For bryan and Foote.

[S Foote.]

Well then Bryan, we agree that hair doesn't `need' androgens, and follicle size has some `independent' control influence.

Here's some free advice for you: in a specific context like this, you should always specify WHAT KIND OF HAIR you're referring to. That's because there's a considerable variation in the response to androgens, from one type of follicle to another.

Occipital scalp hair follicles have very little or no response to androgens, but BEARD hair follicles, on the other hand...

[quote="S Foote.":d2011]But adrogens clearly do `NOT' show the same effects in-vitro as they do in-vivo!

They sure as hell DO, Stephen.[/quote:d2011]

No they don't Bryan, people can read the studies for themselves! Your just trying to save face here, and failing miserably :wink:

Now are you going to provide links or specific quotes from the study you refered to or not?

What's up Bryan, chicken? :roll:

We all know that androgens in some way `change' terminal scalp follicles into male pattern baldness follicles in-vivo.

But they do `NOT' `change the same terminal follicle cells into male pattern baldness follicle cells in-vitro!!

Not overnight in a petri dish, no. It takes longer than that...

Bryan

NO, NO, NO, Bryan!!

`WHAT' takes longer than that??????????

`WHAT' time related mechanism are you refering to??????????

Just trying to claim that some `magic' mystery mechanism `will' eventually change the results of an experiment to suit your argument, is plainly ridiculous.

Thats not science Bryan, it's just your wishfull thinking :roll:

S Foote.

 

[Bryan]

Two things Bryan.

First, eyebrow hair is quite obviously increased by androgens, thats a common observation, particularly as we age.

What makes you think that's an androgen-mediated effect?

Secondly, that study you quote is just another support for the fact that androgens don't directly effect follicles, untill an indirect effect has already `changed' follicles in to male pattern baldness `mode' 8)

Ok, let's hear your explanation, then! The central point here is that they were NEIGHBORING follicles! How can the (alleged) edema affect one follicle, but not another one that's less than a millimeter away??

Why do you have to twist what i say Bryan? What the hell has scalp growth in young girls got to do with my theory of DHT related male pattern baldness. How does this conflict with what i have said?

I insist you answer that point Bryan.

I think I explained it clearly enough for ANY person to be able to understand it, even you. Go back and re-read it.

My theory explains how you can go from terminal hair growth to vellous growth over a short distance.

???

How can there be MASSIVE differences in "edema" over a distance of just millimeters? Are you daft??

I explained to you only a few days ago Bryan, that in my theory the edema does not act directly. Yet here you are again pretending that i claim edema is the only factor in my theory!

I know, I know...it's the contact inhibition CAUSED by the edema. But you're just trying to evade the issue. You still can't explain why one follicle would be affected, but not another one only a millimeter away.

Bryan

 

[S Foote.]

Two things Bryan.

First, eyebrow hair is quite obviously increased by androgens, thats a common observation, particularly as we age.

What makes you think that's an androgen-mediated effect?

Because it effects men Bryan!

Secondly, that study you quote is just another support for the fact that androgens don't directly effect follicles, untill an indirect effect has already `changed' follicles in to male pattern baldness `mode' 8)

Ok, let's hear your explanation, then! The central point here is that they were NEIGHBORING follicles! How can the (alleged) edema affect one follicle, but not another one that's less than a millimeter away??

[quote="S Foote.":c26b4]Why do you have to twist what i say Bryan? What the hell has scalp growth in young girls got to do with my theory of DHT related male pattern baldness. How does this conflict with what i have said?

I insist you answer that point Bryan.

I think I explained it clearly for ANY person to be able to understand it, even you. Go back and re-read it.[/quote:c26b4]

Re-read what? I have seen no such argument from you, so explain your point clearly, and stop trying to evade the question!

My theory explains how you can go from terminal hair growth to vellous growth over a short distance.

???

How can there be MASSIVE differences in "edema" over a distance of just millimeters? Are you daft??

There is no difference in edema, the difference is in the phase of the hair cycle as i have explained to you many times.

I explained to you only a few days ago Bryan, that in my theory the edema does not act directly. Yet here you are again pretending that i claim edema is the only factor in my theory!

I know, I know...it's the contact inhibition CAUSED by the edema. But you're just trying to evade the issue. You still can't explain why one follicle would be affected, but not another one only a millimeter away.

Bryan

As i have said many times before, contact inhibition only restricts follicle growth in the anagen `GROWTH' phase of the hair cycle. Any increase in the local tissue pressure will only result in hair loss when the follicle re-enters anagen. It will not effect follicles that are fully grown and still in anagen.

These follicles in different stages of the hair cycle can be `RIGHT' next to each other!!! As the human anagen phase of scalp follicles can last for years, the hair thinning and loss in response to increased pressure can also last for years, which is what we see in male pattern baldness!!! 8)

Clear enough now Bryan??? :roll:

S Foote.

 

[Bryan]

[quote="S Foote.":42213]My theory explains how you can go from terminal hair growth to vellous growth over a short distance.

???

How can there be MASSIVE differences in "edema" over a distance of just millimeters? Are you daft??

There is no difference in edema, the difference is in the phase of the hair cycle as i have explained to you many times.[/quote:42213]

????????

What in the HELL are you talking about???

I'm talking about how there's NO HAIR GROWTH AT ALL in young girls in the sideburn/beard area, and yet THICK HAIR GROWTH a few millimeters away in their scalp!! Are you completely unable to understand the simple arguments I've been presenting to you??

[quote="S Foote.":42213]I explained to you only a few days ago Bryan, that in my theory the edema does not act directly. Yet here you are again pretending that i claim edema is the only factor in my theory!

I know, I know...it's the contact inhibition CAUSED by the edema. But you're just trying to evade the issue. You still can't explain why one follicle would be affected, but not another one only a millimeter away.

As i have said many times before, contact inhibition only restricts follicle growth in the anagen `GROWTH' phase of the hair cycle. Any increase in the local tissue pressure will only result in hair loss when the follicle re-enters anagen. It will not effect follicles that are fully grown and still in anagen.

These follicles in different stages of the hair cycle can be `RIGHT' next to each other!!! As the human anagen phase of scalp follicles can last for years, the hair thinning and loss in response to increased pressure can also last for years, which is what we see in male pattern baldness!!! 8) [/quote:42213]

Those hair follicles were both in ANAGEN, and they were both GROWING. Explain to me why ONE would be sensitive to testosterone, but not the other one only a millimeter away!!

Bryan

 

[Footy]

[quote="S Foote.":d9609]My theory explains how you can go from terminal hair growth to vellous growth over a short distance.

???

How can there be MASSIVE differences in "edema" over a distance of just millimeters? Are you daft??

There is no difference in edema, the difference is in the phase of the hair cycle as i have explained to you many times.

????????

What in the HELL are you talking about???

I'm talking about how there's NO HAIR GROWTH AT ALL in young girls in the sideburn/beard area, and yet THICK HAIR GROWTH a few millimeters away in their scalp!! Are you completely unable to understand the simple arguments I've been presenting to you??[/quote:d9609]

First off Bryan, for some reason i have not been able to log on to gourmetstylewellness.com using my normal user name today. I have had some problems with my account recently, and i have contacted admin about the problem.

OK, down to business :wink:

What the hell are you talking about here?? Tell me how the hell terminal hair growth even `one' millimeter' away from vellous growth conflicts with my theory?? I have explained how my theory accounts for this time after time. If you don't get it thats OK, just don't try to pretend i haven't answered the point for God's sake!

[quote="S Foote.":d9609]I explained to you only a few days ago Bryan, that in my theory the edema does not act directly. Yet here you are again pretending that i claim edema is the only factor in my theory!

I know, I know...it's the contact inhibition CAUSED by the edema. But you're just trying to evade the issue. You still can't explain why one follicle would be affected, but not another one only a millimeter away.

As i have said many times before, contact inhibition only restricts follicle growth in the anagen `GROWTH' phase of the hair cycle. Any increase in the local tissue pressure will only result in hair loss when the follicle re-enters anagen. It will not effect follicles that are fully grown and still in anagen.

These follicles in different stages of the hair cycle can be `RIGHT' next to each other!!! As the human anagen phase of scalp follicles can last for years, the hair thinning and loss in response to increased pressure can also last for years, which is what we see in male pattern baldness!!! 8)

Those hair follicles were both in ANAGEN, and they were both GROWING. Explain to me why ONE would be sensitive to testosterone, but not the other one only a millimeter away!!

Bryan[/quote:d9609]

We only have your word for that Bryan! Yet again i ask you to provide proper reference to the text of the study you quoted?

Put up or shut up!

S Foote.

 

[Bryan]

What the hell are you talking about here?? Tell me how the hell terminal hair growth even `one' millimeter' away from vellous growth conflicts with my theory?? I have explained how my theory accounts for this time after time. If you don't get it thats OK, just don't try to pretend i haven't answered the point for God's sake!

You have said that the effect of androgens on human hair growth (ALL hair growth) is INDIRECT, not DIRECT. You have said that hair grows thickly in areas where the "plumbing" equation (blood pressure feed, versus lymphatic drainage) is such that the local fluid pressure in the tissues is minimized.

Ok, now go back and re-read what I said before. How can you explain how the tissue "fluid pressure" could change so drastically over the space of a few millimeters? :wink:

Those hair follicles were both in ANAGEN, and they were both GROWING. Explain to me why ONE would be sensitive to testosterone, but not the other one only a millimeter away!!

Bryan

We only have your word for that Bryan! Yet again i ask you to provide proper reference to the text of the study you quoted?

Put up or shut up!

Both the testosterone-sensitive follicles and the testosterone INsensitive follicles started growing in culture. They obviously were in anagen.

Bryan

 

[Footy]

What the hell are you talking about here?? Tell me how the hell terminal hair growth even `one' millimeter' away from vellous growth conflicts with my theory?? I have explained how my theory accounts for this time after time. If you don't get it thats OK, just don't try to pretend i haven't answered the point for God's sake!

You have said that the effect of androgens on human hair growth (ALL hair growth) is INDIRECT, not DIRECT. You have said that hair grows thickly in areas where the "plumbing" equation (blood pressure feed, versus lymphatic drainage) is such that the local fluid pressure in the tissues is minimized.

Ok, now go back and re-read what I said before. How can you explain how the tissue "fluid pressure" could change so drastically over the space of a few millimeters? :wink:

Those hair follicles were both in ANAGEN, and they were both GROWING. Explain to me why ONE would be sensitive to testosterone, but not the other one only a millimeter away!!

Bryan

Please see my post below Bryan.

We only have your word for that Bryan! Yet again i ask you to provide proper reference to the text of the study you quoted?

Put up or shut up!

Both the testosterone-sensitive follicles and the testosterone INsensitive follicles started growing in culture. They obviously were in anagen.

Bryan

No Bryan, my point is was one sample terminal and the other male pattern baldness, in-vivo, `PRIOR' to culturing???

S Foote.

 

[Footy]

It seems i owe you an apology Bryan!

After my reference to eyebrow growth, and your point about terminal growth next to vellous, i wrote a post on notepad to cut&paste later. I don't often do that, but i had been getting cut off line a lot that day. I had thought i had subsequently posted this, but i was distracted and it turns out i overlooked it sorry. :roll:

This is it.

__________________________________________


The central point of my theory is the `in-built' response of the growing anagen follicle to resistence from the surrounding tissue. The growth of any organ is limited by the normal characteristic of contact inhibition. Through contact inhibition, the growing cells meet resistence from the existing cells around this growth. Once a `certain' degree of resistence is meet, the growing cells stop growing.

This characteristic of the contact inhibition of cell growth, is built in to `ALL' normal cells. One of the clinical problems with cancer cells is that they invade other tissues and interfere with other organs, because they have lost `normal' contact inhibition.

I think it is pretty safe to assume that the level of resistence from surrounding tissue, at which growing cells are `switched off' by contact inhibition is a constant. However, other factors can come into play, increasing or reducing the resistence of the surrounding tissue, and so the size of the growing `organ' before contact inhibition kicks in.

Given the `design' of hair follicles and the way the hair cycle works, the `natural' resistence of the tissue around hair follicles, and induced changes in this, `will' create changes in anagen follicle size through contact inhibition, given the basic physics of the system.

It should also be remembered that the hair cycle produces a fresh `batch' of follicle cells each anagen phase, and if these are effected by contact inhibition, this particular batch are likely to retain this induced growth restriction `programing'! Such a characteristic is demonstrated by these cells in-vitro.

However, exposure to androgens of follicle cells in-vitro, does `NOT' directly induce any growth restriction!

The best and most realistic analogy to describe contact inhibition within the follicle `system', is the analogy with a simple party baloon.

If you try to push your finger into a party baloon, a couple of factors are involved in how much `resistence' there is.

Firstly there is the `natural' resistence to movement of the structure of the baloon (the skin). This will offer a `certain' amount of resistence to your finger trying to push into the baloon.

Secondly there is the amount of air pressure in the baloon. This pressure `backs up' the natural resistence of the structure or `skin' of the baloon.

If the structure or skin of the baloon is `weak', the resistence to your finger will be reduced, and you can penetrate the baloon with less resistence. If the pressure in the baloon is also low, the best conditions exist for the maximum penetration of your finger before a `certain' resistence is meet.

Also, if the structure or skin is `weak', any slight changes in internal pressure will make more of a difference to this resistence. If the stucture is `harder' or `tougher' is would take more of a change in pressure to effect the overall resistence.

The other important characteristic of this kind of `system', is that the resistence increases the deeper you push your finger into the baloon! This is a very relevant factor when considering the same principles in the dermis in regard to anagen follicle enlargement.

For the structure or skin of the baloon, consider the dermal tissue. For the pressure behind the skin of the baloon, consider the fluid pressure in the dermal tissue. For your finger, consider the growing anagen follicle trying to push into the dermal tissue!

If the normal contact inhibition of cell growth happens at a constant value of resistence, both the `natural' resistence of the dermal tissue in a particular area, `and' the local tissue fluid pressure, will combine to determine the point at which the resistence to follicle growth reaches the point at which contact inhibition `activates'.

I think hair follicles evolved to take account of contact inhibition of anagen enlargement, to link hair growth with the primary `Hydraulic' temperature control in mammals. This primary temprerature control in the dermis, reduces fluid pressure in cold climates, and increases it in hot climates. This change in resistence `adjusts' hair growth accordingly, and is the reason in evolution for this effect on hair according to my theory.

Why did evolution not just develope a surface structure to produce hair? Why do we have this `pocket' in the dermal tissue system? I think the answer is in this hair growth control system.

I think that apart from rare conditions that can effect the basic hair cycle itself, all hair growth in all species is controlled by the local resistence to anagen enlargement through contact inhibition.

In humans i suggest the factor of the local tissue `toughness' is the major factor in our hair patterns. This can produce the terminal hair growth we see next to vellous growth. Often you can see some intermediate `shorter' growth at this border. Those with Norwood 1 (No loss), can pull back their hair and see shorter hairs in the hairline area.

There is a good example of this mechanism in eyebrow growth.

Eyebrows are seemingly `islands' of hair growth with no apparent association with anything else. But there is a precise association with another factor if you `feel' the tissue this growth comes from!

This hair growth corresponds with an area of `weak' tissue'. You can feel this `softness' compared to the tissue above and below. Boxers can tell us all about how this tissue is easily split!

The tissue resistence factor described above, explains eyebrow hair growth.

I suggest that we have long terminal hair growth on our scalps because of `weak' tissue, and lower fluid pressures in this area, at least pre-puberty. In older bald men, you can often see if you look closely, a change in the surface of the scalp tissue that corresponds to the original hair line.

The down side to this area of weak scalp tissue that produces terminal growth, is that any slight increase in fluid pressure in this area, will more easily increase the resistence of weak tissue as described above. This will more `easily' create smaller follicles through contact inhibition, {male pattern baldness}.

I suggest the primary influence of DHT on changing hair patterns, is through inducing changes in the local tissue pressures.

Again i suggest that the growth of the anagen hair follicle has evolved around the local tissue resistence, and follicles are `very' sensitive to this factor. It doesn't mean that the natural tissue `toughness' differences are going to be obvious, or indeed any changes in the local tissue pressures. But i suggest the evidence is there if we look close enough, as in the eyebrow example.


Going back to the `baloon' analogy. If your finger was able to penetrate to the maximum depth, and then a `tough' structure formed inside the baloon around the `mould' your finger made, any future changes in pressure would not effect `future' finger penetrations. The tough `mould' would preserve the space for your finger!

This is how transplanted anagen follicles survive according to my theory, because of the tough fibrose `shell' formed around it at the time of initial healing.

This post is intended to clear up some points raised about my theory.

________________________________________________________

I will try to read any posts as soon as i can, but i am still having some connection and other computer problems. I hope to resolve these over the weekend.

S Foote.

 

[Bryan]

I understand your theory, Stephen. I've read your various explanations (like the one above) many times. But you haven't addressed my specific question: why would ONE follicle show the alleged effects of contact inhibition (sensitivity to testosterone), while its neighbor a very short distance away (a millimeter or so) does not?

Bryan

 

[Dave001]

I have a quick little question for you´s.

Do you think that maybe scalp hair needs a certain exposure to DHT?

My theory [....]
However there are follicles that need DHT - body hair and I think that even scalp hair needs a certain amount.

I realize that it's fashionable nowadays for one to have his own unique "theory" for every phenomenon, but what you describe is really not a theory but a conjecture, and a poor one at that.

 

[Dave001]

I agree totally with your theory.

I'm saddened that you've been taken-in by such an eccentric theory. If you seriously think that some hypothetical "indirect effect" of androgens can explain the HUGE difference between the thick, luxuriant scalp hair growth of a person with CAIS (complete androgen insensitivity syndrome) and their very minimal (if any) body hair growth, well...I guess there's just not much I can say in response that will convince you.

Bryan

S Foote wrote:

> You have to understand that while Bryan is entitled to his `personal'
> opinion, this is not a `qualified' opinion.

LOL. What is a "qualified opinion"? And more important, who is the judge?

> Bryan is not a scientist, and he has been asked many times on hair
> loss forums what he actually `does', and he has always refused to
> respond

If you were ever to make a remark such as that within scientific
circles, you would be dealt a severe punishment. You need to develop a
better fallback strategy for your intellectual deficiency. Content is
not worthy of merit if it can't stand on its own, and the quality of
information is not determined by the quantity of acronyms that follow
its author's name.

> More and more scientists are now questioning the current theory that

Bullshit.

> Bryan believes is `gospel'. Here is an extract from the reply i got
> from Dr Sawaya, a recognised expert in hair research, on my theory. I
> have posted her full response before.
>
> She said:
>
> "It is a very complex process, but your thoughts are very organized
> and on the right path, similar to what others have been proposing,
> and in some ways yours are more straightforward. I think you've done
> a good job in thinking this through...... Hope this helps... regards
> Marty Sawaya"

I seriously doubt that she agrees with your delusional conjecture, but,
it wouldn't make it any more correct if she did.

> Note that she says my ideas are similar to what others are now
> proposing.

Great, where is the data? You also provided no context to your alleged
information exchanged.

<snip>

 

[Dave001]

[quote="S Foote.":80d17]You admit yourself that follicles don't `need' androgens. In androgen insensitivity syndrome, we still get a `range' of different size follicles from terminal to vellous!!

By what `MECHANISM' can you explain differently sized follicles in the complete absense of any action of androgens Bryan?

Dunno all the reasons. Genetics are an obvious factor, of course. Why would you ask such an odd question? It's much like asking, why are some men taller than others?

[quote="S Foote.":80d17]At the very least, this demonstrates some `OTHER' mechanism of control of follicle size!

Of course.[/quote:80d17]

Well then Bryan, we agree that hair doesn't `need' androgens, and follicle size has some `independent' control influence.

It seems you are learning something after all Bryan :lol:

How do you know that androgens don't `indirectly' effect this `independent' mechanism?????????

The `interpretation' of the in-vitro study results you support Bryan, is typical of the bad science traditional in hair loss research. This is a classic case of trying to `read' what you want into studies instead of what is `actually' shown!!

In this case, people have got this notion into their heads that follicles `MUST' be effected `directly' by androgens because of the `interpretation' that was placed on `EARLY' transplantation results.

It's not just that. It's also the direct stimulation/suppression of hair follicles by androgens in vitro. They show exactly the same effects in vitro that they do in vivo.

But adrogens clearly do `NOT' show the same effects in-vitro as they do in-vivo!

We all know that androgens in some way `change' terminal scalp follicles into male pattern baldness follicles in-vivo.

But they do `NOT' `change the same terminal follicle cells into male pattern baldness follicle cells in-vitro!!

In fact as you are well aware, androgens do not `directly change' the pre-existing growth characteristics of `ANY' follicle cell sample in-vitro![/quote:80d17]

<snip>


Randall, V. A., M. J. Thornton, et al. (1994). "Androgen action in cultured dermal papilla cells from human hair follicles." Skin Pharmacology 7(1-2): 20-6.

"Androgens are major regulators of human hair growth with paradoxically different effects on hair follicles depending on their body site. They stimulate terminal growth in many regions including the face, have no effect on eyelashes, but may cause inhibition and balding on the scalp in genetically disposed individuals. How this occurs is unknown. However, androgens may act on the hair follicle via the cells of the dermal papilla; these would then influence the other cells of the hair follicle by altering the production of regulatory substances such as growth factors and/or extracellular matrix components. Therefore, primary lines of dermal papilla cells have been established from androgen-sensitive hair follicles, such as beard, and control, relatively androgen-independent, non-balding scalp cells and their mechanism of androgen action has been compared. Isolated beard dermal papillae were larger than those from scalp follicles. Although dermal papilla cells did not respond to in vitro androgens by alterations in growth, androgen-dependent dermal papilla cells contained higher levels of specific, low capacity, high affinity androgen receptors than non-balding scalp cells. The ability of the cells to metabolise testosterone to 5 alpha-dihydrotestosterone in culture also varied in parallel to that predicted from studies of hair growth in the 5 alpha-reductase deficiency syndrome. These results support the hypothesis that androgens act via the dermal papilla. They also show that dermal papilla cells retain differences in gene expression in culture which appear to correspond with their androgenic response in vivo. [emphasis added]..."

 

[michael barry]

Ive got an answer for you Bryan.

According to Stephen's theory the reason one follicle shows the effect of contact inhibition (small vellus hair) and one thats a millimeter away does not is that hairs are asynchronous and go into catagen and telogen at different times (sometimes by several years). This is why we can lose 50% of our hair in a given area before it "receeds" and why women with diffuse thinning may not notice it until its really advanced. There is still plenty of big anagen-phase follicles that are unaffected by fluid pressure yet as its only in the early anagen phase when the dermal papilla expands when contact inhibition can effectively shrink the size of the future follicle.

Im NOT SAYING Stephen's theory is right, but that is why, according to his theory, that the phenomena you describe (big hair next to little one in male pattern baldness) would take place.

Have got to say this to you and Dave001 though.................STEPHENS THEORY ISNT HURTING ANYONE, ARMANDO'S THEORY ISNT HURTING ANYONE. The theory I read the other night about vitamin D and hairloss and skin color, isnt hurting anyone, the theory about fibroblasts Ive read isnt hurting anyone. The theory about isufficient blood flow being a factor in hair loss isnt either. IT ISNT TAKING MONEY AWAY FROM RESEARCH YOU BELIEVE IN OR SUPPORT. So why all the hostility towards it? Very few people read these esoteric research forums and most believe the abject party line as put out by transplant mills and Merk that your hair is genetically programmed to run x cycles, start becoming sensitive to DHT, shrivel up and die and there is nothing you can do about it other than cut circulating DHT levels or get plugs anyway.
If Stephen was trying to sell some gimmick device along with his theory, I'd be ticked and think he was scamming people. However, when Ive wrote him and asked what would be an effective method at hair maintenance as per his ideas he simply suggested inversion therapy could improve lymphatic drainage, cold water rinses after shampooing, perhaps and ice pack, and noted that some electromagnetic devices (as used in treating lydophomea on the lydophomea's web page) are now used to treat edema in other areas of the body. Its not like he tried to sell me something or make money. Whether his theory is right or even laughably wrong, he is not hurting anyone with it.

Lots of people are looking for reasons into male pattern baldness now as ethnic groups like Arabs who typically dont bald move into the West and start suffering from it like whites do. Ive seen a few Hispanic young men with receeding lines here in America myself and thought they NEVER balded. More Asians are balding now as the Japanese are painfully aware of (I work for a Japanese company and see this EVERY DAY). So some are looking for answers to see if they can delay baldness with dietary or cultural habits. No harm in this.

 

[Footy]

I understand your theory, Stephen. I've read your various explanations (like the one above) many times. But you haven't addressed my specific question: why would ONE follicle show the alleged effects of contact inhibition (sensitivity to testosterone), while its neighbor a very short distance away (a millimeter or so) does not?

Bryan

I think you `DO' understand my proposed explaination for this Bryan :wink:

Michael Barry understands it, as he demonstrates in his last post in this thread.

Quote:

"Ive got an answer for you Bryan.

According to Stephen's theory the reason one follicle shows the effect of contact inhibition (small vellus hair) and one thats a millimeter away does not is that hairs are asynchronous and go into catagen and telogen at different times (sometimes by several years). This is why we can lose 50% of our hair in a given area before it "receeds" and why women with diffuse thinning may not notice it until its really advanced. There is still plenty of big anagen-phase follicles that are unaffected by fluid pressure yet as its only in the early anagen phase when the dermal papilla expands when contact inhibition can effectively shrink the size of the future follicle. "

That's it in a nutshell, thank you Michael.

I'am pretty sure others reading this will also understand this argument, and i think the only reason you claim to not understand this Bryan, is that you have no answer to it!

S Foote.

 

[Footy]

I agree totally with your theory.

I'm saddened that you've been taken-in by such an eccentric theory. If you seriously think that some hypothetical "indirect effect" of androgens can explain the HUGE difference between the thick, luxuriant scalp hair growth of a person with CAIS (complete androgen insensitivity syndrome) and their very minimal (if any) body hair growth, well...I guess there's just not much I can say in response that will convince you.

Bryan

S Foote wrote:

> You have to understand that while Bryan is entitled to his `personal'
> opinion, this is not a `qualified' opinion.

LOL. What is a "qualified opinion"? And more important, who is the judge?

> Bryan is not a scientist, and he has been asked many times on hair
> loss forums what he actually `does', and he has always refused to
> respond

If you were ever to make a remark such as that within scientific
circles, you would be dealt a severe punishment. You need to develop a
better fallback strategy for your intellectual deficiency. Content is
not worthy of merit if it can't stand on its own, and the quality of
information is not determined by the quantity of acronyms that follow
its author's name.

> More and more scientists are now questioning the current theory that

Bullshit.

Well well what have we here?

Bryan, i would have a quite word with your `mini me' here, before he embarasses himself any further 8)

[Bryan believes is `gospel'. Here is an extract from the reply i got
> from Dr Sawaya, a recognised expert in hair research, on my theory. I
> have posted her full response before.
>
> She said:
>
> "It is a very complex process, but your thoughts are very organized
> and on the right path, similar to what others have been proposing,
> and in some ways yours are more straightforward. I think you've done
> a good job in thinking this through...... Hope this helps... regards
> Marty Sawaya"

I seriously doubt that she agrees with your delusional conjecture, but,
it wouldn't make it any more correct if she did.

> Note that she says my ideas are similar to what others are now
> proposing.

Great, where is the data? You also provided no context to your alleged
information exchanged.

Here is the background for your information.

I am an engineer, and i developed my theory from my own experience of hair transplantation and my engineering (whole system) experience.

In proposing my theory i have tried to follow the scientific rules, and i have had two papers published on my theory in the journal "Medical Hypotheses".

I have always sought the opinion of recognised experts in the field on my theory, and my posted comments from Dr Sawaya came from these enquiries. I will post my letter sent to recognised experts, and their responses below.

The `qualification' in the pursuit of science, is in the response of the scientific community to your proposals by recognised experts. I will post those i have recieved so far below as i said. During the time i have been proposing my theory, i have also been asked if i would be a referee for papers submitted to a leading dermatology journal. I declined this offer as i feel i am not experienced enough in the field to judge other peoples work.

Now Dave, i will ask you the same question i have asked Bryan, that you so casually dismiss above!

What is `YOUR' qualification??

You come on these forums talking in psuedo scientific sentences, that reach no conclusion, and post `scientific studies' as if they give you a personal credibility. :roll: :roll:

You post an in-vitro abstract here and emphasise text that means `nothing' at all in `TRUE' scientific terms! All these in-vitro tests `ACTUALLY' prove is that direct exposure to androgens change `NOTHING'.

You are full of `s**t Dave!

The common factor with all you `pretend' scientists, is that your sentence constuction and spelling is immaculate, but the actual content of what you say is pure crap 8)

I ask you again, What qualifies your opinions over anyone else's on these forums????????????

S Foote.

 

[Footy]

This is my letter to recognised experts in the field of male pattern baldness on my theory, and the two responses to date.

_______________________________________________


Dear ---------

I would welcome your opinion on a factor that must, given accepted physiology, have the `final say' in the size of the in vivo anagen follicle. This factor is the basic mechanism in multi-cellular biology of contact inhibition.

My opinion on the role of contact inhibition in anagen follicle size, and the advantages of this in the evolution and function of hair, can be seen here http://www.hairsite2.com/library/abst-167.htm A slightly modified version of this paper was published in Medical Hypotheses (2002) 59 (5), 522-526. doi:10.1016/S0306-9877(02)00259-1, available on line at http://www.idealibrary.com


The basic reasoning goes like this.

The amount of hair produced is directly related to the period of anagen, and the size achived by the anagen follicle. In male pattern baldness, the anagen period is shortened, resulting in miniaturised follicles.

In multi-cellular biology, any organ `building' is subject to the ultimate control of normal contact inhibition. Contact inhibition ensures that organs can only be as large as the available space allows. This prevents biological structures from interfering with each other.

As the anagen follicle starts to enlarge, it has to push the surrounding dermal tissue aside. The greater the resistence to movement of the dermal tissue, the earlier normal contact inhibition will `kick in'. If the resistence is high, the anagen enlargement period will be turned off early by contact inhibition, resulting in miniaturised follicles. If the resistence is low, anagen enlargement can continue for longer, resulting in larger follicles and increased hair growth.

The only factor that could `modify' the resistence to movement of the dermal tissue, is the fluid pressure within it. If the fluid pressure is high, the tissue rigidity is increased, and therefore its resistence to movement. Likewise, if the fluid pressure is low, so is the resistence to movement.

This mechanism makes a link with high fluid pressure and reduced hair growth, and low fluid pressure and increased hair growth. In my opinion, hair follicles evolved to `read' the fluid pressure in surrounding tissue to adjust hair production in line with other temperature controls in evolving mammals. Please see "The hydraulic dermal model" section of my paper.

A role of contact inhibition mediated through hydraulic changes in male pattern baldness, does not conflict with in-vitro observations, or the donor dominance observed in transplanted grafts. Sample follicle cells `switched off' by contact inhibition, have been fundamentally altered compared to cells that continue to multiply. EG: samples from terminal hair producing follicles. Any different in-vitro response of such samples to androgens, or other substances is to be expected! The observed Hypoxia in follicle grafts demonstrates no `active' circulation within these grafts. No active circulation means no hydraulic changes! The grafts will remain in the `as transplanted state', demonstrating donor dominance.

In male pattern baldness we have hair loss, immune infiltrate and immune sensitivity, ultimate fibrosis, and tissue thickening. These are all recognised factors in edemous tissue. http://www.lymphoedema.org.au/lymphoed.htm

One way to increase hair growth according to this mechanism, is to increase the resistence of follicle cells to contact inhibition? The danger here is that these cells would then be far more likely to become tumorous. In my opinion, the results of Fuchs in manipulating the Wnt pathway, confirms a central role of contact inhibition in follicle developement. http://www.hhmi.org/fuchs/index.html

If you look at other cases of hair loss, the common factor in these conditions is an increase in tissue fluid pressure for one reason or another!

As far as HM like procedures are concerned, i think the implantation itself could create `one off' conditions? There is bound to be some kind of healing process here, and this could very likely allow increased cell multiplication initially, and the developement of a large anagen follicle. We know that an `over production' of cells can occour during the healing process, scar tissue for example?

This predicts a potential problem with follicles generated by HM? If these follicles cycle normally, come the next anagen phase, these would then also come under the influence of normal contact inhibition. If the scalp conditions have not changed, large HM generated follicles could only last for one cycle?

I would welcome your comments on this proposal.

Best Regards,

Stephen Foote.

_____________________________________________

From Dr Carl Bazan, a transplantation expert and leading researcher in hair multiplication.


"Dear Stephen:
Your note is very interesting. I have been following your work on the hydraulics of tissue (regarding mostly on scalp physiology).
I find your work is brilliant and it must be continued since it may open one of the gates we need for solving the problem.
Our research deals with some of the proposed ideas. We find contact inhibition is a true factor in the dermal model. In respect to HM, and particularly my own method that is called SIT (scalp impregnation therapy) the life expectancy and normal cycling of the follicular complex is of utmost importance. We expect an anagen telogen catagen cycle to be repetitive and self adjusting to the environment while conserving donor dominance. We have so much to do. Keep it up.
Best of luck (and hard work),

Dr. Carl
http://www.itzan.com
(Mexico)"

______________________________________________

From Dr Sawaya, who is well known as a leading hair biology researcher.



"Alot of good points are brought up regarding the hair follicle growth and the fact that anagen is a bit predetermined by the previous hair cycle and the "clock" that is set or how long the matrix cells can grow and divide, making a big, anagen follicle, or a smaller and smaller follicle with each hair cycle. The idea of pressure changes from localized factors is interesting as the problem with male pattern hair loss is the fibrosis/scarring that takes place so that the follicles and surrounding tissues are damaged and cannot regenerate.
Male pattern hair loss is not supposed to be a scarring, cicatricial process, but it is a mixed inflammatory process in that many people do have inflammatory changes but usually in the middle follicle, and not as much in the lower follicle, as in alopecia areata.

Overall, these are interesting arguments to stimulate anagen follicles, keeping in mind that there are many substages of anagen, each similar to the cell cycle in carrying out a specific function for a certain period of time.
Many researchers are working on similar concepts with use of growth factors to see if there is any certain one or mix of them that can effect the process.

It is a very complex process, but your thoughts are very organized and on the right path, similar to what others have been proposing, and in some ways yours are more straightforward. I think you've done a good job in thinking this through......
Hope this helps...
regards
Marty Sawaya"

___________________________________________________

S Foote.

 

[Bryan]

I think you `DO' understand my proposed explaination for this Bryan :wink:

Michael Barry understands it, as he demonstrates in his last post in this thread.

Quote:

"Ive got an answer for you Bryan.

According to Stephen's theory the reason one follicle shows the effect of contact inhibition (small vellus hair) and one thats a millimeter away does not is that hairs are asynchronous and go into catagen and telogen at different times (sometimes by several years). This is why we can lose 50% of our hair in a given area before it "receeds" and why women with diffuse thinning may not notice it until its really advanced. There is still plenty of big anagen-phase follicles that are unaffected by fluid pressure yet as its only in the early anagen phase when the dermal papilla expands when contact inhibition can effectively shrink the size of the future follicle. "

That's it in a nutshell, thank you Michael.

HUH?? That doesn't even make sense. Are the two of you claiming that even in balding scalp, follicles first grow BIG thick hairs early in the anagen phase, then they suddenly SHRINK down to vellus (sounds like a 1950's movie title: "The Incredible Shrinking Hair" ), or even become non-existent?? Is that REALLY what your story is?? Do you realize what a ridiculous claim that is?

Bryan

 

[michael barry]

Stephen's theory doesnt claim that at all Bryan. His theory is that in the three major phases of the hair cycle: telogen, catagen and anagen that its only in the anagen phase that the dermal papilla "gets bigger" as the keratinocytes therein begin to manufacture the new follicle after the last one fell out. During this time early in the anagen phase, if edema is taking place in the scalp and the skin in that area is under more fluid pressure because of the lymph nodes arent draining it as well as they do in people without male pattern baldness, the dermal papilla cant expand because when it tries to there is too much fluid pressure pushing against it and the intercellular instructions are to "cease and desist" more or less and grow a very small follicle instead of a big one like the one that just grew and fell out a few weeks back. This is according to Stephen's theory. Im not saying that its a proven fact. I'd love to see it studied. I'd like all the theories to get plenty of study to be truthfull as its only by eliminating competing theories can we possibly find a way to counterract baldness more effectively.

Anyway, the follicles that might be right next door to our new small and weak follicle may only be in year 2 or 3 of a 6 year anagen phase and will not enter the resting and shedding phase for 3 or 4 more years. According to theory, when they do go through rest/shed however, they will grow another small hair like our previous example for the same reason. The new anagen phase for these two small hairs will be shorter, and then they make a hair that is practically a vellus hair and only visible under close inspection. Stephen's main idea is that male pattern baldness is unrecognized lydophomea (Im proboably spelling that wrong, but dont feel like looking it up) in the scalp tissue which symptoms very closely mirror male pattern baldness symtoms wherever edema occurs on the body (inflammation, itchiness, swelling, redness, tightness, fibrosis). Stephen has only suggested the common treatments for edema to me as a way of slowing the progression of my own male pattern baldness. Doesnt mean he is right or wrong, but he obviously has spent a lot of time researching his hypothesis and I really dont feel he would come online and defend it so vigorously if he really didnt want it studied because he didnt feel he was onto something.

If it makes you feel any better however, if you put a gun to my head..........I still lean to men and women with pattern alopecia as just having too many androgen receptors on their follicles (I fully realize that is the most simplistic solution and would be glad to be wrong on it). It would seem like science could come up with a topical or pill that could more effectively inhibit the receptors from accepting DHT by now if that is all there is to baldness. Im not crazy about the half tablet of propecia that I have to take every day proboably anymore than you are using the very expensive shampoo proxiphen Byran. It is however, seemingly ridiculous to me that we have "hair cycle clocks" in the cells of our follicles that say "its cycle 11 now, time to start 'being sensitive' to DHT and shrivel up and disappear". [/i]

 

[Bryan]

Stephen's theory doesnt claim that at all Bryan. His theory is that in the three major phases of the hair cycle: telogen, catagen and anagen that its only in the anagen phase that the dermal papilla "gets bigger" as the keratinocytes therein begin to manufacture the new follicle after the last one fell out. During this time early in the anagen phase, if edema is taking place in the scalp and the skin in that area is under more fluid pressure because of the lymph nodes arent draining it as well as they do in people without male pattern baldness, the dermal papilla cant expand because when it tries to there is too much fluid pressure pushing against it and the intercellular instructions are to "cease and desist" more or less and grow a very small follicle instead of a big one like the one that just grew and fell out a few weeks back. This is according to Stephen's theory.

So I repeat my question: why would ONE follicle be affected by that pressure, but not another neighboring one?

Anyway, the follicles that might be right next door to our new small and weak follicle may only be in year 2 or 3 of a 6 year anagen phase and will not enter the resting and shedding phase for 3 or 4 more years.

What does THAT have to do with anything?? It's still been attempting to grow and still been stifled in that attempt (supposedly) for those 2 or 3 years, because of the alleged fluid pressure.

According to theory, when they do go through rest/shed however, they will grow another small hair like our previous example for the same reason.

I don't understand. What reason is THAT?? Stephen previously said (or at least strongly implied) that going through a rest/shed period sort of "resets" the follicle back to a clean slate. He's repeatedly said that only GROWING follicles (in anagen) are subject to the alleged contact inhibition from fluid pressure.

It really does sound like both of you are now just making stuff up, in an effort to make this theory work.

Bryan

 

[michael barry]

I think you are engaged in an effort of obfusciation for whatever unkown reason Bryan. Youre really smart, and if even I understand Stephen's idea......................I know you do.

Gosh, Its not threatening anyone for Pete's sake.

Number ONE point I want to make is that I dont KNOW if its right or not. I'd like to see it studied like Id like to see many theories studied in more detail (including yours Bryan as youre a smart guy).

I still stand by what Ive been saying about drug company/cosmetic company research into baldness also. They ought to have to publish what the hell the find out since male pattern baldness is classified as a disease. Everyone is trying to turn a buck of male pattern baldness because they know how bad men dont wanna be male pattern baldness and whats found is guarded like a dragon hoarding its gold. Its a wonder of just how much info Revlon may know that Pfizer doesnt or Anderans or Intercyclex or Merk or foreign companies, etc. and just how much they could help each other come up with an effective treatment if the scientists at these various entities werent like a bunch of blind men feeling and elephant wondering what the hell they have their hands on. Cancer research findings (another admittedly infinitely more serious disease, but still a disease) are published for peer review pronto.

Im guessing you feel you and Stephen have some sort of intellectual rivalry and thats great, but what youre doing would be like him acting as if donor dominance didnt make sense to him (on a theoretical abstract paper) and concluding the theory couldnt be true because of that. Right or Wrong, by his theory (unproven of course) he's well explained how 50% of terminals in a given area can be lost (or miniaturized to the point of cosmetic unacceptibility) and still fit the hydrolic dermal model.

By the way Bryan..............youre a smart guy. Just what is your explanation of male pattern baldness? Just a paragraph or two