A Review of male pattern baldness Research.

[S Foote.]

SFoote..if you're still around..wondering what you think about this: http://www.cosmeticsdesign-europe.c...nd-suggests-pine-cone-extract-may-be-the-cure

Sorry I did miss this post.

I think we already have the most powerful natural lymphatic booster there is, DHT.

DHT grows hair over the larger area of the body, the reverse effect in the scalp is easily explained by known fluid dynamic effects. I think it all boils down to a local over production of DHT in the large follicles of the hairy scalp and the beard area. This upsets the lymphatic drainage balance at the end of the system, the male pattern baldness area.

Think about it, most of the dermal DHT is produced in hair follicles. Larger hair follicles have more DHT producing cells. In the bald scalp the miniaturised follicles just don't have the capacity to produce the same amount of DHT as hairy scalp. Yet there is more DHT in the bald scalp?

The simple answer to this is increased fluid levels in the bald scalp. This means increased levels of anything in this fluid including DHT, and by the way PGD2. Increased levels of mast cells that produce PGD2 have been recognised in cases of increased tissue fluid levels for a long time. So has hypoxia and every other recognised factor in the male pattern baldness scalp.

This is why topical 5ARI inhibitors do very little when applied to the bald area, you would get a better result by using these on the hairy scalp and beard area.

I would like to make an important point here.

There can be no doubt that hair follicle enlargement in-vivo, is subject to the same spatial growth controls as any other normal tissue growth.

I have contacted many scientists in hair research and general physiology about this, including some hair scientists well known on these forums, and not one is willing to go on the record and try to deny this.

People should understand there is no way around this if you want really effective hair loss treatments. The veterans on the forums will know I argued years ago that the cell based research intended to grow new "resistant" follicles, would fail because of the influence of spatial growth controls. I have yet to be proven wrong.

None of the current research takes account of this factor, and despite the hype until they do they will go nowhere. In fact as I said the current published studies that fail to include spatial growth controls are misleading and should be retracted.

 

[Armando Jose]

Hi, hello my friend, good to see you again

You have all my respect, your idea is good but why womens don't suffer common hairloss so normally as men?
are these spacial growth controls so differents?

 

[S Foote.]

Hi, hello my friend, good to see you again

You have all my respect, your idea is good but why womens don't suffer common hairloss so normally as men?
are these spacial growth controls so differents?

Hi Armando.

Normal spatial growth controls are exactly the same in all normal tissues. They are based upon a certain amount of external pressure switching off tissue growth. The only difference in male and female hair loss is the cause of the pressure rise. The scalp in both sexes is vulnerable to tissue fluid pressure increases by a number of pathways. In men it is mainly DHT creating local lymphedema.

In Women other hormones come into play here, and the pressure increase is generally lower than in men. That's why Women have more diffuse loss than men. You notice men go through a period of diffuse loss but this goes on to baldness as the pressure gets higher.

Its exactly the same mechanism in both sexes, increased fluid pressure, but for different reasons and at different rates. I refer to this in my article.

 

[Armando Jose]

Thank you Sir.

I doubt that pilosebaceous hormones are so diferent in women and men, because all they are created inside of it. But is your idea and I respect it.

 

[Pereira]

S Foote, as a almost 10years user I've seen a lot of topics of promising researches not reaching the expected results.
I really liked your way of thinking.. it make sense.

 

[plisk]

S foote this is very interesting and i appreciate outside the box thinking

Is what you are suggesting then, that topical AR antagonists should be spread everywhere else BUT the male pattern baldness area of the scalp?

I have some ru58841 liquid and am willing to try this, i could do without that tuft of hair growing on my upper back lol

Also what role do you think wounding plays in this?

EDIT: f*** now that i think of it, this does go a long way to explaining the correlation between balding men and heavy beard and body hair growth.

 

[Trouse]

I got doubly screwed. I have bad diffuse thinning but I have just average body hair and my facial hair isn't thick enough to really grow out and style. A beard would help me tremendously and I could avoid the cancer patient look, but I really am just follicularly challenged I suppose.

 

[S Foote.]

S foote this is very interesting and i appreciate outside the box thinking

Is what you are suggesting then, that topical AR antagonists should be spread everywhere else BUT the male pattern baldness area of the scalp?

I have some ru58841 liquid and am willing to try this, i could do without that tuft of hair growing on my upper back lol

Also what role do you think wounding plays in this?

EDIT: f*** now that i think of it, this does go a long way to explaining the correlation between balding men and heavy beard and body hair growth.

Thanks for your comments. First in my opinion it is the current hair loss research that is out of the box. This has failed to keep up with progress in general physiology, in terms of knowledge about spatial growth controls and tissue engineering principles.

Yes but not AR antagonists 5ARI inhibitors (topical Finasteride etc) We don't want to effect androgen receptor function just reduce local DHT production. As for the male pattern baldness area itself, massage perhaps anti fibrotics to help repair the damage and increase scalp flexibility..

The wounding issue is interesting because there is some evidence that spatial controls are relaxed slightly during the healing process. I did have a reference to this that I cant find right now. This relaxation allows easier tissue rebuilding, but is certainly not permanent, and any effect on hair follicles wont be permanent either.

 

[S Foote.]

S Foote, as a almost 10years user I've seen a lot of topics of promising researches not reaching the expected results.
I really liked your way of thinking.. it make sense.

Thanks for your comments.

 

[S Foote.]

Thank you Sir.

I doubt that pilosebaceous hormones are so diferent in women and men, because all they are created inside of it. But is your idea and I respect it.

With respect Armando, I don't think pilosebaceous hormones have anything to do with it. How can this explain the opposite effect on body hair growth? Or the other changes in the bald scalp on immunology, hypoxia, sweating capacity etc?

 

[Armando Jose]

In Women other hormones come into play here, and the pressure increase is generally lower than in men

My coment arise when you point at the difference between women and men in comon baldness, IMO the main hormones acting in the pilosebaceous unit (hair) are made inside it, not flowing in the blood.

 

[S Foote.]

My coment arise when you point at the difference between women and men in comon baldness, IMO the main hormones acting in the pilosebaceous unit (hair) are made inside it, not flowing in the blood.

Well this still seems to be the general assumption in hair research, and the basis of all the current planed treatments we read about here. Its been around sixty years now that people have been working on treatments based on this assumption, how are we doing so far?

As far as I am aware there has been only one study where actual human male pattern baldness follicles significantly enlarged in an in-vivo situation. One thing this clearly demonstrated was that internal hormones were not responsible for keeping these follicles in a miniaturised state. It was clearly the external conditions that allowed this re-enlargement. I discuss this study in my article.

 

[hairblues]

The constant bombardment of DHT at a certain point can cause inflammation by constantly overstimulating the androgen receptors. This causes immune response inflammation if you are genetically sensitive, which causes itching, redness, scaring and shrinking of the follicles, causing miniaturization and eventually hair loss.

Question is why do some boys start balding in their early teens but some men start balding in their 50-60s?

I mean their both susceptible to male pattern baldness yet one experiences it decades early/later. I'm guessing that dht can be equated to a genetic ticking "bomb" in which at some point in a mans life it'll trigger (in essence tell) the follicle to die.

*shrugs shoulders*

Who knows...

This is interesting I a woman and was told by hair transplant surgeon that my low iron levels (ferritin) 'unmasked' my Androgenetic Alopecia meaning it triggered it prematurely or made it more aggressive than it normally would have been...I do not know if this iron is a factor for men I doubt it because i am sure it would be everywhere if googled BUT if this was a trigger/agrivator for me and other women then their is probably something in regards to men as well.
Upping my iron is not going to cure Androgenetic Alopecia but both the surgeon is confident it will dramatically help to fill in my hair and make me responsive to treatments ( a lot of women with low ferritin do not respond well to treatments)
I am cautiously optimistic and am currently doing other treatments as well..

Their needs to be more research for commonalities.

 

[Armando Jose]

Well this still seems to be the general assumption in hair research, and the basis of all the current planed treatments we read about here. Its been around sixty years now that people have been working on treatments based on this assumption, how are we doing so far?

As far as I am aware there has been only one study where actual human male pattern baldness follicles significantly enlarged in an in-vivo situation. One thing this clearly demonstrated was that internal hormones were not responsible for keeping these follicles in a miniaturised state. It was clearly the external conditions that allowed this re-enlargement. I discuss this study in my article.

Are you refering this article?
An Evolved Hair Growth Mechanism in Mammals, Implications in Human Physiology ?
"The most important implications of this mechanism are in gender related auto-immune conditions. These can be debilitating and sometimes fatal. It is accepted that sex hormones must play a role here, and research continues to identify the hormonal link (19). "
The link refers this article 19. Zandman-Goddard, G., Peeva, E., & Shoenfeld, Y. (2007). Gender and autoimmunity. Autoimmunity reviews, 6(6), 366-372


or this another
A Review of the issues in historic and current hair research, and an overlooked connection

"An Important Testable Link with Gender Related Disease

The indication here that the androgen DHT significantly increases lymphatic drainage has important implications. It is not currently thought that there is any significant gender difference in lymphatic efficiency. However such a difference would make a lot of sense of some serious gender related diseases, especially female susceptibility to autoimmune disease.

We know that lympedema has a pronounced effect upon the prevailing tissue immunology, increasing immune sensitivity and the chances of secondary immune reactions. Such a gender difference in lymphatic efficiency would in simple terms suggest that compared to men, women have low level tissue lymphedema. This is consistent with the recognised differences in gender immunology http://www.ncbi.nlm.nih.gov/pubmed/3907369

It has been accepted for a long time that sex hormones must be involved in female disposition to autoimmune disease, this connection indicates DHT as a major player here. This important question would be quite easy to test by those in the position to do so.

There is an existing study of lymphatic efficiency that also supports this gender difference. This state’s quote “Unexpectedly, three of the four parameters were significantly lower in women compared to men”. http://www.ncbi.nlm.nih.gov/pubmed/9327386

This study tested lymphatic efficiency in the forearms of men and women. There are topical DHT creams and the prior use of these on women in such a study, could test if DHT is responsible for this gender difference. I can see no technical reason why this important question could not be tested, given the will to do so?"

 

[Folliwake]

@S Foote.

First of all, I would like to thank you for taking the time to write what you believe to be actual contributing factors to hereditary hair loss or pattern hair loss. However, I do find some flaws in your theories:

1. You mention that a miniaturised hair follicle thrives in an immunodeficient mouse, which suggests that the environment of the human scalp is a major factor in the miniaturisation process. However, when a miniaturising hair follicle from someone’s scalp was transplanted into their forearm as well as a non-miniaturised hair follicle, the miniaturising hair follicle still continued to miniaturise and the non-miniaturised hair follicle continued to thrive:


"In male pattern baldness the "balding clock" in the follicle or in its very close surrounding keeps time even when the follicle is transplanted to the skin of the forearm. The presence or absence of the galea aponeurotica does not influence the balding process in male pattern baldness. Nor does any supposed increased tension of the scalp or its muscles or a diminished vascular supply to the scalp have an effect on balding."



If we take the belief that a hair transplant works because of the scar tissue around the hair follicle which allows it to eventually grow properly then the miniaturised hair follicle transplanted into the forearm should have not continued to miniaturise.

Thus, I think that we really can’t draw significant assumptions about human hair loss from studies done on any mice! You also do state that the mice are not a good model to draw conclusions about human hair loss so I don’t know why you have used them to base some of your theories of human hair loss on:

“So far we are all aware that what happens in mice and tissue culture, means very little when it comes to human male pattern baldness.”


2. You say that you think pattern hair loss is mainly to do with insufficient lymph drainage in the scalp. However, cold ice and even inverting one’s head can increase lymph drainage. I know that many people have put ice packs on their head for 6 to 8 months in order to try to achieve some hair regrowth and not regrown a single hair. Yet, I also know that putting ice on the scalp during chemotherapy can save up to 80% of hair loss, but stopping hair loss and regrowing hair are 2 different things. You also dismiss inverting one’s head as something which can aid in combatting hair loss, but if lymph drainage does indeed have a role to play in hair loss then inverting one’s head for a period of time is something to be recommended.

 

[S Foote.]

@S Foote.

First of all, I would like to thank you for taking the time to write what you believe to be actual contributing factors to hereditary hair loss or pattern hair loss. However, I do find some flaws in your theories:

1. You mention that a miniaturised hair follicle thrives in an immunodeficient mouse, which suggests that the environment of the human scalp is a major factor in the miniaturisation process. However, when a miniaturising hair follicle from someone’s scalp was transplanted into their forearm as well as a non-miniaturised hair follicle, the miniaturising hair follicle still continued to miniaturise and the non-miniaturised hair follicle continued to thrive:


"In male pattern baldness the "balding clock" in the follicle or in its very close surrounding keeps time even when the follicle is transplanted to the skin of the forearm. The presence or absence of the galea aponeurotica does not influence the balding process in male pattern baldness. Nor does any supposed increased tension of the scalp or its muscles or a diminished vascular supply to the scalp have an effect on balding."



If we take the belief that a hair transplant works because of the scar tissue around the hair follicle which allows it to eventually grow properly then the miniaturised hair follicle transplanted into the forearm should have not continued to miniaturise.

Thus, I think that we really can’t draw significant assumptions about human hair loss from studies done on any mice! You also do state that the mice are not a good model to draw conclusions about human hair loss so I don’t know why you have used them to base some of your theories of human hair loss on:

“So far we are all aware that what happens in mice and tissue culture, means very little when it comes to human male pattern baldness.”


2. You say that you think pattern hair loss is mainly to do with insufficient lymph drainage in the scalp. However, cold ice and even inverting one’s head can increase lymph drainage. I know that many people have put ice packs on their head for 6 to 8 months in order to try to achieve some hair regrowth and not regrown a single hair. Yet, I also know that putting ice on the scalp during chemotherapy can save up to 80% of hair loss, but stopping hair loss and regrowing hair are 2 different things. You also dismiss inverting one’s head as something which can aid in combatting hair loss, but if lymph drainage does indeed have a role to play in hair loss then inverting one’s head for a period of time is something to be recommended.

Thanks for your comments and the points you raise.

You will note that in my article I clearly state that it is possible to design transplantation experiments that would answer these issues properly. Was it just the one miniaturising follicle transplanted to the forearm? At what stage of miniaturisation was this follicle or follicles?

I would expect that any existing growth restricting chemistry induced by spatial controls in a follicle, to be maintained at transplantation until the follicle entered a new cycle. Then you would only get a new miniaturised follicle because of the miniaturised fibrotic scaffold created by the transplantation. This study does not contradict the tissue scaffold idea in transplantation, that is now a recognised factor in tissue engineering in-vivo.

Mouse studies that use a treatment to effect mouse hair growth (like the recent PGD2 study) are irrelevant to male pattern baldness. The big difference in the study I quote in my article is they used Human hair follicles in the mice. Any study that sees a significant regrowth of Human male pattern baldness follicles in an in-vivo model, is very relevant to Human male pattern baldness and has to be explained. The claimed differences in male pattern baldness follicles just cannot explain this, and are effectively refuted by this study. Why should these follicles not enlarge in the Human forearm, but significantly enlarge in the mouse tissue? The difference clearly has to be in the surrounding tissue, not in the follicle itself.

I agree preventing hair loss and re-growing lost hair are two different things. I think this is because once tissue edema gets established it is a lot harder to fix. There is also increased fibrosis longer term that adds to the problem.

I don't remember ever dismissing inverting the head for the reasons you state, and it is something I do myself combined with massage. We can "help" increase lymphatic drainage by these methods, but you have to deal with the actual cause of lymphatic restriction to make any real difference.

 

[S Foote.]

Are you refering this article?
An Evolved Hair Growth Mechanism in Mammals, Implications in Human Physiology ?
"The most important implications of this mechanism are in gender related auto-immune conditions. These can be debilitating and sometimes fatal. It is accepted that sex hormones must play a role here, and research continues to identify the hormonal link (19). "
The link refers this article 19. Zandman-Goddard, G., Peeva, E., & Shoenfeld, Y. (2007). Gender and autoimmunity. Autoimmunity reviews, 6(6), 366-372


or this another
A Review of the issues in historic and current hair research, and an overlooked connection

"An Important Testable Link with Gender Related Disease

The indication here that the androgen DHT significantly increases lymphatic drainage has important implications. It is not currently thought that there is any significant gender difference in lymphatic efficiency. However such a difference would make a lot of sense of some serious gender related diseases, especially female susceptibility to autoimmune disease.

We know that lympedema has a pronounced effect upon the prevailing tissue immunology, increasing immune sensitivity and the chances of secondary immune reactions. Such a gender difference in lymphatic efficiency would in simple terms suggest that compared to men, women have low level tissue lymphedema. This is consistent with the recognised differences in gender immunology http://www.ncbi.nlm.nih.gov/pubmed/3907369

It has been accepted for a long time that sex hormones must be involved in female disposition to autoimmune disease, this connection indicates DHT as a major player here. This important question would be quite easy to test by those in the position to do so.

There is an existing study of lymphatic efficiency that also supports this gender difference. This state’s quote “Unexpectedly, three of the four parameters were significantly lower in women compared to men”. http://www.ncbi.nlm.nih.gov/pubmed/9327386

This study tested lymphatic efficiency in the forearms of men and women. There are topical DHT creams and the prior use of these on women in such a study, could test if DHT is responsible for this gender difference. I can see no technical reason why this important question could not be tested, given the will to do so?"

Yes Armando, what is the point you are trying to make here?

 

[FuianoMonster]

I have started inversions and scalp massage for about a week and noticing some hairs that were dormant are awakening.
So what are the causes of lymphatic restriction? Any way to fix this?

 

[Armando Jose]

The changes in hair growth pattern after autologous hair transplantation.
Lee SH1, Kim DW, Jun JB, Lee SJ, Kim JC, Kim NH.
Author information
Abstract
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.

 

[Armando Jose]

The changes in hair growth pattern after autologous hair transplantation.
Lee SH1, Kim DW, Jun JB, Lee SJ, Kim JC, Kim NH.
Author information
Abstract
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.