Thaory abot Common baldness. Att. Mr. Foote or friends

[Armando Jose]

To Stephen Foote:
Theory:
http://www.sciencedirect.com/science?_o ... 24567eac4f

Patent:
http://www.freshpatents.com/Prevention- ... 243153.php

http://www.freshpatents.com/Prevention- ... escription

Is it interesting acording to your own theory?
It is a pitty that this Dr. did not mention sebum flow
Have a nice day
Armando

 

[Bryan]

Oh Jesus Christ...don't give any encouragement to Stephen Foote! :mrgreen:

 

[sphlanx2006]

Can someone say if there is any scientific value to this?

 

[xcvq]

I guess when you get a hair transplant the transplanted hairs are immune to pressure.

 

[Bryan]

I guess when you get a hair transplant the transplanted hairs are immune to pressure.

Funny, that. And yet when you transplant a BALDING hair follicle, it continues to go bald at the same rate. Funny how that works, isn't it?

 

[bobs]

Bryan, has that actually been done?

I don't doubt that the hair would continue to thin wherever it was moved but still...

that really is the million dollar question, why hairs react so differently to androgens. Odd enough we might never find out considering none of the currently researched treatments deal with that.

 

[Bryan]

Bryan, has that actually been done?

You betcha it's been done! It was thoroughly tested in the famous and much-discussed Nordstrom study, in which balding frontal hair follicles were transplanted to the arm of the same individual, and they continued to go bald at the same rate. The obvious conclusion is that balding doesn't have anything to do with the LOCATION of the follicles. It shows that balding is caused by something inherent to each individual hair follicle.

You can do a search on the word "Nordstrom" here on HairLossTalk.com, and find some huge threads about it. It's especially revealing to see the desperate lengths that Stephen Foote went to, to try to discount that study. But in the end, of course, he had utterly no way to try to make it fit into his own theory about contact inhibition.

I don't doubt that the hair would continue to thin wherever it was moved but still...

Yeah, it's hard to argue with the fact that hair follicles apparently continue to go bald, REGARDLESS of where you transplant them, isn't it?

that really is the million dollar question, why hairs react so differently to androgens. Odd enough we might never find out considering none of the currently researched treatments deal with that.

Well, doctors and researchers ARE interested in that, and they're continuing to work on it...

 

[bobs]

Could it be that once the hair starts thinning it continues to, no matter where it is moved? But if you had moved it pre-balding it would not thin, even if it was destined to go bald? That sounds far-stretched I know but has it been discussed?

 

[Armando Jose]

IMHO, It is neccesary make more deep studies in thi issue

Armando

Nordström RE.
Synchronous balding of scalp and hair-bearing grafts of scalp transplanted to the skin of the arm in male pattern baldness.
Acta Derm Venereol. 1979;59(3):266-8. No abstract available.
PMID: 87090 [PubMed - indexed for MEDLINE]

Dermatol Surg. 1999 Aug;25(8):605-9.
The changes in hair growth pattern after autologous hair transplantation.
Lee SH, Kim DW, Jun JB, Lee SJ, Kim JC, Kim NH.
Department of Dermatology, Kyungpook National University, School of Medicine, Taegu, South Korea.
BACKGROUND: Recently donor dominance has been emphasized in autologous hair transplantation while the influence of the recipient site has been considered negligible. In fact, there have been few studies that show this. OBJECTIVE: This study was performed to examine the influence of the recipient site on transplanted hairs. A clinical study of 19 leprosy patients was performed. These patients had received single hair transplantation due to madarosis and were admitted to The Leprosy Mission, Jesus Hospital, Taegu, Korea, or had visited its outpatient clinic. METHODS: In this study, the rate of growth, thickness of shaft, and graying rate between the transplanted eyebrow hair in the recipient site and scalp hair near the donor site were compared to observe the changes in the growth pattern of the hairs after transplantation. RESULTS: For most of the patients, the growth rate and graying rate of transplanted hairs were lower than those of hairs in the donor site. CONCLUSION: It seems that the recipient site may have an influence on the transplanted hairs. Further studies are needed, including clinical, histopathologic, and molecular biological methods.
PMID: 10491042 [PubMed - indexed for MEDLINE]


Dermatol Surg. 2002 Sep;28(9):795-8; discussion 798-9.
Does the recipient site influence the hair growth characteristics in hair transplantation?
Hwang S, Kim JC, Ryu HS, Cha YC, Lee SJ, Na GY, Kim DW.
Department of Dermatology, Kyungpook National University School of Medicine, Taegu, Korea.
BACKGROUND: Recently hair transplantation has been widely applied not only to correct androgenetic alopecia, but also to correct hair loss on other parts of the body such as the eyebrows and pubic area. It is believed that the transplanted hairs will maintain their integrity and characteristics after transplantation to new nonscalp sites. OBJECTIVE: To evaluate whether the transplanted hairs maintain their hair growth characteristics after transplantation to a new anatomic site other than the scalp. METHODS: Three study designs were used. Study I: Hair transplantation from the author's occipital scalp to his lower leg was performed and clinical evaluations were made at both 6 months and at 3 years after the transplantation. Study II: After finding changes in hair growth characteristics, transplanted hairs were harvested from the leg and retransplanted to the left side of the nape of the neck (group A). As a control study, occipital hairs were transplanted to the opposite side (group B). Observations were made at 6 months after the operation. Study III: An observational study was done in 12 patients with androgenetic alopecia about 1 year after transplantation of occipital hair to frontal scalp. At each step, survival rates were documented and the rate of growth and the diameter of the shafts were measured for both recipient and donor sites. RESULTS: Study I: Surviving hairs on the lower leg showed a lower growth rate (8.2 +/- 0.9 mm/month), but the same diameter (0.086 +/- 0.018 mm) compared with occipital hairs (16.0 +/- 1.1 mm/month, 0.088 +/- 0.016 mm). The survival rate 3 years after transplantation was 60.2%. Study II: There was no significant difference in the growth rate, shaft diameter, and survival rate between retransplanted hairs (group A) and controls (group B). Groups A and B showed a lower growth rate, but the same diameter, compared with occipital hairs. Study III: There was no significant difference in the growth rate and shaft diameter between the transplanted hairs on the frontal scalp and the occipital hairs. CONCLUSION: These results strongly suggest that the recipient site affects some characteristics of transplanted hairs, such as their growth and survival rates.
PMID: 12269871 [PubMed - indexed for MEDLINE]

 

[S Foote.]

Thanks for the link Armando, i have emailed the author.

Just a warning to newbies about Bryan (i'am a scientist) Shelton.

Bryan's brand of "science" can only exist on internet forums. He is not concerned with any genuine reasoning, just trying to impress people on forums with how clever he is. Anyone who knows anything about "real" scientific reasoning see's Bryan for the arogant fool he is.

Yet again right here he proves this.

Bryan said in this thread quote:

"Yeah, it's hard to argue with the fact that hair follicles apparently continue to go bald, REGARDLESS of where you transplant them, isn't it?"

Yet he HIMSELF started a thread that disproves this statment!

http://www.hairlosshelp.com/forums/mess ... fm?catid=1

Here balding human male pattern baldness follicles were transplanted and regrew! These complete follicles with a sheath of original tissue around them regrew when transplanted into tissue having the "right" conditions (whatever this is)

So how the hell can the growth control in male pattern baldness follicles be "inside" these transplanted follicles, or even close around them? There was certainly more than enough androgens available to maintain male pattern baldness "directly" in this study, as Bryan HIMSELF pointed out if you read the linked tread!

You are a complete sham Bryan!

You will never get through to arogant idiots like Bryan Shelton so i dont bother trying anymore.

S Foote.

 

[S Foote.]

One more thing!

When internet "expert" Bryan Shelton laughs at papers that go against the great Bryan's opinion, people should check out the qualifications of the people Bryan is laughing at?

Here are the published papers of the author of this "pressure" theory.

http://scholar.google.com/scholar?q=%22 ... Ustuner%22

The mans an expert on tissue transplantation for God's sake!!

Tell us all about your qualifications and published papers Bryan :roll:

S Foote.

 

[Bryan]

Could it be that once the hair starts thinning it continues to, no matter where it is moved? But if you had moved it pre-balding it would not thin, even if it was destined to go bald? That sounds far-stretched I know but has it been discussed?

I don't recall if that specific idea has ever been discussed. But in any event, I'm not sure what the relevance of that idea would be.

 

[Bryan]

Bryan said in this thread quote:

"Yeah, it's hard to argue with the fact that hair follicles apparently continue to go bald, REGARDLESS of where you transplant them, isn't it?"

Yet he HIMSELF started a thread that disproves this statment!

http://www.hairlosshelp.com/forums/mess ... fm?catid=1

Sorry, Stephen, but that link doesn't work. Don't you bother to double-check your work after posting? OOPS....how silly of me to even ask that question. It's obvious that truth and accuracy have never been major concerns in anything you post!

Here balding human male pattern baldness follicles were transplanted and regrew! These complete follicles with a sheath of original tissue around them regrew when transplanted into tissue having the "right" conditions (whatever this is)

If it's the study I think it is, they only partially regrew. And a lot of it very likely has to do with the fact that the hairs were transplanted onto SCID mice (you conveniently forgot to mention that one little fact! ).

So how the hell can the growth control in male pattern baldness follicles be "inside" these transplanted follicles, or even close around them? There was certainly more than enough androgens available to maintain male pattern baldness "directly" in this study, as Bryan HIMSELF pointed out if you read the linked tread!

Show me where I "pointed out" such a thing. I'll thank you not to put words in my mouth, Stephen.

 

[michael barry]

Stephen,

Have you seen the getfitinib "regrowth" photo? The one in the front of a bald man's head?


Have you seen the getfitnib nose hair photo? Where that cancer patient had whisker-like dark hairs all over there nose?




I really and truly believe Follica is about to have a real solution for baldness based on their experiments. So does TAGOHL.

Its actually pretty simple. They will dermabrade the scalp, and use a topical immunosouppressant cream (probably the one used for eczema already in use) and use a EGF-receptor antagnonizing drug that is used for cancer patients in the cream formulation. That is really "it". Any thing else in their patent is just adjuvants to increase yield, but not necessary (anti-inflammatories, minoxidil, anti-histamines).



If you've not seen the head regrowth photo...................its really "new" hair. The guy was going grey, but had dark brown to black hair right in the front of his bald head. Sunburn is almost assuredly the reason he got the growth up there because it induced a state of re-epilithialization and he got on getfinib at just the right time after re-epilithialization was complete---so the keratinocytes were covering the wound just like the patent says. He'd been on chemo so his immune system couldn't respond to the inflammation----hence he got a bunch of hair on long long long bald scalp (he was a Norwood 6 or so).



There is verbiage in their patent about using the ectodsypslasin DNA sequences. That is probably way in the future, but ectodsypslasin goes along with the androgen receptor gene when skin is growing over a fetus' head in the mother's womb in the first trimester and probably shapes the wreath area as well as helps encode for the level of androgen receptor expression in target organs there. Hopefully, they will be able to one day silence this gene while the make the new hair in this embryonic "window" when the new hairs are made out of your skin's stem cells. There was a good interview with Cotsarialis on NBC's "The Today Show" discussing all of this with Dr. Nancy Snyderman (the NBC medical correspondent) and Matt Lauer. The ball is really rolling on this thing at this point.



IN their initial experiments, Follica was able to simply abrade human skin grafted onto SCID mice, and get hair to be formed where there was none (it was discarded donor-area skin from a hair transplant that had its follicles removed in the surgery). They found they could get much more hair (and larger hairs) if they blocked epidermal growth factor. Daphne Zohar stated in an interview that Follica would be using two FDA approved drugs with their procedure that have been approved for things "other than hairgrowth". Im almost certain from reading their patents that these two will be a topical immunosuppressant (they name five of them in their patent--rampycin, tacromilius, pimecromilus, cyclosporin, and one other) and an EGF-antagonist (almost assuredly getfitinib). The patent claims they will be able to generate hair growth in scars, on eyebrows etc. It worked everywhere on the mice, even genetically hairless mice.


I think you should view this as good news for yourself, no matter what it does to your theory.

 

[S Foote.]

I will post the link again.

I hope it works this time then people can read your U turn opinions for themselves Bryan :roll:

http://www.hairlosshelp.com/forums/mess ... &forumid=1

I have now read the full paper Armando linked, and this well published tissue transplantation expert, claims the same reasons for hair transplantation results as i have.

But i have tried to explain this to you many times Bryan, and i am not wasting any more time on you. People who may be interested in my arguments can search this site.

Thanks for the info Michael. I do like to see progress in better treatments for male pattern baldness as most others here do.

S Foote.

 

[michael barry]

Stephen,

I'll stick that study here for you so you have a HairLossTalk.com link to it. But first-------------did you know that there is a hairtransplant tool that you can buy that you could use on yourself to move a vellus hair or two and see if it regenerates? Look up DHI (Direct Hair Implant). Some doctors simply use small guage sharpened needles. You could move a couple of your own vellus hairs into a lateral slit YOURSELF and test your hypothesis. http://www.youtube.com/watch?v=3lCbAsAHf0U



Here is Bryan's old post:
The study below has been cited a few times by various people on hairloss sites over the last couple of years, but I've read the whole thing, and I want to present some of the interesting details from it. First of all, here's the abstract:

J Am Acad Dermatol. 2003 May;48(5):752-9.

"Transplants from balding and hairy androgenetic alopecia scalp regrow hair comparably well on immunodeficient mice"

Krajcik RA, Vogelman JH, Malloy VL, Orentreich N.

"Human hair follicles were grafted onto 2 strains of immunodeficient mice to compare the regeneration potential of vellus (miniaturized, balding) and terminal (hairy, nonbalding) follicles from males and a female exhibiting pattern baldness. Each mouse had transplants of both types of follicles from a single donor for direct comparison. Grafted follicles from 2 male donors resulted in nonsignificant differences in mean length (52 mm vs 54 mm) and mean diameter (99 microm vs 93 microm) at 22 weeks for hairs originating from balding and hairy scalp, respectively, corresponding to 400% versus 62% of the mean pretransplantation diameters. Follicles from the female donor transplanted to several mice also resulted in nonsignificant differences in length (43 mm vs 37 mm) for hairs from balding and hairy scalp, respectively, during a period of 22 weeks. The mean diameter of the originally vellus hairs increased 3-fold, whereas the terminal hairs plateaued at approximately 50% of pretransplantation diameter, resulting in a final balding hair volume double that of the nonbalding hairs. This report shows that miniaturized hair follicles of pattern alopecia can quickly regenerate once removed from the human scalp and can grow as well as or better than terminal follicles from the same individual."

The abstract gives the salient points: they found that fine vellus hairs from balding human scalps had an EXCEPTIONAL ability to regenerate, when transplanted onto test mice that had severe immune deficiency (they use those for transplant experiments so that the mice don't suffer rejection of the foreign tissue). In fact, after about 5 to 6 months, transplanted follicles with vellus hairs regrew to the same size as the transplanted terminal hairs in one set of mice, and actually grew LARGER than the terminal hairs in another set of mice (for which phenomenon they don't yet have any explanation)! Here's an extended excerpt from the Discussion section at the end in which they speculate about the various implications of their findings:

"...The phenomenon occurring in the xenograft experiments reported here is quite different and dramatic: hypotrophic anagen and telogen hairs from balding scalp exhibiting only vellus hairs in situ regenerate very quickly. By six months, the ratio of the diameters of grafted to pretransplant vellus hairs exceeds 3:1 (Fig 3). Histologic examination of post-transplantation follicles from balding scalp also shows fully developed anagen follicles at six months (Fig 2). The regeneration of vellus follicles occurs just as quickly on male as on female mice (data not shown); this suggests that a factor or factors other than androgen withdrawal may be involved but does not necessarily rule out that differences in androgen levels, availablity, or both between human beings and mice account in part or entirely for the rapid vellus-to-terminal transformation of balding follicles. For instance, the activity of the 5a-R enzyme(s) may be greatly reduced or absent in the transplanted follicles, thereby, limiting exposure of the follicles to DHT. The accelerated transformation of vellus follicles on immunodeficient mice might correspond to responses seen in balding men treated with oral finasteride who are exceptionally good responders. However, in our clinical experience, females with Androgenetic Alopecia, including the female in study II, frequently have normal androgen and androgen-binding globulin levels for their age and sex. It is difficult to argue that lower systemic androgen levels in the female mouse environment (or higher in the male mice) causes the rapid regeneration of vellus hair follicles from the human female. Therefore, the existence of an inhibitor factor other than androgens, particularly in women showing diffuse/pattern alopecia, that is lacking in the nude mouse seems plausible. This could be some other steroid, hormone, cytokine, neuropeptide, or an immunologically related factor."

I think that last part about the "immunologically related factor" is an understatement! After reading this paper, it now seems likely that the immune system is an even bigger factor in male pattern baldness than was previously thought. I personally had always assumed that the putative attack on hair follicles by the immune system was something that happens relatively late in the game, but this study is awfully compelling. But oddly enough, you see very little about this aspect of balding in the medical literature. Dr. Proctor, OTOH, has talked about it for years on alt.baldspot.

So what really is the point of bringing this up in the first place, this issue "Of Mice and Men"?? Well, I think it can be a source of great hope for all of us! It proves that there exists the POTENTIAL for our poor follicles to regenerate completely all on their own, if only we can figure out how to let that happen. It appears that we may not have to wait for far-off and possibly risky genetic treatments, or puzzle-out all those very complex mesenchymal-epithelial interactions (HM, in other words), or depend on other high-tech treatments. We may find simpler, safer ways to do it, with the additional clues provided by this fascinating study.

 

[michael barry]

http://www.hairsite.com/hair-loss/forum ... nswer.html


I hope the getfitinib pictures are in that thread.


LOOK at that thread!!!!!!!!!!!!!!!!!!!!!!!



Terminal hair growth on the nose.


Terminal hair growth in a long-bald frontal lobe of a man's head.

 

[Armando Jose]

´+1

 

[S Foote.]

I would just like to make a point here, but I don't intend to get into anymore unconstructive debates on these forums.

There is a very important scientific rule, that any valid theory must satisfy. This is a good description quote.

"Parsimony: When there are multiple explanations of a phenomenon, scientists must always accept the simplest or logically most economical explanation. This concept is called parsimony or “Occam’s razor.” Parsimony prevents scientists from pursuing overly complex or outlandish theories with endless number of concepts and relationships that may explain a little bit of everything but nothing in particular."

What this means in DHT related changes in hair growth, is that you must explain "ALL" the changes in hair growth and the surrounding tissue, by just "ONE" initial action of DHT. The changes that must be explained here are below.

How DHT increases hair growth in particular areas of the body consistently, and why only in some individuals DHT causes scalp hair loss again in particular areas. You also have to explain how this "SAME" action of DHT creates the noted scalp immunological changes, fibrosis and hypoxia. Then you have to explain why your proposed action of DHT increases sweating capacity in bald areas, and reduces this in areas where DHT increases hair growth. Not forgetting why your explanation increases levels of DHT in bald areas, and why manipulating WNT's makes a difference to hair growth. Finally your proposed action of DHT must explain why some transplantation procedures work whilst others don't.

The "official" explanation of genetic differences within the follicles, just cannot do what the scientific method dictates here. It requires many different mechanisms to explain all the changes involved. I would also be interested to hear how the supporters of the calcification, skull thickening, and Galea theories, can explain all these changes by just one action of DHT? I think not.

There is only one initial action of DHT that answers all these questions. This is that DHT increases the pumping efficiency of lymphatic vessels. From this one initial action, you can explain all these changes using basic text book physiology. You don't even need to know what's happening at the genetic/ molecullar level.
My article that raises this issue with the current research is here.

https://www.researchgate.net/publication/324829427_TISSUE_SCIENCE_PUBLISHED_ARTICLE

My review/discussion paper that elaborates on these questions is here.

https://www.academia.edu/17570665/A...nt_Hair_Research_and_an_Overlooked_Connection.

People may say OK what can be done here? Well these are my thoughts based upon this indicated action of DHT, and Human lymphatic physiology. The solution to male pattern baldness could be a lot more straightforward, cheaper, safer, and more effective than is currently thought. We need to reduce DHT in the hairy areas of the scalp and beard area, and increase DHT levels in the bald scalp itself.

I think the noted increased levels of DHT in the bald scalp, is the bodies way of trying to reduce the higher tissue fluid pressure here. The problem is that the action of DHT lower down, is in effect "blocking the pipework". Taking Propecia will reduce this blockage lower down, but will also reduce DHT production in the bald scalp where it is needed. So in theory if you take Propecia, you will get a significant boost in scalp hair growth by also applying DHT cream to the balding areas. I think this situation is why topical Finasteride in bald areas, does very little for scalp hair growth, it is just being applied in the wrong place.

I see the future here as using topical 5ARI's (shampoos and lotions), on the hairy areas of the head, and topical DHT on the balding areas. In established male pattern baldness, massage and lasers could help get rid of the fibrosis, that interferes with follicle re-enlargement.

Over twenty years ago I argued on the forums, that hair loss treatment research would fail to produce results in Humans, for as long as it failed to take account of the common spatial growth controls that must apply here. So far I have been proven right, and I am sorry to say the same fate will apply to all the current treatment research proposals. People should realise that this is not just my opinion, the current hair loss research clearly goes against the recognised science in tissue growth physiology, as my first article linked above points out.

 

[WheeljackG1]

I would just like to make a point here, but I don't intend to get into anymore unconstructive debates on these forums.

There is a very important scientific rule, that any valid theory must satisfy. This is a good description quote.

"Parsimony: When there are multiple explanations of a phenomenon, scientists must always accept the simplest or logically most economical explanation. This concept is called parsimony or “Occam’s razor.” Parsimony prevents scientists from pursuing overly complex or outlandish theories with endless number of concepts and relationships that may explain a little bit of everything but nothing in particular."

What this means in DHT related changes in hair growth, is that you must explain "ALL" the changes in hair growth and the surrounding tissue, by just "ONE" initial action of DHT. The changes that must be explained here are below.

How DHT increases hair growth in particular areas of the body consistently, and why only in some individuals DHT causes scalp hair loss again in particular areas. You also have to explain how this "SAME" action of DHT creates the noted scalp immunological changes, fibrosis and hypoxia. Then you have to explain why your proposed action of DHT increases sweating capacity in bald areas, and reduces this in areas where DHT increases hair growth. Not forgetting why your explanation increases levels of DHT in bald areas, and why manipulating WNT's makes a difference to hair growth. Finally your proposed action of DHT must explain why some transplantation procedures work whilst others don't.

The "official" explanation of genetic differences within the follicles, just cannot do what the scientific method dictates here. It requires many different mechanisms to explain all the changes involved. I would also be interested to hear how the supporters of the calcification, skull thickening, and Galea theories, can explain all these changes by just one action of DHT? I think not.

There is only one initial action of DHT that answers all these questions. This is that DHT increases the pumping efficiency of lymphatic vessels. From this one initial action, you can explain all these changes using basic text book physiology. You don't even need to know what's happening at the genetic/ molecullar level.
My article that raises this issue with the current research is here.

https://www.researchgate.net/publication/324829427_TISSUE_SCIENCE_PUBLISHED_ARTICLE

My review/discussion paper that elaborates on these questions is here.

https://www.academia.edu/17570665/A...nt_Hair_Research_and_an_Overlooked_Connection.

People may say OK what can be done here? Well these are my thoughts based upon this indicated action of DHT, and Human lymphatic physiology. The solution to male pattern baldness could be a lot more straightforward, cheaper, safer, and more effective than is currently thought. We need to reduce DHT in the hairy areas of the scalp and beard area, and increase DHT levels in the bald scalp itself.

I think the noted increased levels of DHT in the bald scalp, is the bodies way of trying to reduce the higher tissue fluid pressure here. The problem is that the action of DHT lower down, is in effect "blocking the pipework". Taking Propecia will reduce this blockage lower down, but will also reduce DHT production in the bald scalp where it is needed. So in theory if you take Propecia, you will get a significant boost in scalp hair growth by also applying DHT cream to the balding areas. I think this situation is why topical Finasteride in bald areas, does very little for scalp hair growth, it is just being applied in the wrong place.

I see the future here as using topical 5ARI's (shampoos and lotions), on the hairy areas of the head, and topical DHT on the balding areas. In established male pattern baldness, massage and lasers could help get rid of the fibrosis, that interferes with follicle re-enlargement.

Over twenty years ago I argued on the forums, that hair loss treatment research would fail to produce results in Humans, for as long as it failed to take account of the common spatial growth controls that must apply here. So far I have been proven right, and I am sorry to say the same fate will apply to all the current treatment research proposals. People should realise that this is not just my opinion, the current hair loss research clearly goes against the recognised science in tissue growth physiology, as my first article linked above points out.

Sorry if you stated, I'm sick and my brain isn't working on full gears right now, what are you basing the theories on? Experience? Or just studying?