Dispensing with the current outdated donor dominance theory.

[S Foote.]

The current donor dominance theory of the results in hair transplantation, is very clear in what it claims. This is that the hair follicles at the back and sides of the head are basicaly `different' to those in the male pattern baldness area. Because of this, when they are transplanted to the male pattern baldness area they survive the balding process that goes on in the male pattern baldness area.

This notion of `different' follicles, came about because of early experiments involving hair transplantation by respected scientists like Orentreich and Nordstrom. These studies have recently been discussed here.

Nordstrom used grafts of 4mm in diameter, and studied these for 21 months. Orentreich reportedly used 4 to 6mm diameter grafts, and studied these for around 2 to 2 1/2 years.

Both these reputable scientists reported no significant loss of hair in these grafts when transplanted from the back of the head into the balding area, over the time period of the studies. This is a `VERY' important observation!

The problem over the period since these early experiments is that further more longer term observations concerning transplantation, have been limited within the transplantation industry. Any potential `problem' with the current `donor dominance' theory they are `selling', would likely be dismissed as not related to the basic theory of what they are selling!

Even so, some hard `FACTS' have emerged since the early studies on transplantation, that completely disprove the current notion of `differently' programed hair follicles.

Modern day knowledge now recognises that a `balding' process happens in grafts transplanted into the male pattern baldness area, from the alledged `resistent' area at the back of the head!!

This is described as`doughnutting'. This loss of the transplanted hair starts in the middle of the larger grafts, as used in the early studies, and continues to receed outwards in these grafts. This effects grafts of 3mm in diameter upwards, and is a consistent factor in these larger grafts. Over time, the only hair that remains in these grafts is around the edges!

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

The transplantation industry tries to explain this through hypoxia, (a lack of oxygen in the centre of these large grafts}.

However, recognised physiology rejects the `hypoxia hypothesis' completely!.

If hypoxia is going to have an adverse effect on cell growth, it has this effect very quickly. This study shows that hypoxia induces a nine fold increase in production of TGF beta-1, from dermal fibroblasts in tissue culture within 72 hours!!

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

The role of TGF beta-1 in reducing hair follicle growth is claimed as a central factor in male pattern baldness.

http://www.ncbi.nlm.nih.gov/entrez/quer ... query_hl=3

So if hypoxia `was' going to reduce hair growth in these large grafts, it would do so within weeks at the outside. Follicles in these grafts would certainly `NOT' survive the periods as reported in the early studies of around 2 years!

Most significantly, deliberately induced hypoxia in the male pattern baldness scalp, has been shown to `improve' hair follicle condition considerably!

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

To recap then, the `hard' evidence shows a slow loss of follicles starting from the centre and receeding outwards, in the very graft types that were claimed to `prove' the current donor dominance theory. Hypoxia can be ruled out as the cause of this balding process, because of the timeframe, and the quoted studies.

So what we are left with is that these grafts when transplanted into the male pattern baldness area, `ALSO' suffer from male pattern baldness!!

This body of evidence, conclusively `disproves' the current donor doninance theory, as it is currently presented!

The only transplanted follicles that are not effected by male pattern baldness long term, are those transplanted anagen follicles that have had a healing process occour directly adjacent to, or around them.

This is a consistent factor in grafts of any size, and because of this, the transplantation industry has reached the conclusion that `small' is better.

This evidence strongly suggests that the protection of transplanted follicles from miniaturization in the male pattern baldness area, is related to changes induced by the healing process in the tissue `around' the follicles, and not to any `difference' in the follicles themselves!

S Foote.

 

[Bryan]

Re: Dispensing with the current outdated donor dominance the

Stephen, let me say right at the start that I'm going to make every effort to be as pleasant and respectful to you in this reply as I reasonably can!

Nordstrom used grafts of 4mm in diameter, and studied these for 21 months. Orentreich reportedly used 4 to 6mm diameter grafts, and studied these for around 2 to 2 1/2 years.

Both these reputable scientists reported no significant loss of hair in these grafts when transplanted from the back of the head into the balding area, over the time period of the studies. This is a `VERY' important observation!

That's not QUITE true. More on that important issue a little later in this post.

The problem over the period since these early experiments is that further more longer term observations concerning transplantation, have been limited within the transplantation industry. Any potential `problem' with the current `donor dominance' theory they are `selling', would likely be dismissed as not related to the basic theory of what they are selling!

I'd be curious to know if you really think that there's some kind of "cover-up" out there among all the millions of men who have had hair transplants, or some mutual decision to remain quiet about their results. Do you really think that their transplanted follicles are continuing to bald? Don't you think word would have gotten out about it by now, if that were the case?

Modern day knowledge now recognises that a `balding' process happens in grafts transplanted into the male pattern baldness area, from the alledged `resistent' area at the back of the head!!

Do you think it's fair and accurate to describe it as a BALDING process per se, or is it more accurate to acknowledge that SOME transplanted follicles (even perfectly NORMAL ones) will fail to "take", and fall out for various reasons, both known and unknown (including, possibly, the accepted "hypoxia" explanation)?

This is described as`doughnutting'. This loss of the transplanted hair starts in the middle of the larger grafts, as used in the early studies, and continues to receed outwards in these grafts. This effects grafts of 3mm in diameter upwards, and is a consistent factor in these larger grafts. Over time, the only hair that remains in these grafts is around the edges!

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

The transplantation industry tries to explain this through hypoxia, (a lack of oxygen in the centre of these large grafts}.

However, recognised physiology rejects the `hypoxia hypothesis' completely!.

If hypoxia is going to have an adverse effect on cell growth, it has this effect very quickly. This study shows that hypoxia induces a nine fold increase in production of TGF beta-1, from dermal fibroblasts in tissue culture within 72 hours!!

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

Yes, but so what?? You can't predict the exact timetable for the loss of transplanted hairs, based only on the results of the TGF beta-1 increase in some in vitro experiment! Remember, male pattern baldness usually develops over a period of YEARS!

In my opinion, the "hypoxia" explanation for "doughnutting" is a quite plausible one.

So if hypoxia `was' going to reduce hair growth in these large grafts, it would do so within weeks at the outside. Follicles in these grafts would certainly `NOT' survive the periods as reported in the early studies of around 2 years!

Stephen, you seem to be a little confused about the facts in these experiments, and I'm going to try to explain it to you, the way I see it:

I think that the (alleged) hypoxia DOES reduce hair growth within weeks. I think the numbers reported by Nordstrom (Orentreich didn't give any actual before-and after numbers, he just reported the overall effect of either continued growth or continued balding) start with the POST-HYPOXIA counts, if you know what I mean. Here's yet another excerpt from the study, the first three sentences from 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 graphs were then excised for histological examination.

See what I mean? The very first count at 5 months was almost certainly already POST-HYPOXIA, and _all_ the grafts were already diminished equally by that one common factor. The subsequent haircounts at 10 months and 21 months, on the other hand, were a clear manifestation of either continued male pattern baldness (in the case of the frontal grafts), or continued normal growth (in the case of the occipital graft).

Most significantly, deliberately induced hypoxia in the male pattern baldness scalp, has been shown to `improve' hair follicle condition considerably!

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

You need to keep in mind that that particular study, and more importantly its INTERPRETATION, are highly controversial. The author himself suggested that it worked by reducing the supply of androgens in the blood, if I recall correctly. In any event, I keep that study around mainly as a counter to all the people who like to claim that minoxidil works by increasing blood supply to the scalp. I throw that study up to them, just in an effort to challenge their assumptions! :wink: Frankly, I'd like to see it duplicated by someone else, before I can fully believe it myself.

To recap then, the `hard' evidence shows a slow loss of follicles starting from the centre and receeding outwards, in the very graft types that were claimed to `prove' the current donor dominance theory. Hypoxia can be ruled out as the cause of this balding process, because of the timeframe, and the quoted studies.

Not by any stretch can hypoxia be "ruled out". I hope you'll acknowledge my explanation above.

So what we are left with is that these grafts when transplanted into the male pattern baldness area, `ALSO' suffer from male pattern baldness!!

This body of evidence, conclusively `disproves' the current donor doninance theory, as it is currently presented!

Uh, no it doesn't. Not by a long-shot. What you have completely failed to explain is why the numbers of hairs in the transplanted grafts in the Nordstrom experiment (after the initial 5-month period during which hypoxia undoubtedly took its toll on ALL the grafts equally) subsequently COMPLETELY DIVERGED in their natural course: the frontal hairs DECLINED sharply, while the occipital hairs actually INCREASED slightly. You need to acknowledge that you have no explanation for that, according to your theory. For the rest of us, the explanation is clear: there's some fundamental difference between balding and non-balding follicles that exists within the follicles themselves (or, as Nordstrom is careful to acknowlege, their "very close surrounding"). It has nothing to do with edema or contact-inhibition, as these studies make perfectly clear.

Bryan

 

[S Foote.]

Let's keep this as concise and to the point as we can Bryan, because hypoxia is very simply a factor that the current donor dominance theory cannot be reconciled with!!

Most significantly, deliberately induced hypoxia in the male pattern baldness scalp, has been shown to `improve' hair follicle condition considerably!

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

You need to keep in mind that that particular study, and more importantly its INTERPRETATION, are highly controversial. The author himself suggested that it worked by reducing the supply of androgens in the blood, if I recall correctly. In any event, I keep that study around mainly as a counter to all the people who like to claim that minoxidil works by increasing blood supply to the scalp. I throw that study up to them, just in an effort to challenge their assumptions! :wink: Frankly, I'd like to see it duplicated by someone else, before I can fully believe it myself.

I agree that there are a number of interpretations that could be placed on the study, as to the cause and effect details.

But, and this is a `BIG BUT', for the purposes of `this particular' argument, the facts of that study are very clear!

Hypoxia `IS' induced in the balding scalp, and follicle condition `DOES' improve significantly!

This is directly against the suggestion that hypoxia in grafts is `killing' follicles! Also you may be interested in another study that shows induced hypoxia significantly increases VEGF in tissue. You have claimed in the past that increased VEGF is implicated as a possible mechanism of minoxidil's effect, and healthy hair growth in general!

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

More support for hypoxia increasing hair growth `NOT' reducing it : : :wink:

To recap then, the `hard' evidence shows a slow loss of follicles starting from the centre and receeding outwards, in the very graft types that were claimed to `prove' the current donor dominance theory. Hypoxia can be ruled out as the cause of this balding process, because of the timeframe, and the quoted studies.

Not by any stretch can hypoxia be "ruled out". I hope you'll acknowledge my explanation above.

With respect Bryan, the speculation in your explaination just doesn't fit the recognised facts in the matter.

The initial fall out in transplantation described as `shock' fall out, effects all the transplanted follicles and those close by. Even if this is related to initial hypoxia during healing, and really this is highly unlikely, the follicles in the grafts `recover'.

These follicles can then grow normally for a long time as the studies show. This initial loss and recovery, can in no way be linked to the later balding process in the greater area of these larger grafts.

So what we are left with is that these grafts when transplanted into the male pattern baldness area, `ALSO' suffer from male pattern baldness!!

This body of evidence, conclusively `disproves' the current donor doninance theory, as it is currently presented!

Uh, no it doesn't. Not by a long-shot. What you have completely failed to explain is why the numbers of hairs in the transplanted grafts in the Nordstrom experiment (after the initial 5-month period during which hypoxia undoubtedly took its toll on ALL the grafts equally) subsequently COMPLETELY DIVERGED in their natural course: the frontal hairs DECLINED sharply, while the occipital hairs actually INCREASED slightly. You need to acknowledge that you have no explanation for that, according to your theory. For the rest of us, the explanation is clear: there's some fundamental difference between balding and non-balding follicles that exists within the follicles themselves (or, as Nordstrom is careful to acknowlege, their "very close surrounding"). It has nothing to do with edema or contact-inhibition, as these studies make perfectly clear.

Bryan

The scalp to body transplant study by Nordstrom `CAN' be explained by my theory, and i have explained to you the principles involved before!

But this `particular' point is not about scalp to body transplantation Bryan. This is about `normal' transplantation to the male pattern baldness area, and the fact that balding developes in these grafts when the current donor dominance idea says it won't!!

You ask me if i think the transplantation industry would try to cover up anything that would dismiss the current donor dominance idea?

Damm right they would!!

They are selling a procedure based on the currently accepted ideas of donor dominance. If this is shown to be `wrong', everyone who has ever been dissapointed with the results of transplantation, will have legal grounds to sue. Can you imagine the legal consequenses? :shock:

I find it very telling that the transplantation industry chooses to find another name for this recognised balding process in large `plugs' over time. Let's call it `doughnutting' or anything else, just as long as we don't use the word `balding' ! 8)

The period of this balding process in these grafts is the same as male pattern baldness, as is the recession from the centre outwards. Hypoxia as the excuse for this just has no basis in recognised scientific fact.

So how can you possibly reconcile this `balding' with the current donor dominance theory? Simple answer, you can't 8)

S Foote.

 

[michael barry]

I can personally attest that some implants do miniaturize because some of mine are. Some of my old micro-grafts (I had 100 implants----an exceedingly small procedure done in 95' in my temple area behind my hairline to "buff-up" the area because I was promised that propecia would keep me from ever losing another hair {obvioiusly I knew nothing back then}) are indeed now miniaturizing. They grow hair that is smaller in circumference and somewhat wavy and short as compared to the straight hair I have. Gonna have to be electrolosying these out over the next few years.

Bryan mentioned the "millions" of men who have had transplants. Last figures I saw were about 250,000 per year. I really have to wonder how happy some of these guys will be 20-25 years from now when they are in their mid-40's and 50's. I think tons of guys went out and got transplants for receeded temples just like I did years ago when propecia was new thinking they'd never lose any more hair. These guys will discover that that is a huge mistake. I hope if I convey anything to any of these men in these forums it is this salient fact:::::: IF YOU GO HORSESHOE BALD SOMEDAY, TRANSPLANTS WILL LOOK LIKE A 'CURIOUS' COMBOVER. Some of your hippocratic wreath thins, to not notice this on bald men is an act of willful ignorance. So, how much of that hair transplanted will thin eventually also? Just guessing at some hippocratic-wreath bald men Ive seen I'd have to guess at least 20% will eventually go as I have seen some pitifully thin hippocratic wreaths (think of the director Ron Howard, physician Andrew Weil, actor Patrick Stewart------these men would have been pitiful candidates for transplants and would be woefully sorry now if they had had them in their 20's).

Whether Stephen's or Armando's alternative theories of male pattern baldness are correct or not, hair transplantation+propecia isnt a cure for baldness by a longshot and cause much anxiety over the long term. I personally am still leaning to the belief that bald people may have hair with too many androgen receptors and intake more androgens into the dermal papilla than people who dont lose hair or lose it too late in life, but obviously have no way to prove it. It would be interesting to take a man without male pattern baldness and shoot his scalp up daily with DHT and andro and see what happened in 5 years. I suspect he'd be thinning, but who knows. This is the real reason why I think the Japanese (I work with a few of them) are balding so much more often and sooner now..........extra androgens in the diet drenching the receptors with more DHT. But Im very open to new ideas. Im curious also as to why procyanidrin solutions that are available and popular in ther very scientifically advanced and reasonable country of Japan arent really sold here yet except on the internet, but then again grape seed extract applied topically wouldnt get a Pharmaceutical paid because thats not really a drug would it?

Stephen is right about one thing, the current situation in hair replacement gets docs paid huge money (for surgeries they let assistants perform about half of), drug companies get paid, and snake oilers to laugh all the way to the bank. Its hard to believe we can clone a cow and remake an entire face, grow bone marrow from stem cells, but not MAKE more hair from what we have yet. Infuriating to be honest

 

[S Foote.]

Thanks for your input Michael.

My personal interest in the mechanisms of male pattern baldness, started after my own transplantation experience as i have refered to before.

S Foote.

 

[Bryan]

I agree that there are a number of interpretations that could be placed on the study, as to the cause and effect details.

But, and this is a `BIG BUT', for the purposes of `this particular' argument, the facts of that study are very clear!

Hypoxia `IS' induced in the balding scalp, and follicle condition `DOES' improve significantly!

This is directly against the suggestion that hypoxia in grafts is `killing' follicles!

I repeat what I said before: I'd like to see somebody else DUPLICATE the findings of that one rather obscure study. YOU only know about it because I posted about it and scanned it for you to read, and _I_ only know about it because Dr. Proctor mentioned it occasionally on alt.baldspot. I have NEVER seen any other reference to it in the medical literature on hairloss, and I've read hundreds of studies on it. It's a rather weak piece of evidence on which to base a claim about the accepted explanation for "doughnutting", isn't it? :wink:

Oh well...who really knows?? I guess the bottom-line is that we really don't know for sure WHAT causes "doughnutting" in hair transplants.

The scalp to body transplant study by Nordstrom `CAN' be explained by my theory, and i have explained to you the principles involved before!

No you haven't. You STILL have not explained why the non-balding occipital follicles in Norstrom's experiment continued to grow normally (the number of hairs actually INCREASED slightly, from the first count to the last count), whereas the ones from the front DECLINED SHARPLY. I will keep asking you this question until you finally acknowledge it and respond to it, so you might as well bite the bullet and answer.

But this `particular' point is not about scalp to body transplantation Bryan. This is about `normal' transplantation to the male pattern baldness area, and the fact that balding developes in these grafts when the current donor dominance idea says it won't!!

So the bottom-line is that you must think there's a huge COVER-UP in the hair transplantation industry, and it's apparently being perpetuated by the patients who've had it performed on them. Do you have any evidence to back all that up, other than just that it's something required by your theory? :wink:

Bryan

 

[Boru]

To S Foote, Bryan and Michael, this is the most interesting debate I have read yet. There is something here which may explain why I have been able to wake up some of my long dormant follicles (20 years full male pattern baldness).
I thought that increased oxygen supply would be a key factor in improving follicle energy. Have I been riding on a red herring? Dr Marechai's article, published in 1977 is worth further consideration.
I decided against transplants years ago, because a friend had a very bad result.
Still, I am gradually improving my hair growth and condition, whether or not improved oxygen supply is helping or hindering.
I keep an open mind.
Boru

 

[S Foote.]

I agree that there are a number of interpretations that could be placed on the study, as to the cause and effect details.

But, and this is a `BIG BUT', for the purposes of `this particular' argument, the facts of that study are very clear!

Hypoxia `IS' induced in the balding scalp, and follicle condition `DOES' improve significantly!

This is directly against the suggestion that hypoxia in grafts is `killing' follicles!

I repeat what I said before: I'd like to see somebody else DUPLICATE the findings of that one rather obscure study. YOU only know about it because I posted about it and scanned it for you to read, and _I_ only know about it because Dr. Proctor mentioned it occasionally on alt.baldspot. I have NEVER seen any other reference to it in the medical literature on hairloss, and I've read hundreds of studies on it. It's a rather weak piece of evidence on which to base a claim about the accepted explanation for "doughnutting", isn't it? :wink:

Well Bryan at least we agree on one thing, and that is the serious need for `DUPLICATION' of experiments, and i would add, a lot more `independent' research to properly answer these questions!

Your unsubstantiated claim above that the accepted explaination for what is called `doughnutting' in grafts is hypoxia, is typical of the bad science that seems `traditional' in hair loss research! Transplantation people just `claim' hypoxia as the cause with no hard evidence for this, and you recommend we just go along with this?

This is certainly not an explaination that would be accepted outside of hair loss research by medical scientists! This just goes against everything known about the effects of hypoxia, and just the recognised time scale involved in this `BALDING' rules out hypoxia!

Oh well...who really knows?? I guess the bottom-line is that we really don't know for sure WHAT causes "doughnutting" in hair transplants.

It is clearly a continuation of the male balding process in these grafts, nothing else fits the physiology of it and the timescale! :wink:

The scalp to body transplant study by Nordstrom `CAN' be explained by my theory, and i have explained to you the principles involved before!

No you haven't. You STILL have not explained why the non-balding occipital follicles in Norstrom's experiment continued to grow normally (the number of hairs actually INCREASED slightly, from the first count to the last count), whereas the ones from the front DECLINED SHARPLY. I will keep asking you this question until you finally acknowledge it and respond to it, so you might as well bite the bullet and answer.

I had thought you understood how my theory explains this, because of our previous debates? OK, here it is `again' :roll:

According to my theory, it is the `pressure' conditions in the tissue around the follicles, that effects their growth in anagen through normal contact inhibition. Any such `change' in tissue pressure will `NOT' effect existing scalp follicles already in anagen. Such a pressure change will only effect these follicles when they go through another normal cycle and re-enter anagen.

The balding tissue transplanted to the body in Norstrom's experiment, is `swollen' tissue. The edema that started the balding process, has `already' condemed the remaining follicles in these `large' grafts. As soon as they enter anagen again, the tissue `re-modeling' and micro- fibrosis caused by the prior edema, is `still' going to cause further balding as subsequent follicles try to re-enlarge in anagen again.

The now better drainage conditions in the surrounding body tissue, may over time allow some growth improvement, `BUT' because of the large size of the grafts used in Norstrom's study, this would likely take a lot longer than the duration of Norstrom's observations, and also depend on the pre-existing fibrotic conditions. Fibrosis was not a recognised factor in male pattern baldness at the time of this study!!!!!!

In contrast, the `healthy' follicle grafts transplanted to the body, are devoid of any pre-existing adverse tissue conditions like follicle fibrosis, and would likely benefit from the reduced fluid pressure `feed' into these grafts created by the transplantation process itself.

This seemed to be the case as these grafts improved growth slightly.

This is how my theory explains Norstroms observations with these large grafts over the test period.

Now this diversion from the point has been answered, whether you accept this answer or not Bryan :wink:

The balding process over time in `normal' transplantation to the bald area (doughnutting!}, is explained by my theory as follows.

These healthy `larger' grafts transplanted to the bald scalp, also have a reduced fluid `feed' as described above. But over time the increased fluid pressure in the surrounding bald tissue does penetrate and `swell' this graft tissue. The swelling and so the movement of dermal cells into the follicles `space' that causes the problem, is greater where the transplanted tissue is less well supported by the ring of scar tissue around these larger grafts. This is the center of these grafts.

So according to my theory, the first place the slowly increasing pressure will effect these large grafts is in the center, working outwards.

Refer to Fig 3, in my paper. http://www.hairsite2.com/library/abst-167.htm

Incidently, this also explains the raised centers of these grafts over time, or the so called `cobblestoning'.

This is exactly what is seen in these larger grafts over time. The only follicles that survive in these grafts, or in `ANY' other transplantation method for that matter, are those transplanted anagen follicles that have had a `space' protecting fibrose scarring process around them.

That is those right at the edges of larger grafts, or very close to the scar formation as the later smaller grafts experience. Such a fibrose `scaffold' is recognised as allowing organ enlargement in physiology, as i have referenced before.

What Norstrom `should' have done, is to have transplanted healthy `plugs' from the back of the head, both to the body as his original experiment, `AND' to the bald area in the same individuals!

If the bald area transplants `doughnutted' over time and the body transplants didn't, we would know for sure that the conditions in the surrounding tissue are the cause of the `difference'. The current theory you support would be really scewed then Bryan 8)

Incidently and quite ironicaly, a study by the `Orentreich foundation' clearly showed that under the right conditions, transplanted balding human follicles can regenerate!

http://www.hairsite4.com/dc/dcboard.php ... 8612&page=

Again, it isn't always what is in these studies but what isn't! There is no mention in the abstract at least, about the size of grafts used, or the androgenic status of these mice.

But this `particular' point is not about scalp to body transplantation Bryan. This is about `normal' transplantation to the male pattern baldness area, and the fact that balding developes in these grafts when the current donor dominance idea says it won't!!

So the bottom-line is that you must think there's a huge COVER-UP in the hair transplantation industry, and it's apparently being perpetuated by the patients who've had it performed on them. Do you have any evidence to back all that up, other than just that it's something required by your theory? :wink:

Bryan

Huh????????

Get with the program will you Bryan!

The transplant industry is `NOT' denying this balding in grafts, there are many references to this.

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

They don't deny it, they just make up a pathetic un-scientific excuse for it!! :roll:

S Foote.

 

[michael barry]

Stephen and Bryan,
If vellus hairs were transplanted to immune-deficient mice and they grew to normal size right along with non-male pattern baldness hairs also transplanted..........................
.......................... that would seem to indicate that our immune systems have MUCH to do with male pattern baldness? Correct?


I mean, if left in the donors head, the vellus hairs or miniaturized hairs were dying right? But they regrew on the immune-deficient mice. Perhaps after DHT gets in "too much" and its levels are "to high" within the follicle proper, the genetic instructions sent out precipitate the immune system over responding and killing the weak follicle? Guys have any comments?

 

[Bryan]

Your unsubstantiated claim above that the accepted explaination for what is called `doughnutting' in grafts is hypoxia, is typical of the bad science that seems `traditional' in hair loss research! Transplantation people just `claim' hypoxia as the cause with no hard evidence for this, and you recommend we just go along with this?

This is certainly not an explaination that would be accepted outside of hair loss research by medical scientists! This just goes against everything known about the effects of hypoxia, and just the recognised time scale involved in this `BALDING' rules out hypoxia!

Really? Please provide evidence for that claim. It's easy just to give lip-service to your theory, but it's another matter to back it up with scientific EVIDENCE. What supposedly are the "known effects" of hypoxia, and how does the time scale here supposedly "rule it out"?

According to my theory, it is the `pressure' conditions in the tissue around the follicles, that effects their growth in anagen through normal contact inhibition. Any such `change' in tissue pressure will `NOT' effect existing scalp follicles already in anagen. Such a pressure change will only effect these follicles when they go through another normal cycle and re-enter anagen.

Why is that?? Please explain that claim. Why would it have to go through another cycle, first?

The balding tissue transplanted to the body in Norstrom's experiment, is `swollen' tissue. The edema that started the balding process, has `already' condemed the remaining follicles in these `large' grafts. As soon as they enter anagen again, the tissue `re-modeling' and micro- fibrosis caused by the prior edema, is `still' going to cause further balding as subsequent follicles try to re-enlarge in anagen again.

The now better drainage conditions in the surrounding body tissue, may over time allow some growth improvement, `BUT' because of the large size of the grafts used in Norstrom's study, this would likely take a lot longer than the duration of Norstrom's observations, and also depend on the pre-existing fibrotic conditions.

Ok, so your excuse...er, sorry...I meant explanation in this case is that the prior damage (fibrosis) to the follicle is continuing to inhibit its growth, even though it's now in a location devoid of "edema". Unfortunately, there's one little hitch in that explanation, and it has to do with the study that you cited yourself later on in this post, the one about balding human follicles transplanted into the skin of immunodeficient mice! Here's the problem in a nutshell: why didn't the fibrosis prevent THOSE follicles from enlarging greatly and growing normally? :wink:

This is how my theory explains Norstroms observations with these large grafts over the test period.

Not very impressive, Stephen. Still more theorizing with a distinctly ad hoc flavor. Sorry.

The balding process over time in `normal' transplantation to the bald area (doughnutting!}, is explained by my theory as follows.

The ALLEGED balding process. I personally don't think it has anything to do with balding. You only refer to it that because there's no other way, within the confines of your eccentric theory.

These healthy `larger' grafts transplanted to the bald scalp, also have a reduced fluid `feed' as described above. But over time the increased fluid pressure in the surrounding bald tissue does penetrate and `swell' this graft tissue. The swelling and so the movement of dermal cells into the follicles `space' that causes the problem, is greater where the transplanted tissue is less well supported by the ring of scar tissue around these larger grafts. This is the center of these grafts.

HUH?? That's just more ad hoc excuse-making. Even if a follicle is up against a "wall" of fibrosis on one side, it's still going to be subjected to the increased fluid pressure. You're grasping at straws.

What Norstrom `should' have done, is to have transplanted healthy `plugs' from the back of the head, both to the body as his original experiment, `AND' to the bald area in the same individuals!

If the bald area transplants `doughnutted' over time and the body transplants didn't, we would know for sure that the conditions in the surrounding tissue are the cause of the `difference'. The current theory you support would be really scewed then Bryan 8)

Nordstrom didn't do that experiment, but Orentreich DID. He transplanted non-balding follicles to both balding and non-balding areas, and they grew comparably well. It's YOUR theory which is screwed-up. 8)

Incidently and quite ironicaly, a study by the `Orentreich foundation' clearly showed that under the right conditions, transplanted balding human follicles can regenerate!

http://www.hairsite4.com/dc/dcboard.php ... 8612&page=

Yes. I've read that full steady, and I've been meaning to post about it on the hairloss sites. It appears to be strong evidence for the putative immune component of balding, not "edema" or "contact inhibition".

Again, it isn't always what is in these studies but what isn't! There is no mention in the abstract at least, about the size of grafts used, or the androgenic status of these mice.

From the study: "Tissue was removed by 2-mm, full-thickness, punch excisions from both balding and hairy areas of the scalp..." I don't want to go into any more detail about that study right now. I'll do that when I post about it in the near future on both HairLossTalk.com and HLH.

The transplant industry is `NOT' denying this balding in grafts, there are many references to this.

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

They don't deny it, they just make up a pathetic un-scientific excuse for it!! :roll:

Again, you piss me off when you keep referring to it as "balding". That's only your goofy CLAIM, for which you've presented no credible evidence.

Bryan

 

[Bryan]

Stephen and Bryan,
If vellus hairs were transplanted to immune-deficient mice and they grew to normal size right along with non-male pattern baldness hairs also transplanted..........................
.......................... that would seem to indicate that our immune systems have MUCH to do with male pattern baldness? Correct?

Yes, it seems to make a rather strong case for that!

I mean, if left in the donors head, the vellus hairs or miniaturized hairs were dying right? But they regrew on the immune-deficient mice. Perhaps after DHT gets in "too much" and its levels are "to high" within the follicle proper, the genetic instructions sent out precipitate the immune system over responding and killing the weak follicle? Guys have any comments?

Dr. Proctor has said for years on alt.baldspot that androgens seem to "mark" the hair follicles in some way that makes them draw the attention of the immune system. Until now, I've always thought that the alleged immune component in balding (if it really exists at all) is something that happens very late in the game; but now, that mouse study makes it seem like a very real phenomenon that plays a serious role in male pattern baldness.

Bryan

 

[S Foote.]

Your unsubstantiated claim above that the accepted explaination for what is called `doughnutting' in grafts is hypoxia, is typical of the bad science that seems `traditional' in hair loss research! Transplantation people just `claim' hypoxia as the cause with no hard evidence for this, and you recommend we just go along with this?

This is certainly not an explaination that would be accepted outside of hair loss research by medical scientists! This just goes against everything known about the effects of hypoxia, and just the recognised time scale involved in this `BALDING' rules out hypoxia!

Really? Please provide evidence for that claim. It's easy just to give lip-service to your theory, but it's another matter to back it up with scientific EVIDENCE. What supposedly are the "known effects" of hypoxia, and how does the time scale here supposedly "rule it out"?

The scientific evidence lies in everything `KNOWN' about the effects of hypoxia Bryan. Do some basic research before you make these claims 8)

Hypoxia induced into tissue cultures, creates major changes in the cells expression of substances within `HOURS'. In-vivo induced hypoxia has any effect it is `going' to have likewise very quickly. Look it up for yourself Bryan :roll:

There is no way that hypoxia induced by the circulation changes caused at the time of transplantation, can then `kick in' only after 3 or 4 years!The whole idea is ridiculous given known physiology :wink:

According to my theory, it is the `pressure' conditions in the tissue around the follicles, that effects their growth in anagen through normal contact inhibition. Any such `change' in tissue pressure will `NOT' effect existing scalp follicles already in anagen. Such a pressure change will only effect these follicles when they go through another normal cycle and re-enter anagen.

Why is that?? Please explain that claim. Why would it have to go through another cycle, first?

Normal contact inhibition only effects `growing' organs. An increase in resistence of dermal cells caused by rising fluid pressures, will only restrict the growth of enlarging follicles, not those already enlarged.

The balding tissue transplanted to the body in Norstrom's experiment, is `swollen' tissue. The edema that started the balding process, has `already' condemed the remaining follicles in these `large' grafts. As soon as they enter anagen again, the tissue `re-modeling' and micro- fibrosis caused by the prior edema, is `still' going to cause further balding as subsequent follicles try to re-enlarge in anagen again.

The now better drainage conditions in the surrounding body tissue, may over time allow some growth improvement, `BUT' because of the large size of the grafts used in Norstrom's study, this would likely take a lot longer than the duration of Norstrom's observations, and also depend on the pre-existing fibrotic conditions.

Ok, so your excuse...er, sorry...I meant explanation in this case is that the prior damage (fibrosis) to the follicle is continuing to inhibit its growth, even though it's now in a location devoid of "edema". Unfortunately, there's one little hitch in that explanation, and it has to do with the study that you cited yourself later on in this post, the one about balding human follicles transplanted into the skin of immunodeficient mice! Here's the problem in a nutshell: why didn't the fibrosis prevent THOSE follicles from enlarging greatly and growing normally? :wink:

Let's get to the point here Bryan.

You can pick all you like about my theory, but it is based on recognised mechanisms in physiology. Not the pure fantasy required by the current theory. Just to be clear, i will elaborate on your comment below.

These healthy `larger' grafts transplanted to the bald scalp, also have a reduced fluid `feed' as described above. But over time the increased fluid pressure in the surrounding bald tissue does penetrate and `swell' this graft tissue. The swelling and so the movement of dermal cells into the follicles `space' that causes the problem, is greater where the transplanted tissue is less well supported by the ring of scar tissue around these larger grafts. This is the center of these grafts.

HUH?? That's just more ad hoc excuse-making. Even if a follicle is up against a "wall" of fibrosis on one side, it's still going to be subjected to the increased fluid pressure. You're grasping at straws.

My theory is not to do with fluid pressure acting directly on the follicles, as you well know if you were honest Bryan!

It is about how this pressure increases the resistence to movement of dermal cells required to allow follicle enlargement.

The fibrose tissue `fibers' produced at the healing of grafts , extends far enough into the grafts to form a fibrose `shell' around the transplanted anagen follicles at the edges. In my opinion it is this `scaffold' that protects these follicles from the pressure that creates male pattern baldness.

Now i really don't care what you think about the issue of transplantation as it relates to my theory!

The immuno deficient mice study here, is very telling. I have said before, it is common knowledge that edema and immunology are closely linked. One can change the other and vice versa.

In these mice, the formation of fibrose tissue that `locks' follicle size in the as transplanted state (according to my theory), is greatly restricted. Fibrosis is a consequence `OF' immune system activity, just read these forums if you don't believe me! :wink:

So in these mice the fibrose `scaffold' is reduced, allowing the re-enlargement of these male pattern baldness follicles in line with the local pressure conditions, simple. 8)

By your own previous admission Bryan you `CANNOT' explain this mouse study by your theory. You admit what the scientists think, that is that the immunology in human male pattern baldness is down the line from `actual' follicle miniaturisation.

On top of that blow to your theory, the immune component is missing in the macaque studies you love to quote. My theory can explain this little fly in your ointment Bryan, yours can't!

If you are now doing a `U' turn on the immunology question, you have a lot of explaining to do!!

The transplant industry is `NOT' denying this balding in grafts, there are many references to this.

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

They don't deny it, they just make up a pathetic un-scientific excuse for it!! :roll:

Again, you piss me off when you keep referring to it as "balding". That's only your goofy CLAIM, for which you've presented no credible evidence.

Bryan

You have got to be joking Bryan :lol:

I'am sorry an accurate description of what happens in these grafts `pisses' you off :roll:

Let's see? The hair in these grafts thins and receeds from the center outwards over time, and becomes permanently lost.

The `CORRECT' term for this procces is `BALDING'

You just don't like it Bryan simply because your theory cannot explain it scientificaly.

S Foote.

 

[Bryan]

[quote="S Foote.":f36da]Your unsubstantiated claim above that the accepted explaination for what is called `doughnutting' in grafts is hypoxia, is typical of the bad science that seems `traditional' in hair loss research! Transplantation people just `claim' hypoxia as the cause with no hard evidence for this, and you recommend we just go along with this?

This is certainly not an explaination that would be accepted outside of hair loss research by medical scientists! This just goes against everything known about the effects of hypoxia, and just the recognised time scale involved in this `BALDING' rules out hypoxia!

Really? Please provide evidence for that claim. It's easy just to give lip-service to your theory, but it's another matter to back it up with scientific EVIDENCE. What supposedly are the "known effects" of hypoxia, and how does the time scale here supposedly "rule it out"?

The scientific evidence lies in everything `KNOWN' about the effects of hypoxia Bryan. Do some basic research before you make these claims 8)

Hypoxia induced into tissue cultures, creates major changes in the cells expression of substances within `HOURS'. In-vivo induced hypoxia has any effect it is `going' to have likewise very quickly. Look it up for yourself Bryan :roll: [/quote:f36da]

So how do you know that that DOESN'T happen in hair transplants within hours?

There is no way that hypoxia induced by the circulation changes caused at the time of transplantation, can then `kick in' only after 3 or 4 years!The whole idea is ridiculous given known physiology :wink:

Who's claiming that it DOES "kick in" after 3 or 4 years?

Normal contact inhibition only effects `growing' organs. An increase in resistence of dermal cells caused by rising fluid pressures, will only restrict the growth of enlarging follicles, not those already enlarged.

That seems like a rather arbitrary assumption to me. I see no a priori reason why it wouldn't also affect follicles that are relatively static in size. If there's pressure on the static cells, then it seems that surely the (alleged) contact inhibition would alter growth factors in such a way as to suppress them.

HUH?? That's just more ad hoc excuse-making. Even if a follicle is up against a "wall" of fibrosis on one side, it's still going to be subjected to the increased fluid pressure. You're grasping at straws.

My theory is not to do with fluid pressure acting directly on the follicles, as you well know if you were honest Bryan!

It is about how this pressure increases the resistence to movement of dermal cells required to allow follicle enlargement.

The fibrose tissue `fibers' produced at the healing of grafts , extends far enough into the grafts to form a fibrose `shell' around the transplanted anagen follicles at the edges. In my opinion it is this `scaffold' that protects these follicles from the pressure that creates male pattern baldness.

Hmmm.... "The pressure doesn't act directly on cells, but it increases the resistance to their movement." Stephen, that's getting too Alice in Wonderland for me!

I suppose according to you, if I strap lead weights on my belt and jump overboard in the North Atlantic, by the time I sink to the depths of the wreckage of the Titanic, the pressure won't bother me as long as I don't try to move around!

By your own previous admission Bryan you `CANNOT' explain this mouse study by your theory. You admit what the scientists think, that is that the immunology in human male pattern baldness is down the line from `actual' follicle miniaturisation.

That study does make it appear that the immune component is a more important one in balding than _I_ previously thought, although other people have always thought that it was important. Dr. Proctor has mentioned it for YEARS on alt.baldspot. However, I'd like to see that study duplicated by others.

On top of that blow to your theory...

It's not a "blow" to my theory, it's just an indication perhaps that the importance of the various relative factors in balding may need to be readjusted some. I've always acknowledged the immune component of balding, it's just that I've usually thought that it was something that happened relatively late in male pattern baldness.

...the immune component is missing in the macaque studies you love to quote.

Who sez it's "missing"? I believe there's been some material presented about macaque follicular inflammation, sometime in the past.

Let's see? The hair in these grafts thins and receeds from the center outwards over time, and becomes permanently lost.

The `CORRECT' term for this procces is `BALDING'

What is the timeline for the "doughnutting" effect? BE SPECIFIC.

Bryan

 

[S Foote.]

[quote="S Foote.":5dfe1]Your unsubstantiated claim above that the accepted explaination for what is called `doughnutting' in grafts is hypoxia, is typical of the bad science that seems `traditional' in hair loss research! Transplantation people just `claim' hypoxia as the cause with no hard evidence for this, and you recommend we just go along with this?

This is certainly not an explaination that would be accepted outside of hair loss research by medical scientists! This just goes against everything known about the effects of hypoxia, and just the recognised time scale involved in this `BALDING' rules out hypoxia!

Really? Please provide evidence for that claim. It's easy just to give lip-service to your theory, but it's another matter to back it up with scientific EVIDENCE. What supposedly are the "known effects" of hypoxia, and how does the time scale here supposedly "rule it out"?

The scientific evidence lies in everything `KNOWN' about the effects of hypoxia Bryan. Do some basic research before you make these claims 8)

Hypoxia induced into tissue cultures, creates major changes in the cells expression of substances within `HOURS'. In-vivo induced hypoxia has any effect it is `going' to have likewise very quickly. Look it up for yourself Bryan :roll:

So how do you know that that DOESN'T happen in hair transplants within hours?

There is no way that hypoxia induced by the circulation changes caused at the time of transplantation, can then `kick in' only after 3 or 4 years!The whole idea is ridiculous given known physiology :wink:

Who's claiming that it DOES "kick in" after 3 or 4 years?[/quote:5dfe1]

The timeframe of the studies previously quoted, clearly show that no thinning of the grafts was noticed in the 18 months to 2 years of the studies. So how can hypoxia possibly be involved when it has it's effects within hours!

Something is `kicking in' within 3 or 4 years to create the balding process in the studied grafts refered to as `doughnutting'.

It sure as hell isn't hypoxia, and is perfectly consistent with the timeframe of male pattern baldness.

If you want to argue about the recognised control on `growing' organ size determined by normal contact inhibition, study it!! My arguments are based on recognised `basic' principles in multicellular physiology. You really need to brush up on your `basic textbook' knowledge Bryan :wink:

I'am not going to waste my time trying to educate you on the subject ! :roll:

S Foote.

 

[Bryan]

The timeframe of the studies previously quoted, clearly show that no thinning of the grafts was noticed in the 18 months to 2 years of the studies. So how can hypoxia possibly be involved when it has it's effects within hours!

That's EXACTLY my point. Nobody (that I'm aware of) is CLAIMING that there is "hypoxia" involved from 18 months to 2 years! :wink:

Something is `kicking in' within 3 or 4 years to create the balding process in the studied grafts refered to as `doughnutting'.

And I'm asking you AGAIN to provide me a specific TIMELINE of the "doughnutting" effect. Something from the MEDICAL LITERATURE, not just your own febrile claims and accusations! Prove to me that it happens around 3 to 4 years.

I'am not going to waste my time trying to educate you on the subject ! :roll:

What's wrong, Stephen? Are you bailing out of the discussion, now that I'm forcing you to provide SPECIFIC REFERENCES for your claims about the timeline of the "doughnutting" effect??

Bryan

 

[Footy]

The timeframe of the studies previously quoted, clearly show that no thinning of the grafts was noticed in the 18 months to 2 years of the studies. So how can hypoxia possibly be involved when it has it's effects within hours!

That's EXACTLY my point. Nobody (that I'm aware of) is CLAIMING that there is "hypoxia" involved from 18 months to 2 years! :wink:

[quote="S Foote.":c4d32]Something is `kicking in' within 3 or 4 years to create the balding process in the studied grafts refered to as `doughnutting'.

And I'm asking you AGAIN to provide me a specific TIMELINE of the "doughnutting" effect. Something from the MEDICAL LITERATURE, not just your own febrile claims and accusations! Prove to me that it happens around 3 to 4 years.

I'am not going to waste my time trying to educate you on the subject ! :roll:

What's wrong, Stephen? Are you bailing out of the discussion, now that I'm forcing you to provide SPECIFIC REFERENCES for your claims about the timeline of the "doughnutting" effect??

Bryan[/quote:c4d32]

Oh no you don't Bryan!

Don't you miss-quote me here 8)

You know damm well my reference to not educating you, was in the context of basic human physiology, `NOT' the `doughnutting' issue!

The `specific references' you ask for, you already know about for Christ's sake. What are you trying to do here? You are making it very clear to everyone reading this that you are playing a `ego' game here, that has nothing to do with the `science' you claim to be interested in!

The early studies we talked about using the larger grafts now `KNOWN' to bald with time, had no such balding observed in the period of the studies.

As these studies were for up to 2 years, we can conclude that the `balding' process in these grafts generaly starts later than 2 years. This completely rules out hypoxia as the cause of this balding, and is more realisticaly a continuation of male pattern baldness based on the timescale.

Can you offer us `ANY' other explaination for this `long term' balding in these grafts Bryan?

No you can't!

S Foote.

 

[Bryan]

The `specific references' you ask for, you already know about for Christ's sake.

Nope. I do NOT know about them, because I've never seen any, and you haven't presented any.

What are you trying to do here? You are making it very clear to everyone reading this that you are playing a `ego' game here, that has nothing to do with the `science' you claim to be interested in!

ROTFLMAO!!! I think we can all take that as an admission that you STILL don't have any specific scientific references to the timeline of "doughnutting", or continued alleged "balding" of transplanted hair follicles, or anything else you want to call it! :lol: :lol: :lol:

The early studies we talked about using the larger grafts now `KNOWN' to bald with time, had no such balding observed in the period of the studies.

Well, at least you got the SECOND part of that sentence right, but you still haven't been able to cough-up any support for the claim in the FIRST part! :wink:

As these studies were for up to 2 years, we can conclude that the `balding' process in these grafts generaly starts later than 2 years. This completely rules out hypoxia as the cause of this balding, and is more realisticaly a continuation of male pattern baldness based on the timescale.

Can you offer us `ANY' other explaination for this `long term' balding in these grafts Bryan?

Find me some scientific evidence that it happens at all, Stephen.

Bryan

 

[Footy]

The `specific references' you ask for, you already know about for Christ's sake.

Nope. I do NOT know about them, because I've never seen any, and you haven't presented any.

You were the one who posted the Orentriech study Bryan! Did you actually read that?

He used grafts of 4mm diameter or over, and noted no balding in these when re-located to the bald scalp over a period of study of around two years.

We now know that grafts of these sizes `DO' bald with time, so the time frame has to be over two years, and outside of any effects of hypoxia. :wink:

All the data is there to support my argument in studies `YOU' posted Bryan!!

Try interpreting them scientificaly 8)

You have yet to provide me with your explaination of the continued `BALDING' process in these grafts that is now widely accepted in the transplantation industry Bryan?

This is because you can't explain this in terms of the theory you support, simple :wink:

S Foote.

 

[Bryan]

We now know that grafts of these sizes `DO' bald with time, so the time frame has to be over two years, and outside of any effects of hypoxia. :wink:

All the data is there to support my argument in studies `YOU' posted Bryan!!

There is no such data at all. I believe in the phenomenon called "doughnutting", but it's apparently something that happens very early after transplantation (like a matter of weeks or perhaps a month or two).

You're making stuff up, based on what you WANT to believe. Get back to us when you have scientific EVIDENCE for your claims, not just sheer speculation.

Bryan

 

[Footy]

We now know that grafts of these sizes `DO' bald with time, so the time frame has to be over two years, and outside of any effects of hypoxia. :wink:

All the data is there to support my argument in studies `YOU' posted Bryan!!

There is no such data at all. I believe in the phenomenon called "doughnutting", but it's apparently something that happens very early after transplantation (like a matter of weeks or perhaps a month or two).

You're making stuff up, based on what you WANT to believe. Get back to us when you have scientific EVIDENCE for your claims, not just sheer speculation.

Bryan

Your blatant hypocrisy is now clear for all to see Bryan!

Above for all to see you say:

"There is no such data at all. I believe in the phenomenon called "doughnutting", but it's apparently something that happens very early after transplantation (like a matter of weeks or perhaps a month or two)."

But in the original thread here:

http://www.hairlosstalk.com/discussions ... 71&start=0

You say this in response to my point:



S Foote. wrote:
If you remember Bryan, my argument is based on the conditions in the `VERY CLOSE SURROUNDING' of the follicle! I have explained my own thoughts on this influence in previous threads, however there is something here you just `CANNOT' explain by your notion of the `mechanism' involved being `in' the follicles themselves!!

Again as in the last `old' study you posted, the graft size used was `large', that is 4mm plugs. Again, no mention was made of cental hair loss in the alledged `DHT resistent' plugs over the period of the hair counts (21 months).

Bryan wrote:
Of course not. Because there WASN'T any.

S Foote. wrote:
But we now know that in 4mm grafts, a `balding' proccess `DOES' happen over time, the doughnutting effect as it is called is well documented, as i have referenced before.

Bryan wrote:
Please cite some references for it. It must be an uncommon phenomenon, if it didn't happen to either Orentreich or Nordstrom.

__________________________________________

So first you deny the hair loss refered to as `doughnutting' exists at all, because the study `YOU' posted didn't refer to it. You also tried to claim it must be some kind of rare phenomenon. Yet this is a very `COMMON' phenomenon widely accepted even in the transplantation industry, as the references i provided at the time clearly confirmed!!


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

Now you are trying to say that this happens very quickly in these grafts. Which is `COMPLETELY' against everything you have said before, and the references `COMPLETELY' refute!!!!!!!!!!!!!



Your desperate attempts to save face on these forums, break every scientific rule in the book Bryan!

Just tell us all why the majority of the hair transplanted in these grafts `BALDS', just like the original hair Bryan? The hypoxia excuse is a scientific nonsense.

If you expect people here to take you seriously, answer the question in a proper scientific way, and cut all the bullshit!

S Foote.