For Stephen Foote, from a Doctor

[michael barry]

Doctor,

Ive pointed out what you just raised to Stephen before. He disagrees with the examining doctor's conclusions. Stephen found that study (the one you used) initially about a year back.



Wook,

If you look closely at that picture of Larry Craig again, notice how his wreath hair is thin? The other man's wreath hair has so much more density that Craigs. Its hard to believe one could have an edema in an area that rests on pillows every night to me personally. If edema was indeed causing baldness--------------------it would have to be an edema that started effecting the entire cranium from the bottom of the neck upwards from the back, and right above the shaving area all over the forehead.



I, like the other two doctors examining the men with lipedemateous scalps, dont think there is a correlation. Finasteride wouldn't have stabalized one man's hairloss and improved the other mans condition without having an effect on the edema if the two were related. My opinion.













On Bryan's quote: technically you are right Wook...................The real, ubermost, utterly true "problem" in baldness is the genetics withing the hair follicle itself according to the standard theory of baldness. Elvis Presley didn't block his androgen receptors and had good hair at 42 when he died. But the genetics downstream of those androgen receptors seemed to be DHT resistant. However, if we BLOCK those receptors or degrade them, even men with AA should keep the hair they have.


Bryan has a study with a man with cirrhosis who was on oral spironolactone for six years, and began regrowing scalp hair all over his bald head. He had been bald for thirty years. Kinda hard to imagine that spironolactone would orally reduce edema that well isn't it?

 

[michael barry]

"They stab it with their steely knives, but they just can't kill the beast"


--------The Eagles, "Hotel California"

 

[IBM]

michael barry you dont understand. finasteride is fundamental. So i would propose is taking finasteride, raising estrogens and lower testosterone to half.

 

[docj077]

Doctor,

Ive pointed out what you just raised to Stephen before. He disagrees with the examining doctor's conclusions. Stephen found that study (the one you used) initially about a year back.

Actually, I found that study for him and the histological slides that are present in the study are undeniable. A conclusion is one thing, but physical proof of the pathology is quite another.

He can say what he wants, but that still doesn't make him a "professional" with regards to any meaning of that particular word.

I still chuckle when he mentions lipedematous alopecia as being an example of the phenomenon that he's trying to prove exists. The guy needs a good dermatopathology book and a five year old to paraphrase it in an understandable way for him.


It's also important to note that a Andrews' Diseases of the Skin: Clinical Dermatology makes a very specific reference to the actions of androgens, and believe or not, TGF-beta in the tenth edition of their textbook. He can say what he wants about a single study, but a peer reviewed and respected manual of medicine trumps his opinion anyday.

 

[Nathaniel]

michael barry you dont understand. finasteride is fundamental. So i would propose is taking finasteride, raising estrogens and lower testosterone to half.

Yeah that would work very well but you will no longer be a *man*. It depends what you want. There was a guy here (can't remember his name) who was taking androcur, dutasteride and estrogen patches!

 

[michael barry]

Nathaniel,

I too think the side effect and the physical risk are way, way, way to high to take a bunch of estrogen and cut ones testosterone in half. Might as well get friggin' castrated. I dont want to keep my hair that bad.


IBM, you already are taking oral spironolactone.......................finas, oral spironolactone is an awful lot. Topical spironolactone cream applied twice a day would probably be just as good---------------and you wouldn't have side effects.

 

[Bryan]

DHT is the primary culprit in baldness. Cutting T in half gets you about a fifty percent reduction in DHT hypothetically...

I have a study in which a group of patients were castrated, and their serum before-and-after testosterone and DHT levels were measured. Testosterone dropped profoundly by an average of about 95%, of course, but DHT dropped by an average of only about 70% (that number was easy for me to remember, because it's so similar to what you get with finasteride).

So the assumption I've always made is that for the body-wide production of DHT, the availability of 5a-reductase is the main bottleneck that limits production, not the availability of the substrate testosterone. I'm not dogmatically claiming that to be the correct interpretation of those numbers, it just seems like a reasonable assumption to me.

 

[Bryan]

Shelton says that the effect of baldness is mainly one of androgen sensitivity where cell receptors play only a small role in baldness, if my interpretation is correct

Actually, people with non-working androgen receptors never go bald and never grow beard hair to amount to much of anything. I'd say thats more than a small role, but the whole shebang wouldn't you? I mean you can have all the DHT on earth, but if your androgen receptors dont work, you dont go bald, and you dont get chest and arm and neck hair, etc.

http://www.hairlosstalk.com/discussions ... ors#359968

It seems that the main difference between the Big 3 - proponents description of the balding process and the Stephen Foote description of male pattern baldness is that the conventional baldness science describes the problem as one of cell receptors, that is to say androgen receptors...

Oh horseshit, Wookster! It has nothing to do with androgen receptors, except very very indirectly. Can't you think of a more sophisticated way to explain it than just that??

You took what I said completely out of context. I've made it plain as day that the big difference between Stephen Foote's theory and the standard theory of balding has nothing to do with the nature of androgen receptors per se, it has to do with WHERE ANDROGENS ELICIT THEIR RESPONSES WHICH LEAD TO BALDING. Stephen Foote says that happens in lymph vessels, the standard theory of balding says it happens directly in hair follicle cells.

 

[wookster]

[...]

One year of finasteride treatment in fact induced improvement of androgenetic alopecia in one patient and stabilization in the other, but it did not affect the lipedematous scalp, which remained unchanged in both cases.


You'll notice that edema can be associated with male pattern baldness, but reversal and maintaince of male pattern baldness does not require reversal of edema. Instead, inhibition of androgen action is required. Thus, edema is not the underlying cause of the reason for continued deterioration.

This appears to be a major stumbling block for Foote's theory. I am not sure it can recover...

 

[wookster]

Shelton says that the effect of baldness is mainly one of androgen sensitivity where cell receptors play only a small role in baldness, if my interpretation is correct

Actually, people with non-working androgen receptors never go bald and never grow beard hair to amount to much of anything. I'd say thats more than a small role, but the whole shebang wouldn't you? I mean you can have all the DHT on earth, but if your androgen receptors dont work, you dont go bald, and you dont get chest and arm and neck hair, etc.

http://www.hairlosstalk.com/discussions ... ors#359968

It seems that the main difference between the Big 3 - proponents description of the balding process and the Stephen Foote description of male pattern baldness is that the conventional baldness science describes the problem as one of cell receptors, that is to say androgen receptors...

Oh horseshit, Wookster! It has nothing to do with androgen receptors, except very very indirectly. Can't you think of a more sophisticated way to explain it than just that??

You took what I said completely out of context. I've made it plain as day that the big difference between Stephen Foote's theory and the standard theory of balding has nothing to do with the nature of androgen receptors per se, it has to do with WHERE ANDROGENS ELICIT THEIR RESPONSES WHICH LEAD TO BALDING. Stephen Foote says that happens in lymph vessels, the standard theory of balding says it happens directly in hair follicle cells.

YOU ...said that hair follicles become sensitive to androgens and nobody can explain how that happens

 

[Bryan]

Yes, I did say that, and I stand by it. What's your point?

 

[wookster]

Yes, I did say that, and I stand by it. What's your point?

You also said it has nothing to do with androgen receptors except very very indirectly...

 

[Bryan]

Yes, and I stand by that, too. Again: what's your point?

 

[wookster]

Yes, and I stand by that, too. Again: what's your point?

Michael Barry says androgen receptors are basically "the whole shebang" and you say that it has nothing to do with androgen receptors except very very indirectly. That was the point until you accused me of taking things out of context :freaked:

Foote says lymphatics and fluid dynamics are really the whole shebang but docj077 says no that aint true - it is the molecular trees within the totality of the forest of biological interactions that really define what is going on with regards to male pattern baldness; the downstream effects of TGF beta do more damage that the initial upstream effect of androgens.

Finasteride grew hair on a spongy lympedemic scalp so edema is not a causative factor but only a consequential one. Androgens must have a direct effect on the hair follicle, where the follicle becomes sensitive to DHT and miniaturizes, then immune response occurs for most but not all balding individuals.

 

[Bryan]

Yes, and I stand by that, too. Again: what's your point?

Michael Barry says androgen receptors are basically "the whole shebang" and you say that it has nothing to do with androgen receptors except very very indirectly. That was the point until you accused me of taking things out of context :freaked:

Do you have a problem with reading comprehension?? I explained to you more than once in plain English that IT'S THE DIFFERENCE BETWEEN THE STANDARD THEORY AND FOOTE'S THEORY THAT HAS NOTHING TO DO WITH ANDROGEN RECEPTORS.

 

[wookster]

Yes, and I stand by that, too. Again: what's your point?

Michael Barry says androgen receptors are basically "the whole shebang" and you say that it has nothing to do with androgen receptors except very very indirectly. That was the point until you accused me of taking things out of context :freaked:

Do you have a problem with reading comprehension?? I explained to you more than once in plain English that IT'S THE DIFFERENCE BETWEEN THE STANDARD THEORY AND FOOTE'S THEORY THAT HAS NOTHING TO DO WITH ANDROGEN RECEPTORS.

Foote's theory does include the upregulation of androgen receptors buddy

 

[Bryan]

Foote's theory does include the upregulation of androgen receptors buddy

I don't recall his ever mentioning that, except maybe possibly in passing. In any event, it's not an ESSENTIAL feature of his theory. Why do you keep beating this dead horse?

 

[wookster]

Foote's theory does include the upregulation of androgen receptors buddy

I don't recall his ever mentioning that, except maybe possibly in passing. In any event, it's not an ESSENTIAL feature of his theory. Why do you keep beating this dead horse?

The key to understand the balding process appears to be in the understanding of how androgens cause body hair vellus follicles to enlarge to terminal - and cause scalp hair terminal follicles to miniaturize to vellus. The scalp hair follicles somehow become very sensitive to androgens and shrink away to nothing. Body hair follicles appear to go into overdrive, creating a Chewbacca effect.

Also, why the horse-shoe effect in baldness?

http://www.hairlosstalk.com/discussions ... c&start=80

I have a question about androgen receptors and the hydraulic theory of baldness:

http://www.ehrs.org/conferenceabstracts ... sawaya.htm

All scalp biopsies from patients obtained 6 months after finasteride treatment revealed intense upregulation of AR expression in comparison to pre-treatment biopsies of the same patient, whereas ERs were not affected, indicating that AR is very sensitive to the affects of 5a-R type II suppression of DHT.

:freaked: :freaked: :freaked:

How does the hydraulic theory of baldness explain this upregulation of androgen receptors due to finasteride and what part do androgen receptors play in the hydraulic/androgenic balding scenario.

It is a good question, and the answer is simple.

My theory also requires that DHT is produced in the dermal tissue. I am suggesting that DHT evolved primarily to increase lymphatic drainage, and that is it's important role as a male hormone.

Any substance that has evolved to increase lymphatic drainage, would have to be largely produced in the outer tissue (the dermis).

Why? Because if such a substance was mainly introduced into lymph vessels towards the core of the body, the increased vessel pumping would restric flow from the outer tissues.

This back pressure effect is what happens in male pattern baldness according to my theory.

The area's of DHT production according to Merck are quote:

"Type I 5 alpha reductase is predominant in the sebaceous glands of most regions of skin, including scalp, and liver. Type I 5 alpha reductase is responsible for approximately one third of circulating DHT.The type II 5 alpha reductase isozyme is primarily found in prostate, seminal vesicles, epididymides, and hair follicles as well as liver, and is responsible for two thirds of circulating DHT."

DHT production largely in the dermis (the biggest organ in the body), ensures an even effect on lymphatic pumping.

The upregulation process in follicles and other DHT producing structures, is natures way of trying to maintain DHT production.

But this dosen't have to mean the physical effect of DHT is designed to happen where it is produced!

Consider this?

If DHT is only going to be used where it is produced, why is there serum DHT?

This is very inefficient, and nature is not normaly so? Also, why is DHT being produced in the liver? What "direct" function is DHT doing there?

The only possible reason for DHT to be produced in the liver, is so it can be released into the circulation for some purpose.

S Foote.

 

[michael barry]

Wook wrote:
[/quote]Michael Barry says androgen receptors are basically "the whole shebang" and you say that it has nothing to do with androgen receptors except very very indirectly. That was the point until you accused me of taking things out of context

Wook,

People with androgen insensitivity dont go bald or lose any hair. We have seen the RU58841 macaque pictures. We know a man who was on oral spironolactone for six years started regrowing hair all over a bald head that had been bald for decades. Therefore, if you can block or downreg androgen receptors "enough", apparently you can keep your hair and possibly regrow a great deal of it over time.
In this vein, I say the androgen receptor topically would be a wonderful way to "stick our finger" in the baldness process. The genetics that cause baldness are (of course) probably in the dermal papilla or whatever part of the follicle is always there through all three major phases, but thats DNA and we are a long way from being able to directly change that topically (unfortunately).

 

[wookster]

Wook,

People with androgen insensitivity dont go bald or lose any hair. We have seen the RU58841 macaque pictures. We know a man who was on oral spironolactone for six years started regrowing hair all over a bald head that had been bald for decades. Therefore, if you can block or downreg androgen receptors "enough", apparently you can keep your hair and possibly regrow a great deal of it over time.
In this vein, I say the androgen receptor topically would be a wonderful way to "stick our finger" in the baldness process. The genetics that cause baldness are (of course) probably in the dermal papilla or whatever part of the follicle is always there through all three major phases, but thats DNA and we are a long way from being able to directly change that topically (unfortunately).

If only we could selectively de-sensitize the male pattern baldness balding follicles, hair loss could be reversed. Fibrosis would probably also be reversed due to the increased collagenase production of the regenerated hair follicles... ?

Gene therapy?

ensativo: