For bryan and Foote.

[Bryan]

You clearly asked me in our initial debate to provide some evidence that contact inhibition in-vivo, "could" be altering the androgen response in-vitro that involves TGF beta-1.

Everyone here can see i have provided a precedent for such a possibility.

No you haven't. You haven't provided any kind of a "precedent" for anything at all. You have utterly failed to show that the cellular response to androgens has ever been altered by ANYTHING, much less contact inhibition specifically. The study that you keep citing over and over doesn't even mention the word "androgens" in its abstract, yet you hilariously keep pointing to it, for some odd reason. Is it out of sheer desperation that you do that? Are you hoping that people will notice the words "contact inhibition" in there, and simply assume (without reading the rest of it) that you really did provide some evidence for your claim? Is that all you've got left, Stephen? Just hoping that people will read your abstracts with a lack of critical thinking? I find that sad...

But no, you now demand absolute "PROOF" of my arguments :roll:

No, Stephen. All I'm asking for is ANY EVIDENCE AT ALL. You don't have any.

So you are saying that just because i cannot offer absolute proof of a mechanism, i should admit defeat ?

No. I'm saying that because you cannot provide ANY EVIDENCE AT ALL for your claim, you should admit defeat.

Bryan

 

[S Foote.]

You clearly asked me in our initial debate to provide some evidence that contact inhibition in-vivo, "could" be altering the androgen response in-vitro that involves TGF beta-1.

Everyone here can see i have provided a precedent for such a possibility.

No you haven't. You haven't provided any kind of a "precedent" for anything at all. You have utterly failed to show that the cellular response to androgens has ever been altered by ANYTHING, much less contact inhibition specifically. The study that you keep citing over and over doesn't even mention the word "androgens" in its abstract, yet you hilariously keep pointing to it, for some odd reason. Is it out of sheer desperation that you do that? Are you hoping that people will notice the words "contact inhibition" in there, and simply assume (without reading the rest of it) that you really did provide some evidence for your claim? Is that all you've got left, Stephen? Just hoping that people will read your abstracts with a lack of critical thinking? I find that sad...

I doubt very much Bryan, that you are swaying any genuine critical thinkers with this distraction of yours :roll:

But no, you now demand absolute "PROOF" of my arguments :roll:

No, Stephen. All I'm asking for is ANY EVIDENCE AT ALL. You don't have any.

[quote="S Foote.":8544b]So you are saying that just because i cannot offer absolute proof of a mechanism, i should admit defeat ?

No. I'm saying that because you cannot provide ANY EVIDENCE AT ALL for your claim, you should admit defeat.

Bryan[/quote:8544b]

So let's consider the question again in a true scientific way shall we? :roll:

The in-vitro tests clearly show that androgens have no direct effect at all in changing pre-male pattern baldness follicles "into" male pattern baldness follicles. When pre-existing male pattern baldness follicles are exposed to androgens in-vitro, this then causes TGF beta-1 to be expressed from the male pattern baldness cells.

So TGF beta-1 is not expressed in follicles prior to male pattern baldness on exposure to androgens, but it is after male pattern baldness.

So the scientific question is "what is causing" changes in the cells ability to express TGF beta-1?

We can be damm sure it is not "androgens" that are "causing" this change, or the in-vitro tests would have shown that!

So it is "NOT" specificaly the role of androgens that is important, "BUT" the change in the follicle cells ability to express TGF beta-1.

Got that now? :roll:

I have provided a demonstrated, recognised pathway by which prior contact inhibition "COULD" cause changes in the cells ability to express TGF beta-1 in response to external influences, including androgens!!!

But no, this is not good enough for you Bryan!

Which is strange given your own on the record explaination for this "change" Bryan!

According to you, the change in androgen response is due to androgens themselves changing the follicle response over time. This genetic "clock" idea has not one shred of evidence or precedent even, to support it.

You cannot post anything scientific at all to support your own idea's, then you dare to try to tell me to give up an argument i have genuine scientific support for! :roll:

The critical thinkers here are not fooled by you Bryan :wink:

I would also add that whilst my particular theory cannot yet be proven absolutely, there is also no genuine science that can rule it out!

On the other hand, the modern body of evidence is increasingly disproving claims made by the theory you support!!!

I have posted questions to you in this thread concerning this emerging evidence against you, and yet again Bryan the critical thinkers can see you continue to dodge the questions. :roll:


S Foote.

 

[S Foote.]

Michael.

Those links on body hair transplants to scalp are very interesting. How can the old donor dominance idea explain those changes?? :wink:

It would be interesting to know the graft sizes used, as i think this is an important factor in the growth equasion.

S Foote.

 

[michael barry]

Stephen,


The Korean docs that moved head hair to the neck, legs, (and moved some hair to one body part, and then the same hair to another body part) concluded this: "1) The survival rate and growth rate of the transplanted hairs is influenced
by the recipient site.
(2) The cycles of the transplanted hairs may change according to the
recipient area. rather than being fixed by the internal clock of hair
follicles.
(3) The hair growth rate may change immediately after transplantation
according to the recipient site and is maintained afterwards.
(4) The volume of transplanted hair follicles may not change regardless
of the recipient site.
(5) Skin thickness and/or blood vascularity play a role in hair growth and survival


What I take from this Stephen is that moving body hair to one's head will see the growth phase lengthen and the hair itself lengthen. So the hair cycle length is determined by the area of the body the hair is located in. Ive SEEN pictures of body hair that grew to six inches in length on the head. BUT...................The THICKNESS of body hair moved to the head seems to stay the same. Interesting stuff to say the least.

 

[Bryan]

So let's consider the question again in a true scientific way shall we? :roll:

The in-vitro tests clearly show that androgens have no direct effect at all in changing pre-male pattern baldness follicles "into" male pattern baldness follicles.

You keep repeating that statement like a parrot, so I'll give the answer I always do:

No, it doesn't happen overnight in a petri dish.

When pre-existing male pattern baldness follicles are exposed to androgens in-vitro, this then causes TGF beta-1 to be expressed from the male pattern baldness cells.

So TGF beta-1 is not expressed in follicles prior to male pattern baldness on exposure to androgens, but it is after male pattern baldness.

So the scientific question is "what is causing" changes in the cells ability to express TGF beta-1?

We can be damm sure it is not "androgens" that are "causing" this change, or the in-vitro tests would have shown that!

No, we CAN'T be "damn sure" of that, because it doesn't happen overnight. If it happens at all, it might take YEARS.

So it is "NOT" specificaly the role of androgens that is important, "BUT" the change in the follicle cells ability to express TGF beta-1.

In the sense that androgens are a requirement and a prerequisite for balding, they sure as hell ARE important. Theoretically, we could stop balding if we knew how to stop the expression of TGF beta-1 (and perhaps other agents) in response to androgens, but we don't know how to do that yet.

I have provided a demonstrated, recognised pathway by which prior contact inhibition "COULD" cause changes in the cells ability to express TGF beta-1 in response to external influences, including androgens!!!

No you haven't. You haven't provided any evidence at all showing that contact inhibition changes the way cells respond to androgens. I'm shocked that you keep repeating that garbage. Just finding one some specific substance that _may_ be involved in both contact inhibition and balding follicles doesn't say a damned thing about whether contact inhibition alters the cellular response to androgens.

But no, this is not good enough for you Bryan!

Which is strange given your own on the record explaination for this "change" Bryan!

According to you, the change in androgen response is due to androgens themselves changing the follicle response over time. This genetic "clock" idea has not one shred of evidence or precedent even, to support it.

I never said that it did. As I've told you REPEATEDLY, those are just hypotheses.

You cannot post anything scientific at all to support your own idea's, then you dare to try to tell me to give up an argument i have genuine scientific support for! :roll:

ROTFLMFAO!!!

I don't know if you remember, but this specific issue started a long time ago when you first criticized ME for not really being able to explain what causes the "transformation" of scalp hair follicles during/after puberty. So I responded by saying, well, neither do YOU! :wink: And you've been in a tizzy ever since, trying to make us all believe that "contact inhibition" can cause that change in hair follicle cells, with absolutely no scientific evidence for it whatsoever. You're just making a fool out of yourself, Stephen.

I would also add that whilst my particular theory cannot yet be proven absolutely, there is also no genuine science that can rule it out!

On the other hand, the modern body of evidence is increasingly disproving claims made by the theory you support!!!

Like what? That Korean transplant stuff that intrigues you so? I'll have more to say about that in a separate post after this one.

I have posted questions to you in this thread concerning this emerging evidence against you, and yet again Bryan the critical thinkers can see you continue to dodge the questions. :roll:

Not only do I not dodge your questions, I have answered many of them REPEATEDLY! :wink:

Bryan

 

[Armando Jose]

(3) The hair growth rate may change immediately after transplantation
according to the recipient site and is maintained afterwards.

I would also add that thickness don't change, only the duration-lenght of hairs. I don't know what would happen in the possible next hair cycle.

Armando

 

[Armando Jose]

S Foote. wrote:
When pre-existing male pattern baldness follicles are exposed to androgens in-vitro, this then causes TGF beta-1 to be expressed from the male pattern baldness cells.

So TGF beta-1 is not expressed in follicles prior to male pattern baldness on exposure to androgens, but it is after male pattern baldness.

So the scientific question is "what is causing" changes in the cells ability to express TGF beta-1?

We can be damm sure it is not "androgens" that are "causing" this change, or the in-vitro tests would have shown that!

Bryan wrote:
No, we CAN'T be "damn sure" of that, because it doesn't happen overnight. If it happens at all, it might take YEARS.


Then, how is possible develope common baldness in teenageers? Current theory talks about the impact of androgens only after puberty.

Possibly my idea of the existence of androgens a lot years befor puberty in the neighboring scalp pilosebaceous unit is right.

Armando

 

[S Foote.]

So let's consider the question again in a true scientific way shall we? :roll:

The in-vitro tests clearly show that androgens have no direct effect at all in changing pre-male pattern baldness follicles "into" male pattern baldness follicles.

You keep repeating that statement like a parrot, so I'll give the answer I always do:

No, it doesn't happen overnight in a petri dish.

[quote="S Foote.":e5ce6]When pre-existing male pattern baldness follicles are exposed to androgens in-vitro, this then causes TGF beta-1 to be expressed from the male pattern baldness cells.

So TGF beta-1 is not expressed in follicles prior to male pattern baldness on exposure to androgens, but it is after male pattern baldness.

So the scientific question is "what is causing" changes in the cells ability to express TGF beta-1?

We can be damm sure it is not "androgens" that are "causing" this change, or the in-vitro tests would have shown that!

No, we CAN'T be "damn sure" of that, because it doesn't happen overnight. If it happens at all, it might take YEARS.

So it is "NOT" specificaly the role of androgens that is important, "BUT" the change in the follicle cells ability to express TGF beta-1.

In the sense that androgens are a requirement and a prerequisite for balding, they sure as hell ARE important. Theoretically, we could stop balding if we knew how to stop the expression of TGF beta-1 (and perhaps other agents) in response to androgens, but we don't know how to do that yet.

I have provided a demonstrated, recognised pathway by which prior contact inhibition "COULD" cause changes in the cells ability to express TGF beta-1 in response to external influences, including androgens!!!

No you haven't. You haven't provided any evidence at all showing that contact inhibition changes the way cells respond to androgens. I'm shocked that you keep repeating that garbage. Just finding one some specific substance that _may_ be involved in both contact inhibition and balding follicles doesn't say a damned thing about whether contact inhibition alters the cellular response to androgens.

But no, this is not good enough for you Bryan!

Which is strange given your own on the record explaination for this "change" Bryan!

According to you, the change in androgen response is due to androgens themselves changing the follicle response over time. This genetic "clock" idea has not one shred of evidence or precedent even, to support it.

I never said that it did. As I've told you REPEATEDLY, those are just hypotheses.

You cannot post anything scientific at all to support your own idea's, then you dare to try to tell me to give up an argument i have genuine scientific support for! :roll:

ROTFLMFAO!!!

I don't know if you remember, but this specific issue started a long time ago when you first criticized ME for not really being able to explain what causes the "transformation" of scalp hair follicles during/after puberty. So I responded by saying, well, neither do YOU! :wink: And you've been in a tizzy ever since, trying to make us all believe that "contact inhibition" can cause that change in hair follicle cells, with absolutely no scientific evidence for it whatsoever. You're just making a fool out of yourself, Stephen.

I would also add that whilst my particular theory cannot yet be proven absolutely, there is also no genuine science that can rule it out!

On the other hand, the modern body of evidence is increasingly disproving claims made by the theory you support!!!

Like what? That Korean transplant stuff that intrigues you so? I'll have more to say about that in a separate post after this one.

I have posted questions to you in this thread concerning this emerging evidence against you, and yet again Bryan the critical thinkers can see you continue to dodge the questions. :roll:

Not only do I not dodge your questions, I have answered many of them REPEATEDLY! :wink:

Bryan[/quote:e5ce6]

This is getting pathetic now :roll:

You continued rants at me are not going to distract people from the real science, despite your repetitions Bryan. :wink:

I can't wait for your attempts to distort the findings of that long term transplantation study 8)

S Foote.

 

[S Foote.]

S Foote. wrote:
When pre-existing male pattern baldness follicles are exposed to androgens in-vitro, this then causes TGF beta-1 to be expressed from the male pattern baldness cells.

So TGF beta-1 is not expressed in follicles prior to male pattern baldness on exposure to androgens, but it is after male pattern baldness.

So the scientific question is "what is causing" changes in the cells ability to express TGF beta-1?

We can be damm sure it is not "androgens" that are "causing" this change, or the in-vitro tests would have shown that!

Bryan wrote:
No, we CAN'T be "damn sure" of that, because it doesn't happen overnight. If it happens at all, it might take YEARS.


Then, how is possible develope common baldness in teenageers? Current theory talks about the impact of androgens only after puberty.

Possibly my idea of the existence of androgens a lot years befor puberty in the neighboring scalp pilosebaceous unit is right.

Armando

With respect Armando i have a question?

If i understand your theory correctly, you claim that sebum flow into the follicle is "plugging" the follicle preventing hair growth right?

If this is true, the sebum pressure would inflate the follicles, they would enlarge.

But we see just the opposite in male pattern baldness, the follicles are miniaturised!

How can your theory explain this?

S Foote.

 

[Bryan]

Michael.

Those links on body hair transplants to scalp are very interesting. How can the old donor dominance idea explain those changes?? :wink:

What exactly do you think it is that it NEEDS to explain, Stephen? You seem to be under the impression that the "old donor dominance idea" assumes that ALL hair growth demonstrates 100% donor dominance in every possible way, but you are wrong. It's specifically male pattern balding which has been convincingly shown to be donor dominant. But if you'd bother to read Orentreich's 1959 paper that first introduced the idea of hair transplants to the world, you'd see that he tested a variety of alopecias and other skin conditions, not just common male pattern balding, and got a variety of different results. Some of them showed donor dominance, some showed recipient dominance, and some seemed to be somewhere in between the two (they showed only partial donor dominance).

So you don't need to feel that your eccentric theory has been in any way vindicated, just because of the body hair-to-scap transplants and the work reported by those Korean docs which did seem to show that the growth of hair transplants is influenced to _some_ degree by the recipient location. I understand that you're so desperate to support your theory that you'll take succor wherever you can find it, but the Korean study is actually pretty small potatoes! :wink:

Bryan

 

[michael barry]

Bryan,

The fact that body hair doesn't enlarge its circumference indicates some fundamental difference between body hair and scalp hair to me (along with the demonstrated fact that DHT _helps_body hair grow). Tissue scaffolds notwithstanding, the body hair would get just as _fat_ as scalp hair if dermal pressure around them were the only difference between the two types of hair.

Head hair on the arm might not grow long, but its still circumferentially fatter than arm hair and retains its color. Thats a problem that Ive read about with the body hair transplants..................the color matching the heads hair.

 

[michael barry]

Cyclosporine in macaque alopecia...............

This abstract describes cyclosporine for dermatitis in the animal, but alopecia was one of the symptoms that got better because of it...[url]http://www.ncbi.nlm.nih.gov/entrez ... query_hl=2[/url]


You know guys, since arthritis is sometimes treated with cyclosporine (and MSM, which is good for arthritis and hair), and some forms of diabetes are also considered autoimmune conditions now (cyclosporine is now used for that in certain circumstances as well), would it be too much of a stretch to consider baldness more of an autoimmune disorder as many docs now do?

I mean, cyclo would help someone not only retain the hair they have (like castration), but probably (like that mouse study indicates and some heart transplant patients have shown) grow more back. Just think too guys (bryan) cyclo is a more delicate immuno suppressant than some stronger ones that we are supposed to have. Thats my own little half-baked hypothesis anyway.

 

[Armando Jose]

S. Foote write:
With respect Armando i have a question?

If i understand your theory correctly, you claim that sebum flow into the follicle is "plugging" the follicle preventing hair growth right?

If this is true, the sebum pressure would inflate the follicles, they would enlarge.

But we see just the opposite in male pattern baldness, the follicles are miniaturised!

How can your theory explain this?

S Foote.

Dear friend;

When sebum plug the follicle, its volumen decrease and its hardness increase.

Armando

 

[Bryan]

When sebum plug the follicle, its volumen decrease

Where'd you get THAT idea, Armando?

By the way, why don't you learn to "quote" other people's text properly? It would make it a lot easier to read your posts.

Bryan

 

[Armando Jose]

Armando Jose wrote:
When sebum plug the follicle, its volumen decrease

Bryan ask:
Where'd you get THAT idea, Armando?


My answer
When sebum is being oxidized, its viscosity increase and its volumen decrease.

Armando

 

[michael barry]

Bryan,

I have read Armando's website a good while ago. What he purports is that wearing your hair short (a buzz cut) sees sebum not ride the hair far enough away from the follicle, and slide back down the hair until the duct where it emerges on the skin gets blocked. Sebum can get rancid (rotten) and plug up the hole there, eventually as the sebaceous gland keeps pumping out sebum, with less "escaping" this hole, some of it flows inward back down into the follicle via the dermal sheath. It then interrupst the flow of stem cells from the arrector pilli-muscle as they make their migration towards the dermal papilla to give new instructions as to when to begin a new anagen phase, etc.

Sebum, getting oxidized and rotten near the papilla, elicits the immune response as the immune systems marker cells which travel the body, looking for invaders, begin to identify it. T-cells show up, and eventually killer cells to I imagine he feels, trying to kill the rotten sebum thats around. This inadvertenly places stress and chemical attack upon the papilla which has some-now-rotten sebum-therein. Keratinocytes are stopped up, etc.

I dont agree with this as Ive seen THOUSANDS of hispanics of various ages (into their forties) who keep the popular hairstyle du jour, the buzz cut, for the past DECADE and not lose their hair. I think the increase in baldness is due to diet (high glycemic index foods) promoting more insulin-resistance and thus increasing the amount of testosterone the adrenal glands produce to deal with the excess insulin. Internal inflammation of tissues is a by product of insulin resistance, so there are more anti-gens in the body also. A lessening of native diets in the East (less soy, green tea, rice <beta sitosterol in that>, veggies, and fruits) and less avacodo in the Western Hemisphere <lots of beta sis in that too> might see an uptick in earlier baldness and more prostate, acne problems also in my opinion. I do not think the Japanese are losing their hair more now due to haircuts. If anything, I think their hairlengths have gotten longer since the 1930's.

 

[michael barry]

Stephen,

This article http://www.blackwell-synergy.com/doi/ab ... 2.110606.x at Blackwell-Synergy describes Proanthocyanidins from barley extract (B3) as able to "Procyanidin B-3, isolated from barley and identified as a hair-growth stimulant, has the potential to counteract inhibitory regulation by TGF-β1"

TGF-Beta 1 is the pathway that you suggests converts scalp hair to being sesitive to androgens directly by when contact inhibiton via heightened fluid levels sqeezes the papilla's cells enough.

Do you have an observation on this? Think the ol' beer and eggs shampoo might have been even better than we knew perhaps? I noticed that Loren Pickart puts barley and hops in his shampoo. Interesting that.






A word on the good Doctor (Pickart). His suggestions on his site are to use 2% minoxidil, folligen 4 to 5 days a week (a 47$ bottle should last 6 months doing this at least), and to put a small coat of emu, fortified with Saw Palmetto oil on to push down the folligen.

Internally, he suggest flaxseed oil (anti-inflammatory), MSM, and either saw palmetto oil extract, nettles, pygeum, soy isoflavones, or propecia as the internal anti-androgen.

Thats an affordable regimine that has internal DHT anti-androgens, and external anti-androgen, a tissue remodelling agent (peptides with the emu), growth stimulation (minoxidil, and his shampoo includes barley proanthocyanidins). Pretty good stuff, and you only buy the folligen from him. You can get everything else elsewhere. Pickart always struck me as honest. I really think he believes the above gives about as much help as you can get for a reasonable price. He seems like he is square on that at this stage in his life (late 60's) and he isnt trying to make a fortune of the hairloss sufferers.

 

[S Foote.]

Michael.

Those links on body hair transplants to scalp are very interesting. How can the old donor dominance idea explain those changes?? :wink:

What exactly do you think it is that it NEEDS to explain, Stephen? You seem to be under the impression that the "old donor dominance idea" assumes that ALL hair growth demonstrates 100% donor dominance in every possible way, but you are wrong. It's specifically male pattern balding which has been convincingly shown to be donor dominant. But if you'd bother to read Orentreich's 1959 paper that first introduced the idea of hair transplants to the world, you'd see that he tested a variety of alopecias and other skin conditions, not just common male pattern balding, and got a variety of different results. Some of them showed donor dominance, some showed recipient dominance, and some seemed to be somewhere in between the two (they showed only partial donor dominance).

So you don't need to feel that your eccentric theory has been in any way vindicated, just because of the body hair-to-scap transplants and the work reported by those Korean docs which did seem to show that the growth of hair transplants is influenced to _some_ degree by the recipient location. I understand that you're so desperate to support your theory that you'll take succor wherever you can find it, but the Korean study is actually pretty small potatoes! :wink:

Bryan

Well no Bryan!

The korean study aside for a moment, (i for one would like to read the full study), you have a more "direct" problem :wink:

The body hair to scalp transplants in commercial use, are using what you claim to be androgen dependent hair!

This is chest hair or hair from other areas that grew in response to androgens. The donor dominance idea you support, clearly claims that this should retain its androgen driven growth characteristic when transplanted to other areas.

But it doesn't does it as Michael has linked :wink:

So the old donor dominance idea's are simply wrong on this count alone 8)

S Foote.

 

[S Foote.]

Bryan,

The fact that body hair doesn't enlarge its circumference indicates some fundamental difference between body hair and scalp hair to me (along with the demonstrated fact that DHT _helps_body hair grow). Tissue scaffolds notwithstanding, the body hair would get just as _fat_ as scalp hair if dermal pressure around them were the only difference between the two types of hair.

Head hair on the arm might not grow long, but its still circumferentially fatter than arm hair and retains its color. Thats a problem that Ive read about with the body hair transplants..................the color matching the heads hair.

Again Michael the size of graft could be important in this, and the healing conditions.

It would be interesting if they tried human body hair transplantation in immuno mice? What would we see then?

S Foote.

 

[S Foote.]

Stephen,

This article http://www.blackwell-synergy.com/doi/ab ... 2.110606.x at Blackwell-Synergy describes Proanthocyanidins from barley extract (B3) as able to "Procyanidin B-3, isolated from barley and identified as a hair-growth stimulant, has the potential to counteract inhibitory regulation by TGF-β1"

TGF-Beta 1 is the pathway that you suggests converts scalp hair to being sesitive to androgens directly by when contact inhibiton via heightened fluid levels sqeezes the papilla's cells enough.

Do you have an observation on this? Think the ol' beer and eggs shampoo might have been even better than we knew perhaps? I noticed that Loren Pickart puts barley and hops in his shampoo. Interesting that.

I think the TGF beta-1/ androgen thing, is only an in-vitro consideration. I seriously don't think this is the mechanism of androgen miniaturisation of follicles in-vivo. I also don't think this pathway "keeps" male pattern baldness follicles miniaturised.

Simply because if it was, the human male pattern baldness follicles transplanted to those immuno mice would have remained miniaturised.

Someone really should do a lot more experimentation with that type of mice and human follicles. We could move forward alot in understanding human hair growth then in my opinion.

As an avid "real ale" person (i used to brew my own beer from the grain), i am all for any such treatment Michael :lol: :lol:

S Foote.