Insulin resistance, PCOS, and male pattern baldness

S Foote.

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idontwanttobebalding said:
S Foote. said:
Has this theoretical treatment grown any hair on the human male pattern baldness scalp yet?


Please understand....I lean more to the "non-direct effect" side....

but, questions must be answered....

there is no light without darkness....

and since no one else is asking you questions.... :whistle:

then I will!

In regards to your question...please check current clinical stage of Follica's approach. It is my understanding that the "wounding" aspect of their treatment is of central importance...however, a topical treatment is an option that, perhaps, may help results. (wounding by a "medical device" speeds FDA approval from my understanding...please correct me if I am wrong!)

I also ran into this study:

http://www.ncbi.nlm.nih.gov/pmc/article ... =pmcentrez

This study speaks to some of the issues we are exploring.....

In this report, we address these key questions in the unperturbed in vivo confines of the normal hair cycle, as well as in response to injury. In so doing, we unearth surprising and dynamic features of the HF-SC niche and its progeny. First, we show that during anagen, the upper ORS remains slow-cycling, like their SC predecessors, while lower ORS cells cycle more rapidly. Moreover, slow-cycling ORS cells survive catagen and contribute mightily to both HG and a new bulge: in fact, they become the main source of SCs used during the next hair cycle. Lacking a DP, the initial bulge ceases to play a major role in homeostasis but can respond to injury. Finally and perhaps most surprisingly, some actively cycling lower ORS cells not only survive catagen, but also home back to the bulge. Like their upper ORS predecessors, these cells retain many HF-SC markers. However, they irreversibly lose their ability to proliferate in normal homeostasis or upon wounding. Instead, they function decisively in hair anchorage during the resting phase and in providing the quiescent signaling cues that control the hair cycle. Our findings define a point along the ORS where cells lose stemness and become irreversibly fated to differentiate or die, and illuminate how downstream SC progeny can provide negative feedback to the niche and restrict SC self-renewal and tissue formation.

Could this help explain where the "negative" growth factors, influenced by androgens "in" the follicle occur, and, how their damaging effects can influence not only the current follicle.......but the "next one" as well?

Anyway.....

what are your thoughts on the above study?

And how does your theory work with it?

Thanks for your interest and the links.

What i suggest is that there are two things going on when it comes to hair growth. There is the normal hair cycle, and the mechanism of contact inhibition. I dont think that the hair cycle in itself is the problem in male pattern baldness, i think the anagen phase is switched off early by external pressure, then this modifies the other phases of the cycle. I think if you change the external pressure, the hair cycle can sort itself out.

My concern with the hair multiplication and cell/genetic manipulation experiments, is that these are not going to get around normal contact inhibition, if this is the problem in male pattern baldness.

No one knows much about the pathways involved in contact inhibition, only that this is a basic reaction to cell division and tissue growth in-vivo. This prevents tissue growth from invading the space of other tissues, and all normal cells react to contact inhibition of growth. The central characteristics of cancer cells is they lose this reaction, and this is how they cause damage to healthy tissues.

We do know that the Wnt's pathway, b-catenin, and TGF beta-1 are linked to the contact inhibition process, and these factors have been suggested as relevant in male pattern baldness. Fuchs did a mouse study where she manipulated Wnt's and b-catenin, and grew significant amounts of hair. The problem was the tumor developement that went with it.

http://www.hhmi.org/fuchs/index.html


In my opinion, there could be ways that HM could work, a wounding process should help because it is thought that contact inhibition is "relaxed" because of injury to allow better healing. Some proposed procedures claim a matrix of some kind to help in tissue growth, basicaly a "mould" that allows tissue growth.

I think there could be easier ways forward with research shifted to the surrounding tissue, and maybe this currect HM research will reach that conclusion?
 

S Foote.

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freakout said:
i know there is a transplant procedure wherein large sections of the scalp at the back are transplanted to the front. Obviously, the front scalp has to be moved to the back.

Does anyone know of such a case and can verify that the bald or balding hairs continued to lose or regrow some hair?

What ever the results of such a case, it could support or throw a hammer on the mouse experiment.

I think the "flap" grafts were dropped because of tissue survival problems. Having had four scalp reductions 30 years ago, i can tell you that over time, the hair recceded back to where it started from. I am sure if genuine experiments were done, this would be proven to be the norm.
 

Bryan

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I'll tell everybody a true story, just as a demonstration of the ridiculous lengths to which Stephen Foote will go: a few years ago, I asked him to explain why it is that excised scalp hair follicles show the same response to androgens in vitro that they do in vivo. Sitting there in a petri dish in a laboratory, they certainly aren't subjected to supposed "contact inhibition", so why would androgens still suppress their growth??

The answer he gave me (I have no idea if he said this with a straight face, or if he was incredibly embarrassed and red-faced while typing it) was that the "contact inhibition" caused the hair follicles to become sensitive (apparently permanently?) to androgens!!! Seriously, that's the actual answer he gave me!! :mrgreen:

I think this is a good example of the extent to which he'll go, just to try to prove his own eccentric theory about "contact inhibition".
 

S Foote.

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Bryan said:
I'll tell everybody a true story, just as a demonstration of the ridiculous lengths to which Stephen Foote will go: a few years ago, I asked him to explain why it is that excised scalp hair follicles show the same response to androgens in vitro that they do in vivo. Sitting there in a petri dish in a laboratory, they certainly aren't subjected to supposed "contact inhibition", so why would androgens still suppress their growth??

The answer he gave me (I have no idea if he said this with a straight face, or if he was incredibly embarrassed and red-faced while typing it) was that the "contact inhibition" caused the hair follicles to become sensitive (apparently permanently?) to androgens!!! Seriously, that's the actual answer he gave me!! :mrgreen:

I think this is a good example of the extent to which he'll go, just to try to prove his own eccentric theory about "contact inhibition".


This kind of outburst is exactly why the smart people on the forums dont take you seriously Bryan.

The in-vitro studies do not reflect what goes on in the body, the immuno mouse study is just the latest nail in the coffin of the relevance of test tube studies. OK, your just to stupid to understand this. People can see your basic stupidity for themselves in this very thread.

I posted a link for you about a study that clearly showed that follicle cells behave very differently in-vivo than they do in-vitro, even before androgens come into it! This was:

"Study of Cell Senescence in Cultured
Primary Balding and Non-Balding
Dermal Papilla Cells
A.W. Bahta
Dermatology (QMUL), London, UK"

Your response was to call this a "pointless" study with no further comment. Pointless just because it didn't agree with you Bryan!

I have posted reactions from scientists to my theory in this thread that prove that i can be taken seriously outside of "internet forums"

Your kind of twisted reasoning can only exist in these forums, and you would be laughed at in the real scientific community, as Dr Yechiels reaction to you proved.

So rant away Bryan. no one who knows about science is listening to you.
 

freakout

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I Broke the Mystery of Male Pattern Baldness

S Foote. said:
I think the "flap" grafts were dropped because of tissue survival problems. Having had four scalp reductions 30 years ago, i can tell you that over time, the hair recceded back to where it started from. I am sure if genuine experiments were done, this would be proven to be the norm.
Thanks. Would you consider scalp reduction 'pulling the recipient site to the donor site or 'pulling a donor to the recipient site? Tough question, huh?. :woot:

The reason I brought up the 'flap' grafts is because I was particularly interested on transplant of the frontal scalp to back. If my theories are correct, they should regrow hair.
 

S Foote.

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Re: I Broke the Mystery of Male Pattern Baldness

freakout said:
S Foote. said:
I think the "flap" grafts were dropped because of tissue survival problems. Having had four scalp reductions 30 years ago, i can tell you that over time, the hair recceded back to where it started from. I am sure if genuine experiments were done, this would be proven to be the norm.
Thanks. Would you consider scalp reduction 'pulling the recipient site to the donor site or 'pulling a donor to the recipient site? Tough question, huh?. :woot:

The reason I brought up the 'flap' grafts is because I was particularly interested on transplant of the frontal scalp to back. If my theories are correct, they should regrow hair.

They are as you describe, "pulling the donor to the recipient site."

Mine were done by a top clinic at the time, and the whole scalp was loosened to avoid what people refered to as "stretch back". Even so over time, the hair moved "up" receeded back to its starting position.

I would be interested in why you think you would get regrowth in the procedure you describe?
 

freakout

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I would be interested in why you think you would get regrowth in the procedure you describe?
The mice experiment came up as a surprise to the researchers. The original intention was to develop more efficient transplant proceduces if i read it right.

The transplanted follicles are contained in biopsies of the scalp of 28 men 11 women all of which regrew hair which labels them as scalp transplants - not just hair follicles transplants.

When they regrew hair, it suggested that nothing was wrong within the pilosesbaeous units; that by merely removing them from the human scalp and transplanting them elsewhere, the units will regrow hair normally - as if nothing was wrong just days before.

We also know that there are several indications that hair growth characteristics are determine by the recipient site - Donor Dominance Takes a Bow. In this case, a follicle was transplanted.

However, if that were true, the follicles should not have regrown hair several inches on the mice since mice maintain hair length just a few centimeters long. However, it suggested that hair growth characteristics is determine by the pilosebeceous units.

Regardless of the donor or recipient site dominance assertions, the outcome of the mice experiments suggested that the root cause of male pattern baldness is being induced from OUTSIDE the pilosebeceous units.

The association of male pattern baldness with several serious diseases and conditions supports the suggestion that male pattern baldness is being induced from OUTSIDE the pilosebeceous units. It is also obvious that whatever is causing male pattern baldness, it has no effect on the 'horseshoe' area (back and sides of the head).

Therefore, if the hair folicles are capable of fixing themselves, as shown in the mice experiments, transplanting balding scalp to the 'horseshoe' area should allow them to fix themselves as well.

However, only an actual procedure can confirm this.

These are the reasons why I never read any argument or study which tend to focus on the scalp particularly within the pilosebeceous units or the follicles.
 

freakout

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S Foote said:
They are as you describe, "pulling the donor to the recipient site."
I don't necessarily describe it as such. I'm not aware EXACTLY how a transplant or a reduction is done.

But the way I see it is this: the donor was pulled and the recipient was thrown away :)
Technically, it moved to a recipient site. But in reality there never was a recipient unless you consider the boney or "tendous" surface of the galea a "recipient". The galea could not be a recipient because it has no direct permanent connection with the scalp.

what is 'contact inhibition'?
 

S Foote.

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freakout said:
I would be interested in why you think you would get regrowth in the procedure you describe?
The mice experiment came up as a surprise to the researchers. The original intention was to develop more efficient transplant proceduces if i read it right.

The transplanted follicles are contained in biopsies of the scalp of 28 men 11 women all of which regrew hair which labels them as scalp transplants - not just hair follicles transplants.

When they regrew hair, it suggested that nothing was wrong within the pilosesbaeous units; that by merely removing them from the human scalp and transplanting them elsewhere, the units will regrow hair normally - as if nothing was wrong just days before.

We also know that there are several indications that hair growth characteristics are determine by the recipient site - Donor Dominance Takes a Bow. In this case, a follicle was transplanted.

However, if that were true, the follicles should not have regrown hair several inches on the mice since mice maintain hair length just a few centimeters long. However, it suggested that hair growth characteristics is determine by the pilosebeceous units.

Regardless of the donor or recipient site dominance assertions, the outcome of the mice experiments suggested that the root cause of male pattern baldness is being induced from OUTSIDE the pilosebeceous units.

The association of male pattern baldness with several serious diseases and conditions supports the suggestion that male pattern baldness is being induced from OUTSIDE the pilosebeceous units. It is also obvious that whatever is causing male pattern baldness, it has no effect on the 'horseshoe' area (back and sides of the head).

Therefore, if the hair folicles are capable of fixing themselves, as shown in the mice experiments, transplanting balding scalp to the 'horseshoe' area should allow them to fix themselves as well.

However, only an actual procedure can confirm this.

These are the reasons why I never read any argument or study which tend to focus on the scalp particularly within the pilosebeceous units or the follicles.


There are transplantation experiments that could be done to resolve these questions. But i cannot see many volunteers for the procedure you describe.

I think you may well see regrowth of bald scalp when moved as a flap to the back of the head. In my opinion this would be because of a reduced blood "feed" to the flap due to the procedure. It has been shown that reducing the feed to the scalp significantly improves the follicles. Bryan has a study describing this scalp arterial ligiture procedure.

There have been reports of bald men who have been accidently scalped, regrowing hair after the scalp is sewn back on. Reduced blood feed would reduce the fluid build up around follicles according to my theory.
 

S Foote.

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freakout said:
S Foote said:
They are as you describe, "pulling the donor to the recipient site."
I don't necessarily describe it as such. I'm not aware EXACTLY how a transplant or a reduction is done.

But the way I see it is this: the donor was pulled and the recipient was thrown away :)
Technically, it moved to a recipient site. But in reality there never was a recipient unless you consider the boney or "tendous" surface of the galea a "recipient". The galea could not be a recipient because it has no direct permanent connection with the scalp.

what is 'contact inhibition'?


Yes, the bald area is cut away and the hairy scalp on the sides of the head is stretched upwards and sewn together to fill in the space. I dont know if the galea is also cut away with the bald area.

Contact inhibition of cell growth is a normal and important restriction on cell multiplication, that all normal cells (including follicle cells) have.

http://en.wikipedia.org/wiki/Contact_inhibition
 

freakout

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S Foote. said:
I think you may well see regrowth of bald scalp when moved as a flap to the back of the head. In my opinion this would be because of a reduced blood "feed" to the flap due to the procedure. It has been shown that reducing the feed to the scalp significantly improves the follicles.
I''ve read this ligature procedure. Effective at about half of patients. Note that this figure is the same sa an independent study done with minoxidil of 52%.

I don't subscribe to the ligature procedure that it restricted blood flow. Ligation will cause a rerouting with the growth of new blood vessels to makeup for the ligature otherwise the scalp will rot and die. There is enough blood flow to supply the the scalp and follicles by the rerouting new blood vessels.

Something else was severed when the ligature procedure was performed. This something was never discussed or brought up in any study I've read.

In fact, two control case studies show limiited blood flow in the general area of the balding scalp have been shown.
http://www.ncbi.nlm.nih.gov/pubmed/2715645
http://www.ncbi.nlm.nih.gov/pubmed/8628793
 

freakout

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S Foote. said:
There have been reports of bald men who have been accidently scalped, regrowing hair after the scalp is sewn back on.

The procedure I'm suggesting does not have to involve 'flaps' but rather small incisions the size of biopsies similar to the ones used in the mice experiment.

I had hope those researchers should have done so since they had the chance with 40 subjects of men and women.

Edited:
S Foote. said:
Reduced blood feed would reduce the fluid build up around follicles according to my theory.
Fluid build up is a consequence - not a normal occurence, if ever there is such a finding. A reduced blood feed would result in atrophy of affected tissues which may result with fluid built up to replace the atrophied tissues.
 

balder

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Blood Pressure and Balding

http://www.nytimes.com/2009/12/08/healt ... 8real.html


In a study published in 2007, for example, researchers looked at 250 men ages 35 to 65. After controlling for age, high cholesterol, smoking and other variables, they found that hypertension was “strongly associatedâ€￾ with male pattern baldness: those with a blood pressure reading above 120 over 80 had twice the risk of the others.

http://www.endocrine-abstracts.org/ea/0 ... 15p143.htm



With the onset of puberty blood pressure increases more in men than in women while boys and girls do not show any gender differences in blood pressure. Androgens are known to play an important role in renal tubular epithelial cell growth, hypertrophy and erythropoetin production and may be important determinants of sex-specific differences in blood pressure. However the exact mechanisms are not clear yet.

 

S Foote.

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freakout said:
S Foote. said:
There have been reports of bald men who have been accidently scalped, regrowing hair after the scalp is sewn back on.

The procedure I'm suggesting does not have to involve 'flaps' but rather small incisions the size of biopsies similar to the ones used in the mice experiment.

I had hope those researchers should have done so since they had the chance with 40 subjects of men and women.

Edited:
[quote="S Foote.":isq8apxa]Reduced blood feed would reduce the fluid build up around follicles according to my theory.
Fluid build up is a consequence - not a normal occurence, if ever there is such a finding. A reduced blood feed would result in atrophy of affected tissues which may result with fluid built up to replace the atrophied tissues.[/quote:isq8apxa]

I am not talking about reducing blood feed to the point of tissue atrophy, and the conditions you describe did not happen in the arterial ligiture study i refered to in this thread.

Also i am not talking about what would be described as clinical edema in the male pattern baldness scalp, but all the known markers for increased edema are there. If you study the effects on tissue of edema, it is known that fibrosis and inflammation go along with this.

This is what happens in the male pattern baldness scalp.
 

S Foote.

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balder said:
Blood Pressure and Balding

http://www.nytimes.com/2009/12/08/healt ... 8real.html


In a study published in 2007, for example, researchers looked at 250 men ages 35 to 65. After controlling for age, high cholesterol, smoking and other variables, they found that hypertension was “strongly associatedâ€￾ with male pattern baldness: those with a blood pressure reading above 120 over 80 had twice the risk of the others.

http://www.endocrine-abstracts.org/ea/0 ... 15p143.htm

[quote:35k6rjt9]

With the onset of puberty blood pressure increases more in men than in women while boys and girls do not show any gender differences in blood pressure. Androgens are known to play an important role in renal tubular epithelial cell growth, hypertrophy and erythropoetin production and may be important determinants of sex-specific differences in blood pressure. However the exact mechanisms are not clear yet.

[/quote:35k6rjt9]


Thanks for the link, my theory predicts this correlation as i have said for a long time.
 

freakout

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S Foote., can you state your theory in a nutshell? Thanks.
 

freakout

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S Foote. said:
This was an early description of the theory.

http://www.hairsite2.com/library/abst-167.htm

Wow, that got my miniscule brain spinning :) So the theory goes that human evolution contributed to the development of male pattern baldness? ... that male pattern baldness's occurence has little to do with environmental condition within a lifetime?

I know summaries can be confusing and absurd or weird but I'm pretty much aware of that but providing concluding statements, regardless of controversies, is the way to get attention. So I'd really prefer to read it in a nutshell.
 

S Foote.

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freakout said:
S Foote. said:
This was an early description of the theory.

http://www.hairsite2.com/library/abst-167.htm

Wow, that got my miniscule brain spinning :) So the theory goes that human evolution contributed to the development of male pattern baldness? ... that male pattern baldness's occurence has little to do with environmental condition within a lifetime?

I know summaries can be confusing and absurd or weird but I'm pretty much aware of that but providing concluding statements, regardless of controversies, is the way to get attention. So I'd really prefer to read it in a nutshell.

OK, as an engineer, i ask questions based on basic common sense.

The very basic idea was this. The growing anagen follicle has to grow into the dermal tissue, so what would happen if the dermal tissue doesn't want to move out of the way?

The conclusion i reached is described in the "Hydraulic dermal model" part of the link i posted.

Forget about scalp hair for a moment and consider this. If you transpose the hydraulic principle i suggest onto humans, you notice that the one consistant thing about androgens is they grow hair in certain areas of the body. These areas all have higer concentrations of lymph vessels close to the follicles.

The implication of the theory is that androgens are increasing lymph drainage, so reducing the local fluid pressure and increasing hair growth.

The odd and "opposite" effect is that in some people, this action can reduce scalp growth. But there is no direct relationship here as to androgen levels or time period, so there has to be another factor.

I think this factor is the complex blood supply/drainage that evolved to service the enlarging brain in higher primates.


Now i dont think there is any evolved purpose in human scalp hair growth, i think this is just a side effect of other more important developements.

Why all this long scalp hair anyway? This is downright dangerous in terms of survival! You wont see or hear the sabre tooth tiger coming with all this hair over your eyes and ears. Unless by the time we got this growth we were smart enough to know to cut it or tie it back, and i think this is the key.

I think the good circulation and drainage that evolved to grow our brains and make us smart, also increased our scalp hair growth. Higher levels of androgens helped us to breed in a sexually competitive environment. The drainage from the scalp can be reduced in this area by androgen increased drainage elsewhere, simple "plumbing" effect because of the complex head feed/ return systems in humans.

This reduced scalp drainage will not build up fluid unless the feed pressure is high. This is why i think there is a proven relationship with high blood pressure and male pattern baldness.

This is as basic as i can describe the theory, hope it is helpful.
 

squeegee

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I think we are on something Stephen! Thanks for your reply..way more clearer now.. I think that that the lympatic system has to do with something with male pattern baldness which explain the horsehoe pattern..But I think that ENOS is part of it.. Endothelial Nitric Oxide Synthase regulates microlymphatic Flow via collecting lymphatics..this is why black females are using Castor oil and Miconazole Nitrate to stimulate hair grow. The problem is when Nitric Oxide becomes impaired or uncoupled, problems are happening..= endothelial dysfunction. Clogged lymphatic system, production of Peroxynitrites and free radicals. Also stimulating lymphatic drainage help a lot the people with acne which is linked with androgen problems.
 
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