For bryan and Foote.

[Bryan]

But you have to remember Michael, that these in-vitro studies are not in any way "safe". The cell's themselves are significantly mutated by the culturing as i have pointed out.

As I clearly explained to you in a previous post, an important aspect of Sawaya's study is that the WHOLE follicles were cultured, not individual cells, and there wasn't any need to "transfect" additional androgen receptors, thus making moot one of your previous objections.

That in-vivo mouse study, is probably the most important in a long time. It clearly refutes the assumptions of "ALL" the in-vitro studies, and shows the danger of making such assumptions in science.

This study of "genuine" male pattern baldness follicles in a "real" mammalian dermal system, completely destroys the current theory, "and" the old donor dominance idea. It clearly proves androgens do "NOT" directly restrict male pattern baldness follicles, in fact these follicles thrive!

As I also clearly explained to you before, it didn't prove any such thing. The level of androgens in those mice wasn't established at all, so there's no point in speculating about it in that study.

There is no evidence at all for any kind of androgen "marking" of follicles for some kind of immune response. In the genuine cases of auto-immune attacks, the "targeted" cells are destroyed! This is what immune responses do! This isn't happening in male pattern baldness.

Oh, so you believe in the "Law of the Excluded Middle", do you, Stephen? There's no middle-ground at all? It's only one extreme or the other? :wink:

In fact macaque studies show male pattern baldness does not "need" any immune involvement at all!

http://www.hairsite4.com/dc/dcboard.php ... ting_type=

Hey, I'm delighted that at the very least you admit that macaque balding is even MORE exclusively associated with the negative effects of androgens than human balding! :wink:

Bryan

 

[S Foote.]

But you have to remember Michael, that these in-vitro studies are not in any way "safe". The cell's themselves are significantly mutated by the culturing as i have pointed out.

As I clearly explained to you in a previous post, an important aspect of Sawaya's study is that the WHOLE follicles were cultured, not individual cells, and there wasn't any need to "transfect" additional androgen receptors, thus making moot one of your previous objections.

So why did real "in-vivo" male pattern baldness follicles in the mouse study, not "directly" respond to androgens as Sawaya's study predicted they should Bryan?

I'am still waiting for your excuse?

That in-vivo mouse study, is probably the most important in a long time. It clearly refutes the assumptions of "ALL" the in-vitro studies, and shows the danger of making such assumptions in science.

This study of "genuine" male pattern baldness follicles in a "real" mammalian dermal system, completely destroys the current theory, "and" the old donor dominance idea. It clearly proves androgens do "NOT" directly restrict male pattern baldness follicles, in fact these follicles thrive!

As I also clearly explained to you before, it didn't prove any such thing. The level of androgens in those mice wasn't established at all, so there's no point in speculating about it in that study.

Now you have "REALLY" blown your credibility, and clearly shown everyone reading this how you twist things to suit your particular argument of the "day"!!!!

I will answer your point with your "OWN" answer to the "SAME" question in your original thread about that study, quote:

--------------------------------------------------------------------------------
Originally posted by: daytona
Could it be that these transplanted vellous hairs recovered to terminal hairs because of the lack of DHT present and not due to an absence of an immune response?
--------------------------------------------------------------------------------


"You're forgetting this important line from the study: "The regeneration of vellus follicles occurs just as quickly on male as on female mice (data not shown); this suggests that a factor or factors other than androgen withdrawal may be involved..."

Furthermore, men with prostate cancer who undergo total androgen ablation with castration and flutamide don't experience dramatic hair regrowth.

Bryan "


You have just finished off any last remaining scientific credibility you had Bryan :wink:

There is no evidence at all for any kind of androgen "marking" of follicles for some kind of immune response. In the genuine cases of auto-immune attacks, the "targeted" cells are destroyed! This is what immune responses do! This isn't happening in male pattern baldness.

Oh, so you believe in the "Law of the Excluded Middle", do you, Stephen? There's no middle-ground at all? It's only one extreme or the other? :wink:

No Bryan, i believe in proper scientific evidence for such claims, and there isn't any!

If you have any post it instead of all this amatuer "guesswork"!

In fact macaque studies show male pattern baldness does not "need" any immune involvement at all!

http://www.hairsite4.com/dc/dcboard.php ... ting_type=

Hey, I'm delighted that at the very least you admit that macaque balding is even MORE exclusively associated with the negative effects of androgens than human balding! :wink:

Bryan

Well of course it is Bryan!!

But the negative scalp effects of androgens in macaques or humans, are certainly "NOT" direct as you try to claim against overwhelming evidence to the contrary!

All the evidence clearly points to an "indirect" action of androgens in male pattern baldness, as i have said all along!

So again Bryan, tell us all how that mouse study supports your "direct action of androgens" claim in this thread? I'am still waiting! :roll:

S Foote.

 

[Bryan]

http://www.stophairlossnow.co.uk/News/News143.htm[/url]

http://www.ncbi.nlm.nih.gov/entrez/quer ... t=Abstract[/quote:276ca]

ROTFLMFAO!!!!

Is that the best you can do, Stephen? Find a couple of studies, one of which is about hair follicle formation, and the other briefly mentions "contact inhibition" in its text, and both studies share a mention of one substance (beta catenin), so THAT is how you try to link male pattern baldness with contact inhibition?? LOL!!!

Sometimes I really do feel sorry for you. Seriously.

Bryan

 

[S Foote.]

http://www.stophairlossnow.co.uk/News/News143.htm[/url]

http://www.ncbi.nlm.nih.gov/entrez/quer ... t=Abstract

ROTFLMFAO!!!!

Is that the best you can do, Stephen? Find a couple of studies, one of which is about hair follicle formation, and the other briefly mentions "contact inhibition" in its text, and both studies share a mention of one substance (beta catenin), so THAT is how you try to link male pattern baldness with contact inhibition?? LOL!!!

Sometimes I really do feel sorry for you. Seriously.

Bryan[/quote:ff9f0]

Yeah right :roll:

I said those were for starters Bryan, i have neither the time or the inclination to educate you in proper scientific reasoning.

Besides which, i have already posted that a "real" hands on researcher has confirmed that contact inhibition is a reality in this context.

So you keep on ranting Bryan, it doesn't mean squat in reality. Everyone now knows your just a lot of ignorant talk, or you would have answered my points on the mouse study by now :roll: :wink:

Its Friday night, and i'am outa here 8)

S Foote.

 

[Aplunk1]

Instead of "for starters," why don't you post some actual material that we can read. I want to see some of these findings.

 

[Bryan]

I said those were for starters Bryan, i have neither the time or the inclination to educate you in proper scientific reasoning.

Oh-oh....I think everybody knows what THAT means: we aren't gonna see any real evidence for the involvement of "contact inhibition" in male pattern baldness! :wink:

Bryan

 

[Bryan]

So why did real "in-vivo" male pattern baldness follicles in the mouse study, not "directly" respond to androgens as Sawaya's study predicted they should Bryan?

I've already explained to you several times: maybe the levels of androgens in those mice (both male and female) were too small to have a significant negative effect, or perhaps the total lack of any immune response completely overwhelmed a relatively small negative androgenic effect. We don't really know too much about any of that, because the androgen levels weren't measured. It's all pretty speculative.

Now you have "REALLY" blown your credibility, and clearly shown everyone reading this how you twist things to suit your particular argument of the "day"!!!!

I will answer your point with your "OWN" answer to the "SAME" question in your original thread about that study, quote:

--------------------------------------------------------------------------------
Originally posted by: daytona
Could it be that these transplanted vellous hairs recovered to terminal hairs because of the lack of DHT present and not due to an absence of an immune response?
--------------------------------------------------------------------------------

"You're forgetting this important line from the study: "The regeneration of vellus follicles occurs just as quickly on male as on female mice (data not shown); this suggests that a factor or factors other than androgen withdrawal may be involved..."

Furthermore, men with prostate cancer who undergo total androgen ablation with castration and flutamide don't experience dramatic hair regrowth.

Bryan "

You have just finished off any last remaining scientific credibility you had Bryan :wink:

I don't know how many times I have to explain this to you, but here we go again: we don't KNOW what the levels of androgens in either the male or female mice were, so all this is pretty speculative. The one thing that _does_ seem fairly certain is that there is an immune component to human balding, as Dr. Proctor has been saying for many years.

Bryan

 

[michael barry]

Stephen,
The Almighty God of Hairloss's post on macaque balding where he quotes Dr. Uno's research indicates that Macaque balding is purely androgen driven.

TAGHL states that "We know that macaques respond more favorably to baldness treatments than humans do (especially to antiandrogen treatments). And we know the response rate among macaques is remarkably consistent; i.e., they all get similar results (in contrast to humans, where we see greatly varying results among individuals). So, why do macaques get better and more consistent results? because macaque baldness IS PURELY A GENETIC AND ANDROGEN-DRIVEN DISEASE."

TAGHL goes on to say that "in macaque abldness, inflammation and fibrosis is ABSENT among ALL macaques (source: Uno's study below). This is a key difference between macaque and human baldness. And since infalmmation generates a slew of potent hair growth inhibitors (IL-1, TNF-alpha, TGF-beta1, etc.) and since fibrosis scars the structure of the follicle itself, this explains the difference in results between humans and macaques." He goes on to cite additional human hair UN-healthy factors like stress, smoking, diets, insulin resistance (which lowers globulin and ups testosterone), etc....


Stephen, maque baldness must be purely androgenic. Since it happens SO fast, perhaps macaques just have too many androgen receptors. TAGHL and Uno have presented enough info for us to dismiss immuno/edema concerns from this type of creature.

I think Bryan's citing of Sawaya's RU58841 study CONCLUSIVELY shown that androgens at least "somewhat weaken" hairs directly. Both of you guys (and me too) dont think male hormone directly kills follicles alone anymore. Bryan believes they (like Dr. Proctor notes with the immune cells clustering in higher than normal numbers around male pattern baldness follicles) directly "mark" the follicle for immune attack. Dr. Richard Lee (of minoxidil.com) said that spironolactone is effective (he believes more effective than finasteride) because it blocks hair's androgen receptors, with which he believes DHT binds to in such a way that gets the immune system to see the follicle as a "foreign body" which it tries to kill.


My impression is that head hair in male pattern baldness people gets weakened a little by androgens (23% protien activity, 12% DNA/RNA)...................................................and then either a immune response or edema finishes off the hairs to where they are vellus hair, and eventually slick baldness.

I wish you both had labs, staffs, and human test subject to work with so you could gain satisfaction in figuring this out. I know its frustrating to have to theoreticize using the scientific record, but its all we have. Have a great weekend, this has been an illuminating thread.

 

[powersam]

the main problem i would have with bryans theory is it does not explain why you only lose the hair on the top of the head. why do those hairs go and not the ones on the side? footes theory in my mind goes some way toward explaining this

the main problem i have with footes theory is why everyone with dht in their system doesnt go bald. if it is due to fluid pressure around the follicle then this pressure would exist in anyone with dht in their system so why do some people lose their hair and others not? bryans theory in my mind goes some way toward explaining this

nb/ i and probably most other people on this forum cannot follow the discussions between you two due to lack of knowledge and i apologise if i've completely missed something or misunderstood altogether

 

[michael barry]

Power Sam,
I believe temporal hair has been shown to have a higher amount of androgen receptors than hair on the back and sides of the head. I know that a variant of the androgen receptor gene discovered by German scientists is present in over 98% of male pattern baldness men that they studied vs. only 76.-something% of non-male pattern baldness men. Its thought among researchers that male pattern baldness involves inheriting 4-5 genes and how they interact among each other.
Tom Hagerty (who I think knows volumes about hair) noted that it is not "theoretical speculation" and "all this can be seen by an electron microscope" referring to the images of "abnormal streamers underneath the follicles appear to be a STRUCTURAL barrier for the DOWN-GROWTH of anagen follicels. Moreover, severe inflammatroy involvement in the streamers causes SUPPRESSIVE growth of the follicular bulb and Dermal papilla cells". ------those micorographic images are availbable in Uno's $160 book THE HISTOPATHOLOGY OF HAIRLOSS which Amazon was out of last time I checked (I was gonna buy it).

This certainly looks like a type of PHYSICAL contact inhibiton to me anyway.........stopping the new anagen follicle from getting as fat (thick hair shaft) and diving as deep for a better blood/oxygen supply as it needs to have. Seemingly starting at the temples first, where there are more androgen receptors. NOTE: Stephen thinks the DHT formed in the root sheath of the follicle (where type 2 alpha reductase resides in all of us) and the alpha five reductase type 1 that is in the sebocytes of the skin and the sebaceous glands must get made, and much of it not only bind with DP receptor sites, but "fall down" to the lymphatic node pumps, and screw up the plumbing in your scalp......causing a mild pitting edema there, thats just enough to cause the conditions described in the above paragraph. Im pretty much assuming that according to Stephen's theory, Dutasteride would be quite a bit better for hairloss than Propecia would beacuse Propecia claims to stop 65-70% of serum DHT, and (according to Merk's OWN literature 38% of scalp DHT......although Bryan has noted other studies show it to be much higher than that), Dutasteride gets something like 90% of blood DHT and Glaxo-Smith-Kline claims 58% of scalp DHT.........which may be much higher than that also.

I wish I knew of a substance that would rid the scalp of Testosterone.....I dont think we need it up there. I know spironolactone inhibits T formation, but for only the 4 hours or so after application. Ive been telling guys for a while that I think taking propecia, and topically applying sprio twice a day would be a safe way to cut androgen transcription by a big amount on their heads and to apply prox-n (I checked with proctor and he said this is OK) for an approach thats effective and really cheap if you buy Indian Proscar from Genhair, make your own spironolactone, and buy prox-n. Hell, thats not 40 bucks a month for all of it........not bad ; ).

 

[S Foote.]

Instead of "for starters," why don't you post some actual material that we can read. I want to see some of these findings.

What i am arguing here is not so much specific research about contact inhibition in male pattern baldness, but the basic fact that "ALL" normal cell growth "IS" limited "BY" contact inhibition. The only cells that do not stop multipying in response to "pressure" from surrounding cells, are cancer cells.

The link i posted to Fuchs work, described the effects in mice of manipulating certain molecular pathways, Wnt's and Beta catenin. These allowed increased follicle size and increased hair growth. These mice also developed tumors!

Although we don't know all the details of the mechanisms involved in contact inhibition, we do know that both Wnt's and beta catenin are involved!

Hair follicles are unique in that they are the only organ in the body that goes through a shrinkage and re-enlargement process, (the hair cycle).

When follicles shrink in the resting phase, they give up the space in the dermal tissue they occupied in the anagen phase. The dermal cells move into this space. When the follicle again enters the growth phase, it has to push these dermal cells out of the way.

Any increase in the resistence to this of the dermal cells, "MUST" result in a smaller anagen follicle through normal contact inhibition.

There is one clear example of contact inhibition in follicle growth , i will refer to this in my reply to Bryan.

S Foote.

 

[S Foote.]

I said those were for starters Bryan, i have neither the time or the inclination to educate you in proper scientific reasoning.

Oh-oh....I think everybody knows what THAT means: we aren't gonna see any real evidence for the involvement of "contact inhibition" in male pattern baldness! :wink:

Bryan

You have already seen this evidence for yourself Bryan, but it seems you are just to dumb to understand it. :roll:

Here it is again from that Uno post i linked before.

http://www.hairsite4.com/dc/dcboard.php ... ting_type=

Quote:


"In alopecia skin, tha abnormal streamers underneath the follicles appear to be a structural barrier for the down-growth of anagen follicles. "

So what physiological factor is preventing these follicles from just "forcing" past this physical barrier Bryan?

It's called the "normal contact inhibition" of cell growth Bryan. :wink:

S Foote.

 

[S Foote.]

So why did real "in-vivo" male pattern baldness follicles in the mouse study, not "directly" respond to androgens as Sawaya's study predicted they should Bryan?

I've already explained to you several times: maybe the levels of androgens in those mice (both male and female) were too small to have a significant negative effect, or perhaps the total lack of any immune response completely overwhelmed a relatively small negative androgenic effect. We don't really know too much about any of that, because the androgen levels weren't measured. It's all pretty speculative.

[quote="S Foote.":b2546]Now you have "REALLY" blown your credibility, and clearly shown everyone reading this how you twist things to suit your particular argument of the "day"!!!!

I will answer your point with your "OWN" answer to the "SAME" question in your original thread about that study, quote:

--------------------------------------------------------------------------------
Originally posted by: daytona
Could it be that these transplanted vellous hairs recovered to terminal hairs because of the lack of DHT present and not due to an absence of an immune response?
--------------------------------------------------------------------------------

"You're forgetting this important line from the study: "The regeneration of vellus follicles occurs just as quickly on male as on female mice (data not shown); this suggests that a factor or factors other than androgen withdrawal may be involved..."

Furthermore, men with prostate cancer who undergo total androgen ablation with castration and flutamide don't experience dramatic hair regrowth.

Bryan "

You have just finished off any last remaining scientific credibility you had Bryan :wink:

I don't know how many times I have to explain this to you, but here we go again: we don't KNOW what the levels of androgens in either the male or female mice were, so all this is pretty speculative. The one thing that _does_ seem fairly certain is that there is an immune component to human balding, as Dr. Proctor has been saying for many years.

Bryan[/quote:b2546]

But everyone here can see that was "NOT" your opinion in your original posting of that study Bryan :roll:

How do you expect to be taken seriously when you so obviously change your opinions depending on your arguments in different threads :roll: :roll:

You are getting pathetic here Bryan. There was certainly no immune component in the in-vitro studies, "YOU" claimed in this very thread "PROVED" the in-vivo effect of androgens! So trying to claim that now, is just showing everyone your desperation to try to rescue some personal credibility. :wink:


S Foote.

 

[S Foote.]

Stephen,
The Almighty God of Hairloss's post on macaque balding where he quotes Dr. Uno's research indicates that Macaque balding is purely androgen driven.

TAGHL states that "We know that macaques respond more favorably to baldness treatments than humans do (especially to antiandrogen treatments). And we know the response rate among macaques is remarkably consistent; i.e., they all get similar results (in contrast to humans, where we see greatly varying results among individuals). So, why do macaques get better and more consistent results? because macaque baldness IS PURELY A GENETIC AND ANDROGEN-DRIVEN DISEASE."

TAGHL goes on to say that "in macaque abldness, inflammation and fibrosis is ABSENT among ALL macaques (source: Uno's study below). This is a key difference between macaque and human baldness. And since infalmmation generates a slew of potent hair growth inhibitors (IL-1, TNF-alpha, TGF-beta1, etc.) and since fibrosis scars the structure of the follicle itself, this explains the difference in results between humans and macaques." He goes on to cite additional human hair UN-healthy factors like stress, smoking, diets, insulin resistance (which lowers globulin and ups testosterone), etc....


Stephen, maque baldness must be purely androgenic. Since it happens SO fast, perhaps macaques just have too many androgen receptors. TAGHL and Uno have presented enough info for us to dismiss immuno/edema concerns from this type of creature.

I think Bryan's citing of Sawaya's RU58841 study CONCLUSIVELY shown that androgens at least "somewhat weaken" hairs directly. Both of you guys (and me too) dont think male hormone directly kills follicles alone anymore. Bryan believes they (like Dr. Proctor notes with the immune cells clustering in higher than normal numbers around male pattern baldness follicles) directly "mark" the follicle for immune attack. Dr. Richard Lee (of minoxidil.com) said that spironolactone is effective (he believes more effective than finasteride) because it blocks hair's androgen receptors, with which he believes DHT binds to in such a way that gets the immune system to see the follicle as a "foreign body" which it tries to kill.


My impression is that head hair in male pattern baldness people gets weakened a little by androgens (23% protien activity, 12% DNA/RNA)...................................................and then either a immune response or edema finishes off the hairs to where they are vellus hair, and eventually slick baldness.

I wish you both had labs, staffs, and human test subject to work with so you could gain satisfaction in figuring this out. I know its frustrating to have to theoreticize using the scientific record, but its all we have. Have a great weekend, this has been an illuminating thread.

Michael.

That mouse study, was the perfect test of "ALL" the claims of Bryan relating to the in-vitro studies.

All the proposed "direct" effects of androgens were completely refuted by this study, end of story!

There was "NO" immunology in the test tube, and "NO" immunology in these mice. So nothing at all to fudge the issue.

Androgens did "NOT AT ALL DIRECTLY" restrict the in-vivo growth of male pattern baldness follicles, as Bryan claimed in this thread!

Nothing else reported in test tube experiments, means squat in offering any "percieved" suppport to the current theory in the light of this in-vivo study, simple.

You say quote:

"Stephen, maque baldness must be purely androgenic. Since it happens SO fast, perhaps macaques just have too many androgen receptors. TAGHL and Uno have presented enough info for us to dismiss immuno/edema concerns from this type of creature. "

No Michael, the lack of what is classed as clinical edema, doesn't mean there is no increase in tissue fluid pressure!

Even in humans that develope immunology related to edema, you could not classify the bald area as clinicaly edemous.

It's just a matter of the degree of pressure in the tissue.

S Foote.

 

[S Foote.]

the main problem i would have with bryans theory is it does not explain why you only lose the hair on the top of the head. why do those hairs go and not the ones on the side? footes theory in my mind goes some way toward explaining this

the main problem i have with footes theory is why everyone with dht in their system doesnt go bald. if it is due to fluid pressure around the follicle then this pressure would exist in anyone with dht in their system so why do some people lose their hair and others not? bryans theory in my mind goes some way toward explaining this

nb/ i and probably most other people on this forum cannot follow the discussions between you two due to lack of knowledge and i apologise if i've completely missed something or misunderstood altogether

The difference in individuals according to my theory, is not the level of DHT but the blood pressure feeding the scalp.

I suggest a certain level of DHT will reduce lymphatic drainage from the male pattern baldness area. But if the individual has a lower blood pressure "feed" to the scalp, this would not cause edema.

However, if an individual has a higher blood pressure, this would increase the chance of DHT causing scalp edema through reduced drainage of this higher fluid "feed" rate.


Thats the "genetic" difference according to my theory.

S Foote.

 

[Bryan]

the main problem i would have with bryans theory is it does not explain why you only lose the hair on the top of the head. why do those hairs go and not the ones on the side?

Well, that's begging the question. The answer is that the hair on top of your hair goes and not other hair (beard hair, for example) because only the hair on top of your head is androgen-sensitive.

The proper question to ask is this: why are some hairs androgen-sensitive, and others aren't? Nobody knows the answer to that question yet.

Bryan

 

[Bryan]

Power Sam,
I believe temporal hair has been shown to have a higher amount of androgen receptors than hair on the back and sides of the head. I know that a variant of the androgen receptor gene discovered by German scientists is present in over 98% of male pattern baldness men that they studied vs. only 76.-something% of non-male pattern baldness men.

I don't think that's what Sam was referring to. Differences in numbers and types of androgen receptors would help explain the differences in the SEVERITY of the androgenic response, but they don't explain the QUALITATIVE differences in the androgenic response. In other words, they don't explain why androgens stimulate beard hair, but suppress scalp hair.

Bryan

 

[Bryan]

Instead of "for starters," why don't you post some actual material that we can read. I want to see some of these findings.

What i am arguing here is not so much specific research about contact inhibition in male pattern baldness, but the basic fact that "ALL" normal cell growth "IS" limited "BY" contact inhibition.

Thanks for that pearl of wisdom, but now why don't you provide what was actually ASKED of you: evidence that "contact inhibition" is actually involved in male pattern baldness.

Bryan

 

[Bryan]

http://www.hairsite4.com/dc/dcboard.php ... ting_type=[/url]

Quote:

"In alopecia skin, tha abnormal streamers underneath the follicles appear to be a structural barrier for the down-growth of anagen follicles. "

So what physiological factor is preventing these follicles from just "forcing" past this physical barrier Bryan?

It's called the "normal contact inhibition" of cell growth Bryan. :wink:[/quote:934d0]

Yawn.

So explain to us what causes that physical barrier IN THE FIRST PLACE, Stephen! :wink:

BTW, it looks like someone I know is "to dumb" to speak the Queen's English!

Bryan

 

[Aplunk1]

Burn!