagen "size" of the follicle is only effected by changes in pressure come the next cycle. In the next telogen "miniaturised" phase of the hair cycle, the surrounding tissue has moved into the space previously occupied by the large anagen follicle. When the follicle next enters anagen growth, it has to deal with the resistence of this surrounding tissue again. If this has increased since the last anagen phase, contact inhibition will start earlier in the phase, and the anagen follicle will be smaller.

If the pressure rise takes a long time to develope, and this is possible in physiology, the follicle may go through two or three cycles getting smaller each time.

The remaining full anagen hair isolated in bald spots we talked about, may be follicles that have a very long anagen phase. The info is that human scalp hair can be in anagen for two to twelve years.

It would be interesting if these particular follicles were studied more. According to my theory, the pressure around these should be high enough to miniaturise these in one cycle. They should not show reduced growth over more cycles, because the pressure was enough to fully miniaturise the follicles around them in this area.

But we never seem to get professional experiments that answer this kind of question. Let me ask you a question Bryan?

We have talked about that immune deficient mouse transplantation study before. If this was repeated ensuring that there was more than enough DHT in the tissues to be a fair test, and if the same results happened, would you concede that this disproves the assumpions made about donor dominance and the in-vitro studies?

S Foote.

 

[Bryan]

But we never seem to get professional experiments that answer this kind of question. Let me ask you a question Bryan?

We have talked about that immune deficient mouse transplantation study before. If this was repeated ensuring that there was more than enough DHT in the tissues to be a fair test, and if the same results happened, would you concede that this disproves the assumpions made about donor dominance and the in-vitro studies?

I don't see how one simple mouse test could supposedly "disprove" donor dominance, since THAT has been solidly demonstrated in hair transplant clinics for DECADES, not just in individual experiments by the experts.

 

[S Foote.]

But we never seem to get professional experiments that answer this kind of question. Let me ask you a question Bryan?

We have talked about that immune deficient mouse transplantation study before. If this was repeated ensuring that there was more than enough DHT in the tissues to be a fair test, and if the same results happened, would you concede that this disproves the assumpions made about donor dominance and the in-vitro studies?

I don't see how one simple mouse test could supposedly "disprove" donor dominance, since THAT has been solidly demonstrated in hair transplant clinics for DECADES, not just in individual experiments by the experts.

Well apart from this study, there have been others which clearly show donor dominance is not as "solid" as you assume Bryan.

http://www.newhair.com/resources/mp-200 ... inance.asp

Early in this thread you quoted the study by Nordstrom claiming "it is all in the follicle". However you failed to mention that Nordstrom himself stated the results could be because of an effect "very close to the follicle".

In that mouse study, we have whole human male pattern baldness follicles transplanted in a small piece of human tissue. The fact that they regrew as they did completly disproves that it is "all in the follicle". It "has" to be an effect outside the follicle as Nordstrom suggested it may be! This is very clear.

I am away for a few days so can't post till next week. I just suggest people look at the facts here for themselves.

S Foote.

 

[Bryan]

Well apart from this study, there have been others which clearly show donor dominance is not as "solid" as you assume Bryan.

http://www.newhair.com/resources/mp-200 ... inance.asp

Donor dominance is as "solid" as I've always said. You keep mentioning the results of that Japanese experiment, so I'll keep giving you the same reply: the term "donor dominance" (in this context) refers specifically to androgenetic alopecia. Here is what Dr. Bernstein HIMSELF says at that link (added emphasis is my own):

"In 1959, Dr. Norman Orentreich...put forth the concept that in androgenetic alopecia 'the transposed grafted skin maintains its integrity and characteristics independent of the recipient site.' "

See what I've been saying to you over and over and over for years? Dr. Orentreich was a careful investigator; he wouldn't simply make the outrageous claim that hair follicles show donor dominance for every last physical characteristic you can think of; he made that claim SPECIFICALLY for androgenetic alopecia, and he was correct! If you read his 1959 paper (mentioned above by Bernstein), you'll plainly see that Orentreich tested other hair problems, too (like alopecia areata), and not all of them displayed donor dominance!! :laugh:

So how many times are you going to keep bringing-up that Japanese experiment as a challenge to donor dominance, and how many times am I going to have to keep explaining to you its total lack of significance?

Early in this thread you quoted the study by Nordstrom claiming "it is all in the follicle". However you failed to mention that Nordstrom himself stated the results could be because of an effect "very close to the follicle".

Yes, that was obviously a very cautious statement by Nordstrom. Like any true scientist, he was acknowledging the vague possibility of another possible explanation, no matter how slight or insignificant it was.

In that mouse study, we have whole human male pattern baldness follicles transplanted in a small piece of human tissue. The fact that they regrew as they did completly disproves that it is "all in the follicle". It "has" to be an effect outside the follicle as Nordstrom suggested it may be! This is very clear.

As I've been saying about that study for a long time, it's interesting, but we can't really draw any conclusions from it, for a number of reasons: it hasn't been duplicated by anybody else; they didn't indicate the levels of androgens in those mice; and it remains unclear what effect (if any) the lack of an immune system had on the hair growth in those mice.

 

[anxious1]

Just a thought,

What about the theory that its not reduced blood flow to the galea, but increased blood flow to the galea.

The increase in blood brings more DHT to the follicles, which in susceptible people creates miniturization based around the shape of the galea.

transplanted hairs from back or sides, in people with the male pattern baldness gene or watever,
aren't programmed to be affected by the DHT so the extra DHT in the blood doesnt bother them, this would explain the usually contradictory 'but how com transplanted hairs are unaffected'.

I have no idea why theyre would be an increase in blood flow to the galea. maybe its related to head size or something.

just a thought, feel free to add to this or disprove it.

 

[Bryan]

What about the theory that its not reduced blood flow to the galea, but increased blood flow to the galea.

The increase in blood brings more DHT to the follicles, which in susceptible people creates miniturization based around the shape of the galea.

As I've explained numerous times over the years, I don't think DHT in the blood has a significant effect on scalp hair, or any other tissue, for that matter. DHT isn't much of an endocrine hormone, it's mainly a paracrine or autocrine hormone.

 

[freakout]

[... we can't really draw any conclusions from (the mouse experiment), for a number of reasons: it hasn't been duplicated by anybody else; they didn't indicate the levels of androgens in those mice; and it remains unclear what effect (if any) the lack of an immune system had on the hair growth in those mice.

It hasn't been duplicated but no one with credibility disputed it.

Of course the male mouse has several hundred times more androgens than female mice. But sensitivity is not dictated by the level of androgens in the male mouse but the number of the supposed presence of androgen receptors in the hair follicles.

The lack of immune system in the mice is insignificant. Hair follicles are immune-previlieged as shown in the Jahoda Transgender experiment.

DNA analysis of the new follicles also showed DNA signitures from both donor and recipient.

Was that intelligent enough for you?

 

[Bryan]

Of course the male mouse has several hundred times more androgens than female mice. But sensitivity is not dictated by the level of androgens in the male mouse but the number of the supposed presence of androgen receptors in the hair follicles.

The "supposed" presence of androgen receptors in hair follicles?? Are you still stuck on the idea that follicles don't have androgen receptors?

Was that intelligent enough for you?

Depends on how you answer my question above! :laugh:

 

[freakout]

Seems to me you're being cornered by a mouse. :bravo:

 

[Bryan]

Seems to me you're being cornered by a mouse. :bravo:

Seriously, I'm curious to hear where you got the idea that hair follicles don't have androgen receptors! Did you see that on one of those crazy Web sites that post all kinds of strange ideas like that, or did you dream it up yourself, or how exactly did you come up with that idea?

 

[freakout]

I will have many crazy ideas until the Androgenetic Alopecia king, Bryan, can come with something to dispute the lowly mouse.

But allow me to rephrase.

Of course the male mouse has several hundred times more androgens than female mice. But sensitivity is not dictated by the level of androgens in the male mouse but the number of androgen receptors in the hair follicles.

The lack of immune system in the mice is insignificant. Hair follicles are immune-previlieged as shown in the Jahoda Transgender experiment.

DNA analysis of the new follicles also showed DNA signitures from both donor and recipient.

There. That should be more appealing to you.

 

[Bryan]

If the androgen receptor is just a conduit, does it really matter how many there are? From my understanding, the sensitivity (the reaction to the presence of androdens) lies in the follicle itself not the receptor.

I wish people would be more careful when they use the word "sensitivity" in this context. To me, it means how strongly a hair follicle reacts to a given amount of androgenic stimulation, regardless of which response it has to androgens (stimulation, or suppression).

A whole bunch of things can determine how "sensitive" it might be to androgens, like how many androgen receptors it has, very complex local chemical factors that determine how strongly androgens bind to those androgen receptors, how much 5a-reductase the cell makes, the specific polymorphism of androgen receptor that the individual has, etc.

The specific response to androgens that a hair follicle has would appear to be mainly determined by genetics. I suppose there are possibly other factors that can have an influence on that, too, but I don't know what they might be at this time.

Now, increased receptors, I would presume , would mean increased exposure and that may have some consequence, I really don't know.

I think it's safe to assume that it would increase the level of the normal response that a particular hair follicle has to androgens!

I have read (I think it was a post by CCS) that by reducing DHT (like when using finasteride.) the follicle can respond by creating more receptors (feedback loop I guess) which seems rather odd to me. :dunno:

That was a famous claim made by Sawaya several years ago. She made a statement about it at a medical conference she was attending. As far as I know, it has never been duplicated in any published study by any other hairloss researcher.

If the hair grows independant of the presence of androgens, why would it show a "need" (for lack of a better term) for androgen exposure by increasing receptors?

Well, it seems obvious that it's a function of hair follicle cells that's INDEPENDENT and SEPARATE from the evolution of balding hair follicles in humans (or the ancestor of humans that first evolved balding). In other words, almost all body hair follicles are stimulated by androgens, which is presumably why they evolved millions of years ago to need androgens, and be programmed to fight a reduction in androgens by making more androgen receptors. But the simple fact that balding evolved much more recently in scalp hair follicles wasn't enough (not yet, anyway) to dispense with that very early "programming" in the scalp hair follicles to make more androgen receptors when androgens decline. Maybe that'll eventually happen in the future! :dunno:

 

[S Foote.]

Well apart from this study, there have been others which clearly show donor dominance is not as "solid" as you assume Bryan.

http://www.newhair.com/resources/mp-200 ... inance.asp

Donor dominance is as "solid" as I've always said. You keep mentioning the results of that Japanese experiment, so I'll keep giving you the same reply: the term "donor dominance" (in this context) refers specifically to androgenetic alopecia. Here is what Dr. Bernstein HIMSELF says at that link (added emphasis is my own):

"In 1959, Dr. Norman Orentreich...put forth the concept that in androgenetic alopecia 'the transposed grafted skin maintains its integrity and characteristics independent of the recipient site.' "

See what I've been saying to you over and over and over for years? Dr. Orentreich was a careful investigator; he wouldn't simply make the outrageous claim that hair follicles show donor dominance for every last physical characteristic you can think of; he made that claim SPECIFICALLY for androgenetic alopecia, and he was correct! If you read his 1959 paper (mentioned above by Bernstein), you'll plainly see that Orentreich tested other hair problems, too (like alopecia areata), and not all of them displayed donor dominance!! :laugh:

So how many times are you going to keep bringing-up that Japanese experiment as a challenge to donor dominance, and how many times am I going to have to keep explaining to you its total lack of significance?

I really dont believe Bryan, that you dont "get" the point here!

If Orentreich was correct about donor dominance in male pattern baldness as you try to claim here, the male pattern baldness grafts to those mice would "NOT" have regrown as they did, end of story.

Whole human male pattern baldness follicles clearly did "NOT" show the donor dominance you claim Bryan, it doesnt get any more straight forward!!

I think you are trying yet again to skirt around a major flaw in your arguments by avoiding the basic obvious points i made.

I dont intend getting involved in this kind of pointless debate again, so i will leave it there. People can see the facts for themselves.


S Foote.