Minoxidil and Insulin

[mindovermatter]

good post

good post, don't know why everyone seems to be bashing you. I think you most eloquently pointed out with clear logic the contradictions in recent studys. Why everything doesn't match up is the result of male pattern baldness being a complex problem scientifically. We should all keep in my that whenever someone does a study, they want it to be a success, hence they want to have something profound to say at the end of it. If they came out and said, "well it looks like this, but we're really not sure" it never would have gotten any attention or be published. So they kind of have to make it sound like they "discovered" something. Not saying that all studys don't have profound discoveries... just something to keep in mind.

first post! woot!

 

[Bryan]

Bryan wrote:
I can't help but notice that you haven't addressed the specifics of what I said about that contact inhibition/TGF beta-1 study. Should I assume that you haven't thought of any way to debunk what I said about it, Stephen? :wink:<


If you are refering to the `flip flop' issue as you like to call it Bryan, i thought i had addressed that? Try this.

No, that's not really what I'm talking about. I'm referring to the fact that contact inhibition and TGF beta-1 have similar effects. You don't seem to want to acknowledge that simple fact! :wink:

When follicle cells that are known to be `future' male pattern baldness follicles are exposed to androgens in-vitro, nothing happens. Direct exposure of these cells to androgens does `NOT' induce any change in their growth response.

Really? How would YOU know? Because it doesn't happen overnight in a petri dish? :wink:

When these cells come from `already' balding follicles, this restricted growth characteristic is maintained by androgens in-vitro.

It's caused AND maintained by androgens.

So, what we can be sure of from this, is that androgens are maintaining the `pre-existing' growth characteristics of follicle cells in-vitro, whatever this may be. I think this is the important thing to remember. Androgens are not `directly' changing the growth characteristics of `any' follicle cell samples.

Of course they are.

The only candidate `mechanism' for the flip flop in-vitro response to androgens of male pattern baldness cells, is normal contact inhibition Bryan!

Where do you get THAT idea?? The study that YOU even quoted yourself shows that 1) Androgens increase the expression of TGF beta-1 in balding hair follicles, and 2) TGF beta-1 inhibits the growth of hair follicles. You seem confused.

Androgens increase the expression of TGF beta-1 in culture. http://www.ncbi.nlm.nih.gov/entrez/quer ... t=Abstract

So TGF beta-1 is androgen inducible from follicle cells.

BTW, you may be overlooking something here that is VERY important. I'm going to let you figure it out for yourself, but here's a little hint for you: BEARD follicles! :wink:

TGF beta-1 is also known to `MAINTAIN' cell samples in- vitro, in the growth restricted state induced by contact inhibition in-vivo. http://www.ncbi.nlm.nih.gov/entrez/quer ... t=Abstract

Give it up, Stephen. Contact inhibition and TGF beta-1 had the same effects in that experiment, so you don't really have a point to make here.

Bryan

 

[Bryan]

A reasonable attempt at misleading people about what i have said on this issue Bryan, but not good enough i'am afraid!

I have explained to you before Bryan, that it is not the increased fluid pressure itself that is acting `directly' here. It is the effect of this in `pushing' dermal tissue cells in towards the `hollow' space that the enlarging anagen follicle is trying to create.

That differs only in nuance from what I said.

The `scaffold' principle is well known in providing a template for cellular growth.

A scaffold provides protection from `interference' by other structures from preventing cellular growth through normal contact inhibition. The advantages of a scaffold template for cell multiplication is recognised by professional science, and has been discussed in the context of hair multiplication research. http://www.hairsite4.com/dc/dcboard.php ... 2515&page=

I didn't read through that entire thread. Was anything really mentioned about contact inhibition? How would such a "scaffold" prevent contact inhibition? How would it prevent cell-to-cell contact?

My suggestion is that transplanted anagen follicles can survive and cycle, because a natural scarring `scaffold' is created by the healing process during the transplantation procedure.

But you've got to explain why balding follicles continue to bald, even when transplanted! :wink:

Yes Bryan, this does mean that you should be able to `auto- graft' pre-balding follicles back into the male pattern baldness area with sucess, and i wish someone would try this!

Your theory would be completely scewed then wouldn't it!!

Only if it actually worked. I think it has the same chance as the proverbial "snowball in Hell".

Bryan

 

[thin=depressed]

"Glucose is the vehicle by which energy gets from digested food to the cells of the body. In Type I diabetes mellitus, insufficient insulin is available to help get glucose out of the blood and into the cells of the body. " I researched a bit into glucose and insulin's relationship and it turns out that the insulin - hairloss connection may also include glucose because its a chain effect with glucose being the catalyst as well as adenosine.

 

[S Foote.]

You know Bryan, i always grin when i see these point dodging, psuedo scientific posts of yours!

Just for the record, i am not out to score points on these forums. I have my own hair loss experiences, and i have heard bulls**t spoken on the subject from people far more qualified than you!

I really don't care if people agree with my opinions on this subject or not. If i am on the right track with my personal ideas, time will tell!

If you are so desperate to maintain some kind of personal percieved internet `expert' status, then i just feel sorry for you! Personaly i have a life outside of these forums.

I don't mind getting involved in meaningful discussions, and arguing points in a proper scientific manner. But time after time, you demonstrate that you are not interested in `true' science. All you are interested in is trying to convince people of your personal opinion, and you will distract and distort as you see fit to achieve this!

I have made my points, and all i would ask of people is to consider these in the light of accepted scientific principles. Don't take what `ANYONE' on these forums, including me says as being valid. Educate yourselves on what is scientificaly valid and what is not!

There are just a few points i would make about your latest repetitive post Bryan.


>>Bryan wrote:
I can't help but notice that you haven't addressed the specifics of what I said about that contact inhibition/TGF beta-1 study. Should I assume that you haven't thought of any way to debunk what I said about it, Stephen? <<

S Foote wrote:
If you are refering to the `flip flop' issue as you like to call it Bryan, i thought i had addressed that? Try this.

>>Bryan wrote:
No, that's not really what I'm talking about. I'm referring to the fact that contact inhibition and TGF beta-1 have similar effects. You don't seem to want to acknowledge that simple fact!<<

Anyone who has read my posts on this Bryan, can see for themselves that `I' was the one who pointed out that TGF beta-1 and contact inhibition have similar effects! Thats the whole essense of the precedent i quoted!!

What the hell are you talking about here?????

S Foote. wrote:
When follicle cells that are known to be `future' male pattern baldness follicles are exposed to androgens in-vitro, nothing happens. Direct exposure of these cells to androgens does `NOT' induce any change in their growth response.

>>Bryan wrote:
Really? How would YOU know? Because it doesn't happen overnight in a petri dish? <<

S Foote. wrote:
When these cells come from `already' balding follicles, this restricted growth characteristic is maintained by androgens in-vitro.

>>Bryan wrote:
It's caused AND maintained by androgens.<<


S Foote. wrote:
So, what we can be sure of from this, is that androgens are maintaining the `pre-existing' growth characteristics of follicle cells in-vitro, whatever this may be. I think this is the important thing to remember. Androgens are not `directly' changing the growth characteristics of `any' follicle cell samples.

>>Bryan wrote:
Of course they are.<<

I have been asking you to provide us with some hard evidence for this `opinion' of yours throughout this thread Bryan. But you just can't do this!!!

Lets put these ridiculous statements of yours in their true context Bryan.

You believe that androgens directly transform normal follicles into male pattern baldness follicles. But the in-vitro testing clearly shows that androgens `DONT' do this! So instead of accepting the `ACTUAL' results of the testing, you decide to believe that given time, the results would `change' to suit your theory! Just what kind of Micky Mouse `science' is this Bryan?

I could bolt a silver lady mascot on the hood of my Ford `wishing' that it will turn into a Rolls Royce. When it doesn't, i should not take this as a sign that i am wrong in my thinking, because i `KNOW' that the silver lady mascot is `ASSOCIATED' with Rolls Royces!

Instead of just `wishing' androgens directly convert normal follicles into male pattern baldness follicles, just give us some `hard' evidence Bryan!

Anything remotely scientific would be a major improvement on your `wishes'!


S Foote. wrote:
Androgens increase the expression of TGF beta-1 in culture. http://www.ncbi.nlm.nih.gov/entrez/quer ... t=Abstract

So TGF beta-1 is androgen inducible from follicle cells.

>>Bryan wrote:
BTW, you may be overlooking something here that is VERY important. I'm going to let you figure it out for yourself, but here's a little hint for you: BEARD follicles!<<

I'm shaking in my boot's Bryan! Go on supprise me with yet another misinterpretation of the facts!



S Foote. wrote:
TGF beta-1 is also known to `MAINTAIN' cell samples in- vitro, in the growth restricted state induced by contact inhibition in-vivo. http://www.ncbi.nlm.nih.gov/entrez/quer ... t=Abstract

>>Bryan wrote:
Give it up, Stephen. Contact inhibition and TGF beta-1 had the same effects in that experiment, so you don't really have a point to make here<<


The point you keep missing Bryan is that they `DO' have the same effect. That was the point i made!!



S Foote. wrote:
The `scaffold' principle is well known in providing a template for cellular growth.

A scaffold provides protection from `interference' by other structures from preventing cellular growth through normal contact inhibition. The advantages of a scaffold template for cell multiplication is recognised by professional science, and has been discussed in the context of hair multiplication research. http://www.hairsite4.com/dc/dcboard.php ... 2515&page=

>>Bryan wrote:
I didn't read through that entire thread. Was anything really mentioned about contact inhibition? How would such a "scaffold" prevent contact inhibition? How would it prevent cell-to-cell contact?<<

Well it isn't really hard to figure out is it!

Why do scientists bother to construct scaffolds to assist in cell multiplication, if the cells could form the necessary structure themselves without interference??

You should do your homework Bryan!

S Foote. wrote:
My suggestion is that transplanted anagen follicles can survive and cycle, because a natural scarring `scaffold' is created by the healing process during the transplantation procedure.

>>Bryan wrote:
But you've got to explain why balding follicles continue to bald, even when transplanted!<<

But the latest research dosen't agree does it Bryan?

How come male pattern baldness follicles increase growth when transplanted into mice? These are not androgen deficient mice, so `YOU' have to explain that! http://www.hairsite4.com/dc/dcboard.php ... 8612&page=

You also have to explain the latest body hair transplatation results that go completely against your argument! http://www.hairsite8.com/woods/chest1.htm

If you want people to take you seriously Bryan, you should stop trying to distract from the issues. I asked you for your explaination for the Hypoxia paradox, and again you just ignored the question!

Just answer this question, and stop trying to shift the discussion to my theory! Your just not fooling anyone with these tactics!

S Foote.

 

[Bryan]

>>Bryan wrote:
No, that's not really what I'm talking about. I'm referring to the fact that contact inhibition and TGF beta-1 have similar effects. You don't seem to want to acknowledge that simple fact!<<

Anyone who has read my posts on this Bryan, can see for themselves that `I' was the one who pointed out that TGF beta-1 and contact inhibition have similar effects! Thats the whole essense of the precedent i quoted!!

What the hell are you talking about here?????

What I'm talking about is that you keep trying to blame the growth-inhibitive effects seen in androgenetic alopecia on CONTACT INHIBITION, rather than on ANDROGENS themselves. Don't try to pretend you don't know what I mean.

Lets put these ridiculous statements of yours in their true context Bryan.

You believe that androgens directly transform normal follicles into male pattern baldness follicles. But the in-vitro testing clearly shows that androgens `DONT' do this!

I notice you ignored the statement I made where I said that because it doesn't happen overnight in a petri dish, you think it can't happen at all! :wink:

Instead of just `wishing' androgens directly convert normal follicles into male pattern baldness follicles, just give us some `hard' evidence Bryan!

I can't do that, and neither can YOU explain how and why follicles eventually become sensitive to androgens in vitro. We're in the very same boat on that particular issue, Stephen.

>>Bryan wrote:
BTW, you may be overlooking something here that is VERY important. I'm going to let you figure it out for yourself, but here's a little hint for you: BEARD follicles!<<

I'm shaking in my boot's Bryan! Go on supprise me with yet another misinterpretation of the facts!

You're probably assuming that ALL hair follicles express TGF beta-1 in response to androgens, but you need to understand that it's probably only androgen-sensitive SCALP follicles that do so.

S Foote. wrote:
TGF beta-1 is also known to `MAINTAIN' cell samples in- vitro, in the growth restricted state induced by contact inhibition in-vivo. http://www.ncbi.nlm.nih.gov/entrez/quer ... t=Abstract

>>Bryan wrote:
Give it up, Stephen. Contact inhibition and TGF beta-1 had the same effects in that experiment, so you don't really have a point to make here<<

The point you keep missing Bryan is that they `DO' have the same effect. That was the point i made!!

So stop trying to blame balding on contact inhibition, instead of androgens!

S Foote. wrote:
The `scaffold' principle is well known in providing a template for cellular growth.

A scaffold provides protection from `interference' by other structures from preventing cellular growth through normal contact inhibition. The advantages of a scaffold template for cell multiplication is recognised by professional science, and has been discussed in the context of hair multiplication research. http://www.hairsite4.com/dc/dcboard.php ... 2515&page=

Yes, but where is the reference to contact inhibition in that link??? They seem to be concerned only with the DIRECTION that new hair follicles grow, and how to force them to grow in the proper direction with the proper "scaffolding". You have a penchant for taking other ideas and twisting them around to try to make them look like they have something to do with your contact inhibition theory.

>>Bryan wrote:
But you've got to explain why balding follicles continue to bald, even when transplanted!<<

But the latest research dosen't agree does it Bryan?

How come male pattern baldness follicles increase growth when transplanted into mice? These are not androgen deficient mice, so `YOU' have to explain that! http://www.hairsite4.com/dc/dcboard.php ... 8612&page=

That's a very interesting study, but the circumstances are so unusual and contrived that it's difficult to draw any firm conclusions. It may say more about the auto-immune aspects of balding than the androgenic aspects, since those mice were immuno-deficient.

You also have to explain the latest body hair transplatation results that go completely against your argument! http://www.hairsite8.com/woods/chest1.htm

I've already commented on that in the past, but I'll do it again: it's also interesting, but inconclusive. It doesn't seem all that outrageous to me that the location to which a hair follicle is transplanted could have _some_ influence on the length to which the resulting hair grows; however, that's a far cry from what YOU believe, which is that the resulting hair could actually wither and die from contact inhibition.

If you want people to take you seriously Bryan, you should stop trying to distract from the issues. I asked you for your explaination for the Hypoxia paradox, and again you just ignored the question!

I ignored something you said about the peculiarities of hair transplants for the simple reason that I don't really follow all the grisly details of hair transplantations, except for the all-important fact of "donor-dominance" (which is a HUGE thorn in your side). I didn't know enough about the specifics of what you were talking about to make any comment and I didn't feel like doing a few hours of research just for that one issue, so I just let it go.

I did notice, however, that you probably misconstrued what that doctor said in that "artery-ligature" study from back in the 1970's. As usual, you attempted to connect that with contact inhibition and even implied that the author himself explained the results that way, but that's not the case. If I remember correctly, the author's own theory was that reducing the blood flow to the scalp was reducing its supply of circulating androgens to the hair follicles. His own idea had nothing to do with YOUR eccentric theory.

Bryan

 

[S Foote.]

>>Bryan wrote:
No, that's not really what I'm talking about. I'm referring to the fact that contact inhibition and TGF beta-1 have similar effects. You don't seem to want to acknowledge that simple fact!<<

Anyone who has read my posts on this Bryan, can see for themselves that `I' was the one who pointed out that TGF beta-1 and contact inhibition have similar effects! Thats the whole essense of the precedent i quoted!!

What the hell are you talking about here?????

What I'm talking about is that you keep trying to blame the growth-inhibitive effects seen in androgenetic alopecia on CONTACT INHIBITION, rather than on ANDROGENS themselves. Don't try to pretend you don't know what I mean.

HUH???, I am saying that the evidence suggests that androgens induce early contact inhibition within follicles in male pattern baldness in-vivo. These effected follicle cells `THEN' maintain this characteristic when tested with androgens in-vitro, because of androgen inducable TGFbeta-1.

The study i posted clearly demonstrates that TGF beta-1 has this effect upon prior contact inhibited cells. Here is another sudy that confirms the release of TGF beta-1 by male pattern baldness cells in-vitro. http://www.fasebj.org/cgi/content/full/16/14/1967

So the clinical experiments show a proven pathway that could explain the in-vitro response of male pattern baldness cells to androgens in-vitro.

To be clear so you don't get confused again Bryan, i am proposing that the indirect action of androgens in-vivo, induce restricted growth in male pattern baldness follicles through early contact inhibition of the enlarging anagen follicle. The expression of TGF beta-1 by androgens from these male pattern baldness cells in-vitro, then maintains this growth restriction characteristic.

Lets put these ridiculous statements of yours in their true context Bryan.

You believe that androgens directly transform normal follicles into male pattern baldness follicles. But the in-vitro testing clearly shows that androgens `DONT' do this!

]I notice you ignored the statement I made where I said that because it doesn't happen overnight in a petri dish, you think it can't happen at all! :wink:

I ignored that comment Bryan, because is is just part of your wishfull thinking!

You are saying that it doesn't happen overnight, to try to imply that it `DOES' happen eventually! Yet again Bryan, you have not one shred of evidence, or even the remotest precedent for your assumption!

The possible mechanism i quote above for what we see in the in-vitro tests, is based on `proven' biological effects, not un-scientific wishfull thinking!

Instead of just `wishing' androgens directly convert normal follicles into male pattern baldness follicles, just give us some `hard' evidence Bryan!

I can't do that, and neither can YOU explain how and why follicles eventually become sensitive to androgens in vitro. We're in the very same boat on that particular issue, Stephen.

We are very far from being in the same boat on this Bryan. I have explained this above by known mechanisms, you can't explain it period!

>>Bryan wrote:
BTW, you may be overlooking something here that is VERY important. I'm going to let you figure it out for yourself, but here's a little hint for you: BEARD follicles!<<

I'm shaking in my boot's Bryan! Go on supprise me with yet another misinterpretation of the facts!

You're probably assuming that ALL hair follicles express TGF beta-1 in response to androgens, but you need to understand that it's probably only androgen-sensitive SCALP follicles that do so.

But your notion of `androgen sensitive scalp follicles', as you put it Bryan, has been dis-proven!

The `actual' in-vitro testing on `pre-balding' samples from the future male pattern baldness area, clearly shows that they are `NOT' directly androgen sensitive, as i keep pointing out!

If it is only existing male pattern baldness cells that express TGF beta-1, the capacity to do this `MUST' have been induced by an in-direct action of androgens in-vivo.

S Foote. wrote:
TGF beta-1 is also known to `MAINTAIN' cell samples in- vitro, in the growth restricted state induced by contact inhibition in-vivo. http://www.ncbi.nlm.nih.gov/entrez/quer ... t=Abstract

>>Bryan wrote:
Give it up, Stephen. Contact inhibition and TGF beta-1 had the same effects in that experiment, so you don't really have a point to make here<<

The point you keep missing Bryan is that they `DO' have the same effect. That was the point i made!!

So stop trying to blame balding on contact inhibition, instead of androgens!

How can you possibly say that Bryan, you know damm well that i think androgens are the cause of male pattern baldness (via normal contact inhibition).

S Foote. wrote:
The `scaffold' principle is well known in providing a template for cellular growth.

A scaffold provides protection from `interference' by other structures from preventing cellular growth through normal contact inhibition. The advantages of a scaffold template for cell multiplication is recognised by professional science, and has been discussed in the context of hair multiplication research. http://www.hairsite4.com/dc/dcboard.php ... 2515&page=

Yes, but where is the reference to contact inhibition in that link??? They seem to be concerned only with the DIRECTION that new hair follicles grow, and how to force them to grow in the proper direction with the proper "scaffolding". You have a penchant for taking other ideas and twisting them around to try to make them look like they have something to do with your contact inhibition theory.

Jezz!

I have a penchant for researching exsisting biological principles, to support my proposed mechanisms Bryan. It's called referencing in support of an argument, you should try it sometime Bryan!

The scaffold principle is a natural aid to cell migration and tissue building. During the healing process, natural fibrin scaffolds help in the tissue rebuilding. There are `MANY' papers on this principle.

You want to know how a scaffold, or more accurately a matrix can protect cells from contact inhibition? read this. http://www.pubmedcentral.nih.gov/articl ... tid=122571

I am suggesting that a similar matrix of fibrose scar tissue forming around transplanted follicles, can protect this `space' for future anagen enlargements.

>>Bryan wrote:
But you've got to explain why balding follicles continue to bald, even when transplanted!<<

But the latest research dosen't agree does it Bryan?

How come male pattern baldness follicles increase growth when transplanted into mice? These are not androgen deficient mice, so `YOU' have to explain that! http://www.hairsite4.com/dc/dcboard.php ... 8612&page=

That's a very interesting study, but the circumstances are so unusual and contrived that it's difficult to draw any firm conclusions. It may say more about the auto-immune aspects of balding than the androgenic aspects, since those mice were immuno-deficient.

You also have to explain the latest body hair transplatation results that go completely against your argument! http://www.hairsite8.com/woods/chest1.htm

I've already commented on that in the past, but I'll do it again: it's also interesting, but inconclusive. It doesn't seem all that outrageous to me that the location to which a hair follicle is transplanted could have _some_ influence on the length to which the resulting hair grows; however, that's a far cry from what YOU believe, which is that the resulting hair could actually wither and die from contact inhibition.

The immuno-deficient mice are used to avoid rejection in this kind of experiment. There is no evidence that the immune status of these mice is `causing' the re-enlargement of human male pattern baldness follicles!. In fact, you yourself have said in the past that you go along with the immune effects in male pattern baldness being an associated and not a `causal' factor. Are you now changing your position Bryan?

As for the body hair experiments, these completely blow your donor dominance idea out of the water! The very phrase `donor dominance' means the characteristics of the transplanted follicles `dominates'!!! But the body hair experiments prove otherwise. You can't have it both ways Bryan!

Where do you get this from, quote: "however, that's a far cry from what YOU believe, which is that the resulting hair could actually wither and die from contact inhibition." Where have i said that? I am sayiing that transplanted follicles are protected from contact inhibition!

If you want people to take you seriously Bryan, you should stop trying to distract from the issues. I asked you for your explaination for the Hypoxia paradox, and again you just ignored the question!

I ignored something you said about the peculiarities of hair transplants for the simple reason that I don't really follow all the grisly details of hair transplantations, except for the all-important fact of "donor-dominance" (which is a HUGE thorn in your side). I didn't know enough about the specifics of what you were talking about to make any comment and I didn't feel like doing a few hours of research just for that one issue, so I just let it go.

The `all important fact of donor dominance' as you put it, is not a `thorn in my side', as the body hair transplants, and the quoted mouse experiment dis-prove lt Bryan, simple!

I did notice, however, that you probably misconstrued what that doctor said in that "artery-ligature" study from back in the 1970's. As usual, you attempted to connect that with contact inhibition and even implied that the author himself explained the results that way, but that's not the case. If I remember correctly, the author's own theory was that reducing the blood flow to the scalp was reducing its supply of circulating androgens to the hair follicles. His own idea had nothing to do with YOUR eccentric theory.

Why do you always try to mislead people Bryan? You accuse me of implying that the author `agreed' with me! Show us all the post? Thats a blatent lie Bryan!

I said that the reduced fluid `feed' to the scalp, and the improvement in follicle size and condition, was in line with my theory.

Again Bryan, referencing experiments to support an argument. is called `SCIENCE'

As for the word `eccentric', i don't think you understand it's meaning!!

I argue my points referencing precedents for my proposed mechanisms. You argue your personal opinion using `fantasy' guesswork about genetic clocks, and you dare to call me eccentric!

Well some recognised experts, who's comments on my theory i have posted before, don't think i'am eccentric. So please don't claim that i am scientificly `eccentric' unless you are going to tell us all of your qualification to reach such a conclusion Bryan?

S Foote.

 

[Old Baldy]

Stephen: I don't mean to be a jacka** or smart aleck. But, what is your suggested regimen for curing male pattern baldness.

It think you are a very smart man but it's time for you to tell us what regimen(s) to adopt to cure male pattern baldness.

Bryan has the luxury of falling back on the "DHT" studies. I have the luxury of falling back on the "DHT" studies.

What is your suggested regimen to combat male pattern baldness?

Enough of this fu**ing bantering back and forth, PLEASE tell us how to thwart contact inhibition.

And you to Bryan, you're a very smart man, what the he** is your suggested regimen for Godsakes! Put it "on paper" for us.

Please guys!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!

Then I"LL have the LUXURY of falling back on both of you. 8)

 

[Bryan]

HUH???, I am saying that the evidence suggests that androgens induce early contact inhibition within follicles in male pattern baldness in-vivo. These effected follicle cells `THEN' maintain this characteristic when tested with androgens in-vitro, because of androgen inducable TGFbeta-1.

The study i posted clearly demonstrates that TGF beta-1 has this effect upon prior contact inhibited cells. Here is another sudy that confirms the release of TGF beta-1 by male pattern baldness cells in-vitro. http://www.fasebj.org/cgi/content/full/16/14/1967

So the clinical experiments show a proven pathway that could explain the in-vitro response of male pattern baldness cells to androgens in-vitro.

That's a ridiculous theory. How long do those hair follicles have to be out of a person's scalp and sitting in a petri dish before they lose their status as being "prior contact inhibited" cells, to then be "maintained" in that same state by androgens? I'd like to know what your answer to THAT is! :wink:

You want to know how a scaffold, or more accurately a matrix can protect cells from contact inhibition? read this. http://www.pubmedcentral.nih.gov/articl ... tid=122571

I am suggesting that a similar matrix of fibrose scar tissue forming around transplanted follicles, can protect this `space' for future anagen enlargements.

Hey, haven't you forgotten something?? How about the part where that same scar tissue sort of "locks-in" the excessive fluid pressure around balding follicles, so that they continue balding even when transplanted to non-balding areas of scalp? What a wonderfully convincing part of your theory! :x

As for the body hair experiments, these completely blow your donor dominance idea out of the water! The very phrase `donor dominance' means the characteristics of the transplanted follicles `dominates'!!! But the body hair experiments prove otherwise. You can't have it both ways Bryan!

Stephen, I know you're anxious to take succor from any source you can, considering how the available evidence is so overwhelmingly against your theory; therefore, I can understand why you feel the need to make a REALLY BIG DEAL out of the fact that "donor dominance" may not be fully 100% in effect, but maybe only 90% or so!

Where do you get this from, quote: "however, that's a far cry from what YOU believe, which is that the resulting hair could actually wither and die from contact inhibition." Where have i said that? I am sayiing that transplanted follicles are protected from contact inhibition!

I wasn't referring to transplanted hairs. I was referring to normal hairs in situ.

Bryan

 

[S Foote.]

Stephen: I don't mean to be a jacka** or smart aleck. But, what is your suggested regimen for curing male pattern baldness.

It think you are a very smart man but it's time for you to tell us what regimen(s) to adopt to cure male pattern baldness.

Bryan has the luxury of falling back on the "DHT" studies. I have the luxury of falling back on the "DHT" studies.

What is your suggested regimen to combat male pattern baldness?

Enough of this fu**ing bantering back and forth, PLEASE tell us how to thwart contact inhibition.

And you to Bryan, you're a very smart man, what the he** is your suggested regimen for Godsakes! Put it "on paper" for us.

Please guys!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!

Then I"LL have the LUXURY of falling back on both of you. 8)

Good question Old Baldy!

I have just got back home after a hard day. It's a busy time of year for me, and i have some family issues to deal with as well. It's now 10-10 pm here in England, and i am `knackered' as we say here.

Your question deserves a considered response, and i will post a reply either tommorow or over the weekend. I will also reply to Bryans latest distraction then as well.

Good night!

S Foote.

 

[S Foote.]

HUH???, I am saying that the evidence suggests that androgens induce early contact inhibition within follicles in male pattern baldness in-vivo. These effected follicle cells `THEN' maintain this characteristic when tested with androgens in-vitro, because of androgen inducable TGFbeta-1.

The study i posted clearly demonstrates that TGF beta-1 has this effect upon prior contact inhibited cells. Here is another sudy that confirms the release of TGF beta-1 by male pattern baldness cells in-vitro. http://www.fasebj.org/cgi/content/full/16/14/1967

So the clinical experiments show a proven pathway that could explain the in-vitro response of male pattern baldness cells to androgens in-vitro.

That's a ridiculous theory. How long do those hair follicles have to be out of a person's scalp and sitting in a petri dish before they lose their status as being "prior contact inhibited" cells, to then be "maintained" in that same state by androgens? I'd like to know what your answer to THAT is! :wink:

But the conclusion of the authors of that study is quite clear Bryan. Perhaps you should tell `THEM' where they are going wrong!

You want to know how a scaffold, or more accurately a matrix can protect cells from contact inhibition? read this. http://www.pubmedcentral.nih.gov/articl ... tid=122571

I am suggesting that a similar matrix of fibrose scar tissue forming around transplanted follicles, can protect this `space' for future anagen enlargements.

Hey, haven't you forgotten something?? How about the part where that same scar tissue sort of "locks-in" the excessive fluid pressure around balding follicles, so that they continue balding even when transplanted to non-balding areas of scalp? What a wonderfully convincing part of your theory! :x

Firstly Bryan, i would like a citation in support of your claim above. That is that balding follicles continue to get smaller after transplantation to hairy areas. Be `VERY' specific Bryan! I want to see evidence that these follicles continue to miniaturize!!!

Secondly,this is a demonstration to the people reading this thread, of how you try to twist things when you can't answer the points Bryan. I have always said that i think the `primary' factor is the scaring issue. This was in my original paper, `before' i even discussed my theory on these sites!!
http://www.hairsite2.com/library/abst-167.htm You are well aware of this!!

Quote: "There is however a significant difference between the successful plug grafts and unsuccessful scalp reduction. This is the 'wall' of scar tissue that forms around each plug graft. According to the hydraulic hair growth mechanism, this scar tissue should reinforce the graft against expansion. There could also be a secondary factor of reduced blood flow into the graft because of the scar tissue."

As for the body hair experiments, these completely blow your donor dominance idea out of the water! The very phrase `donor dominance' means the characteristics of the transplanted follicles `dominates'!!! But the body hair experiments prove otherwise. You can't have it both ways Bryan!

Stephen, I know you're anxious to take succor from any source you can, considering how the available evidence is so overwhelmingly against your theory; therefore, I can understand why you feel the need to make a REALLY BIG DEAL out of the fact that "donor dominance" may not be fully 100% in effect, but maybe only 90% or so!

I'am not `anxious' about anything Bryan! If you truly believe that the available evidence supports your opinion, you are sadly dilusional!

Just because `you' say something is so, doesn't mean it is!!!

The people following these threads are not as stupid as you would wish!

Quite simply, your donor dominance theory says that the growth characteristics of androgen `sensitive' follicles, is controlled by androgens `within' the follicles. Your theory has `NO' margin whatsoever for an `overulling' action of the surrounding tissue!

When a supporter of a theory has to keep `bending' it to suit new evidence, it's a sad day for science Bryan!

Where do you get this from, quote: "however, that's a far cry from what YOU believe, which is that the resulting hair could actually wither and die from contact inhibition." Where have i said that? I am sayiing that transplanted follicles are protected from contact inhibition!

I wasn't referring to transplanted hairs. I was referring to normal hairs in situ.

Bryan

You really do jump about Bryan!

What we are seeing in androgen related changes in hair growth/loss, is changes in the size of follicles.

Can you suggest any other `recognised' physiological mechanism that can logicaly change the size of the `WHOLE' follicle organ, besides contact inhibition?

I will post about Old Baldies point tommorow.

S Foote.

 

[Bryan]

That's a ridiculous theory. How long do those hair follicles have to be out of a person's scalp and sitting in a petri dish before they lose their status as being "prior contact inhibited" cells, to then be "maintained" in that same state by androgens? I'd like to know what your answer to THAT is! :wink:

But the conclusion of the authors of that study is quite clear Bryan. Perhaps you should tell `THEM' where they are going wrong!

HUH??? What the hell are you talking about, Stephen?? What they said in their study doesn't have a damned thing to do with what I asked you above! ANSWER THE QUESTION I ASKED YOU! Once you answer that question, I will have some follow-up questions for you.

Hey, haven't you forgotten something?? How about the part where that same scar tissue sort of "locks-in" the excessive fluid pressure around balding follicles, so that they continue balding even when transplanted to non-balding areas of scalp? What a wonderfully convincing part of your theory! :x

Firstly Bryan, i would like a citation in support of your claim above. That is that balding follicles continue to get smaller after transplantation to hairy areas. Be `VERY' specific Bryan! I want to see evidence that these follicles continue to miniaturize!!!

Well, Orentreich didn't actually state that they continue to miniaturize, he just stated that they "remained bald". Here's the citation: ""Autografts in Alopecia and Other Selected Dermatological Conditions", Norman Orentreich, Annals of the New York Academy of Sciences 1959; 83: 463-479.

Secondly,this is a demonstration to the people reading this thread, of how you try to twist things when you can't answer the points Bryan. I have always said that i think the `primary' factor is the scaring issue. This was in my original paper, `before' i even discussed my theory on these sites!!

???

What the Sam Hell are you talking about, Stephen?? I have _always_ acknowledged the part of your theory about scarring (BTW, your inability to spell "scarring" is SCARING me )! Hell, I've made fun of it on numerous occasions as a perfect example of a completely ad hoc theory! Don't you remember?? :wink:

Stephen, I know you're anxious to take succor from any source you can, considering how the available evidence is so overwhelmingly against your theory; therefore, I can understand why you feel the need to make a REALLY BIG DEAL out of the fact that "donor dominance" may not be fully 100% in effect, but maybe only 90% or so!

Quite simply, your donor dominance theory says that the growth characteristics of androgen `sensitive' follicles, is controlled by androgens `within' the follicles. Your theory has `NO' margin whatsoever for an `overulling' action of the surrounding tissue!

Excuse me, but YOU aren't the arbitrator of how much "margin" there is in any particular scientific theory! :-x As I've explained to you a number of times, hirsutism (just as an example) isn't perfectly 100% controlled by a very thorough inhibition of androgens. There's more to hairgrowth than just androgens, Stephen, although as James Hamilton so brilliantly observed many many years ago, they _are_ a prerequisite and incitant for androgenetic alopecia. But if you start monkeying around with other unusual mad-scientist experiments like transplanting a hair follicle to a wildly different body location, it doesn't seem all THAT unusual to me that it may take on slightly different growth patterns than it had previously. But that's nowhere nearly as significant (for your eccentric theory) as the fact that its response to androgens remains the same, and its growth remains RELATIVELY the same (+/- 10% or so), regardless of its new location. YOU, on the other hand, have the screwball idea that a hair follicle can go from 100% to 0%, just because of its location in an area of alleged "edema"!!

I wasn't referring to transplanted hairs. I was referring to normal hairs in situ.

You really do jump about Bryan!

What we are seeing in androgen related changes in hair growth/loss, is changes in the size of follicles.

Can you suggest any other `recognised' physiological mechanism that can logicaly change the size of the `WHOLE' follicle organ, besides contact inhibition?

Yes. Androgenetic alopecia.

Bryan

 

[oni]

lol! is this a pissing post for two or can anyone.........

 

[S Foote.]

Stephen: I don't mean to be a jacka** or smart aleck. But, what is your suggested regimen for curing male pattern baldness.

It think you are a very smart man but it's time for you to tell us what regimen(s) to adopt to cure male pattern baldness.

Bryan has the luxury of falling back on the "DHT" studies. I have the luxury of falling back on the "DHT" studies.

What is your suggested regimen to combat male pattern baldness?

Enough of this fu**ing bantering back and forth, PLEASE tell us how to thwart contact inhibition.

And you to Bryan, you're a very smart man, what the he** is your suggested regimen for Godsakes! Put it "on paper" for us.

Please guys!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!

Then I"LL have the LUXURY of falling back on both of you. 8)

According to the Hydraulic theory, it is the systematic levels of DHT that `trigger' male pattern baldness in the individual, not the DHT within the balding follicles themselves.

Perhaps the most significant contribution of DHT in male pattern baldness, comes from the dermal tissue of the head in general, not that produced in the balding follicles. This DHT produced in the follicles of the whole scalp and beard, and the sebaceous glands, feeds into the local lymphatics, and an excess of DHT here can create lymphedema of the male pattern baldness area, triggering the male pattern baldness process as i have described.

Once edema forms in the male pattern baldness area, it can be self maintaining by processes already known in lymphedema. http://www.lymphoedema.org.au/

So the other area that has to be tackled besides the DHT `trigger', is the self maintaining effect of the edema, largely by the induced changes in the local immunology.

So, we need at least to reduce DHT production at the local dermal production in the `whole' head. We also need to do something about the induced inflamation, and anything else that reduced the tissue fluid levels at the hair follicle level, would be a good thing.

In my opinion, the treatment experience to-date, has reached a similar conclusion with the promotion on these sites of the `big three'!

People recommend a systematic 5ARI, along with topical anti-inflammatory regimes including Nazoral, and finally Minoxidil. I regard Minoxidil as a aid because it reduces the fluid level from the surface tissue around the follicles.

It should be increasingly obvious to people that using a topical 5ARI on the bald area, is far less effective than a systematic 5ARI, indicating more of a `systematic', and therefore indirect effect of DHT.

The only effect these topical 5ARI's have in my opinion, depends on the `local' absorbtion into the hairy areas of the scalp. If you don't want to use a systematic 5ARI, then the topicals will be much more effective if used `all over' the hairy areas of the head, according to my theory.

I would recommend the 1% Nizoral, and other anti-inflammatories based on peoples experiences on these sites.

I also think that devices like the laser comb can be beneficial, as these devices are known to reduce edema. That is how the laser comb works in male pattern baldness according to the Hydraulic theory.

I don't really like to recommend specific treatments, because i cannot try some of these myself because of personal health problems. So be aware i am talking here at the theoretical level based on my theory!

In my opinion, one significant part of the equation is being neglected in these treatments. The quoted treatments help with the drainage side of the `fluid' equasion. In trying to reduce scalp fluid levels, which is what is necessary according to the theory, it would help a lot to reduce the fluid `feed'.

I think this is why such an improvement in scalp conditions, and the hair follicles was seen in the arterial ligature procedure. http://www.geocities.com/bryan50001/artery_ligature.htm This significantly reduces the fluid `feed' to the male pattern baldness area.

Again, speaking `theoreticaly', this procedure should drasticaly improve the response of the individual to the other treatments above.

In the future it may be that a surgical `re-plumbing' to improve both the drainage from the scalp, and reduce the feed to the scalp, would avoid the influence of DHT altogether!

I'am sure Bryan will have a few things to say here, but just remember this.

If the current theory was right, topical 5ARI's would be more effective than systematic 5ARI's, because the topicals act `directly' at the heart of the `problem'! That is on the DHT produced within the follicles. But anyone familiar with the posts on hair loss sites, knows different!

Also, the major drug companies would have developed topical anti-androgens that would have stopped male pattern baldness in it's tracks, (according to the current theory). Are we so naive as to believe they haven't experimented with such treatments?

So where are they?

S Foote.

 

[S Foote.]

lol! is this a pissing post for two or can anyone.........

Yes, having to go over things with Bryan time and time again, does get boring!

Bryan.

I have said my piece, and if you don't understand my points, so be it. People can see for themselves by the effectiveness of treatments, that the direct theory is coming apart at the seams! See my post to Old Baldy.

If you insist on quoting 60 year old studies whilst ignoring the implications of the latest research, go ahead! Other people know better!

Judging from your irrational obsession with spelling errors, you should be posting on `essay' discussion forums Bryan, at least thats something you have a talent for!!

I certainly can't fault your writing style, or spelling Bryan. It's just a pity that the `ACTUAL' content of what you say is meaningless in a scientific context!

I must say your tactic of wearing people down with your repetitive posts, is very effective in making sure you have the last word!

I really have better things to do than try to educate you in the skills of deduction and original thinking.

S Foote.

 

[Bryan]

Oh, so you're not going to attempt to answer a tough new question I have for you, which I have never asked you before until now? Somehow I'm not terribly surprised! :wink:

A great American was once famous for saying "If you can't take the heat, stay out of the kitchen." You obviously can no longer take the heat.

Bryan

 

[Old Baldy]

Thanks for the info. Stephen. I like your use of the word "replumbing". From all I've read, replumbing of the scalp circulatory system is important. I guess I'm doing all I can right now. Thanks for the info.

If I wrote all I'm trying to do to "install" a new plumbing system you'd shake your head and take an aspirin!! :lol:

I would think we should be very careful if we try to diminish the "feed" to the scalp. The coming and going of fluids is natural. We should try to improve scalp health to make that coming and going more efficient. I have no problem with taking finasteride. internally, no side effects and it is a rather harmless drug from all I've read.

I think that aspirin you'd take if you saw all I'm trying to do for scalp health is more "dangerous" than finasteride.

 

[S Foote.]

Oh, so you're not going to attempt to answer a tough new question I have for you, which I have never asked you before until now? Somehow I'm not terribly surprised! :wink:

A great American was once famous for saying "If you can't take the heat, stay out of the kitchen." You obviously can no longer take the heat.

Bryan

OK Bryan ask your question!

I don't have any problem answering your questions, but often when i have answered, you just throw the same question at me again and again!

Just try to make it relevant to the context, and i will answer it. 8)

S Foote.

 

[S Foote.]

I would just like to respond to a few important points Bryan.


S Foote wrote:
Firstly Bryan, i would like a citation in support of your claim above. That is that balding follicles continue to get smaller after transplantation to hairy areas. Be `VERY' specific Bryan! I want to see evidence that these follicles continue to miniaturize!!!

>>Bryan wrote:
Well, Orentreich didn't actually state that they continue to miniaturize, he just stated that they "remained bald". Here's the citation: ""Autografts in Alopecia and Other Selected Dermatological Conditions", Norman Orentreich, Annals of the New York Academy of Sciences 1959; 83: 463-479.<<

Then please don't ever claim again that balding follicles "continue to bald" when transplanted into hairy areas! You have clearly mis-quoted the article, not very scientific Bryan!

How can you know that the miniaturisation continues without more comprehensive studies??? These follicles could have increased in size slightly. Not perhaps in a cosmeticaly significant way, but such an observation would be in line with modern day body hair transplantation, and might have added to further understanding!

When Orentreich did this research some `40' odd years ago, did he note the non long term survival of transplanted follicles in the larger grafts? When he made his `donor dominance' conclusions, did he double check this conclusion by experimenting with other types of transplantation like scalp reduction?

I'am sure you have the full study Bryan, so you tell us!

You seem to have a high regard for these old `pioneer's' of the current theory, but i don't share your respect for them at all! As i have said before, these early experiments should have been followed up to prove the conclusions beyond doubt. But such experiments in transplantation are only just now begining to happen!!

Since these early `assumptions', a lot of desperate vunerable people, have been left scarred (Spelling OK?) by failed transplant techniques based on Orentreich's `assumption'.

S Foote wrote:
Quite simply, your donor dominance theory says that the growth characteristics of androgen `sensitive' follicles, is controlled by androgens `within' the follicles. Your theory has `NO' margin whatsoever for an `overulling' action of the surrounding tissue!

>>Bryan Wrote:
Excuse me, but YOU aren't the arbitrator of how much "margin" there is in any particular scientific theory! As I've explained to you a number of times, hirsutism (just as an example) isn't perfectly 100% controlled by a very thorough inhibition of androgens. There's more to hairgrowth than just androgens, Stephen, although as James Hamilton so brilliantly observed many many years ago, they _are_ a prerequisite and incitant for androgenetic alopecia.<<

So finally you agree with me Bryan!! Of course there are `external' factors, and androgens are a prerequisite for the process. Thats what i have been saying!

`YOU' are the one who claimed earlier that the growth process is controlled `internally' by paracrine or autocrine mechanisms. You just can't have it both ways Bryan, and you can't squirm your way out of this point!!

If as you claimed earlier, androgens `directly' control follicle size by effecting the `internal' production of follicle cell growth signaling molecules, there is no possible way transplantation could effect this, simple!

That was the point you have consistantly argued as to why transplants work in the first place. That is that your `donor dominance' idea means the conditions in the surrounding tissue don't `CHANGE' things!!

You may `NOW' try to throw other factors in the `mix', but that just won't wash with the theory you claim!


S Foote wrote:
Can you suggest any other `recognised' physiological mechanism that can logicaly change the size of the `WHOLE' follicle organ, besides contact inhibition?

>>Bryan wrote:
Yes. Androgenetic alopecia.<<

Androgenic alopecia is the name of a physical condition Bryan, it is `NOT' descriptive of any `MECHANISM' of follicle miniaturization. Try again!

S Foote.

 

[thin=depressed]

--------------------------------------------------------------------------------

M119 -- 6/5/99 updated 3/22/00

HAIR LOSS AND INSULIN

Gabe Mirkin, M.D.

Exciting new research shows that high blood levels of insulin and its growth factors may cause male pattern baldness in which men and women lose hair from the top and front of their heads, while hair on the sides of their scalp continue to grow luxuriously. A study from Harvard School of Public Health shows that men who have the highest blood levels of insulin like growth factor-1 are the ones most likely to suffer male pattern baldness. Women who have high levels of insulin (polycystic ovary syndrome) are the ones most likely to lose hair from the tops of their heads. It still is early in the research, but evidence is accumulating that male-pattern baldness may be caused by high levels of insulin that are produced by eating huge amounts of sugary and floured foods such as bakery products and pastas. We need research to show if male pattern baldness can be prevented by avoiding flour and sugar, eating fruits only with meals and taking drugs such as Glucophage, Actos and Avandia that lower insulin levels.

Signorello LB et al. Hormones and hair patterning in men: A role for insulin-like growth factor-1. Journal of the American Academy of Dermatology February, 1999;40:200-203

I just got done eating a bowl of pasta and finished it off with a boston cream donut.OH sh*t