For bryan and Foote.

[Footy]

Bryan. In response to the two points being discussed.

The first point about the `oddball' terminal follicles, that can exist in the heart of the male pattern baldness area for long periods. I suspect that there hasn't been any specific research following on from that study you quoted, aimed at answering this question?

From the viewpoint of my theory, this would propose that what is actually `oddball' about these particular follicles, is that they have an exeptionally long anagen phase. This is why they do not miniaturise, as this requires a `re-cycling' as i have explained.

But you are right in thinking Bryan that my theory would be wrong, if it could be shown that these follicles are surviving in the male pattern baldness area through `normal' cycling. So the real question here is are there studies that can `PROVE' that these `odd' follicles are cycling at the same average rate as the male pattern baldness follicles next door?

Stephen, I just dug-out that study again and re-read it, and I misremembered the details of those 'oddball' follicles. Their comments are a little bit vague, but what they seem to be saying is that they found both androgen-sensitive and androgen INsensitive follicles in the occipital region of the scalp, not in the vertex. Sorry I screwed-up on that particular detail!

However, that still doesn't let your theory off the hook. You still have no really good way of explaining why some follicles in a particular geographic region of the scalp show the effects of contact inhibition, while others do not. The only tentative explanation you have is (once again) that the alleged "edema" sets in at some midpoint between cycles of those follicles. That hypothesis obviously doesn't work for someone who's been balding for a long period of time.

No Bryan, that is not what i said. :roll:

The build up in fluid pressure can take a long time itself. It is quite clearly not something that happens instantly. This combined with the long anagen period, explains the thinning and recession we see in male pattern baldness. This senario also explains the gradual shortening of male pattern baldness hairs over more than one cycle, the pressure and so resistence to anagen enlargement increases with time.

You don't agree and thats fine. Again we had just better agree to disagree Bryan. :lol:

But these observations do put a big hole in the `direct' theory you support Bryan???????????????????

How can any `direct' mechanism of androgen induced follicle miniaturisation, create this `GRADUAL' miniaturisation over more than one cycle?

If as you claim, androgens are directly interacting with genetic expression within follicle cells to effect growth, this would be an instant effect! The androgen induced change in gene expression you claim causes male pattern baldness, is either on or off! There is just no room in your theory for miniaturisation over more than one cycle!

Please divert, sorry i mean explain?? :wink:

As far as the current theory you support goes Bryan, this particular study `again' shows that androgens do not `DIRECTLY' convert non male pattern baldness follicles into male pattern baldness follicles, which is the very heart of this theory!!

How does it show that? Please explain.

I based that on your now accepted error above, in regard to that study.

You ask me to provide evidence for the time line i claim rules out hypoxia, as the cause of this hair loss. Here it is!

There is one other factor that occours in transplanted grafts, this was even noted by Nordstrom in the study you posted Bryan! It is this factor that proves a timeline that rules out hypoxia as the cause of the `doughnutting' hair loss.

This is a quote from that Nordstrom study out of the results section.

"The hairs in the hair-bearing grafts gradually fell off over a couple of weeks and started to grow again after about 3 months as is normally seen in punch hair grafting.

5, 10 and 21 months after transplantation the numbers of hairs in the transplants were counted. The grafts were then excised for histological examination. In the graft taken from the occipital region the number and macroscopical quality of the hairs remained unchanged"

The initial `shock' hair loss in grafts is a fact, and normally seen as Nordstrom said.

Nordstrom also confirms the common observation that there is around a 3 month period before hair in these grafts starts growing again.

Any conditions of oxygen starvation (hypoxia) in these grafts will be well established before 3 months, so the regrowing hair should reflect this by growing back with this `doughnutting' pattern of loss in the centre.

But as Nordstrom noted, this didn't happen! In fact he reports above that even after 21 months the terminal hair bearing occipital graft, showed `NO' loss!

You are very subtly MISINTERPRETING what Nordstrom said, and I'm going to explain this to you once and for all so that we can get past this point of confusion! :wink:

Nordstrom only did haircounts at months 5, 10, and 21, and he reported the EXACT numbers for those haircounts. But the only thing those numbers demonstrate is that THERE WAS NO FURTHER LOSS AFTER THE FIFTH MONTH in the graft that came from the non-balding donor area. I'm trying to get you to understand that in my opinion, doughnutting DID occur (and quite possibly caused by hypoxia, just like the medical establishment claims), and it occurred DURING THE FIRST 5 MONTHS. The results of Nordstrom's careful little experiment are perfectly consistent with both the standard medical theory of male pattern baldness, and the real-world observations of "doughnutting".

Do you understand my position, now?

No, no, no Bryan!

Just read all those links i provided you with, about the hair loss patern in grafts called `doughnutting'!

Doughnutting refers to a `permanent' recession of hair from the center of these grafts outward, until there is just hair growth left around the edges!

Are you trying to tell me that this happens within five months? If so Nordstrom and Orentreich would have SEEN it!!

The `balding' in these grafts refered to as `doughnutting', happens over a period `outside' of both Nordstrom and Orentreich's studies, which automaticaly rules out hypoxia! :wink:

I would say this Bryan.

I wish Nordstrom had also transplanted occipital 4mm grafts to the male pattern baldness area in this individual, and followed this up for a few years!

I am willing to bet that the 4mm occipital grafts to the forearm, would `NOT' doughnut over time, but the same grafts to the male pattern baldness area `WOULD'!

This is because i think it is the conditions in the surrounding tissue that determine the fate of large anagen follicles, in the absense of a protective `scaffold'.

Well, at the very least Orentreich did something fairly CLOSE to that. Even though he didn't report specific haircount numbers like Nordstom did, I think he would have noticed if there were a differential effect of the growth rates of the grafts, depending on the recipient site. But his conclusion at the end was unequivocal: "hair to hair" grew hair; "hair to bald" grew hair; "bald to bald" remained bald; and "bald to hair" remained bald.

Bryan

The `BIG' problem you continue to have in quoting these old studies Bryan, is that they did not notice the doughnutting in these grafts that is recognised today!

So yet again Bryan, explain this longer term hair loss according to the theory you support? 8)

S Foote.

 

[Footy]

Dave, listen up.

The problem is, you have yet to raise any specific points regarding my theory you have a problem with?

The problem is that you don't have a theory. It is readily dispensed of by Occam's razor.

Your "Hydraulic Dermal Model" is a complete joke. Your entire "theory" is presented in descriptive lay terminology, and demonstrates no fundamental understanding or knowledge of fluid or hydrodynamics, subjects which cannot be discussed meaningfully in nonmathematical language.

If you want your theory to be taken seriously, tell me where it is presented.

You really are a case Dave :roll:

You are completely full of s**t

You can post all the big words and psuedo scientific phrases you like, but you ain't impressing anyone 8)

I have already posted the link to my paper, and the full text of my letter to experts for you. If you don't understand this, thats your problem. The responses i also posted, at `LEAST' made it clear that professional scientists understood what i said :roll:

I don't think you have the faintest idea what `Ockham's razor' ACTUALLY is!! You can't even spell it properly! :roll: Here's a link to it, read it and learn something :wink:

http://phyun5.ucr.edu/~wudka/Physics7/N ... node5.html

Once you have read this Dave, come back and tell us all how the current theory of male pattern baldness explains `ALL' the related factors in the male pattern baldness scalp, according to Ockhams razor????

I can't wait :wink:

S Foote.

 

[Dave001]

Dave, listen up.

The problem is, you have yet to raise any specific points regarding my theory you have a problem with?

The problem is that you don't have a theory. It is readily dispensed of by Occam's razor.

Your "Hydraulic Dermal Model" is a complete joke. Your entire "theory" is presented in descriptive lay terminology, and demonstrates no fundamental understanding or knowledge of fluid or hydrodynamics, subjects which cannot be discussed meaningfully in nonmathematical language.

If you want your theory to be taken seriously, tell me where it is presented.

You really are a case Dave :roll:

You are completely full of s**t

You can post all the big words and psuedo scientific phrases you like, but you ain't impressing anyone 8)

I have already posted the link to my paper, and the full text of my letter to experts for you. If you don't understand this, thats your problem. The responses i also posted, at `LEAST' made it clear that professional scientists understood what i said :roll:

Your paper has many words in it, but says NOTHING. Why don't you provide us all with some entertainment by telling us the where and how you measured the fluid pressure, as well as the values you arrived at. What is the interstitial fluid pressure (heard of Pascal, idiot? Bernoulli?) surrounding the hair follicle? How did you measure it?

Here's an idea: why don't you present your theory in some of the newsgroups in the sci.* hierarchy (e.g., sci.physics, sci.chem, sc.math)? You won't do that because you would instantly be called on your bullshit. Your theory hinges on rheology, which you obviously don't know the FIRST thing about! There's not ONE single equation to accompany your entire theory. You can not bullshit your way in physical chemistry. Sorry pal, but you've tried to cross over into the hard sciences, and you're knee deep in sh*t.

I don't think you have the faintest idea what `Ockham's razor' ACTUALLY is!! You can't even spell it properly! :roll: Here's a link to it, read it and learn something :wink:

Hey moron, "Occam's razor" can be spelled BOTH ways. In fact, my usage is the more frequently used spelling. Ever heard of a dictionary? Congratulations on making yourself look like an even bigger idiot.

Google results for "Ockham's razor": 111,000 hits
"Did you mean: 'Occam's razor'"
"Occam's razor" 167,000 hits


Fool.

 

[Dave001]

Bryan wrote:

Yeah. I wonder if some intrepid soul who is going in for a "follicular-unit" transplant anyway would volunteer to test that for us?? All they'd have to do is have two or three BALDING follicles moved slightly to a new position in the same balding area, and see what happens over the next couple years or so! That wouldn't interfere in any way with the regular transplants being done, and wouldn't add significantly to the cost at all! Any volunteers out there who are about to have transplants done??

Why waste a few grafts?! :wink:

No sh*t. Isn't it scary to think anyone could take this fool seriously? (No offense intended to Bryan, who has already made it clear that the interest is a research project of the driving forces behind the minds of delusional freaks, in somewhat different words :wink

 

[Bryan]

No Bryan, that is not what i said. :roll:

The build up in fluid pressure can take a long time itself. It is quite clearly not something that happens instantly. This combined with the long anagen period, explains the thinning and recession we see in male pattern baldness. This senario also explains the gradual shortening of male pattern baldness hairs over more than one cycle, the pressure and so resistence to anagen enlargement increases with time.

Yes, but you're dodging the issue again: what you said certainly would explain the overall slow progress of balding (assuming your theory were correct in the first place), but THAT AIN'T WHAT I ASKED YOU. I asked you to explain the DIFFERENTIAL EFFECT from one neighboring follicle to another. The only way you can attempt to explain why one follicle supposedly shows the effects of contact inhibition, but not a neighboring one, is to assume that the alleged "pressure" sets in relatively suddenly, in between cycles of those neighboring follicles. You might as well bite the bullet and admit that, Stephen. I'm not going to let you slip out of this.

How can any `direct' mechanism of androgen induced follicle miniaturisation, create this `GRADUAL' miniaturisation over more than one cycle?

If as you claim, androgens are directly interacting with genetic expression within follicle cells to effect growth, this would be an instant effect! The androgen induced change in gene expression you claim causes male pattern baldness, is either on or off! There is just no room in your theory for miniaturisation over more than one cycle!

ROTFLMAO!! I won't even dignify that with a response...

You are very subtly MISINTERPRETING what Nordstrom said, and I'm going to explain this to you once and for all so that we can get past this point of confusion! :wink:

Nordstrom only did haircounts at months 5, 10, and 21, and he reported the EXACT numbers for those haircounts. But the only thing those numbers demonstrate is that THERE WAS NO FURTHER LOSS AFTER THE FIFTH MONTH in the graft that came from the non-balding donor area. I'm trying to get you to understand that in my opinion, doughnutting DID occur (and quite possibly caused by hypoxia, just like the medical establishment claims), and it occurred DURING THE FIRST 5 MONTHS. The results of Nordstrom's careful little experiment are perfectly consistent with both the standard medical theory of male pattern baldness, and the real-world observations of "doughnutting".

Do you understand my position, now?

No, no, no Bryan!

Just read all those links i provided you with, about the hair loss patern in grafts called `doughnutting'!

I have. Several times! :wink:

Doughnutting refers to a `permanent' recession of hair from the center of these grafts outward, until there is just hair growth left around the edges!

Are you trying to tell me that this happens within five months? If so Nordstrom and Orentreich would have SEEN it!!

They probably DID see such an effect. Can you prove they DIDN'T? :wink:

The `balding' in these grafts refered to as `doughnutting', happens over a period `outside' of both Nordstrom and Orentreich's studies, which automaticaly rules out hypoxia! :wink:

Really? Then PROVE IT. Cite me some evidence (I've now requested that evidence from you about a half-dozen times, to no avail).

The `BIG' problem you continue to have in quoting these old studies Bryan, is that they did not notice the doughnutting in these grafts that is recognised today!

How would YOU know?? Prove to me that they didn't notice any doughnutting. And give me a TIMELINE for the doughnutting.

So yet again Bryan, explain this longer term hair loss according to the theory you support? 8)

There apparently WASN'T any hairloss in the long term (after the first 5 months or so). So I guess it all comes down to only one possible explanation which supports your theory: you're accusing Orentreich and Nordstrom of falsifying the results of their studies. I'm not terribly surprised that that's the bottom-line for you.

Bryan

 

[michael barry]

I have some test study questions Im sure someone can answer........


1.> Have in vitro test been performed to see if body hair responds to DHT directly?

2.> When in vitro tests are performed on head hair, and androgen is added to them, and their growth isnt effected, how much of the philosebaceous unit was involved? Was the skin sample large enough to include the arrector pilli and sebaceous gland, the skin surface and enough area under the papilla to include any typical expansion that would occur in early anagen enlargement? Microcapillaries that feed the follicle involved in the test tube also?



I do feel the need to mention to Byran that the guy who had the unsuccessfull transplants had regular male pattern baldness fibrosis and not a fibrosis scaffold as Stephen makes mention of according to his theory. I remember back in 1990 when I went to a Doctor to get on propecia and he told me that new drugs where being developed that would proboably cure baldness that they would only be good for men who were just starting to bald, because for already shiny bald men he said "you cant grow hair on an eggshell". That amused me a bit, but that Doctor claimed that nobody knew why transplants worked either so I didnt take him too seriously as I thought the guy was making more money helping old ladies deal with wrinkles and just seen him as a prescription writer for me.........was funny at the time though, you had to be there.

 

[Bryan]

I have some test study questions Im sure someone can answer........

1.> Have in vitro test been performed to see if body hair responds to DHT directly?

Hmmm.... I'm sure there's a number of them around, but here's an interesting one (albeit somewhat INDIRECT, because the main purpose of it was to test the effects of RU58841 on both scalp hair and body hair): "RU58841, a new therapeutic agent affecting androgen receptor molecular interactions in human hair follicles", M.E. Sawaya, from the book "Hair Research for the Next Millenium", 1996. Here's a fascinating excerpt from this study, showing the differential effects of antiandrogens (and, by extension, androgens themselves) on body hair and beard hair (emphasis added is my own):

"...The study of beard and scalp hair follicles of 6 male donors in longer term culture (up to 14 days) appeared to be an interesting model. The whole follicles were mounted in a collagen matrix. The study revealed significant differences (p<0.005) when the follicles were cultured in DHT (10 nM and 100 nM) in the absence or presence of 1 uM RU58841 added, i.e.:

a) in the presence of RU58841 hair follicle growth rates were found to be increased by 23% for scalp follicles but a 16% decrease was noted in beard follicles.

b) protein, DNA, and RNA polymerase II activity revealed increases in scalp (25%, 12%, and 12% respectively) and respectively equivalent relative decreases in beard hair follicles.

c) thioredoxin reductase activity, a sulfhydryl-reducing enzyme important for keratin protein synthesis, increased by 16% in scalp follicles after 14 days in culture but decreased by 10% in beard hair follicles."

Isn't that really cool?? :lol: Stephen Foote always used to bug me to explain the EXACT ways that androgens affect hair follicles, and above are some examples of the specific ways that androgens (and antiandrogens) have differential effects on scalp hair follicles and body hair follicles.

At the end of the study in the Conclusion section, Sawaya goes on to say: "The model system using human hair follicles from scalp and beard in a 14 days culture system is a novel approach in testing drugs and compounds for their effectiveness in stimulating scalp or inhibiting beard hair growth....other ongoing studies using animal models such as the teady bear hamster, mouse androgenetic alopecia model, and macaque monkey and other human models (see elsewhere in this volume) revealed similar findings with regard to RU58841."

2.> When in vitro tests are performed on head hair, and androgen is added to them, and their growth isnt effected, how much of the philosebaceous unit was involved? Was the skin sample large enough to include the arrector pilli and sebaceous gland, the skin surface and enough area under the papilla to include any typical expansion that would occur in early anagen enlargement? Microcapillaries that feed the follicle involved in the test tube also?

Sure. The 4-mm grafts used by Nordstrom are quite large by today's standards. They got the entire follicle. However, note that Nordstrom removed certain parts in his experiment:

"...The galea aponeurotica and excess fat under the follicles were trimmed away."

He removed the galea, which some people have claimed to be the CAUSE of balding.

I do feel the need to mention to Byran that the guy who had the unsuccessfull transplants had regular male pattern baldness fibrosis and not a fibrosis scaffold as Stephen makes mention of according to his theory.

I understand. In any event, Nordstrom's transplanted balding follicles CONTINUED to bald right on schedule, even with the assistance of the "fibrosis scaffold" that formed as a result. That's the bottom-line! :wink:

Bryan

 

[Old Baldy]

Bryan wrote:

Yeah. I wonder if some intrepid soul who is going in for a "follicular-unit" transplant anyway would volunteer to test that for us?? All they'd have to do is have two or three BALDING follicles moved slightly to a new position in the same balding area, and see what happens over the next couple years or so! That wouldn't interfere in any way with the regular transplants being done, and wouldn't add significantly to the cost at all! Any volunteers out there who are about to have transplants done??

Why waste a few grafts?! :wink:

No sh*t. Isn't it scary to think anyone could take this fool seriously? (No offense intended to Bryan, who has already made it clear that the interest is a research project of the driving forces behind the minds of delusional freaks, in somewhat different words :wink

You know Dave, I asked Stephen what he thought would be a good treatment(s) a while back and his (summarized) answer was to use those things that improve scalp health. His answer for treating male pattern baldness was rational and made sense. You know, reduce inflammation, provide the growth factors, improve blood vessel function, etc.

Obviously I go further with the DHT effect but attempting to stop the ensuing cascade of events was what I took to be Stephen's main thrust. (I could be wrong Stephen - correct me if I remembered your answer erroneously.)

So Dave, although we have problems with Stephen's theory on the cause of male pattern baldness, etc., I couldn't take issue with his suggested treatment(s). (Unless I understood his advice erroneously.)

Doctor Proctor feels factors other than DHT play a MAJOR role in male pattern baldness progression (as I know you know also).

So, in the end, Stephen's suggested treatment(s) are pretty "mainstream". (Unless, as stated, I misunderstood him.)

If I remember correctly, Stephen even believed DHT was the triggering event.

Bryan and Stephen disagree on the cause, (you know, androgen sensitivity versus androgen sensitivity PLUS constriction), I don't know that they are far apart on the treatment aspect? Maybe I'm wrong Dave.

You know, I'm not sure Bryan really disagrees with the androgen sensitivity PLUS constriction theory? I mean, maybe Bryan just feels constriction isn't that influential? Maybe a minor player rather than a major player? Then again, maybe a "no player". :wink:

Vice versa for Stephen's opinion on the effects of androgens.

I think we all agree that those things that improve blood vessel health/function are positives in the fight against male pattern baldness? Well, at least I do.

 

[Footy]

Dave, listen up.

The problem is, you have yet to raise any specific points regarding my theory you have a problem with?

The problem is that you don't have a theory. It is readily dispensed of by Occam's razor.

Your "Hydraulic Dermal Model" is a complete joke. Your entire "theory" is presented in descriptive lay terminology, and demonstrates no fundamental understanding or knowledge of fluid or hydrodynamics, subjects which cannot be discussed meaningfully in nonmathematical language.

If you want your theory to be taken seriously, tell me where it is presented.

You really are a case Dave :roll:

You are completely full of s**t

You can post all the big words and psuedo scientific phrases you like, but you ain't impressing anyone 8)

I have already posted the link to my paper, and the full text of my letter to experts for you. If you don't understand this, thats your problem. The responses i also posted, at `LEAST' made it clear that professional scientists understood what i said :roll:

Your paper has many words in it, but says NOTHING. Why don't you provide us all with some entertainment by telling us the where and how you measured the fluid pressure, as well as the values you arrived at. What is the interstitial fluid pressure (heard of Pascal, idiot? Bernoulli?) surrounding the hair follicle? How did you measure it?

Here's an idea: why don't you present your theory in some of the newsgroups in the sci.* hierarchy (e.g., sci.physics, sci.chem, sc.math)? You won't do that because you would instantly be called on your bullshit. Your theory hinges on rheology, which you obviously don't know the FIRST thing about! There's not ONE single equation to accompany your entire theory. You can not bullshit your way in physical chemistry. Sorry pal, but you've tried to cross over into the hard sciences, and you're knee deep in sh*t.

I don't think you have the faintest idea what `Ockham's razor' ACTUALLY is!! You can't even spell it properly! :roll: Here's a link to it, read it and learn something :wink:

Hey moron, "Occam's razor" can be spelled BOTH ways. In fact, my usage is the more frequently used spelling. Ever heard of a dictionary? Congratulations on making yourself look like an even bigger idiot.

Google results for "Ockham's razor": 111,000 hits
"Did you mean: 'Occam's razor'"
"Occam's razor" 167,000 hits


Fool.

OK bigmouth, enough of your sad posing here :roll:

You raised the principle of Ockhams razor and claimed it refutes my theory. But we are all still waiting for you to tell us `exactly' how Ockhams razor refutes my theory?

I also asked you to tell us how the current theory you support, explains the observations in the male pattern baldness scalp, according to the principles of Ockhams razor???

So instead of just posting all these psuedo scientific phrases you found on Google, just support your claims with some `REAL' science!!!!!!!

You just can't do this, because you are just an attention seeking internet `pretend' scientist!

As if there aren't enough of these on these forums allready :roll: :roll:

S Foote.

 

[Footy]

No Bryan, that is not what i said. :roll:

The build up in fluid pressure can take a long time itself. It is quite clearly not something that happens instantly. This combined with the long anagen period, explains the thinning and recession we see in male pattern baldness. This senario also explains the gradual shortening of male pattern baldness hairs over more than one cycle, the pressure and so resistence to anagen enlargement increases with time.

Yes, but you're dodging the issue again: what you said certainly would explain the overall slow progress of balding (assuming your theory were correct in the first place), but THAT AIN'T WHAT I ASKED YOU. I asked you to explain the DIFFERENTIAL EFFECT from one neighboring follicle to another. The only way you can attempt to explain why one follicle supposedly shows the effects of contact inhibition, but not a neighboring one, is to assume that the alleged "pressure" sets in relatively suddenly, in between cycles of those neighboring follicles. You might as well bite the bullet and admit that, Stephen. I'm not going to let you slip out of this.

OK Bryan, you want to do this the hard way lets do it. I have explained this point to you over and over, it is all related to the long period {many years} of the human hair cycle. Others reading these threads have `got' the point of my argument, but you haven't (apparently)? :wink:

So now i will ask you to show `ME' hard evidence for a specific time period between one follicle starting to bald, and the same effect on follicles `next door'?

You are labouring this here, so `YOU' provide me with `SPECIFIC' time differentials `proven' in specific studies??

How can any `direct' mechanism of androgen induced follicle miniaturisation, create this `GRADUAL' miniaturisation over more than one cycle?

If as you claim, androgens are directly interacting with genetic expression within follicle cells to effect growth, this would be an instant effect! The androgen induced change in gene expression you claim causes male pattern baldness, is either on or off! There is just no room in your theory for miniaturisation over more than one cycle!

ROTFLMAO!! I won't even dignify that with a response...

The simple truth is you `CANNOT' explain this by your theory Bryan and your not fooling anyone here with this response 8)

Doughnutting refers to a `permanent' recession of hair from the center of these grafts outward, until there is just hair growth left around the edges!

Are you trying to tell me that this happens within five months? If so Nordstrom and Orentreich would have SEEN it!!

They probably DID see such an effect. Can you prove they DIDN'T? :wink:

The `balding' in these grafts refered to as `doughnutting', happens over a period `outside' of both Nordstrom and Orentreich's studies, which automaticaly rules out hypoxia! :wink:

Really? Then PROVE IT. Cite me some evidence (I've now requested that evidence from you about a half-dozen times, to no avail).

The `BIG' problem you continue to have in quoting these old studies Bryan, is that they did not notice the doughnutting in these grafts that is recognised today!

How would YOU know?? Prove to me that they didn't notice any doughnutting. And give me a TIMELINE for the doughnutting.

So yet again Bryan, explain this longer term hair loss according to the theory you support? 8)

There apparently WASN'T any hairloss in the long term (after the first 5 months or so). So I guess it all comes down to only one possible explanation which supports your theory: you're accusing Orentreich and Nordstrom of falsifying the results of their studies. I'm not terribly surprised that that's the bottom-line for you.

Bryan

Your continued dancing around a very simple point is just becoming more and more ridiculous Bryan. Your desperate primary interest, in the preservation of some kind of percieved personal `expertise' over the `actual' science, is now clear to everyone :wink:

This is a very clear issue Bryan! If you do a Google search for "hair transplantation doughnutting", all the information you get describes this as a loss of hair growth in larger grafts as used by Nordstrom and Orentreich, untill there is just hair growing around the edges of these grafts.

Now did Nordstrom and Orentreich see this during the period of their respective studies????????

Just cut and paste the text from these studies that shows they observed the type of loss in these grafts, refered to as doughnutting Bryan!!

I recognise Nordstrom and Orentreich as reputable scientists Bryan. If they didn't report `doughnutting' as now recognised by the transplantation industry, we can be sure it didn't happen during the period of their studies!

If it didn't happen in this time frame, the pattern of loss refered to as doughnutting, `CANNOT' be related to conditions of hypoxia induced at the time of the transplantation, simple! :roll:

You are the one who is questioning the expertise of these respected scientists Bryan! You are trying to claim here that `doughnutting' happened early on in these grafts, and these scientists just didn't notice it!

You are not a stupid person Bryan, but it seems you would rather just avoid anything that proves you wrong, than admit the science of the matter. :roll:

S Foote.

 

[Footy]

I have some test study questions Im sure someone can answer........

1.> Have in vitro test been performed to see if body hair responds to DHT directly?

Hmmm.... I'm sure there's a number of them around, but here's an interesting one (albeit somewhat INDIRECT, because the main purpose of it was to test the effects of RU58841 on both scalp hair and body hair): "RU58841, a new therapeutic agent affecting androgen receptor molecular interactions in human hair follicles", M.E. Sawaya, from the book "Hair Research for the Next Millenium", 1996. Here's a fascinating excerpt from this study, showing the differential effects of antiandrogens (and, by extension, androgens themselves) on body hair and beard hair (emphasis added is my own):

"...The study of beard and scalp hair follicles of 6 male donors in longer term culture (up to 14 days) appeared to be an interesting model. The whole follicles were mounted in a collagen matrix. The study revealed significant differences (p<0.005) when the follicles were cultured in DHT (10 nM and 100 nM) in the absence or presence of 1 uM RU58841 added, i.e.:

a) in the presence of RU58841 hair follicle growth rates were found to be increased by 23% for scalp follicles but a 16% decrease was noted in beard follicles.

b) protein, DNA, and RNA polymerase II activity revealed increases in scalp (25%, 12%, and 12% respectively) and respectively equivalent relative decreases in beard hair follicles.

c) thioredoxin reductase activity, a sulfhydryl-reducing enzyme important for keratin protein synthesis, increased by 16% in scalp follicles after 14 days in culture but decreased by 10% in beard hair follicles."

Isn't that really cool?? :lol: Stephen Foote always used to bug me to explain the EXACT ways that androgens affect hair follicles, and above are some examples of the specific ways that androgens (and antiandrogens) have differential effects on scalp hair follicles and body hair follicles.

At the end of the study in the Conclusion section, Sawaya goes on to say: "The model system using human hair follicles from scalp and beard in a 14 days culture system is a novel approach in testing drugs and compounds for their effectiveness in stimulating scalp or inhibiting beard hair growth....other ongoing studies using animal models such as the teady bear hamster, mouse androgenetic alopecia model, and macaque monkey and other human models (see elsewhere in this volume) revealed similar findings with regard to RU58841."

[quote="michael barry":5e4c5]2.> When in vitro tests are performed on head hair, and androgen is added to them, and their growth isnt effected, how much of the philosebaceous unit was involved? Was the skin sample large enough to include the arrector pilli and sebaceous gland, the skin surface and enough area under the papilla to include any typical expansion that would occur in early anagen enlargement? Microcapillaries that feed the follicle involved in the test tube also?

Sure. The 4-mm grafts used by Nordstrom are quite large by today's standards. They got the entire follicle. However, note that Nordstrom removed certain parts in his experiment:

"...The galea aponeurotica and excess fat under the follicles were trimmed away."

He removed the galea, which some people have claimed to be the CAUSE of balding.

I do feel the need to mention to Byran that the guy who had the unsuccessfull transplants had regular male pattern baldness fibrosis and not a fibrosis scaffold as Stephen makes mention of according to his theory.

I understand. In any event, Nordstrom's transplanted balding follicles CONTINUED to bald right on schedule, even with the assistance of the "fibrosis scaffold" that formed as a result. That's the bottom-line! :wink:

Bryan[/quote:5e4c5]

First Bryan, i dont see anything in any of these `ground breaking' studies you keep posting, that show that androgens `CONVERT' the existing growth characteristics of follicles, into a `different' growth characteristic???

This is what the current theory you support `actually' requires, and you just can't come up with without inventing fantasy mechanisms! :wink:

Secondly, you are very well aware that the scaffold principle i have described to you time and time again, states that the formation of such a scaffold will maintain the pre-existing growth characteristics of transplanted follicles. This is consistant with what is currently refered to as `donor dominance' :wink:

Now i have a life outside of these forums, and i am much in demand socially :lol: :lol:

So i probably won't post again till next week :lol:

S Foote.

 

[Bryan]

I think all the relevant information has now been presented by both sides, including the "closing arguments". I'll leave it up to each individual reader here to decide for himself the credibility of your theory! :wink:

Bryan

 

[michael barry]

Here are some articles that were googled from "in vitro and androgen and hair".

joe.endocrinology-journals.org/cgi/content/abstract/156/1/59


ncbi.nlm-gnih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids+7748741&dopt+Abstract



ehrs.org/conferenceabstracts/2003 barcelona/guestlectures/L-17-itami.htm


content.karger.com/ProdukteDB/produckte.asp?

Aktion=showPDF&ProduktNr=220436&Ausgabe=227989&Artiklnr=
53266&filename=53266.pdf


Have got to be honest guys, all of these papers seemed to indicate that basically androgen inception on the dermal papilla makes terminal hairs in the scalp turn to vellus hairs and it makes body hair turn from vellus to terminal hairs, with the exception of one of them which stated that no change was seen in vitro of the scalp follicles. The rest pretty much say they did.

I found one study that supported my little idea, but forgot the address. My idea was that follicles from the temporal and frontal areas of the scalp in balding guys simply have more androgen receptors. THis study pretty much stated than men typically have more androgen receptors in temporal and frontal scalp hair follicles than women do. Thats been my own wild *** guess on baldness pretty much from the start.


When Stephen gets the time, I'd really like to see the in vitro study he has been referring to that witnessed no change in the follicle in a test tube when androgens were added. Bryan has posted studies concerning RU5388, but they only proved that the growth RATE was increased when adding the androgen receptor blocker to head hair. I want to see where it shrinks the follicle to vellus in a study to conclude personally whether or not androgens act directly on hair. If they do, Im pretty much at the end of my yellow brick road of studying hair loss as thats whats garnered my interest in a few alternative theories of baldness.

 

[Bryan]

Here are some articles that were googled from "in vitro and androgen and hair".

joe.endocrinology-journals.org/cgi/content/abstract/156/1/59

ncbi.nlm-gnih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids+7748741&dopt+Abstract

ehrs.org/conferenceabstracts/2003 barcelona/guestlectures/L-17-itami.htm
content.karger.com/ProdukteDB/produckte.asp?

Aktion=showPDF&ProduktNr=220436&Ausgabe=227989&Artiklnr=
53266&filename=53266.pdf

Excuse me, Michael, but didn't you notice that those aren't legitimate links?? :wink:

Have got to be honest guys, all of these papers seemed to indicate that basically androgen inception on the dermal papilla makes terminal hairs in the scalp turn to vellus hairs and it makes body hair turn from vellus to terminal hairs, with the exception of one of them which stated that no change was seen in vitro of the scalp follicles. The rest pretty much say they did.

Yep. The total body of evidence is overwhelmingly in support of the standard medical view of balding.

I found one study that supported my little idea, but forgot the address. My idea was that follicles from the temporal and frontal areas of the scalp in balding guys simply have more androgen receptors. THis study pretty much stated than men typically have more androgen receptors in temporal and frontal scalp hair follicles than women do. Thats been my own wild *** guess on baldness pretty much from the start.

Sure, but the REAL question is why androgens stimulate most body hair growth, but suppress most scalp hair growth. That remains to be elucidated.

When Stephen gets the time, I'd really like to see the in vitro study he has been referring to that witnessed no change in the follicle in a test tube when androgens were added.

He's just referring to the RU58841 study with stumptailed macaques which found evidence that androgens instigate balding by causing the dermal papillae to alter their production of growth factors/inhibitors, which then diffuse out to the rest of the follicle and cause them to shrivel up.

The one other casual observation in that study which caused Stephen to wet his pants in delight is that they also observed that hair follicles from YOUNG macaques (prior to puberty) didn't seem to be sensitive to androgens. Ever since then, Stephen has been citing that in almost every post of his, just because nobody knows exactly how or when follicles start to become sensitive. Just that one little part of that one little study is what he now hangs his hat on, and he thinks that's what destroys the entire standard medical establishment view of human balding! :wink:

Bryan has posted studies concerning RU5388, but they only proved that the growth RATE was increased when adding the androgen receptor blocker to head hair. I want to see where it shrinks the follicle to vellus in a study to conclude personally whether or not androgens act directly on hair. If they do, Im pretty much at the end of my yellow brick road of studying hair loss as thats whats garnered my interest in a few alternative theories of baldness.

Here's a study showing that androgens reduce the growth rate of human scalp hair follicle cells in vitro:

Acta Derm Venereol. 1990;70(4):338-41.

"In vitro effects of testosterone, dihydrotestosterone and estradiol on cell growth of human hair bulb papilla cells and hair root sheath fibroblasts."

Arai A, von Hintzenstern J, Kiesewetter F, Schell H, Hornstein OP.

Department of Dermatology, University of Erlangen-Nuremberg, Federal Republic of Germany.

The influence of testosterone, dihydrotestosterone (each 10 ng/ml up to 300 ng/ml) and estradiol (0.2 ng/ml up to 10 ng/ml) on the growth behaviour (cell count, [3H]thymidine uptake, cell doubling time) of subcultured human hair bulb papilla cells and hair root sheath fibroblasts was studied. Papilla cells and root sheath fibroblasts were isolated by microdissection from the same anagen hair follicles obtained from biopsies of androgen-sensitive scalp regions in 6 healthy male subjects. Dihydrotestosterone and testosterone concentrations above 30 ng/ml significantly reduced the growth of both cell types; lower doses had no effect. Estradiol had no distinct influence on the growth curves of either cell type up to 10 ng/ml, whereas higher concentrations significantly increased the growth of both cell types as shown by [3H]thymidine uptake. Papilla cells reacted more sensitively than root sheath fibroblast to dihydrotestosterone and testosterone, as shown by the growth curves, [3H]thymidine uptake, and cell doubling time.

 

[michael barry]

Sorry about the links. Im not a great computer person and honestly dont know how to send them. Had to write em' down and type em' out myself. If you google the same keywords though, they'll come up on the first few pages.


Casual unrelated observation: Was out today and seen a 5-6 hippocratic wreath bald guys in their 60's. A couple of the guys had wreaths that were only about 2 inches wide in the very back over the classic "donor" area. Shiny bald, hair only went about 2 inches above ears and maybe 3-3 1/2 behind ear. This reminded me of the huge problems of hair transplantation. One simply doesnt know how far their baldness will go. If these men had plugs done in their 20's, they would look outrageous at this age, litterally like a rag doll, but worse. Until science can manufacture at least 30-40 thousand follicles to go with the perhaps 30 thousand follicles almost all men keep, hair transplant's are just a huge risk.

 

[Boru]

Sorry about the links. Im not a great computer person and honestly dont know how to send them. Had to write em' down and type em' out myself. If you google the same keywords though, they'll come up on the first few pages.


Casual unrelated observation: Was out today and seen a 5-6 hippocratic wreath bald guys in their 60's. A couple of the guys had wreaths that were only about 2 inches wide in the very back over the classic "donor" area. Shiny bald, hair only went about 2 inches above ears and maybe 3-3 1/2 behind ear. This reminded me of the huge problems of hair transplantation. One simply doesnt know how far their baldness will go. If these men had plugs done in their 20's, they would look outrageous at this age, litterally like a rag doll, but worse. Until science can manufacture at least 30-40 thousand follicles to go with the perhaps 30 thousand follicles almost all men keep, hair transplant's are just a huge risk.

You are absolutely correct. hair transplant's would also tramautise the very scalp areas which I have proved can be restored, given the right combination of stimulii. I do not believe that there is enough potential donor material around the wreath area to create a good permanent hairline at the front and temples never mind the crown. It makes my discovery all the more amazing to me.
Boru

 

[Footy]

I think all the relevant information has now been presented by both sides, including the "closing arguments". I'll leave it up to each individual reader here to decide for himself the credibility of your theory! :wink:

Bryan

So you are conceding this important point then Bryan!

Just to be sure i will ask you one last time, as you haven't answered my question Bryan!

How can you explain the long term balding in the larger(over 3mm) grafts, transplanted to the balding scalp, as anything other than a continuation of male pattern baldness?

S Foote.

 

[Footy]

Here are some articles that were googled from "in vitro and androgen and hair".

joe.endocrinology-journals.org/cgi/content/abstract/156/1/59


ncbi.nlm-gnih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids+7748741&dopt+Abstract



ehrs.org/conferenceabstracts/2003 barcelona/guestlectures/L-17-itami.htm


content.karger.com/ProdukteDB/produckte.asp?

Aktion=showPDF&ProduktNr=220436&Ausgabe=227989&Artiklnr=
53266&filename=53266.pdf


Have got to be honest guys, all of these papers seemed to indicate that basically androgen inception on the dermal papilla makes terminal hairs in the scalp turn to vellus hairs and it makes body hair turn from vellus to terminal hairs, with the exception of one of them which stated that no change was seen in vitro of the scalp follicles. The rest pretty much say they did.

I found one study that supported my little idea, but forgot the address. My idea was that follicles from the temporal and frontal areas of the scalp in balding guys simply have more androgen receptors. THis study pretty much stated than men typically have more androgen receptors in temporal and frontal scalp hair follicles than women do. Thats been my own wild *** guess on baldness pretty much from the start.


When Stephen gets the time, I'd really like to see the in vitro study he has been referring to that witnessed no change in the follicle in a test tube when androgens were added. Bryan has posted studies concerning RU5388, but they only proved that the growth RATE was increased when adding the androgen receptor blocker to head hair. I want to see where it shrinks the follicle to vellus in a study to conclude personally whether or not androgens act directly on hair. If they do, Im pretty much at the end of my yellow brick road of studying hair loss as thats whats garnered my interest in a few alternative theories of baldness.

Michael.

The important point i am trying to get across here, is about a common assumption, refered to in your statement above quote:

"Have got to be honest guys, all of these papers seemed to indicate that basically androgen inception on the dermal papilla makes terminal hairs in the scalp turn to vellus hairs and it makes body hair turn from vellus to terminal hairs,"

The important point about the in-vitro studies, is that the `ONLY' thing they `DO' actually `PROVE', is that androgens `DO NOT DIRECTLY MAKE' terminal hairs on the scalp `turn' into vellous follicles, or turn body vellous follicles into terminal follicles!!

Here are a couple of links that show this.

http://endo.endojournals.org/cgi/content/full/138/1/356

http://www.fasebj.org/cgi/content/full/16/14/1967

In all the in-vitro studies i can find, androgens do not `directly change' any follicle cells from one growth rate into another growth rate. All they are doing is `allowing' these different samples to express their pre-existing growth rate in-vitro.

There is a world of difference in what is happening in-vitro, to what `everbody' knows is happening in-vivo!

The basic undeniable facts are these.

We know androgens `DO' change the growth rates of follicles in-vivo (in the body). The in-vitro studies `PROVE' that this change is not caused `directly' by androgens, so the effect of androgens that changes the growth rates of follicles has to be `IN-DIRECT', simple. :wink:

Just because androgens in-vitro `support' the pre-existing growth characteristics of the different follicles, doesn't mean anything in terms of what we want to know! Cream cheese could support the pre-existing growth characteristics of different follicles in-vitro!!

So does this mean cream cheese `CAUSES' male pattern baldness?? Of course not!!

The current `direct' theory of androgen induced growth changes in follicles, has been tested in-vitro, and found to be wrong!

What is extraordinary in scientific terms, is that the people who support the current `direct' theory, have decided to `make up' a way to get around the experimental results that don't suit their theory!

This is a proposed `genetic clock' that will at some time `change' follicle cells proven to not respond directly to androgens, `into' cells that `DO'?????

This whole `un-testable fantasy' notion, would be instantly thown out in any other area of science!

Just think about this?

I put a silver lady mascot on the hood of my Ford, and it didn't turn into a Roll's Royce. I then said it would turn into a Roll's Royce given `time', because we all know the silver lady mascot is associated with Roll's Royces.

Would you believe me?

This is what Bryan wants you to believe about the in-vitro follicle tests! :roll:

Bryan can, and `will' post all the in-vitro studies he likes. But he wont find any that show androgens `directly' change the growth characteristics of hair follicles! This in itself shows the current theory of `pre-disposed' follicles to be just plain wrong!

S Foote.

 

[michael barry]

Stephen, that second study seemed to indicate that TGF-B1 made epithelial cells slow down. If insulin-like hormones like this affect baldness, Im assuming cutting down on sugar, white flour, and all the other stuff they tell diabetics to stay away from might be helpful for guys with male pattern baldness.

Gotta be honest, am not to crazy about studies using pre-and post pubescent maques though. Dont they just receed straight back and not the classic Norwood that people do?


I still wonder if the microcapillaries that feed the hair follicle are degenerated by the male pattern baldness process and this is the main way baldness is achieved also. I cant get over that study that showed out of 100+ guys, that the AVERAGE blood flow was 2.6 times less in the balding guys scalps. Thats such a huge, obvious difference.

 

[michael barry]

Upon further consideration.........Stephen do you think that perhaps DHT could be like the effect liquor has on a person? One drink=great, 2=better, 5=nauseated, 12=alchohol poisoning, 14=DEAD?


What do scientists that you have read speculate about androgens added directly to hair in vitro surrounded by collagen that doesnt shrink to vellus when experiments are performed? Do they all postulate about a hair cycle clock, or believe that on cycle number X or Y the bald genes express themselves? Do any of them have alternate theories of baldness also?