For bryan and Foote.

[Bryan]

I think you are engaged in an effort of obfusciation for whatever unkown reason Bryan. Youre really smart, and if even I understand Stephen's idea......................I know you do.

You think _I_ am the one doing the "obfuscating" by asking the questions above?? And you think you know the answers to them? If so, why didn't you actually ANSWER them?

...by his theory (unproven of course) he's well explained how 50% of terminals in a given area can be lost (or miniaturized to the point of cosmetic unacceptibility) and still fit the hydrolic dermal model.

No, he hasn't done that. Not at all. Neither have you.

Bryan

 

[Footy]

I think you are engaged in an effort of obfusciation for whatever unkown reason Bryan. Youre really smart, and if even I understand Stephen's idea......................I know you do.

You think _I_ am the one doing the "obfuscating" by asking the questions above?? And you think you know the answers to them? If so, why didn't you actually ANSWER them?

http://www.keratin.com/aa/aa008.shtml[/url]

I know you all ready know all this Bryan, but i repeat this because i don't want any more excuses from you on this point 8)

I would add that full anagen production of terminal hair is reached reletively early in the human anagen phase, certainly no longer than a year. The full transition to the largest the follicle will get in anagen, is demonstrated by the amount of taper in the initial hair shaft.

So, we can have two follicles in terminal hair producing anagen `right' next to each other. One of these could have say one year of anagen left, whilst the other may have say six years of anagen left.

At this point an increase in the local fluid pressure happens. However, this has no immediate effect on these anagen follicles through contact inhibition, as both follicles are `fully grown' already.

Then after a year, one follicle enters the telogen/categen regression and rest phase, which lasts for around four months before the next anagen phase of this particular follicle starts.

This is when the re-growth of this follicle becomes effected, and restricted by the changes in the pressure in the tissue around it. This follicle will at this time show a reduced anagen growth and reduced hair production, according to my theory.

But the other follicle next to it will continue to produce terminal hair for four and a half years or so.

This is how you can get balding follicles `right next to' non balding follicles Bryan! :roll:

The other factor is of course that the increases in scalp fluid pressure build up from the extremities of the lymphatic system outwards, according to my theory. This in itself can take time to extend over the full male pattern baldness area.

Between them, these factors logicaly explain initial thinning, and ultimate recession in male pattern baldness.

Have you got it now Bryan? :wink:

S Foote.

 

[Footy]

I noticed you posted this on Farrels site Bryan {where you feel safe from scientific reality!}

Quote:

"I remember well the EXACT moment I stopped discussing things with Ernie several years ago. It was a moment when I realized with a flash of Zen clarity (truly a satori experience) that Ernie just doesn't have the intellect to understand hairloss theory, no matter how hard I might try to explain it to him.

Stephen, on the other hand, is a smart guy. He understands technical material. His only personal foible is the inability to see that a cherished pet theory of his is unworkable. It's a matter of deadly PRIDE, I suppose, not a lack of intellect."

______________________________________________

You have the nerve to try to claim that i just defend my theory `at all costs', in the face of evidence that it is `unworkable'!!!!!!!!!

Then you post this desperate drivel on the issue of transplantation, that anyone with any sense can see right through!


http://www.hairlosstalk.com/discussions ... 725#159725

The day you can actually and `specificaly', show me `GENUINE' scientific evidence against my theory, i will willingly hold my hands up!

Until then Bryan, people who `REALLY' understand science and the proper interpretation of studies, remain unimpressed with your efforts :x

S Foote

 

[Bryan]

I would add that full anagen production of terminal hair is reached reletively early in the human anagen phase, certainly no longer than a year. The full transition to the largest the follicle will get in anagen, is demonstrated by the amount of taper in the initial hair shaft.

Agreed.

So, we can have two follicles in terminal hair producing anagen `right' next to each other. One of these could have say one year of anagen left, whilst the other may have say six years of anagen left.

Agreed.

At this point an increase in the local fluid pressure happens. However, this has no immediate effect on these anagen follicles through contact inhibition, as both follicles are `fully grown' already.

WHOA THERE, pardner (that's how we talk, here in Texas )!

What the hell do you mean, "an increase...happens"?? Are you talking about a sudden ONSET of balding in an individual who previously had a full head of hair?? What about an individual who has BEEN balding for a long time and (according to your theory) has a now permanent increase in scalp fluid pressure?? Let's not attempt to gloss-over the details here by slipping-in an important detail like that...

Then after a year, one follicle enters the telogen/categen regression and rest phase, which lasts for around four months before the next anagen phase of this particular follicle starts.

This is when the re-growth of this follicle becomes effected, and restricted by the changes in the pressure in the tissue around it. This follicle will at this time show a reduced anagen growth and reduced hair production, according to my theory.

But the other follicle next to it will continue to produce terminal hair for four and a half years or so.

This is how you can get balding follicles `right next to' non balding follicles Bryan! :roll:

Yes, but your explanation necessarily ASSUMES an obviously contrived situation: it requires that the increased "fluid pressure" DEVELOPS relatively suddenly during the existence of two fully-grown anagen hairs, after which one of them goes relatively quickly back into telogen, sheds that old hair, then attempts to grow a new one which (supposedly) will then show the signs of contact inhibition (sensitivity to testosterone).

That's all rather typical of your ad hoc explanations: it REQUIRES that specific stipulation about a relatively sudden onset of balding. It certainly doesn't explain anything when the person has been balding for a long time (10-20 years, or longer).

The other factor is of course that the increases in scalp fluid pressure build up from the extremities of the lymphatic system outwards, according to my theory. This in itself can take time to extend over the full male pattern baldness area.

Another very feeble attempt at an explanation. I said in PLAIN ENGLISH that the two hairs can be very close together, like only a millimeter apart. I pointed that out SPECIFICALLY so that you'd be unable to claim that there may be extra "fluid pressure" in one part of the scalp, but not in another part that's several inches away. You didn't think I'd let you get away with THAT, did you? :wink:

Bryan

 

[Footy]

I would add that full anagen production of terminal hair is reached reletively early in the human anagen phase, certainly no longer than a year. The full transition to the largest the follicle will get in anagen, is demonstrated by the amount of taper in the initial hair shaft.

Agreed.

So, we can have two follicles in terminal hair producing anagen `right' next to each other. One of these could have say one year of anagen left, whilst the other may have say six years of anagen left.

Agreed.

At this point an increase in the local fluid pressure happens. However, this has no immediate effect on these anagen follicles through contact inhibition, as both follicles are `fully grown' already.

WHOA THERE, pardner (that's how we talk, here in Texas )!

What the hell do you mean, "an increase...happens"?? Are you talking about a sudden ONSET of balding in an individual who previously had a full head of hair?? What about an individual who has BEEN balding for a long time and (according to your theory) has a now permanent increase in scalp fluid pressure?? Let's not attempt to gloss-over the details here by slipping-in an important detail like that...

Then after a year, one follicle enters the telogen/categen regression and rest phase, which lasts for around four months before the next anagen phase of this particular follicle starts.

This is when the re-growth of this follicle becomes effected, and restricted by the changes in the pressure in the tissue around it. This follicle will at this time show a reduced anagen growth and reduced hair production, according to my theory.

But the other follicle next to it will continue to produce terminal hair for four and a half years or so.

This is how you can get balding follicles `right next to' non balding follicles Bryan! :roll:

Yes, but your explanation necessarily ASSUMES an obviously contrived situation: it requires that the increased "fluid pressure" DEVELOPS relatively suddenly during the existence of two fully-grown anagen hairs, after which one of them goes relatively quickly back into telogen, sheds that old hair, then attempts to grow a new one which (supposedly) will then show the signs of contact inhibition (sensitivity to testosterone).

That's all rather typical of your ad hoc explanations: it REQUIRES that specific stipulation about a relatively sudden onset of balding. It certainly doesn't explain anything when the person has been balding for a long time (10-20 years, or longer).

The other factor is of course that the increases in scalp fluid pressure build up from the extremities of the lymphatic system outwards, according to my theory. This in itself can take time to extend over the full male pattern baldness area.

Another very feeble attempt at an explanation. I said in PLAIN ENGLISH that the two hairs can be very close together, like only a millimeter apart. I pointed that out SPECIFICALLY so that you'd be unable to claim that there may be extra "fluid pressure" in one part of the scalp, but not in another part that's several inches away. You didn't think I'd let you get away with THAT, did you? :wink:

Bryan

Thats absolute bullshit as you well know Bryan!

Your not fooling the knowledgable people on this forum Bryan, no matter how hard you try :wink:

All the answers to your questions have been explained to you over and over again.

This constant psuedo scientific rubbish you churn out might impress the less informed people who read these forums, but if you think you are fooling anyone else you are sadly mistaken :roll:

The points i raised in my last post, are based on fully accepted human physiology. You know Bryan, i am really starting to think that you just don't understand these points, is that your problem?

I had thought that you did understand at least `something' of `REAL' science, but i am now not so sure?

This pathetic psuedo scientific ranting by you and your `mini me' Dave001 on Farrels censored site, is a good example of the fantasy world you live in :wink:

http://www.hairlosshelp.com/forums/mess ... TARTPAGE=2

I have shown what accepted experts think about my theory, and i just smile everytime i see your latest `expert' opinions, and `back patting' indulged in by you `psuedo's' :roll:

Your comments about my theory on a site where you know i can't respond just say more about you than i could ever say!

If you really want people to think you have `some' scientific credibility. just answer the question i have asked you over and over!

That is why do the very grafts used in transplantation that you claim `prove' donor dominance, `Actually' BALD in the same way as the original hair?

You have all the data and references that show this, so just stop pretending you don't!

If you want credibility here, just answer the question Bryan?

S Foote.

 

[Bryan]

Thats absolute bullshit as you well know Bryan!

Your not fooling the knowledgable people on this forum Bryan, no matter how hard you try :wink:

All the answers to your questions have been explained to you over and over again.

REALLY??? ROTFLMAO!! This is the FIRST time that you and I have discussed your attempted "explanation" above about the timing of hairs in anagen and how one can be balding but not the other, etc.

BTW, how come you don't ANSWER the points I raised above in response, but only continue a diatribe of insults against me, instead? :wink:

The points i raised in my last post, are based on fully accepted human physiology.

Why didn't you ANSWER what I said in my reply? Cat got your tongue (do they use that expression in England?), Stephen?

Your comments about my theory on a site where you know i can't respond just say more about you than i could ever say!

Hey, now we're on a site where you CAN reply, Stephen! Why don't you start with what I said above?? :wink:

If you really want people to think you have `some' scientific credibility. just answer the question i have asked you over and over!

That is why do the very grafts used in transplantation that you claim `prove' donor dominance, `Actually' BALD in the same way as the original hair?

You have all the data and references that show this, so just stop pretending you don't!

I'm telling you yet again: THERE IS NO EVIDENCE that transplanted hairs bald in the same way as the original hair. Prove me wrong and SHOW ME ANY SUCH EVIDENCE.

I can understand your anger and frustration in the last couple of posts: you're stuck in a logical rut, with no escape. You know it, I know it, and all the other readers here know it.

Bryan

 

[Dave001]

Footy wrote:

[...]

> In proposing my theory i have tried to follow the scientific rules,

Seems you may have glanced over a few.

> and i have had two papers published on my theory in the journal
> "Medical Hypotheses".

One less journal I'll be reading.

[...]

> The `qualification' in the pursuit of science, is in the response of
> the scientific community to your proposals by recognised experts. I

Doesn't veracity count for anything?

All you're really saying is that the level of one's qualification is subjectively determined by his audience, which only reinforces what I've already said. Further, you cannot recursively apply your standard of qualification to a community without presupposing expertise somewhere along the way.

[...]

> You come on these forums talking in psuedo scientific sentences, that

Can you provide an example of a pseudoscientific sentence that I've used? Please contrast it with a scientific sentence so that everyone can learn the difference.

> reach no conclusion, and post `scientific studies' as if they give
> you a personal credibility. :roll: :roll:

What sort of conclusion were you hoping for that I failed to offer? Again, examples are appreciated.

> You post an in-vitro abstract here and emphasise text that means
> `nothing' at all in `TRUE' scientific terms! All these in-vitro tests
> `ACTUALLY' prove is that direct exposure to androgens change
> `NOTHING'.

What's with the excessive use of quotation marks (or 'inverted commas' as some of you Brits prefer)?

> You are full of `s**t Dave!

I had no idea that my diet was high in salt.

[...]

> I ask you again, What qualifies your opinions over anyone else's on
> these forums????????????

Absolutely nothing. There are no presupposed qualifications of any kind in an open forum such as this. I expect the reader to hold my posts to the same standard of criticism that he would anyone's. So should you.

 

[Footy]

Dave, listen up.

You are just as entitled to your own opinion and interpretation as anyone else on these forums.

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

If you had questioned and debated my theory in a proper scientific manner, i wouldn't have a problem with that.

But so far all you have done is `rubbish' it with sarcastic unspecific `one liners' as in your last post.

If you are not prepared as it seems your not, to go on the record with your `SPECIFIC' objections to my theory, then just shut up!

Bryan is quite capable of defending himself here, if you have nothing scientific to say, just stay on Farrels censored site.

S Foote.

 

[Footy]

Thats absolute bullshit as you well know Bryan!

Your not fooling the knowledgable people on this forum Bryan, no matter how hard you try :wink:

All the answers to your questions have been explained to you over and over again.

REALLY??? ROTFLMAO!! This is the FIRST time that you and I have discussed your attempted "explanation" above about the timing of hairs in anagen and how one can be balding but not the other, etc.

BTW, how come you don't ANSWER the points I raised above in response, but only continue a diatribe of insults against me, instead? :wink:

The points i raised in my last post, are based on fully accepted human physiology.

Why didn't you ANSWER what I said in my reply? Cat got your tongue (do they use that expression in England?), Stephen?

It just gets frustrating when you clearly distort and avoid the issues Bryan. It's also clear from my PM's that a growing number of people also think this!

But in this post i am going to give you the benefit of the doubt, and use your own comments here to demonstrate where you are going wrong :wink:

The biggest flaw you have in your arguments Bryan, is that you lack the basic knowledge of general human physiology that scientists are taught as a `background'. This is important because it allows them to judge study implications, and explainations based on this well established background experience of `real' physiology!

This is why more and more `real' scientists are not happy with the current explainations offered for the causes of male pattern baldness. Simply because in order to make the current theory work, mechanisms have to be invented that have no precedent in known physiology. For example the `magic' genetic clock that `has' to run independently in `EACH' follicle, but goes against every recognised principle in known physiology!

Dr Sawaya refered to this `new' thinking in the letter i posted. There is now even data emerging that is causing the transplantation industry to question the current notion of `donor dominance'.

http://www.hairlosstalk.com/newsletter/article181.htm

Now Bryan, as an example of your deliberate avoiding the point in these matters, i described how an increase in fluid pressure will effect follicles when they `re-cycle', i made this very clear! Then you said, quote:

"What the hell do you mean, "an increase...happens"?? Are you talking about a sudden ONSET of balding in an individual who previously had a full head of hair?? What about an individual who has BEEN balding for a long time and (according to your theory) has a now permanent increase in scalp fluid pressure?? Let's not attempt to gloss-over the details here by slipping-in an important detail like that... "

How can you possibly be serious in this response to my description? Just how can my explaination of balding over a period of `YEARS', be genuinely interpreted by you as a `sudden' process???? Likewise, i explained how the combination of the hair cycle period, and the slow build up and progression of edema, explains the long term balding you are now shouting about above!

My argument was based on `accepted' knowledge in the time periods of the human hair cycle, and the known effects of lymphedema in particular.

http://www.lymphoedema.org.au/index.htm


I really haven't got the time to educate you in `BASIC' physiology Bryan. If you want to be credible in your arguments, just learn something about this!!

Your breathtaking ignorance on the very basics in interpretation of evidence in science, is demonstrated below :roll:

If you really want people to think you have `some' scientific credibility. just answer the question i have asked you over and over!

That is why do the very grafts used in transplantation that you claim `prove' donor dominance, `Actually' BALD in the same way as the original hair?

You have all the data and references that show this, so just stop pretending you don't!

I'm telling you yet again: THERE IS NO EVIDENCE that transplanted hairs bald in the same way as the original hair. Prove me wrong and SHOW ME ANY SUCH EVIDENCE.

Here we go again. People can see by reading prior posts, that i have posted all this before in response to Bryan's `denial' syndrome :roll:

The continued balding of aledged `resistent' follicles in grafts transplanted to the balding scalp, is common knowledge, and `WIDELY' accepted in the transplantation industry. Take your pick Bryan!

http://www.google.co.uk/search?hair loss=en&ie ... arch&meta=

Quote from this article.

http://www.hairtransplantadviser.org/repair.htm

" In doughnutting, the centers of grafts get insufficient oxygen following transplantation and therefore, the follicles in the central portion of the grafts fail to survive. This results in hair growing only in the periphery of the grafts. This was a common phenomenon in 4- and 5-mm plugs, but can also be noted in grafts 3-mm in size."

This balding is described as doughnutting by the transplantation industry, and it is `suggested' that oxygen starvation {hypoxia{, is responsible for this.

The problem is that if hypoxia is known to have it's effects on tissues `very' quickly.

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

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

The studies by the respected hair loss researchers Orentriech and Nordstrom, both posted by `YOU' Bryan, confirm that the hair in these grafts survives for long enough (over 18 months at least}, to completely rule out hypoxia as a `cause of this recognised balding process.

http://www.hairlosstalk.com/discussions ... hp?t=17571

In fact, the only specific study into the effects of hypoxia, again posted by `YOU' Bryan, clearly shows that hypoxia actually increases hair growth!!

http://www.geocities.com/bryan50001/artery_ligature.htm

What i am doing here Bryan is considering the implications of the `whole' body of evidence. You should try this sometime! :wink:

I can understand your anger and frustration in the last couple of posts: you're stuck in a logical rut, with no escape. You know it, I know it, and all the other readers here know it.

Bryan

You wish Bryan. 8)

S Foote.

 

[Bryan]

Now Bryan, as an example of your deliberate avoiding the point in these matters, i described how an increase in fluid pressure will effect follicles when they `re-cycle', i made this very clear! Then you said, quote:

"What the hell do you mean, "an increase...happens"?? Are you talking about a sudden ONSET of balding in an individual who previously had a full head of hair?? What about an individual who has BEEN balding for a long time and (according to your theory) has a now permanent increase in scalp fluid pressure?? Let's not attempt to gloss-over the details here by slipping-in an important detail like that... "

How can you possibly be serious in this response to my description? Just how can my explaination of balding over a period of `YEARS', be genuinely interpreted by you as a `sudden' process???? Likewise, i explained how the combination of the hair cycle period, and the slow build up and progression of edema, explains the long term balding you are now shouting about above!

You're still stalling, and everybody following this thread can see it. I'm going to explain it to you again, and don't try to dodge the point:

The slowness or quickness of balding is a RELATIVE thing. For your theory to be able to explain how two side-by-side follicles can have such opposite characteristics (one is suppressed by testosterone, the other isn't), you MUST assume that the "edema" BEGAN when one of the follicles was already fully grown, but the other was not. And even then, that disparity would only last for a relatively short period of time (the duration of the rest of the anagen phase in that first follicle). After that, and for the rest of that person's life, the two side-by-side follicles would have the IDENTICAL characteristic of being suppressed by testosterone. See what I mean? Your theory cannot explain how that situation could arise in a scalp which has been balding for a relatively LONG period of time (10-20 years or more).

The continued balding of aledged `resistent' follicles in grafts transplanted to the balding scalp, is common knowledge, and `WIDELY' accepted in the transplantation industry. Take your pick Bryan!

http://www.google.co.uk/search?hair loss=en&ie ... arch&meta=

Quote from this article.

http://www.hairtransplantadviser.org/repair.htm

" In doughnutting, the centers of grafts get insufficient oxygen following transplantation and therefore, the follicles in the central portion of the grafts fail to survive. This results in hair growing only in the periphery of the grafts. This was a common phenomenon in 4- and 5-mm plugs, but can also be noted in grafts 3-mm in size."

This balding is described as doughnutting by the transplantation industry, and it is `suggested' that oxygen starvation {hypoxia{, is responsible for this.

The problem is that if hypoxia is known to have it's effects on tissues `very' quickly.

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

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

The studies by the respected hair loss researchers Orentriech and Nordstrom, both posted by `YOU' Bryan, confirm that the hair in these grafts survives for long enough (over 18 months at least}, to completely rule out hypoxia as a `cause of this recognised balding process.

I'm rapidly growing tired of your continuing to dodge the issue. I'm giving you ONE LAST CHANCE to acknowledge what I've been telling you. If you don't respond this time in good faith, then this conversation will be over, with no hard feelings.

I'm going to state this as simply as I possibly can: I believe that the phenomenon of "doughnutting" exists, and I think it happens pretty quickly, like in the first few weeks, or possibly a month or two. After that, I believe that transplanted non-balding grafts continue to grow normally, with no further loss of follicles. I challenge you to find evidence to the contrary of either of those assumptions. Put up or shut-up.

If your only reply to this is to once again post those same links to sites that discuss "doughnutting" without specifying an actual TIMELINE, then this dialogue between you and me will be finished.

Bryan

 

[Footy]

Now Bryan, as an example of your deliberate avoiding the point in these matters, i described how an increase in fluid pressure will effect follicles when they `re-cycle', i made this very clear! Then you said, quote:

"What the hell do you mean, "an increase...happens"?? Are you talking about a sudden ONSET of balding in an individual who previously had a full head of hair?? What about an individual who has BEEN balding for a long time and (according to your theory) has a now permanent increase in scalp fluid pressure?? Let's not attempt to gloss-over the details here by slipping-in an important detail like that... "

How can you possibly be serious in this response to my description? Just how can my explaination of balding over a period of `YEARS', be genuinely interpreted by you as a `sudden' process???? Likewise, i explained how the combination of the hair cycle period, and the slow build up and progression of edema, explains the long term balding you are now shouting about above!

You're still stalling, and everybody following this thread can see it. I'm going to explain it to you again, and don't try to dodge the point:

The slowness or quickness of balding is a RELATIVE thing. For your theory to be able to explain how two side-by-side follicles can have such opposite characteristics (one is suppressed by testosterone, the other isn't), you MUST assume that the "edema" BEGAN when one of the follicles was already fully grown, but the other was not. And even then, that disparity would only last for a relatively short period of time (the duration of the rest of the anagen phase in that first follicle). After that, and for the rest of that person's life, the two side-by-side follicles would have the IDENTICAL characteristic of being suppressed by testosterone. See what I mean? Your theory cannot explain how that situation could arise in a scalp which has been balding for a relatively LONG period of time (10-20 years or more).

I just don't think you get the science of this argument at all Bryan, or the basics of my theory??

Firstly, testosterone doesn't `directly' effect side by side follicles, unless these are already balding follicles. The in-vitro tests prove this, because direct exposure to androgens has no effect of growth restriction on follicles prior to male pattern baldness in-vivo. So your claim that side by side follicles have `opposite' characteristics is just not true.

It is also quite clear that both the side by side follicles can both be fully grown whilst having a period of years between their anagen termination points. If you are trying to suggest that human hair follicles continue enlarging `right up to anagen termination', this would mean a continually thickening hair shaft, a tapered hair. This is clearly `NOT' true in humans!

Quite simply Bryan, the local fluid pressure increase explains the initial difuse thinning based on the long period {up to ten years}, of the human hair cycle. This thinning will lead to baldness over that period `IF' the pressure increase is enough to create vellous follicles. Remember Bryan that my theory proposed a Hydraulic `adjustment' mechanism of anagen follicle size. In the individual, a slight increase in pressure over a long period over an increasing area, will reduce follicle size slowly over more than one anagen phase!

Both the duration and extension of increased pressure, is a factor unique to the individual based on their particular `fluid dynamics'.

Are you trying to say here that an individual can have male pattern baldness that just involves thinning, and that this thinning reaches a certain point then remains like that indefinately? If so, show me some citations for your claim.

male pattern baldness is a `progressive' condition Bryan, it gets worse with time!

I had assumed in this debate that you were fully aware of the details of my theory? :roll:

The continued balding of aledged `resistent' follicles in grafts transplanted to the balding scalp, is common knowledge, and `WIDELY' accepted in the transplantation industry. Take your pick Bryan!

http://www.google.co.uk/search?hair loss=en&ie ... arch&meta=

Quote from this article.

http://www.hairtransplantadviser.org/repair.htm

" In doughnutting, the centers of grafts get insufficient oxygen following transplantation and therefore, the follicles in the central portion of the grafts fail to survive. This results in hair growing only in the periphery of the grafts. This was a common phenomenon in 4- and 5-mm plugs, but can also be noted in grafts 3-mm in size."

This balding is described as doughnutting by the transplantation industry, and it is `suggested' that oxygen starvation {hypoxia{, is responsible for this.

The problem is that if hypoxia is known to have it's effects on tissues `very' quickly.

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

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

The studies by the respected hair loss researchers Orentriech and Nordstrom, both posted by `YOU' Bryan, confirm that the hair in these grafts survives for long enough (over 18 months at least}, to completely rule out hypoxia as a `cause of this recognised balding process.

I'm rapidly growing tired of your continuing to dodge the issue. I'm giving you ONE LAST CHANCE to acknowledge what I've been telling you. If you don't respond this time in good faith, then this conversation will be over, with no hard feelings.

I'm going to state this as simply as I possibly can: I believe that the phenomenon of "doughnutting" exists, and I think it happens pretty quickly, like in the first few weeks, or possibly a month or two. After that, I believe that transplanted non-balding grafts continue to grow normally, with no further loss of follicles. I challenge you to find evidence to the contrary of either of those assumptions. Put up or shut-up.

If your only reply to this is to once again post those same links to sites that discuss "doughnutting" without specifying an actual TIMELINE, then this dialogue between you and me will be finished.

Bryan

Bryan, it is clear that you just don't know what the term `doughnutting' refers to in transplantation!

The term doughnutting is used by the transplantation industry to describe a loss of hair in transplanted grafts, `NOT' the induction of hypoxia!. Doughnutting is a description of hair loss, a big hole in the hair growth in these grafts like a doughnut! :roll:

You say you think doughnutting occours quickly in these larger grafts, but it doesn't! Doughnutting refers to a loss of hair! Is that clear now? If not just read the many references i provided you with about this!

Again, in the early studies by Orentriech and Nordstrom using these grafts, no central hair loss or `doughnutting' was observed in periods of up to two years!! A significant loss of hair in these grafts is now widely accepted as referenced, but the very time scale demonstrated rules out hypoxia as a possible cause of this!

So if hypoxia is happening very quickly in these grafts as i agree it would {if it happens at all}, this is having `NO' effect on `actual' hair loss in these grafts, or `doughnutting' as the transplantation industry prefers to call it!.

So if hypoxia is not responsible for this hair loss or `doughnutting', as it cannot be according to the time scale, what is if not male pattern baldness????

Is this clear to you now Bryan? :wink:

S Foote.

 

[Bryan]

I just don't think you get the science of this argument at all Bryan, or the basics of my theory??

Firstly, testosterone doesn't `directly' effect side by side follicles, unless these are already balding follicles. The in-vitro tests prove this, because direct exposure to androgens has no effect of growth restriction on follicles prior to male pattern baldness in-vivo. So your claim that side by side follicles have `opposite' characteristics is just not true.

I understand the basics of your theory. I'm really surprised that YOU don't seem to understand the very simple point that I'm making! Let me describe it again using different words...hopefully you'll understand me, this time:

I previously told you about a study with human subjects in which scalp biopsies were taken, and follicles were grown in vitro with added testosterone. One mildly surprising finding is that while most of those follicles were sensitive to testosterone as expected (their growth was suppressed by testosterone), there was the occasional follicle which was NOT sensitive to testosterone at all. They continued to grow normally, even with the added androgen. Moreover, those non-sensitive follicles weren't localized in some particular area of scalp (at least, as far as I recall), they were just interspersed randomly and unpredictably among the other follicles which WERE sensitive to the testosterone. In other words, there almost certainly were side-by-side pairs of follicles on the scalp, one of which would be sensitive to androgens, while its neighbor a tiny distance away would NOT be sensitive to androgens. Are you with me so far?

Ok, here's the very simple point I'm making: according to your theory, the only way that a follicle can be sensitive to androgens in that fashion is if it has experienced contact inhibition. Correct? :wink: If there are two side-by-side anagen follicles sitting in a person's scalp and one of them is sensitive to androgens (in that fashion) but not the other, then the first one has obviously experienced contact inhibition, but not the second one. Correct? We are then forced to draw an obvious conclusion: the (alleged) edema with resulting contact inhibition must have occured relatively quickly at some point in time BETWEEN the second insensitive follicle's reaching full anagen, and the first sensitive follicle's reaching full anagen. Otherwise, they wouldn't have OPPOSITE characteristics in their responses to androgens. See my point, now?

Another obvious conclusion is that it sets a time-limit on when that phenomenon could occur (side-by-side follicles with opposite characteristics). It couldn't happen in a specific area of scalp that's been balding for a lengthy period of time (10 years or longer). Correct?

Bryan, it is clear that you just don't know what the term `doughnutting' refers to in transplantation!

The term doughnutting is used by the transplantation industry to describe a loss of hair in transplanted grafts, `NOT' the induction of hypoxia!. Doughnutting is a description of hair loss, a big hole in the hair growth in these grafts like a doughnut! :roll:

Of course. The only point you and I differ on is the CAUSE of the doughnutting.

You say you think doughnutting occours quickly in these larger grafts, but it doesn't!

Then provide scientific EVIDENCE that it doesn't occur quickly.

Doughnutting refers to a loss of hair! Is that clear now? If not just read the many references i provided you with about this!

That has ALWAYS been clear. Why are you dwelling on the obvious?

Again, in the early studies by Orentriech and Nordstrom using these grafts, no central hair loss or `doughnutting' was observed in periods of up to two years!! A significant loss of hair in these grafts is now widely accepted as referenced, but the very time scale demonstrated rules out hypoxia as a possible cause of this!

It now appears that you've been missing a fundamental point all this time that I thought was obvious: the very FIRST counting of hairs in the transplanted grafts was done by Nordstrom at the 5-month point, with subsequent countings done at 10 months and 21 months. My own position is that the "doughnutting" actually DID occur in all those grafts, and it occurred well within those first 5 months!! What strongly supports that assumption is the fact that the NUMBERS of hairs in those grafts after 5 months were already fairly small...even the one from the non-balding occipital area was only 13 hairs after 5 months. In the reading I've done of other material on the Web about hair transplantation, the original numbers of hairs in similar-sized grafts right after they were extracted were considerably higher than that, like twice or maybe even three times as high! And, of course, that count actually INCREASED slightly over the course of all the remaining months, while the grafts of balding follicles continued to decline sharply, as expected.

So I think this has been kind of a "Who's on first" comedy routine of misunderstanding between you and me: I've assumed that the "doughnutting" is over and done with within 5 months, and from that point on, hair transplants demonstrate their normal donor dominance, with continued normal growth (for originally non-balding follicles) for decades afterwards. That's why I was growing increasingly frustrated when I kept asking you to PROVE that transplants continue balding, and you kept pointing me right back to those same damned links about "doughnutting" which I've already read a dozen times!

So now I think you probably have a better idea of where I'm coming from. If you still don't agree with me, then I'm asking you to provide scientific EVIDENCE that contradicts my position. Something that will address the TIMELINE of when "doughnutting" occurs.

Bryan

 

[Guest]

:shock:

OK OK OK. Let me make one request... Can somebody tell me what you guys are talking about? I want to follow this thread but I have just started reading it. Can one of you give me a quick summary of what is being said?

 

[Footy]

I just don't think you get the science of this argument at all Bryan, or the basics of my theory??

Firstly, testosterone doesn't `directly' effect side by side follicles, unless these are already balding follicles. The in-vitro tests prove this, because direct exposure to androgens has no effect of growth restriction on follicles prior to male pattern baldness in-vivo. So your claim that side by side follicles have `opposite' characteristics is just not true.

I understand the basics of your theory. I'm really surprised that YOU don't seem to understand the very simple point that I'm making! Let me describe it again using different words...hopefully you'll understand me, this time:

I previously told you about a study with human subjects in which scalp biopsies were taken, and follicles were grown in vitro with added testosterone. One mildly surprising finding is that while most of those follicles were sensitive to testosterone as expected (their growth was suppressed by testosterone), there was the occasional follicle which was NOT sensitive to testosterone at all. They continued to grow normally, even with the added androgen. Moreover, those non-sensitive follicles weren't localized in some particular area of scalp (at least, as far as I recall), they were just interspersed randomly and unpredictably among the other follicles which WERE sensitive to the testosterone. In other words, there almost certainly were side-by-side pairs of follicles on the scalp, one of which would be sensitive to androgens, while its neighbor a tiny distance away would NOT be sensitive to androgens. Are you with me so far?

Ok, here's the very simple point I'm making: according to your theory, the only way that a follicle can be sensitive to androgens in that fashion is if it has experienced contact inhibition. Correct? :wink: If there are two side-by-side anagen follicles sitting in a person's scalp and one of them is sensitive to androgens (in that fashion) but not the other, then the first one has obviously experienced contact inhibition, but not the second one. Correct? We are then forced to draw an obvious conclusion: the (alleged) edema with resulting contact inhibition must have occured relatively quickly at some point in time BETWEEN the second insensitive follicle's reaching full anagen, and the first sensitive follicle's reaching full anagen. Otherwise, they wouldn't have OPPOSITE characteristics in their responses to androgens. See my point, now?

Another obvious conclusion is that it sets a time-limit on when that phenomenon could occur (side-by-side follicles with opposite characteristics). It couldn't happen in a specific area of scalp that's been balding for a lengthy period of time (10 years or longer). Correct?

For the sake of clarity in this debate Bryan, could you post some kind of direct text from the study you refer to above?

You see you are saying that these samples showed a restricted growth to testosterone, apart from some `oddball' follicles that showed no such response.

So presumably you are talking here about samples from male pattern baldness follicles in-vivo, that we know are growth restricted subsequently by testosterone in-vitro, correct?

If so and the `odd' male pattern baldness follicle is not showing such a growth restriction, then why according to the `direct' theory, is it then an `male pattern baldness' follicle in the first place???

Do you get do you get my drift here Bryan? This is an important study by the sounds of it, so please post as much detail about this as you can.

Bryan, it is clear that you just don't know what the term `doughnutting' refers to in transplantation!

The term doughnutting is used by the transplantation industry to describe a loss of hair in transplanted grafts, `NOT' the induction of hypoxia!. Doughnutting is a description of hair loss, a big hole in the hair growth in these grafts like a doughnut! :roll:

Of course. The only point you and I differ on is the CAUSE of the doughnutting.

You say you think doughnutting occours quickly in these larger grafts, but it doesn't!

Then provide scientific EVIDENCE that it doesn't occur quickly.

Doughnutting refers to a loss of hair! Is that clear now? If not just read the many references i provided you with about this!

That has ALWAYS been clear. Why are you dwelling on the obvious?

Again, in the early studies by Orentriech and Nordstrom using these grafts, no central hair loss or `doughnutting' was observed in periods of up to two years!! A significant loss of hair in these grafts is now widely accepted as referenced, but the very time scale demonstrated rules out hypoxia as a possible cause of this!

It now appears that you've been missing a fundamental point all this time that I thought was obvious: the very FIRST counting of hairs in the transplanted grafts was done by Nordstrom at the 5-month point, with subsequent countings done at 10 months and 21 months. My own position is that the "doughnutting" actually DID occur in all those grafts, and it occurred well within those first 5 months!! What strongly supports that assumption is the fact that the NUMBERS of hairs in those grafts after 5 months were already fairly small...even the one from the non-balding occipital area was only 13 hairs after 5 months. In the reading I've done of other material on the Web about hair transplantation, the original numbers of hairs in similar-sized grafts right after they were extracted were considerably higher than that, like twice or maybe even three times as high! And, of course, that count actually INCREASED slightly over the course of all the remaining months, while the grafts of balding follicles continued to decline sharply, as expected.

So I think this has been kind of a "Who's on first" comedy routine of misunderstanding between you and me: I've assumed that the "doughnutting" is over and done with within 5 months, and from that point on, hair transplants demonstrate their normal donor dominance, with continued normal growth (for originally non-balding follicles) for decades afterwards. That's why I was growing increasingly frustrated when I kept asking you to PROVE that transplants continue balding, and you kept pointing me right back to those same damned links about "doughnutting" which I've already read a dozen times!

So now I think you probably have a better idea of where I'm coming from. If you still don't agree with me, then I'm asking you to provide scientific EVIDENCE that contradicts my position. Something that will address the TIMELINE of when "doughnutting" occurs.

Bryan

In this context Bryan, the study you posted in a previous thread by Orentriech, is more informative regarding the `normal' transplantation to the bald area and so the `doughnutting' issue. I have searched for this, but i can't find your original post.

I think this is an important argument, and i want to be very clear in the details to avoid any further confusion.

So if you would again please post as much direct quotation from both Orentreich and Nordstroms papers, i will respond in more detail over the weekend.

S Foote.

 

[Footy]

:shock:

OK OK OK. Let me make one request... Can somebody tell me what you guys are talking about? I want to follow this thread but I have just started reading it. Can one of you give me a quick summary of what is being said?

Hi.

The existing theory of how DHT effects follicles is that the follicles are `different' in the way they respond to DHT. This idea came about a long time ago because hair transplanted from the back of the head `survived' when moved to the balding area.

What i am saying is that since this early assumption, more evidence has come to light that shows that male pattern baldness does in fact happen in the very kind of grafts that the current theory is based on.!

This is what this debate is about.

I am suggesting that a factor other than `geneticaly different' follicles accounts for the survival of `some' of the transplanted follicles.

This is an important issue as the whole current research into male pattern baldness is based on this `genetic difference' idea. I think this idea is wrong, and that is why these forums are full of dissapointment about the performance of treatments based on the current theory.

S Foote.

 

[Bryan]

For the sake of clarity in this debate Bryan, could you post some kind of direct text from the study you refer to above?

At the moment I'm in kind of a hurry, and I only want to post this rather abbreviated reply to you. I'll have a little more to say in a moment about the content of all these studies we've been discusssing.

You see you are saying that these samples showed a restricted growth to testosterone, apart from some `oddball' follicles that showed no such response.

So presumably you are talking here about samples from male pattern baldness follicles in-vivo, that we know are growth restricted subsequently by testosterone in-vitro, correct?

Yes. That's correct.

If so and the `odd' male pattern baldness follicle is not showing such a growth restriction, then why according to the `direct' theory, is it then an `male pattern baldness' follicle in the first place???

Ahh...that's exactly my point, Stephen! It is NOT an male pattern baldness follicle!! :wink:

This supports the casual observation many people have made that there can sometimes be that 'oddball' hair or two growing just fine within an area of pronounced balding. I've noticed that phenomenon, too: despite my own pretty slick baldspot at the back (you can see my photos here on this site), there are nevertheless a few hairs scattered through that area that seem to be fairly healthy! Those renegade hairs that insist on surviving are (presumably) just like the ones in the study which were found to be insensitive to androgens.

I have no explanation for those occasional 'oddball' follicles which are androgen- and male pattern baldness-resistant, even within areas of overt and obvious balding. I've never tried to evade or hide the fact that we simply don't KNOW the reasons why most (but not all) scalp follicles become sensitive to androgens. However, it appears to me that YOU, on the other hand, do in fact have an even tougher time trying to explain that phenomenon; that's because you DO have a central theory that purports to explain all the details of balding. And I have no idea how you could explain why one particular follicle existing within a large area of alleged edema would be spared its effects, while all of its immediate neighbors suffer from alleged contact inhibition.

In this context Bryan, the study you posted in a previous thread by Orentriech, is more informative regarding the `normal' transplantation to the bald area and so the `doughnutting' issue. I have searched for this, but i can't find your original post.

Actually, the great advantage of the Nordstrom study over the Orentreich study is that Nordstrom actually COUNTED hairs in the grafts at regular intervals, and reported them! Orentreich apparently didn't do that...he only reported the gross and obvious progress of the transplants over a period of up to 2 1/2 years, and didn't make a "progress report" every few months, like Nordstom did. So I think Nordstrom's more detailed and precise reporting is probably even more important that Orentreich's somewhat looser reporting.

I think this is an important argument, and i want to be very clear in the details to avoid any further confusion.

So if you would again please post as much direct quotation from both Orentreich and Nordstroms papers, i will respond in more detail over the weekend.

If necessary, I will dig-up the previous posts I made about both Nordstrom and Orentreich, in which I reported many of the details of their studies. Also, I will dig-up that third study about the 'oddball' insensitive follicles and report some of those details, sometime over this weekend. However, Stephen, my offer to you still stands: I'd be happy to snail-mail you paper copies of all three of them, for your careful study and perusal! There's more information in all that stuff than I care to type-out all at once. The Orentreich study in particular is QUITE lengthy. If you Private Message me where to send them, you can study them all to your heart's content.

Bryan

 

[TheBaldingMenace]

Wow! When these two guys go at it's like they should have their own show...the S Foote and Bryan show. Learn from each other guys don't beat each other with a stick :hairy:

 

[Grandpa]

I'm not even going to pretend to grasp any of the specifics you guys are talking about, but I just have a probably really naive question for Foote. From your point of view do you think this same doughnutting would occur in HM follicles? I assume you probably would, and although I'm personally really skeptical about HM coming soon or being any kind of silver bullet I still held out a bit of hope for it. It'd be pretty disheartening to hear the whole effort's been wasted on junk science.

 

[Footy]

Bryan.

I haven't got a lot of time tonight, but i think i may be able to find the relevant details tommorow. If not i may take you up on your offer.

S Foote.

 

[Footy]

I'm not even going to pretend to grasp any of the specifics you guys are talking about, but I just have a probably really naive question for Foote. From your point of view do you think this same doughnutting would occur in HM follicles? I assume you probably would, and although I'm personally really skeptical about HM coming soon or being any kind of silver bullet I still held out a bit of hope for it. It'd be pretty disheartening to hear the whole effort's been wasted on junk science.

Hi.

The point really relevant to modern transplantation in my opinion, is the lesson this `doughnutting' teaches. The term doughnutting was applied to the very common hair loss that occours in the larger plug grafts that were commonly used up until around the late 80's.

Over time, the hair in these grafts thinned from the centre outwards, leaving a ring of hair around the outside of the grafts. Hence the term `doughnutting'.

My argument is that the only hair growth that survives long term in grafts to the male pattern baldness area, is from those anagen follicles that have had a healing process happen around them. I think this is why all the modern grafts have `evolved' into mini grafts.

I am suggesting that a `scaffold', or `mould' of fibrose tissue has formed around these anagen follicles that `saves' this space for future large anagen follicles to grow into! I think this is why `some' transplanted follicles can survive as larger follicles in the male pattern baldness area, against the increased intrusion of dermal cells and early contact inhibition because of increased fluid pressure.

Such natural `scaffolds' are recognised as guides to tissue growth, and are known to modify the contact inhibition response.

http://www.pubmedcentral.nih.gov/articl ... tid=122571

I find it interesting that the leading HM pioneer's are now busy taking out patents on bio-scaffolds?

http://www.hairsite4.com/dc/dcboard.php ... 8995&page=

I see this as a good sign in HM research, and the acceptance of the scaffold principle as hope for reliable HM in the future.

S Foote.