For bryan and Foote.

[Guest]

I have a quick little question for you´s.

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

My theory is that certain people can´t cope with the amount of DHT that they produce - this causes inflammation and that´s when the entire cytokine cascade starts which leads to the irreversible fibrosis. This is what we call male pattern baldness, the pattern depends on how the cells are distributed during embryogenesis or whenever those cells migrate.

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

In short - if you take away 100% of the DHT from a person with diffuse thinning he will keep thining - but without inflammation! So the follicles will become dormant and only produce fine hairs. I´m talking all over the head not just the "DHT insensitive area" which I belive is sensitive but can withstand soo much more DHT because of placement?

 

[S Foote.]

I have a quick little question for you´s.

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

My theory is that certain people can´t cope with the amount of DHT that they produce - this causes inflammation and that´s when the entire cytokine cascade starts which leads to the irreversible fibrosis. This is what we call male pattern baldness, the pattern depends on how the cells are distributed during embryogenesis or whenever those cells migrate.

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

In short - if you take away 100% of the DHT from a person with diffuse thinning he will keep thining - but without inflammation! So the follicles will become dormant and only produce fine hairs. I´m talking all over the head not just the "DHT insensitive area" which I belive is sensitive but can withstand soo much more DHT because of placement?

I think, and as i understand it most scientists tend to agree, that the inflammation is not `directly' linked with the process of male pattern baldness in a causative `chain'.

The evidence is that the increasing inflammatory conditions develope over time `alongside' the follicle miniaturization, and is `NOT' the cause of the follicle miniaturization called male pattern baldness.

Of course the increased fibrosis with time does make attempts to re-enlarge follicles more difficult, so anti-inflammatories have a treatment role in my opinion.

As for the mechanism of DHT that `triggers' male pattern baldness?

We have to remember that DHT consistently `GROWS' hair over the larger part of the body, in a fairly consistent time scale.

The `ODD' thing is that rising levels of DHT trigger male pattern baldness in `some' individuals, and the timescale can vary a lot in different individuals. male pattern baldness is the odd man out in some individuals, and it is against the `general' hair growing nature of DHT. This means another factor, and no i don't think this is differences in the follicles themselves!

So i agree that DHT is `good' for scalp hair growth, up to a certain `systematic' amount in the individual that `flips' some kind of switch to create the `opposite' effect of male pattern baldness.

Question, how many people thought their hair was growing great, a few months before they noticed their first signs of male pattern baldness? I did, and i suggest this is because of increasing DHT!

Given the `WHOLE' body of evidence related to DHT induced hair growth/loss, and the eficacy of treatments to date, it should be increasingly clear to people that DHT is acting `INDIRECTLY' on in-vivo hair growth.

I have made my argument for the mechanism of this, and would add that `only' indirect DHT induced increases in scalp fluid pressure, would explain follicle miniaturization by contact inhibition, the immunology as is recognised in edema and male pattern baldness, and the sweating increase discussed in this forum.

S Foote.

 

[Guest]

I agree totally with your theory.

One question, do you belive that the "dht insensitive" hair goes dormant on finasteride in a reversible process or do you belive that the deregulation is a permanent one?

 

[Armando Jose]

Sorry for my interference but, as Stephen point out:
" So i agree that DHT is `good' for scalp hair growth, up to a certain `systematic' amount in the individual that `flips' some kind of switch to create the `opposite' effect of male pattern baldness. "

I completely agreed, even resembling the Ernie's theory about nutrients.
The key in scalp hairs could be that we don't know when appears the androgens in this zone. I suposse before puberty, in the first year of our existence, and IMO there is not problem with circulating androgens because there are located only in the neighborhood of the pilosebaceous follicle. Scalp hair is asynchronous, its biological signals don't arrive so far.

Now, it's time to know exactly when appears androgens in scalp. In bibliography there is not a unequivocal work regarding this issue. I would like develop a pertinent trial. If my thoughts are correct, the current theory should be revised carefully.

Armando

 

[S Foote.]

I agree totally with your theory.

One question, do you belive that the "dht insensitive" hair goes dormant on finasteride in a reversible process or do you belive that the deregulation is a permanent one?

Could you please clarify what you mean by `DHT insensitive' hair?

I don't think that DHT or other androgens `directly' effect either hair loss or hair growth. The important point of the in-vitro studies that people seem to miss, is that `direct' exposure to androgens, dosen't `change' the pre-existing growth characteristics of `ANY' type of follicle cell sample.

I think this is the important thing to remember, as it is easy to point to `some' molecular change induced by androgens in-vitro, but the bottom line is `no' growth changes are observed!

Because we know DHT `does' create follicle growth `changes', this must be an indirect effect, and `THE' significant effect on hair growth.

Could you please elaborate on your question?

S Foote.

 

[Bryan]

I have a quick little question for you´s.

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

Absolutely not. As I've pointed out numerous times, scalp hair thrives and flourishes in the COMPLETE ABSENCE of androgens.

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

Nope. Scalp hair doesn't need DHT (or other androgens) at all.

In short - if you take away 100% of the DHT from a person with diffuse thinning he will keep thining - but without inflammation! So the follicles will become dormant and only produce fine hairs.

No, that's just not true. Scalp hair follicles don't need androgens at all.

Bryan

 

[Bryan]

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

 

[Bryan]

I don't think that DHT or other androgens `directly' effect either hair loss or hair growth. The important point of the in-vitro studies that people seem to miss, is that `direct' exposure to androgens, dosen't `change' the pre-existing growth characteristics of `ANY' type of follicle cell sample.

I think this is the important thing to remember, as it is easy to point to `some' molecular change induced by androgens in-vitro, but the bottom line is `no' growth changes are observed!

Because we know DHT `does' create follicle growth `changes', this must be an indirect effect, and `THE' significant effect on hair growth.

That's typical of your strange logic: just because we don't (yet) fully understand how androgen-sensitive hair follicles actually BECOME sensitive to them, you jump to the weird conclusion that androgens must not have any direct effect at all, despite the in vitro experiments clearly showing that they do. What a strange non sequitur.

Bryan

 

[Guest]

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

I have to look at my own situation. I started losing hair and gaining a much stronger libido at the same time and this at the age of 28.

Short story. At 28 my hair was Sean Penn like, early Sean Penn but I always had on and off problems with my erection. I didn´t think much of it but once I stopped cardio training my erection came and I started losing hair - not instantly but after oh about 1 year or so. I started taking finasteride and it help but not much. Now I´m back to doing Cardio my hair is better then it has been since before I noticed it was falling out.

Something happened along the way aswell. About 1 month ago I was eating very little, doing alot of cardio and had about Zero sex. My scalp was feeling amazing, my cheast hair which I shave about once a week (stubbles) wasn´t coming back at all and I started shedding. Mainly from the back and sides - which I could easily point to the lack of DHT but then my scalp hair also started feeling limp, very healthy in terms of shine etc but really weak. I started eating better, more sexually activity and today a month later my hair feels much much stronger and my scalp feels really good.

I belive there´s a thin line between too much and not enough DHT in the follicles and I also belive that once the process is underway you need to be much more careful - just like you have to be if you dislocate your shoulder.

 

[S Foote.]

I don't think that DHT or other androgens `directly' effect either hair loss or hair growth. The important point of the in-vitro studies that people seem to miss, is that `direct' exposure to androgens, dosen't `change' the pre-existing growth characteristics of `ANY' type of follicle cell sample.

I think this is the important thing to remember, as it is easy to point to `some' molecular change induced by androgens in-vitro, but the bottom line is `no' growth changes are observed!

Because we know DHT `does' create follicle growth `changes', this must be an indirect effect, and `THE' significant effect on hair growth.

That's typical of your strange logic: just because we don't (yet) fully understand how androgen-sensitive hair follicles actually BECOME sensitive to them, you jump to the weird conclusion that androgens must not have any direct effect at all, despite the in vitro experiments clearly showing that they do. What a strange non sequitur.

Bryan

It isn't `strange' logic Bryan, it's proper scientific reasoning! :wink:

The in-vitro studies clearly show that hair follicles are not `directly' androgen sensitive, nor do they `become' so!

For `anything' to be sensitive to `something', means that some kind of `CHANGE' is induced.

The in-vitro studies clearly show, that `DIRECT' exposure to androgens, does `NOT' change the pre-existing growth characteristics of `ANY' follicle cell type! Be this terminal scalp follicles, pre-balding follicles, balding follicles, beard follicles, or vellous follicles.

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? At the very least, this demonstrates some `OTHER' mechanism of control of follicle size! 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.

So ever since then, the results of further experiments have been interpreted, or more accurately `twisted' to try to `SUIT' this idea!

There is not one scrap of `real' scientific support for the `direct' theory you support Bryan, and as time goes on the `donor dominance' assumption it was based on is also falling apart with modern transplantation knowledge! :wink:

S Foote.

 

[S Foote.]

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

Nesta.

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

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 :wink:

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

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

If these professional scientists were content with the current theory, why would they now be thinking along similar lines to me?

Nuff said 8)

S Foote.

 

[Guest]

S. Foote: Your theory is much more along what I´ve noticed with myself and I too have taken some beating on this forum for "wacky ideas" ( I remember when I tried to explain that you can´t get spironolactone or revivogen dependant the same way you get minoxidil dependant - it´s like saying situps creates dependancy if you want to keep your abs ).

In theory I belive that you can upregulate the amount of testosterone you produce by having alot of sex, eating more and above all other reasons puberty (the same way the level of THS rises with overstimulation). The elevated does of DHT then effects the scalp in such a way that inflammation occurs and once that happens the follicles are damaged.

I don´t know if the inflammation irreversibly changes some part of the follicle or if it´s physical obstruction by fibroblasts but since the cells have such huge capacity to regenarate after going into atrofi I´m betting that the bulk of the damage is done by fibroblasts.

I´m also a bit concerned that the fibroblasts could be the reason why HM won´t be successful in complete bald areas.

Ps. Bryan I think that you have skills it´s just that on this issue and on the issue of topical androgens we just don´t think the same (I belive that the topicals on the market today, with their ethanol carrier do more damage then good).

 

[Bryan]

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.

I belive there´s a thin line between too much and not enough DHT in the follicles and I also belive that once the process is underway you need to be much more careful - just like you have to be if you dislocate your shoulder.

You haven't said a single word about the all-important point which I clearly explained in that paragraph above, so I'll simply repeat it: scalp hair thrives and grows luxuriantly even in the TOTAL ABSENCE of androgens.

Bryan

 

[Bryan]

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?

At the very least, this demonstrates some `OTHER' mechanism of control of follicle size!

Of course.

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.

There is not one scrap of `real' scientific support for the `direct' theory you support Bryan...

ROTFLMFAO!!!

Bryan

 

[Bryan]

Ps. Bryan I think that you have skills it´s just that on this issue and on the issue of topical androgens we just don´t think the same (I belive that the topicals on the market today, with their ethanol carrier do more damage then good).

Really?? That's interesting. How do you explain Price's results with placebo treatments in an alcoholic vehicle, compared to those subjects who got no topical solution at all?

Bryan

 

[jimmystanley]

i agree with bryan...surely hair flourishes with out any androgen related stimulation...look back to pre-testosterone days....but it is also possible that some of the hair on the sides and back of our heads have become androgen dependent and any type of alph 5 inhibitor may be causing them to fall out...? no science here...just an observation.

 

[Bryan]

It's more likely that such hairs are androgen-NEUTRAL. In other words, androgens neither stimulate them nor suppress them. I've read that certain other types of hair are that way, too, like eyebrow hair. Interestingly, there apparently can be mixtures of such follicles in a given location. For example, one fascinating study I have is where they tested random scalp follicles from the same individual, and whereas many of them were found to have the usual sensitivity to androgens (their growth was suppressed by testosterone), an occasional neighboring hair follicle was found NOT to be affected by testosterone, one way or the other (let's see Stephen explain THAT little conundrum)!

It's just so damned ODD how stubbornly he continues to defend his ridiculous little pet theory, even in the face of overwhelming scientific AND circumstantial evidence against it. For example, one marvels at the thick heads of hair on healthy little girls. How many androgens do THEY have circulating in their bloodstreams (cough:nesta:cough)?? And you can draw a pretty clear line of demarcation where that thick scalp hair goes rapidly to vellus, and then to non-existent (in what would be the sideburn/beard area, if they were males). Does Stephen really expect anyone to believe that there are such MASSIVE differences in "edema" in the head area of little girls that would explain such profound differences in the rates of hair growth over the space of less than an inch?? Or is he just floating down a certain well-known river in Egypt? :wink:

Bryan

 

[S Foote.]

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.":3ec88]At the very least, this demonstrates some `OTHER' mechanism of control of follicle size!

Of course.[/quote:3ec88]

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!

You can keep on trying to `add' some magic mechanism to explain this as you regularly do, but that just doesn't wash scientificaly :wink:

There is not one scrap of `real' scientific support for the `direct' theory you support Bryan...

ROTFLMFAO!!!

Bryan

If you `really' think the current theory is sound Bryan, you are just kidding yourself :roll:

S Foote.

 

[Bryan]

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...

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

They sure as hell DO, Stephen.

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

 

[S Foote.]

It's more likely that such hairs are androgen-NEUTRAL. In other words, androgens neither stimulate them nor suppress them. I've read that certain other types of hair are that way, too, like eyebrow hair. Interestingly, there apparently can be mixtures of such follicles in a given location. For example, one fascinating study I have is where they tested random scalp follicles from the same individual, and whereas many of them were found to have the usual sensitivity to androgens (their growth was suppressed by testosterone), an occasional neighboring hair follicle was found NOT to be affected by testosterone, one way or the other (let's see Stephen explain THAT little conundrum)!

Two things Bryan.

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

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)

Post details of that study Bryan, and i will point out to you how it supports my theory and dismisses yours! :lol:

It's just so damned ODD how stubbornly he continues to defend his ridiculous little pet theory, even in the face of overwhelming scientific AND circumstantial evidence against it. For example, one marvels at the thick heads of hair on healthy little girls. How many androgens do THEY have circulating in their bloodstreams (cough:nesta:cough)?? And you can draw a pretty clear line of demarcation where that thick scalp hair goes rapidly to vellus, and then to non-existent (in what would be the sideburn/beard area, if they were males). Does Stephen really expect anyone to believe that there are such MASSIVE differences in "edema" in the head area of little girls that would explain such profound differences in the rates of hair growth over the space of less than an inch?? Or is he just floating down a certain well-known river in Egypt? :wink:

Bryan

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.

My theory explains how you can go from terminal hair growth to vellous growth over a short distance. Actually, eyebrow hair demonstrates my theory very well as i have explained before!!

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!

If you still don't get it Bryan, i will explain it again. Then i will save the post and repost it every time you try to distort my theory in the future!

S Foote.