Continued below.
- - - Updated - - -
The core problem in male pattern baldness is one of tissue growth. The anagen enlargement of the follicles is cut short, and the follicles fail to enlarge further. The smaller follicles then produce less hair.
Basic physics dictate that in order for the follicles to enlarge, the surrounding tissue has to move out of the way, two things cannot occupy the same space at the same time. So there has to be a resistence factor of the surrounding tissue to follicle enlargement.
I will make a simple analogy. Anagen follicle enlargement is like trying to inflate a balloon under water. The higher the water pressure, the harder it is to inflate the balloon. If the pressure inflating the balloon is a constant, changing the external pressure will change the ultimate size the balloon can reach.
It has been demonstrated that normal tissue growth is subject to spacial constraints. Increasing external pressure restricts tissue growth. Reducing external pressure allows increased tissue growth.
http://www.pnas.org/content/111/15/5586.abstract
This physical connection when considered in terms of general dermal physiology, generates the following hypothesis. This is that the hair producing structure in mammals evolved as a re-cycling pocket, to read and respond to the prevailing external resistence. This allows follicle size and hair growth, to automaticaly adjust in line with the mammals primary thermal control system. This and other advantages of the pocket structure of hair follicles in evolution, are detailed in my pdf article with diagrams linked here.
http://thenode.biologists.com/a-consideration-of-mammalian-dermal-evolution/discussion/
In the described original function the different timing of anagen in follicles, and the distortion of follicles already in anagen, creates shedding and thinning of hair when neccesary.
According to this, anagen follicle size is determined by the resistence factor of the local tissue. Any significant change in follicle size, being caused by changes in local tissue fluid pressures created by whatever mechanism.
In male pattern baldness rising fluid pressures over time in the areas concerned, would account for the shedding and thinning patterns and ultimate baldness.
There is evidence that DHT has a significant effect upon tissue fluid pressures and levels, based upon evolution. There is also evidence that in some individuals, DHT can create increased fluid pressure in the male pattern baldness area. The details of how this happens, are for another discussion. The point here being, is increased scalp fluid pressure the actual cause of follicle miniaturisation in male pattern baldness?
DHT induced scalp lymphedema as the primary cause of male pattern baldness, is the only thing that makes sense of and gives order to all the associated scalp conditions.
Changes in immunology, fibrosis, and hypoxia are all recognised downstream effects of lymphedema.
http://www.plosmedicine.org/article/info:doi/10.1371/journal.pmed.0030254#close
The increased sweating capacity and sebaceous gland swelling, is also easily explained by the local increase in tissue fluid pressures. The scalp tightness and taut shiny skin, are something we all know about.
There are also increased levels of DHT in bald scalp tissue, despite a drastic reduction in the local production capacity. Most dermal DHT production is from many DP cells in large follicles. Most of this is lost in miniaturised follicles. However increased tissue fluid levels, also means increased amounts of substances transported in this fluid. This includes DHT.
There is a paradox concerning hypoxia in the bald scalp, that supports increased fluid pressure as the mechanism of male pattern baldness. Some claim hypoxia itself has a causal role in the male pattern baldness process.
http://www.ncbi.nlm.nih.gov/pubmed/8628793
But there is another study that demonstrates that surgicaly induced scalp hypoxia, significantly increases hair growth?
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2536995/
What tells the story is how the hypoxia is produced. In lymphedema, the reduced fluid drainage and stagnation reduces oxygen levels in the tissue. In the the surgical procedure, the limited blood feed reduces the oxygen levels. Lymphedema increases tissue fluid pressure, whilst reduced blood supply reduces tissue fluid pressure. This is the important difference, and the common link with the changes in hair growth.
So how does this explain the results of hair transplantation, and more to the point what can we do to treat male pattern baldness?
Continued below.
- - - Updated - - -
The principle here is that hair follicle enlargement, is controled by the prevailing external tissue resistence. It has already been sugested that the fibrotic tissue that forms over time in male pattern baldness, is a barrier to follicle re- enlargement. This has been suggested as one of the reasons that it is harder to treat male pattern baldness, once it has been established. The reverse principle must also apply.
In transplantation, large follicles are transplanted into the bald area. In the modern small grafts, the healing process results in fibrotic scar tissue around the grafts. Now instead of being a barrier to the enlargement of small follicles, fibrosis becomes a barrier to the external tissue moving in on the large follicles space. This conserves this space for future large anagen follicles.
This would explain why the only large follicles to survive long term in the old large grafts, are those around the edges. That is within the scarring zone.
This also explains the paradox of male pattern baldness follicles re-enlargeing in the quoted mouse study. The lack of immunology in these mice, fails to produce this fibrotic cage around the follicles during healing. The transplanted miniaturised follicles, are then free to re-enlarge within the low resistence conditions in the mouse tissue.
The common factor in the treatments that have a positive effect in male pattern baldness, is that they have some effect on reducing scalp tissue fluid pressures and levels. We are all aware of these treatments.
Reducing levels of DHT with finasteride etc, reduces the primary effect that results in scalp lymphedema.
Minoxidil stimulates the local microcirculation, reducing surface fluid levels (demonstrated by wrinkles).
http://www.ncbi.nlm.nih.gov/pubmed/6239893
Latanoprost was developed to reduce tissue fluid pressure in the eyes. note the lymphatic drainage link.
http://www.ncbi.nlm.nih.gov/pubmed/24049723
Low level laser light, has now been approved for treating lymphedema.
http://www.breastcancer.org/treatment/lymphedema/treatments/laser
Anti-inflammatory drugs do just that. They help to reduce tissue effects, that increase and maintain edema.
We then have all the anecdotes.
There have been all sorts of methods proposed to increase the blood supply to follicles, that claim to have some effect. Scalp exercises, hanging upside down, massage etc.
It is not increasing blood supply that matters, it is improving the scalp circulation to reduce fluid levels.
So what can we do to increase the effectiveness of male pattern baldness treatment?
The quoted mouse study demonstrates that there is nothing basicaly "wrong" with the follicles in male pattern baldness, and given the right conditions they can re-enlarge. So we need to provide the right conditions.
The fluid pressure in tissue is a function of the feed and drainage equation. In this senario, DHT is reducing the drainage side of the equation. So we obviously need to address this. There is the feed side also, and i think the evidence suggests that this can make a significant difference in men who are prone to male pattern baldness.
So we need to increase scalp fluid drainage, reduce scalp fluid feed, and address the scalp fibrosis that increases scalp tissue rigidity.
Continued below.
- - - Updated - - -
On the drainage side of the equation and DHT.
Again without going into detail here about fluid dynamics, and the complex "plumbing" of the human head. The evidence is that there is to much local production of DHT, in the large follicles of the whole scalp and beard area. This is why topical 5ARI inhibitors on the bald area itself have little effect, and why the systematic drugs like finasteride have a better treatment effect. But i dont think it is neccessary to use systematic drugs here.
People were supprised by the treatment effect of shampoo's that have some action upon reducing DHT production. I suggest this is simply because they are treating the whole scalp. So ideally for convinience of use, we need shampoo's and face washes that topicaly reduce local DHT production effectively.
To maximise the increased drainage, we must also address the other side of the equation. This could be more important that the drainage side in reversing male pattern baldness.
With reduced scalp drainage, a higher blood pressure feed is far more likely to create higher scalp fluid pressure. This is in line with the recent study that confirmed a link with coronary heart disese, and vertex balding in male pattern baldness. The common factor being implicated here, is a higher core blood pressure in the individual.
http://bmjopen.bmj.com/content/3/4/e002537.short?g=w_open_current_tab
There have also been anecdotes on the forums, about bald men who have had accidents involving scalp detachment. I cannot find the posts, but the claim is that after scalp re-attachment hair started to regrow. The only difference now being the reduced blood supply to the re-attached scalp.
According to this factor the scalp arterial ligature procedure referenced above, should make a big difference
second part. i though id post it.!!!
https://www.hairlosstalk.com/interact/threads/a-review-of-male-pattern-baldness-research.89751/
in combination with local DHT reduction. This would of course need to be properly studied first for safety, and wider effects upon core blood pressure etc in the male pattern baldness application. But a one off reversable procedure like this, could be much more effective and preferable than any other surgery for male pattern baldness.
Then we are left with dealing with the scalp fibrosis that developes in male pattern baldness. Here again a common factor links male pattern baldness and lymphedema.
In male pattern baldness some claim a good massage technique has a positive edffect. In lymphedema such techniques are used to reduce the fluid levels, and breakdown the fibrotic tissue. Lasers we know show a positive effect in male pattern baldness, and they are also used in lymphedema to again reduce fluid levels and fibrosis. Such things should not be needed long term once the right fluid balance in achieved in the male pattern baldness area.
Somethings to avoid would be heating the scalp, and external irritants that create inflammation. Cold is good, and cool or lukewarm water only should be used for washing the hair.
The external connection here, also explains why the cell based research for male pattern baldness has not gone as expected. Over the last twenty years or so, we have seen these companies come and go. The same thing seems to happen in all these procedures. Initial results seem promising, but then they just dont develope.
I think the problem is these procedures do not address the actual problem. It would be perfectly possible to create new follicles initialy, but these then have to survive the scalp conditions as described above. Without some kind of external protective matrix, they will suffer the same fate as the original follicles. I think that is why these procedures are failing to develope.
We could always mess with the normal tissue growth controls, to make follicles overcome the external resistence. But this would be a very bad idea, and one that would certainly not be licensed in humans. In my opinion these kinds of procedures would be expensive, not effective long term, and potentialy dangerous.
If we can change the external condition that cause follicle miniaturisation, these procedures would not be neccessary anyway.
- - - Updated - - -
The core problem in male pattern baldness is one of tissue growth. The anagen enlargement of the follicles is cut short, and the follicles fail to enlarge further. The smaller follicles then produce less hair.
Basic physics dictate that in order for the follicles to enlarge, the surrounding tissue has to move out of the way, two things cannot occupy the same space at the same time. So there has to be a resistence factor of the surrounding tissue to follicle enlargement.
I will make a simple analogy. Anagen follicle enlargement is like trying to inflate a balloon under water. The higher the water pressure, the harder it is to inflate the balloon. If the pressure inflating the balloon is a constant, changing the external pressure will change the ultimate size the balloon can reach.
It has been demonstrated that normal tissue growth is subject to spacial constraints. Increasing external pressure restricts tissue growth. Reducing external pressure allows increased tissue growth.
http://www.pnas.org/content/111/15/5586.abstract
This physical connection when considered in terms of general dermal physiology, generates the following hypothesis. This is that the hair producing structure in mammals evolved as a re-cycling pocket, to read and respond to the prevailing external resistence. This allows follicle size and hair growth, to automaticaly adjust in line with the mammals primary thermal control system. This and other advantages of the pocket structure of hair follicles in evolution, are detailed in my pdf article with diagrams linked here.
http://thenode.biologists.com/a-consideration-of-mammalian-dermal-evolution/discussion/
In the described original function the different timing of anagen in follicles, and the distortion of follicles already in anagen, creates shedding and thinning of hair when neccesary.
According to this, anagen follicle size is determined by the resistence factor of the local tissue. Any significant change in follicle size, being caused by changes in local tissue fluid pressures created by whatever mechanism.
In male pattern baldness rising fluid pressures over time in the areas concerned, would account for the shedding and thinning patterns and ultimate baldness.
There is evidence that DHT has a significant effect upon tissue fluid pressures and levels, based upon evolution. There is also evidence that in some individuals, DHT can create increased fluid pressure in the male pattern baldness area. The details of how this happens, are for another discussion. The point here being, is increased scalp fluid pressure the actual cause of follicle miniaturisation in male pattern baldness?
DHT induced scalp lymphedema as the primary cause of male pattern baldness, is the only thing that makes sense of and gives order to all the associated scalp conditions.
Changes in immunology, fibrosis, and hypoxia are all recognised downstream effects of lymphedema.
http://www.plosmedicine.org/article/info:doi/10.1371/journal.pmed.0030254#close
The increased sweating capacity and sebaceous gland swelling, is also easily explained by the local increase in tissue fluid pressures. The scalp tightness and taut shiny skin, are something we all know about.
There are also increased levels of DHT in bald scalp tissue, despite a drastic reduction in the local production capacity. Most dermal DHT production is from many DP cells in large follicles. Most of this is lost in miniaturised follicles. However increased tissue fluid levels, also means increased amounts of substances transported in this fluid. This includes DHT.
There is a paradox concerning hypoxia in the bald scalp, that supports increased fluid pressure as the mechanism of male pattern baldness. Some claim hypoxia itself has a causal role in the male pattern baldness process.
http://www.ncbi.nlm.nih.gov/pubmed/8628793
But there is another study that demonstrates that surgicaly induced scalp hypoxia, significantly increases hair growth?
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2536995/
What tells the story is how the hypoxia is produced. In lymphedema, the reduced fluid drainage and stagnation reduces oxygen levels in the tissue. In the the surgical procedure, the limited blood feed reduces the oxygen levels. Lymphedema increases tissue fluid pressure, whilst reduced blood supply reduces tissue fluid pressure. This is the important difference, and the common link with the changes in hair growth.
So how does this explain the results of hair transplantation, and more to the point what can we do to treat male pattern baldness?
Continued below.
- - - Updated - - -
The principle here is that hair follicle enlargement, is controled by the prevailing external tissue resistence. It has already been sugested that the fibrotic tissue that forms over time in male pattern baldness, is a barrier to follicle re- enlargement. This has been suggested as one of the reasons that it is harder to treat male pattern baldness, once it has been established. The reverse principle must also apply.
In transplantation, large follicles are transplanted into the bald area. In the modern small grafts, the healing process results in fibrotic scar tissue around the grafts. Now instead of being a barrier to the enlargement of small follicles, fibrosis becomes a barrier to the external tissue moving in on the large follicles space. This conserves this space for future large anagen follicles.
This would explain why the only large follicles to survive long term in the old large grafts, are those around the edges. That is within the scarring zone.
This also explains the paradox of male pattern baldness follicles re-enlargeing in the quoted mouse study. The lack of immunology in these mice, fails to produce this fibrotic cage around the follicles during healing. The transplanted miniaturised follicles, are then free to re-enlarge within the low resistence conditions in the mouse tissue.
The common factor in the treatments that have a positive effect in male pattern baldness, is that they have some effect on reducing scalp tissue fluid pressures and levels. We are all aware of these treatments.
Reducing levels of DHT with finasteride etc, reduces the primary effect that results in scalp lymphedema.
Minoxidil stimulates the local microcirculation, reducing surface fluid levels (demonstrated by wrinkles).
http://www.ncbi.nlm.nih.gov/pubmed/6239893
Latanoprost was developed to reduce tissue fluid pressure in the eyes. note the lymphatic drainage link.
http://www.ncbi.nlm.nih.gov/pubmed/24049723
Low level laser light, has now been approved for treating lymphedema.
http://www.breastcancer.org/treatment/lymphedema/treatments/laser
Anti-inflammatory drugs do just that. They help to reduce tissue effects, that increase and maintain edema.
We then have all the anecdotes.
There have been all sorts of methods proposed to increase the blood supply to follicles, that claim to have some effect. Scalp exercises, hanging upside down, massage etc.
It is not increasing blood supply that matters, it is improving the scalp circulation to reduce fluid levels.
So what can we do to increase the effectiveness of male pattern baldness treatment?
The quoted mouse study demonstrates that there is nothing basicaly "wrong" with the follicles in male pattern baldness, and given the right conditions they can re-enlarge. So we need to provide the right conditions.
The fluid pressure in tissue is a function of the feed and drainage equation. In this senario, DHT is reducing the drainage side of the equation. So we obviously need to address this. There is the feed side also, and i think the evidence suggests that this can make a significant difference in men who are prone to male pattern baldness.
So we need to increase scalp fluid drainage, reduce scalp fluid feed, and address the scalp fibrosis that increases scalp tissue rigidity.
Continued below.
- - - Updated - - -
On the drainage side of the equation and DHT.
Again without going into detail here about fluid dynamics, and the complex "plumbing" of the human head. The evidence is that there is to much local production of DHT, in the large follicles of the whole scalp and beard area. This is why topical 5ARI inhibitors on the bald area itself have little effect, and why the systematic drugs like finasteride have a better treatment effect. But i dont think it is neccessary to use systematic drugs here.
People were supprised by the treatment effect of shampoo's that have some action upon reducing DHT production. I suggest this is simply because they are treating the whole scalp. So ideally for convinience of use, we need shampoo's and face washes that topicaly reduce local DHT production effectively.
To maximise the increased drainage, we must also address the other side of the equation. This could be more important that the drainage side in reversing male pattern baldness.
With reduced scalp drainage, a higher blood pressure feed is far more likely to create higher scalp fluid pressure. This is in line with the recent study that confirmed a link with coronary heart disese, and vertex balding in male pattern baldness. The common factor being implicated here, is a higher core blood pressure in the individual.
http://bmjopen.bmj.com/content/3/4/e002537.short?g=w_open_current_tab
There have also been anecdotes on the forums, about bald men who have had accidents involving scalp detachment. I cannot find the posts, but the claim is that after scalp re-attachment hair started to regrow. The only difference now being the reduced blood supply to the re-attached scalp.
According to this factor the scalp arterial ligature procedure referenced above, should make a big difference
second part. i though id post it.!!!
https://www.hairlosstalk.com/interact/threads/a-review-of-male-pattern-baldness-research.89751/
in combination with local DHT reduction. This would of course need to be properly studied first for safety, and wider effects upon core blood pressure etc in the male pattern baldness application. But a one off reversable procedure like this, could be much more effective and preferable than any other surgery for male pattern baldness.
Then we are left with dealing with the scalp fibrosis that developes in male pattern baldness. Here again a common factor links male pattern baldness and lymphedema.
In male pattern baldness some claim a good massage technique has a positive edffect. In lymphedema such techniques are used to reduce the fluid levels, and breakdown the fibrotic tissue. Lasers we know show a positive effect in male pattern baldness, and they are also used in lymphedema to again reduce fluid levels and fibrosis. Such things should not be needed long term once the right fluid balance in achieved in the male pattern baldness area.
Somethings to avoid would be heating the scalp, and external irritants that create inflammation. Cold is good, and cool or lukewarm water only should be used for washing the hair.
The external connection here, also explains why the cell based research for male pattern baldness has not gone as expected. Over the last twenty years or so, we have seen these companies come and go. The same thing seems to happen in all these procedures. Initial results seem promising, but then they just dont develope.
I think the problem is these procedures do not address the actual problem. It would be perfectly possible to create new follicles initialy, but these then have to survive the scalp conditions as described above. Without some kind of external protective matrix, they will suffer the same fate as the original follicles. I think that is why these procedures are failing to develope.
We could always mess with the normal tissue growth controls, to make follicles overcome the external resistence. But this would be a very bad idea, and one that would certainly not be licensed in humans. In my opinion these kinds of procedures would be expensive, not effective long term, and potentialy dangerous.
If we can change the external condition that cause follicle miniaturisation, these procedures would not be neccessary anyway.
