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Stephan S. Foote was right!


#1

OK, so maybe the reasons Stephan and Ernie provided for why hair plucking works to increase terminal hairs on the scalp remain unproven, a recent article in Cell sheds a little light on the matter.

I somewhat recently detailed a HM protocol that plucked the entire scalp in order to get plenty of low passaged cells to inject as well as trigger a massive immune (follicle repair) response in the scalp.

Interestingly, it looks like less might equal more when it comes to hair plucking.


#2

Another article: http://www.latimes.com/science/sciencenow/la-sci-sn-hair-regeneration-20150408-story.html

But I am also right, when I say that plucking hairs will use up a follicle’s
fixed number of hair-cycles, eventually causing the follicle being plucked to
stop growing hair (as likely does anything that induces a hair follicle to
enter a new hair-cycle, like the shock from hair transplanting).

So plucking hairs will shorten or even cease the productive lifespan of the follicle
s being plucked. But if–IF–it causes enough neighboring unplucked follicles
in humans to grow again AND continue to grow and cycle normally without additional plucking,
then the sacrifice would be worth it.

[quote][postedby]Originally Posted by James Bond[/postedby]
OK, so maybe the reasons Stephan and Ernie provided for why hair plucking works to increase terminal hairs on the scalp remain unproven, a recent article in Cell sheds a little light on the matter.

I somewhat recently detailed a HM protocol that plucked the entire scalp in order to get plenty of low passaged cells to inject as well as trigger a massive immune (follicle repair) response in the scalp.

Interestingly, it looks like less might equal more when it comes to hair plucking.

http://www.telegraph.co.uk/news/science/science-news/11525367/Cure-for-thinning-hair-Scientists-find-plucking-stimulates-huge-growth.html[/quote]


#3

I wonder if this explains why in the trials of Minoxidil, the trialist who
unknowingly were applying a placebo still grew more hair, although less new hair than
those who were actually applying the real minoxidil.

The reason could be that the repeated rubbing employed to distribute the minoxidil onto the scalp would
have resulted in dislodging some hairs from their follicles, which might have an effect
similar to the plucking done in the mice experiment.


#4

what you are saying about the “fixed hair cycle count” is an hypothesis which, to my knowledge, is completely unproven.

[quote]Another article: http://www.latimes.com/science/sciencenow/la-sci-sn-hair-regeneration-20150408-story.html

But I am also right, when I say that plucking hairs will use up a follicle’s
fixed number of hair-cycles, eventually causing the follicle being plucked to
stop growing hair (as likely does anything that induces a hair follicle to
enter a new hair-cycle, like the shock from hair transplanting).

So plucking hairs will shorten or even cease the productive lifespan of the follicle
s being plucked. But if–IF–it causes enough neighboring unplucked follicles
in humans to grow again AND continue to grow and cycle normally without additional plucking,
then the sacrifice would be worth it.

[postedby]Originally Posted by James Bond[/postedby]
OK, so maybe the reasons Stephan and Ernie provided for why hair plucking works to increase terminal hairs on the scalp remain unproven, a recent article in Cell sheds a little light on the matter.

I somewhat recently detailed a HM protocol that plucked the entire scalp in order to get plenty of low passaged cells to inject as well as trigger a massive immune (follicle repair) response in the scalp.

Interestingly, it looks like less might equal more when it comes to hair plucking.

[postedby]Originally Posted by Ahab[/postedby][/quote]


#5

good point

[quote][postedby]Originally Posted by Ahab[/postedby]
I wonder if this explains why in the trials of Minoxidil, the trialist who
unknowingly were applying a placebo still grew more hair, although less new hair than
those who were actually applying the real minoxidil.

The reason could be that the repeated rubbing employed to distribute the minoxidil onto the scalp would
have resulted in dislodging some hairs from their follicles, which might have an effect
similar to the plucking done in the mice experiment.[/quote]


#6

Hi JB, been a long time.

I don’t remember supporting Ernie’s ideas? If i recall he claimed plucking body hair “diverted nutrients” increasing scalp growth. This is nothing like my proposal.

I do recall predicting that the cell based research would go nowhere, as it doesn’t address the problem. Not being in a position to test things my self, progress has been slow but emerging research does continue to support my claim.

For those who don’t know, i claim the important in-vivo control on follicle size, is something that is already recognized in general physiology. This external pressure control on tissue growth is described here:

My latest updated article describes this connection in terms of evolution, and has further discussion of this effect in transplantation and other current treatments.

https://independent.academia.edu/StephenFoote/Papers


#7

If follicles having a limited-number-of-cycles is completely unproven, it could be because no one’s bothered to experimentally test it.

But there is something called traction alopecia which is supposed to result in hair follicles being “damaged” when hairs are plucked or constantly pulled (which latter might be simply a case of slow-motion plucking), until the “damage” accumulates to the point that the follicle is “scarred” and stops producing hair.

The “scarred” follicle explanation seems to be the medically accepted explanation–but I strongly suspect no one’s actually experimentally tested that notion, either.


#8

I wonder if anyone cares to experiment with this by plucking chest hair or some other body hair?


#9

Well, it’s been observed on MICE, it’s interesting but as we have previously noted you can get virtually anything to grow on mice !


#10

Hi Stephan:

Sorry. I didn’t mean to imply you and Ernie shared a theory. Only that you both had postulated ideas in the past that plucking would induce hair growth (for differing reasons). I don’t recall the specifics of Ernie’s theory, but I do recall being somewhat skeptical of it. Wasn’t he actively experimenting on himself at one point? It’s been a while.


#11

Yes Ernie experimented on himself, wonder what happened to him?

If i recall correctly, my view on plucking was about the recognized over production of cells in response to injury. In the context of HM, the implantation of cells could possible create a follicle because of the injury factor.

But in my opinion, unless an external supporting matrix was produced (as in normal transplantation) the follicles would fail on re-cycling. I think this accounts for the initial hype of a procedure, followed by this not standing the test of time.


#12

What would determine whether a procedure can be commercially successful is simply the ability to produce new, cosmetically viable hair follicles in the skin. Whether or not these follicles can cycle beyond their first instance, they would still be useful as a “temporary fix” to hair loss, and of course additional new follicles could be generated again and again, with each additional round of cell injections.

So the new follicles don’t cycle? The bottom line for selling the procedure to the public is, “So what?” As long as they last long enough to provide visible terminal hair coverage on bald scalp, and can be augmented with further injections, it’s essentially a stopgap cure. That in and of itself would be highly commercially valuable.

I think the problem with companies like Intercytex and Aderans was not just that the new follicles didn’t cycle, it was that these companies simply couldn’t grow enough cosmetically worthy terminal hairs in the first place.

S Foote, regarding your idea that new follicles created from cell injections wouldn’t cycle, that may in fact be true, but why do you seem so certain of this?

I do see some merit in that conclusion, i.e., that the newly-grown follicles might lack the “external” epithelial “matrix” (to use your word), i.e. the epithelial cells which line the follicle and are part of it – since new hairs might be grown purely from a DP cell line, excluding epithelial cells.

In fact, Dr. Xaowei “George” Xu discussed the importance of having BOTH cell lines, i.e., those derived from DP cells, as well as epithelial cells, in de novo grown follicles…

http://www.upenn.edu/pennnews/current/2014-03-13/research/penn-dermatologist-makes-breakthrough-battle-against-hair-loss

That said, I think that if you can grow new follicles in skin using just DP cells, even if you’re lacking the epithelial component which provides the matrix, you’ll still get new hair follicles and can have significant coverage which NO OTHER TREATMENT has ever been able to provide so far. As these new follicles fail, to use your description, more new ones can always be induced with supplemental cell injections, augmenting the existing hair.

As for injected cells being able to unite with existing miniaturizing follicles, they could take advantage of the epithelial cell matrix which already exists, and in that way, possibly revive a cycling follicle.

All of the above, of course, assumes that you are correct, and new follicles grown from DP cells only (without epithelial matrix) fail before being able to recycle. However, I still say even that is a big assumption. At this point I have seen or heard of nothing in evidence that would tell us for sure, one way or the other.


#13

Anything that had produced cosmetically viable amounts of replacement hair for even a few years would have gone to market, cycling or not.

Our current MPB treatment options are too weak to really fight the problem. So we describe them as loss prevention. But they are still so pathetic that they can barely keep a lot of guys above baseline for 5 years - even WITH the permanent commitment. It’s ridiculous. MPB treatment effectiveness has nowhere to go but up.


#14

I’am sorry i should elaborate upon what i meant by failing on cycling.

The whole essence of my proposal is based upon an external tissue growth control, that is already recognized in general physiology. Basic physics dictate that if hair follicles are going to enlarge, the surrounding tissue must move out of the way. The resistance of the surrounding tissue becomes the significant control on ultimate follicle size, through this external pressure control linked in my first post.

My article also linked above offers evidence for this external pressure control being the significant factor in follicle miniaturization in MPB. Cycle by cycle, the follicles become smaller as the external pressure increases.

What this means for HM type cell based procedures, is that they are not addressing the cause of the problem. Lets say you can generate large follicles in the MPB scalp using a cell based procedure. If these cycle normally, during the Telogen regression phase the follicle gives up its space to the surrounding tissue. Come the next anagen enlargement phase, the growing follicle has to push surrounding tissue away again.

This is where HM follicles will experience the same problem as the originals and fail to produce another large follicle. In this scenario you don’t want HM generated follicles to re-cycle, as this is when they become vulnerable.

In my opinion, conventional transplants survive long term because of what happens during the procedure. The healing process around the large transplanted follicles, creates a tough fibrotic natural matrix around these follicles. This preserves the large follicle space against intrusion of surrounding tissue when follicles re-cycle. The generation of such a natural matrix around HM follicles would be the way to go, but then why bother?

According to this external tissue growth control, there is nothing wrong with the original follicles, and given the right external conditions these can re-enlarge.

In my opinion this was demonstrated in the immune deficient mouse study most are aware of on the forums. There are some points i would like to make about this study when i have more time.


#15

The big difference in this particular study, is it used human hair follicles. This is the only study so far in which miniaturized human MPB follicles, fully re-enlarged in an in-vivo study.

In my opinion, understanding exactly why this happened is the real key to the cure for MPB. This is a good article about this study by a leading transplantation doctor.

http://www.miamihair.com/news/ind_article_donor_vs_recipient_dominance_rev/

Apart from the enlargement of MPB follicles, i think there are a couple of other things in this study that point towards what is happening here. I will post more about this later in the week.


#16

S Foote, are you referring to the study posted by James Bond (thread initial post) or to the study by Orentreich?

A careful read of the following article, which I think is one of the best pieces of reporting on the study by Dr Chuong at USC, seems to indicate that the study was done on mice, using mouse follicles only, and not human follicles…

http://www.newscientist.com/article/dn27323-painful-baldness-cure-regenerate-hair-by-plucking-whats-left.html#.VSwtovnF8uc

In fact, it is very common for researchers to graft human tissue onto the backs of mice and other lab animals, to study the effect of something on human tissues, where approval for experiments on actual humans has not yet been granted. One of the MANY examples of that in hair research would be Dr Terskikh’s recent work with stem cells at the Sanford-Burnham Research Institute in San Diego.

However, this does NOT appear to be what was done in Dr Chuong’s study. Correct me if you’re sure I’m wrong, but this research seems to have been done on mice using mouse follicles. Please note the comments by Dr. Nadia Rosenthal from Monash University in Australia.

I wouldn’t give an enormous amount of credence to Dr Norman Orentreich, he is a very conventional, extremely old-school hair transplant surgeon, in fact he’s practically known as the “Father of Hair Transplant Surgery”. How his studies can be seen as revolutionary or compelling in any way, I would have no idea.


#17

The study i am referring to used human scalp follicles transplanted to immune deficient mice, and is discussed and referenced here.

I am posting my interpretation of this below.


#18

A discussion about the mouse study.

In my opinion the immune deficient mouse human transplant study discussed and referenced below, is the most important human MPB study so far. http://www.miamihair.com/news/ind_article_donor_vs_recipient_dominance_rev/

The first thing this study does, is to throw out the old donor dominance notion as its elements have been claimed. The re-enlargement of the transplanted human MPB follicles, refutes all the claims made for the direct androgen pathway in MPB.

The MPB follicles enlarged by around 400%, in the presence of more than enough androgen’s to prevent this (according to the direct action theory). Even so some people continue to speculate about how this could still be explained by the direct androgen effect theory.

You can explain anything you like by adding evermore complication. This has always been the problem with the direct androgen action theory, you have to keep on adding complication to make it fit the facts. This is why genuine science abides by the central rule of parsimony. That is look for the most simple way it is possible to explain things. Science uses this rule, because it has been proven time and time again.

Efforts to explain this study by some change in an androgen related pathway, have another big problem. The large non balding follicles used in this study, also significantly changed size. They went the other way and reduced in size by around 40%.

The current thinking is that these follicles are not effected by androgen’s at all, either directly or indirectly. So to explain the results of this study by direct effects, straightaway you need two different mechanisms. Not good for parsimony.

There is only one known tissue growth control mechanism, that explains these effects with parsimony.

What is very clear from this study, is that follicles of very different sizes, ended up the same size. (No significant size differences). So something in the mouse tissue, is dictating one particular size of hair follicle within that particular tissue.

One characteristic of some strains of immune deficient mice, is that injury produces very little or no scar tissue (fibrosis).

http://www.pnas.org/content/94/20/10663.full.pdf

Normal human transplantation produces a fibrotic matrix of scar tissue around the grafts, isolating these from some external influences. I suggest this did not happen in this particular study.

The small one or two follicle grafts used in this study and the lack of any scar tissue formation around them, means that the follicles are free to adjust their size through the pressure control of tissue growth described previously.

In this case the natural resistance (pressure) of the mouse tissue, allowed for the one particular size of follicle observed in the study.

We know from this study that MPB follicles have the ability to enlarge given the right conditions. Research needs to shift towards reducing the external pressure that keeps these follicles miniaturized. This is the only way forward in my opinion.