For bryan and Foote.

[Bryan]

BTW, I included all the pertinent and relevant information from the Nordstrom study in that thread I started a while back entitled: "Dispensing with old-fashioned male pattern baldness theories, and one NEW one!", which is in this same forum about half-way down the page from here.

I left out some of his discussions of old-fashioned balding treatments, but I included virtually all of the important stuff about his experiment with transplanting scalp grafts to the arm of a male subject. There was a small, crude diagram of the subject's arm with the implanted grafts in his study, but I duplicated all the essential information in the text of my post. So you can review all the important data by re-reading that post.

Bryan

 

[michael barry]

STEPHEN AND BRYAN, Here are some questions regarding hydrolic theory I have, I'll ask em' and you guys can contemplate em'. Hows that?

1.> Stephen, Ive garnered from your posts that you think Male Baldness is usually actually another sometimes genetic (it is, I looked it up) imparement, Lymphoedema of the scalp. However it is not recognized as such. Would I be correct to assume this?

2.> The symptoms of lymphoedema closely mirror male pattern baldness. First there is chronic inflammation which leads to fibrosis and then to hair loss in the part of the body that has edema. I looked that up. This is caused by the lymphatic system not pumping correctly carrying away excess toxins and protiens from the blood back to the neck where it goes back into the lymphatic sytem to whereeverthefuck its supposda' go. This is just a general statement and not a question.

3.> Stephen, do you think a Doctor would recognize lymphoedema on the scalp if asked given that MRI's are considered as an identifying test for this now (Penn University Website)?

4.> The suggested treatments for lymphoedema on the australian society of lymphoedema's homepage included compression bandages (because failing lypmh's only pump when compressed by massage, excercise, or manual pressure). Do you think one could sleep with a bandage firmly around one's head to treat this? Ive seen you link articles that laser light devices, electromagnetic devices, and diuretics can treat lymphoedema, but the Australian web page mentioned compression garments as the foremost treatment and Im assuming thats because its the best? Thoughts?

5.> Ive noticed that you mentioned that midoxodil, which is 60% alchohol (big known diuretic) has a diuretic effect as a topical drug and I have read that the higher doses of minoxodil usually are accompanied by fluid shifting effects like swollen feet and sometimes gynochomastia. Caffeine, another diuretic, keeps popping up on forums as its both a vasolidator and diuretic. Any opinion whether a topical diuretic to shift fluids (containing toxins and protiens) back down the lymphatic system while getting the capillaries to fill with blood and expand with a topical vasolidator to assist the pumping would be useful?

6.> You mention that DHT has a negative pumping effect on scalp tissue in your posts that aggravates the lymphoedema. This is the "indirect" effect of androgens causing hair loss according to your theory. Can you, in layman's terms, give a description of this phenomena or your best guess at it?



Note: I hope by answering the 5 queries above you can present your theory in a way the regualars understand well instead of focusing on Nordstroms and Orenitech's plug graft studies of so many years ago that proboably confuse most readers. By the way, Ive looked into electromagnetic helments, but the company that makes the product, Bx3 Electromagentic Helments have not posted pics of before and after on their site. I aint gonna bite unless those jokers put a few up as thats my policy on hair products.
Bryan, any observations you have would be great as I feel giving these queries a go could "air out" Stephen's ideas for better or ill.

 

[Footy]

Bryan.

In response to the two points being discussed.

The first point about the `oddball' terminal follicles, that can exist in the heart of the male pattern baldness area for long periods. I suspect that there hasn't been any specific research following on from that study you quoted, aimed at answering this question?

From the viewpoint of my theory, this would propose that what is actually `oddball' about these particular follicles, is that they have an exeptionally long anagen phase. This is why they do not miniaturise, as this requires a `re-cycling' as i have explained.

But you are right in thinking Bryan that my theory would be wrong, if it could be shown that these follicles are surviving in the male pattern baldness area through `normal' cycling. So the real question here is are there studies that can `PROVE' that these `odd' follicles are cycling at the same average rate as the male pattern baldness follicles next door?

Such an `extra long' anagen phase of `odd' follicles, is not beyond the bounds of reason. Human anagen is known to be variable anyway, the periods quoted in the literature reflect this.

http://www.pg.com/science/haircare/hair_twh_23.htm

As far as the current theory you support goes Bryan, this particular study `again' shows that androgens do not `DIRECTLY' convert non male pattern baldness follicles into male pattern baldness follicles, which is the very heart of this theory!!

__________________________________________________________

The second point involves the hair loss common in the larger plug grafts, refered to as doughnutting. The real issue of debate here involves the current explaination for this as tissue hypoxia due to the characteristics induced by the procedure itself.

You believe that the hypoxia alledged to cause this very common hair loss in larger grafts, happens very quickly Bryan. I agree that if hypoxia does happen in these grafts, it will happen from `day one'. But whether this effects hair growth is a whole different matter!

You ask me to provide evidence for the time line i claim rules out hypoxia, as the cause of this hair loss. Here it is!

There is one other factor that occours in transplanted grafts, this was even noted by Nordstrom in the study you posted Bryan! It is this factor that proves a timeline that rules out hypoxia as the cause of the `doughnutting' hair loss.

This is a quote from that Nordstrom study out of the results section.

__________________________________________________________

"The hairs in the hair-bearing grafts gradually fell off over a couple of weeks and started to grow again after about 3 months as is normally seen in punch hair grafting.

5, 10 and 21 months after transplantation the numbers of hairs in the transplants were counted. The grafts were then excised for histological examination. In the graft taken from the occipital region the number and macroscopical quality of the hairs remained unchanged"

___________________________________________________________

The initial `shock' hair loss in grafts is a fact, and normally seen as Nordstrom said.

Nordstrom also confirms the common observation that there is around a 3 month period before hair in these grafts starts growing again.

Any conditions of oxygen starvation (hypoxia) in these grafts will be well established before 3 months, so the regrowing hair should reflect this by growing back with this `doughnutting' pattern of loss in the centre.

But as Nordstrom noted, this didn't happen! In fact he reports above that even after 21 months the terminal hair bearing occipital graft, showed `NO' loss!

It is the same 4mm grafts from the non balding occipital region, as used by Nordstrom, that where commonly used in the balding area. It is also these 4mm grafts, and even 3mm grafts that are now known to commonly bald in this doughnutting pattern.

http://www.hairtransplantmedical.com/ha ... repair.htm

Quote:

" This results in hair growing only in the periphery of the grafts. This was a common phenomenon in 4- and 5-mm plugs, but can also be noted in grafts 3-mm in size."

There is one other pure common sense factor that takes this doughnutting out of the time line of hypoxia!

People had these larger grafts done over a number of sessions that could run for up to 2 years. Any hypoxia induced loss would have been noticed by both patient and clinics, and the alarm bells would have stopped the use of these grafts long before they were actually dropped!

I know from my own experience with 4mm grafts that the `doughnutting' hair loss pattern takes years to develope, just like male pattern baldness!!

I would say this Bryan.

I wish Nordstrom had also transplanted occipital 4mm grafts to the male pattern baldness area in this individual, and followed this up for a few years!

I am willing to bet that the 4mm occipital grafts to the forearm, would `NOT' doughnut over time, but the same grafts to the male pattern baldness area `WOULD'!

This is because i think it is the conditions in the surrounding tissue that determine the fate of large anagen follicles, in the absense of a protective `scaffold'.

S Foote.

 

[Boru]

[quote="S Foote.":ffbed]I don't think that DHT or other androgens `directly' effect either hair loss or hair growth. The important point of the in-vitro studies that people seem to miss, is that `direct' exposure to androgens, dosen't `change' the pre-existing growth characteristics of `ANY' type of follicle cell sample.

I think this is the important thing to remember, as it is easy to point to `some' molecular change induced by androgens in-vitro, but the bottom line is `no' growth changes are observed!

Because we know DHT `does' create follicle growth `changes', this must be an indirect effect, and `THE' significant effect on hair growth.

That's typical of your strange logic: just because we don't (yet) fully understand how androgen-sensitive hair follicles actually BECOME sensitive to them, you jump to the weird conclusion that androgens must not have any direct effect at all, despite the in vitro experiments clearly showing that they do. What a strange non sequitur.

Bryan

It isn't `strange' logic Bryan, it's proper scientific reasoning! :wink:

The in-vitro studies clearly show that hair follicles are not `directly' androgen sensitive, nor do they `become' so!

For `anything' to be sensitive to `something', means that some kind of `CHANGE' is induced.

The in-vitro studies clearly show, that `DIRECT' exposure to androgens, does `NOT' change the pre-existing growth characteristics of `ANY' follicle cell type! Be this terminal scalp follicles, pre-balding follicles, balding follicles, beard follicles, or vellous follicles.

You admit yourself that follicles don't `need' androgens. In androgen insensitivity syndrome, we still get a `range' of different size follicles from terminal to vellous!!

By what `MECHANISM' can you explain differently sized follicles in the complete absense of any action of androgens Bryan? At the very least, this demonstrates some `OTHER' mechanism of control of follicle size! How do you know that androgens don't `indirectly' effect this `independent' mechanism?????????

The `interpretation' of the in-vitro study results you support Bryan, is typical of the bad science traditional in hair loss research. This is a classic case of trying to `read' what you want into studies instead of what is `actually' shown!!



In this case, people have got this notion into their heads that follicles `MUST' be effected `directly' by androgens because of the `interpretation' that was placed on `EARLY' transplantation results.

So ever since then, the results of further experiments have been interpreted, or more accurately `twisted' to try to `SUIT' this idea!

There is not one scrap of `real' scientific support for the `direct' theory you support Bryan, and as time goes on the `donor dominance' assumption it was based on is also falling apart with modern transplantation knowledge! :wink:

S Foote.[/quote:ffbed]

Are you implying that the suppression of the 5a reductase enzyme is irelevant in male pattern baldness, because the binding of the DHT to the androgen receptors may not be the culprit for minaturisation? What about the trials of proscar and propecia, which improved hair growth in younger men?
Is there something else about the activity of DHT, or the 5 alpha reductace, other than hitting the follicle receptors, which is being ignored.
Giving this theory a chance, maybe it has an effect on the libido from a systemic point of view.
As I read these opposing points of view, I realise that I have a long way to go to understand fully the reasons why I have been able to grow alot of hair back after twenty years male pattern baldness. However,if the various doctors and specialists at the forefront of the "traditional" science are still guessing about the causes of minaturisation, what hope for me? I just have to do what I do, and wait for more detailed knowledge later. I hope they don't put me in a test tube!

 

[Footy]

>>>STEPHEN AND BRYAN, Here are some questions regarding hydrolic theory I have, I'll ask em' and you guys can contemplate em'. Hows that?<<<

Hi Michael, good questions!

>>>1.> Stephen, Ive garnered from your posts that you think Male Baldness is usually actually another sometimes genetic (it is, I looked it up) imparement, Lymphoedema of the scalp. However it is not recognized as such. Would I be correct to assume this?<<<

Yes you are right in thinking that lymphoedema of the scalp, or any mechanism of different fluid levels effecting hair growth, is not recognised. This is why i am pointing out the evidence for this here.

I think it is only changes in the local tissue fluid pressures that make sense of both DHT related hair loss (male pattern baldness), AND DHT related hair growth. Apart from this, there is a good reason in evolution why hair growth should be adjusted by changes in fluid pressure, and why DHT should effect fluid pressures as a male hormone. I describe this in my paper.

http://www.hairsite2.com/library/abst-167.htm

I think the `genetic' factors here are the genetics that determine an individuals vascular characteristics, and their levels of DHT.

I certainly don't think that hair follicles are programed differently in the way they respond to DHT. Because the in-vitro tests clearly show that androgen exposure does not change the pre-existing growth characteristic of follicle cells.



>>>2.> The symptoms of lymphoedema closely mirror male pattern baldness. First there is chronic inflammation which leads to fibrosis and then to hair loss in the part of the body that has edema. I looked that up. This is caused by the lymphatic system not pumping correctly carrying away excess toxins and protiens from the blood back to the neck where it goes back into the lymphatic sytem to whereeverthefuck its supposda' go. This is just a general statement and not a question.<<<

The only part of this i don't agree with, is that the toxins etc are creating the hair loss directly. I think the evidence is that it is the local fluid pressure that effects the follicle size, because this explains both the DHT related hair growth and the DHT related hair loss.

>>>3.> Stephen, do you think a Doctor would recognize lymphoedema on the scalp if asked given that MRI's are considered as an identifying test for this now (Penn University Website)?<<<

I am pretty sure that the signs of increased fluid levels in the bald scalp could be measured. Remember that the actual `swelling' in the scalp is small compared to the fluid pressure, because the scalp is a thin layer curving around the skull. It is well suported, so it is not as obvious that there is edema here as it would be say in an arm or leg.

Whether you could talk you doctor into doing these tests is something else!

But i think a protein level biopsy would confirm edema. As protein levels vary with tissue fluid levels. There is also the bio-impedence test that is claimed to accurately compare reletive fluid levels in tissues.

For me, the thread here about the study "Beards, Baldness, and Sweat secretion", demonstrates these fluid level differences.

>>>4.> The suggested treatments for lymphoedema on the australian society of lymphoedema's homepage included compression bandages (because failing lypmh's only pump when compressed by massage, excercise, or manual pressure). Do you think one could sleep with a bandage firmly around one's head to treat this? Ive seen you link articles that laser light devices, electromagnetic devices, and diuretics can treat lymphoedema, but the Australian web page mentioned compression garments as the foremost treatment and Im assuming thats because its the best? Thoughts?<<<

I don't really think that would be practical?

I certainly think that massage is good, and ice packs will help. I think that the inversion theropy some recommend, is OK to a point. But i think the `good' part about this is returning to the upright position. A couple of mins inverted, then returning upright, is exercising the scalps drainage vessels.



>>>5.> Ive noticed that you mentioned that midoxodil, which is 60% alchohol (big known diuretic) has a diuretic effect as a topical drug and I have read that the higher doses of minoxodil usually are accompanied by fluid shifting effects like swollen feet and sometimes gynochomastia. Caffeine, another diuretic, keeps popping up on forums as its both a vasolidator and diuretic. Any opinion whether a topical diuretic to shift fluids (containing toxins and protiens) back down the lymphatic system while getting the capillaries to fill with blood and expand with a topical vasolidator to assist the pumping would be useful?<<<

I think minoxidil is usefull in shifting fluid from the periferal tissues (around hair follicles).

http://www.hairsite4.com/dc/dcboard.php ... 051&page=2

But if the minoxidil or it's vehicle cause irritation, this is counter productive.

The best scalp topicals would be those that reduce inflammation and fibrosis, created by the edema, that hinder attempts to reduce the edema.

I think many people on these forums are now experimenting with these topicals.

>>>6.> You mention that DHT has a negative pumping effect on scalp tissue in your posts that aggravates the lymphoedema. This is the "indirect" effect of androgens causing hair loss according to your theory. Can you, in layman's terms, give a description of this phenomena or your best guess at it?<<<

This is quite straight forward if you know how the lymphatic system moves fluid out of tissues. This is a good site.

http://www.jdaross.mcmail.com/lymphatics2.htm

The basics of what i am saying is this.


I think the primary function of DHT as a male hormone, is to increase lymphatic drainage. What this does is to increase the fluid turnover in tissues, increasing nutrient supply and waste product removal in tissues.

This function enhances the tissue building nature of other androgens, and effects other fluid related male functions.

To do this, DHT must be increasing the natural contraction rate of lymphatic vessels. When these vessels contract, fluid is moved through them because of the one way valves in these vessels. (refer to the link).

This would mean that DHT acts through androgen receptors within these vessels, to effect the nervous control of muscle fiber contraction in lymph vessels. DHT is known to have effects on the nervious system.

The technical problem with this system of increasing lymphatic `pumping', involves the one way valves in the vessels, and this is where it gets slightly complicated.

The lymph vessels start in the outer tissues, and ultimately lead to a point where this drained tissue fluid re-enters the blood circulation. If you increase the pumping of a lymph vessel at some point away from its origin in the outer tissues, this will increasingly slam the one way valves shut against the flow from the outer tissue. This means that increased drainage from one part of the vessel. effectively reduces drainage from the very end of the same vessel.

The best analogy i can use here is this.

If you are showering `upstairs', and someone turns on the water `downstairs', you will get a reduced flow, depending on the basic `plumbing'. In other words, the increased flow below, `rob's flow from the end of the system.

I think evolution has taken some account of this factor, in that DHT is introduced into the tissues with a bias towards the ends of the lymph vessels, that is the outer tissues.

The largest producer of DHT, and in effect the largest organ in the body, is the dermal tissue. The other major centres of DHT production are the prostate and liver. These sites of DHT production on the whole produce an even pumping of lymph vessels, avoiding the reduced drainage this can cause from the outer tissues.

But i think another factor comes into play in the human scalp.

This is the evolution of a very complex fluid system to service the human brain. The primary consideration in terms of evolution, is to protect this `large' brain. If this means the local `plumbing' that evolved can cause reduced drainage from the scalp because of the action of DHT, so what!

That would be secondary to the survival of the human brain!

If you look at the layout of the lymphatic vessels of the surface tissue of the human head, the vunerability the scalp drainage is clear.

http://137.222.110.150/calnet/DeepNeck/ ... m#section6

It is just a case of particular circumstances that creates the fluid build up, and male pattern baldness in my opinion.

The large anagen follicles on our scalps are the largest local producers of DHT. This DHT feeds the lower lymph vessels. This increases the pumping of these vessels, reducing fluid levels in the beard area, and promoting beard growth. The enlarging beard follicles increase their DHT production, adding to the pumping of the lower lymph vessels.

When you consider that the lymph vessels in the male pattern baldness area are sparse compared to those lower down according to the diagram, you can see how drainage from these can be reduced as described above.

If an individual has a naturaly higher fluid `feed', that is a higher blood pressure, this reduced drainage can produce edema.

It is known that male pattern baldness is linked to a higher risk of heart problems in later life. I suggest the link is a naturaly higher blood pressure.

This is really the simplest way i can describe my theory. It basicaly just uses recognised physiological mechanisms and fluid dynamic principles, to explain all the aspects of DHT related hair loss/growth.

S Foote.

 

[michael barry]

Stephen, you did a good job with those questions so that others can read your theory and understand it and judge for themselves. Its in laymans terms to which is great.

I have one more observation that I should have made mention of.

On Tom Hagerty's site, he has linked a few articles about microcapillary circulation. I thought about your idea when I seen this. As Im sure you know, the protien VEGF dialates the blood vessels and promotes angiogenisis and better blood flow. This, and fighting the hardening of collagen, and NO release, are speculated to be the main ways minoxidil works.

Docs in this study applied some protien that increased VEGF production in mice and of course their follicle sizes got much bigger in the next anagen phase as opposed to control group. When protien was taken away, follicles were really small again (vellus) next anagen phase. The docs in the study (oversimplification, I think) speculated that male pattern baldness men might just have too few capillaries in their heads.

I thought about your theory and what I know about microcapillaries that feed follicles. The microcapillaries increase about 4 times in size in from the end of catagen to the early stages of anagen to bring more blood to the newly active follicle, so in effect they shrink and grow with the follicle.

Question: Do you think that its possible that the edema is simply squeezing the micro-capillaries so much that they cant really feed nutrients to the follilce (this is what the docs speculated) in addition to inhibiting the early-anagen papilla expansion?

I mention this because of another article by the doctor Ivy Greenwell (proboably sure you heard of her) in which she stated that since skid row winos usually have luxuriant heads of hair as opposed to college professors that the excellent vasolidation effects of alchohol was proboably why. Drunks have the cleanest arteries in the world (and the worst livers). Their artieries are also dialated constantly as well as kept free of plaque by the booze, so much so that the ones on their faces end up bursting. Estrogen acts as a vasolidator also, Greenwell believes that this one of the reasons is why women go bald so much less than men. If you think about it, keeping blood vessels open would also present tension against fluid levels in the scalp, helping press the water and protiens back down the neck where its supposed to go. Wonder if you have a thought or two on this? I thought about how this might relate to hair plugs, but since plugs have tissue scaffolds, and the bottoms of the incisions made are pretty deep in the skin.........by this idea they shouldnt be affected all that much.

Just a stray thought, we all have'em on something as beffudling as male pattern baldness

 

[Armando Jose]

Very interesting post.

I have a question for Stephen, why the different incidence of premature baldness among women and men acording your theory?

TIA

Armando

 

[formercurly]

Stephen, are you suffering from male pattern baldness? If so, have you had any success growing hair back?

I'm just curious to know that but the main reason for my post is the following:

I understand a great deal of your theory and I think it makes a lot of sense. I don't have the time to be reading all the links and also I'm pretty new in this forum, therefore I don't yet have the scientific knowledge about male pattern baldness yet to talk with all these big words, but I would like to voice my opinion and observation which may relate to your theory.

I got the following ideas from a free booklet I recieved by mail years ago from a person named Oleda Baker, which she's a hair stylist and she makes her own hair products. I'm relying just on memory so these are not exact quotes from the booklet. In a nut shell, she states that the cause of male pattern baldness is that in men, the galea (a protective sheet that covers the skull) thickens and causes deprivation of blood supply to the follicles. This supposedly explains why the part of the scalp where male pattern baldness occurs is tighter than the sides and back that is not effected by male pattern baldness. Her remedy is just to massage your head on a daily basis to increase circulation.

MY OPINION:

I can relate to the above because the scalp on the sides and back of MY scalp is loose enough that I can even pinch it, whereas the top is so tight I can barely move it. Is this just a COINCIDENCE? Now my wife's scalp is a lot more loose on the top.

Why that peculiar pattern that starts on the temples and crown?
Well, it probably comes from birth. Haven't you noticed the pattern in which babies grow their hair after their shed as newborns? It resembles that of male pattern baldness don't it? Only in reverse, right? Maybe the follicles on the temples are just genetically weaker or have a naturally shorter anagen phase. As far as the crown is concerned, that is probably the tightest section of the scalp isn't it?

Another important point I have observed is that everywhere else in the body where hair grows, the skin is loose, but on the top of the head, the scalp is tight. Does that scalp tightness have any relation to your theory Stephen? Do you think it's the cause or the effect of male pattern baldness?

 

[Boru]

Stephen, are you suffering from male pattern baldness? If so, have you had any success growing hair back?

I'm just curious to know that but the main reason for my post is the following:

I understand a great deal of your theory and I think it makes a lot of sense. I don't have the time to be reading all the links and also I'm pretty new in this forum, therefore I don't yet have the scientific knowledge about male pattern baldness yet to talk with all these big words, but I would like to voice my opinion and observation which may relate to your theory.

I got the following ideas from a free booklet I recieved by mail years ago from a person named Oleda Baker, which she's a hair stylist and she makes her own hair products. I'm relying just on memory so these are not exact quotes from the booklet. In a nut shell, she states that the cause of male pattern baldness is that in men, the galea (a protective sheet that covers the skull) thickens and causes deprivation of blood supply to the follicles. This supposedly explains why the part of the scalp where male pattern baldness occurs is tighter than the sides and back that is not effected by male pattern baldness. Her remedy is just to massage your head on a daily basis to increase circulation.

MY OPINION:

I can relate to the above because the scalp on the sides and back of MY scalp is loose enough that I can even pinch it, whereas the top is so tight I can barely move it. Is this just a COINCIDENCE? Now my wife's scalp is a lot more loose on the top.

Why that peculiar pattern that starts on the temples and crown?
Well, it probably comes from birth. Haven't you noticed the pattern in which babies grow their hair after their shed as newborns? It resembles that of male pattern baldness don't it? Only in reverse, right? Maybe the follicles on the temples are just genetically weaker or have a naturally shorter anagen phase. As far as the crown is concerned, that is probably the tightest section of the scalp isn't it?

Another important point I have observed is that everywhere else in the body where hair grows, the skin is loose, but on the top of the head, the scalp is tight. Does that scalp tightness have any relation to your theory Stephen? Do you think it's the cause or the effect of male pattern baldness?

I believe that scalp exercises are necessary in conjunction with dutasteride or finasteride minoxidil etc. I have kept my scalp from getting tight (and stopped my chin from going double or my face getting wrinkled) with the scalp and face exercises over the past twenty years. I just needed the finasteride and to develop new methods of microcapillary stimulation, and my hair wanted to grow again.
I was doing this long before Tom Hagerty published his book five years ago. The question is, will young men want to go to the bother of these exercises every day? It only takes a few minutes every now and then, and you get into the habit.
I don't have fewer capillaries, I just have to work harder than non male pattern baldness prone men to keep them healthy. At male pattern baldness is to some degree linked with heart disease, it seems logical to me to conclude that there is a tendency for capillaries to athropy in the male pattern baldness prone area. It is a symptom which should alert us to keep our hearts healthy. Worshiping good fruit and veg is my new religion. No red meat, fenugreek (fed to horses to give them glossy coats) and anything else I can get to look after my heart. Get your arteries unclogged as well. If the efficiency of the main blood supply is put at risk, the capillaries will suffer first.
Boru

 

[Footy]

Hi Michael.

>>>I have one more observation that I should have made mention of.

On Tom Hagerty's site, he has linked a few articles about microcapillary circulation. I thought about your idea when I seen this. As Im sure you know, the protien VEGF dialates the blood vessels and promotes angiogenisis and better blood flow. This, and fighting the hardening of collagen, and NO release, are speculated to be the main ways minoxidil works.

Docs in this study applied some protien that increased VEGF production in mice and of course their follicle sizes got much bigger in the next anagen phase as opposed to control group. When protien was taken away, follicles were really small again (vellus) next anagen phase. The docs in the study (oversimplification, I think) speculated that male pattern baldness men might just have too few capillaries in their heads.

I thought about your theory and what I know about microcapillaries that feed follicles. The microcapillaries increase about 4 times in size in from the end of catagen to the early stages of anagen to bring more blood to the newly active follicle, so in effect they shrink and grow with the follicle.

Question: Do you think that its possible that the edema is simply squeezing the micro-capillaries so much that they cant really feed nutrients to the follilce (this is what the docs speculated) in addition to inhibiting the early-anagen papilla expansion?<<<

I have no doubt the capillaries are effected in male pattern baldness, but i think this is because of the increased fluid pressure, and is another part of the self maintaining effects of edema. A higher fluid pressure `outside' of the capillaries will tend to collapse them, making them less effective in circulation `through' the scalp. This would just add to the edema.

I think VEGF is expanding the scalp capillaries, and creating a significant reduction in the local `flow through' reducing the pressure in the scalp.

As i said, i think it is only DHT related changes in tissue fluid pressures via the lymphatic vessels, that can explain both DHT related hair loss AND hair growth.

The effects we are seeing in the balding scalp are just the result of the increased fluid pressure, and these other factors just add to the problem IMO.

By the way, i agree that the VEGF pathway is probably how minoxidil is working in hair growth.

S Foote.

 

[Footy]

Very interesting post.

I have a question for Stephen, why the different incidence of premature baldness among women and men acording your theory?

TIA

Armando

Hi Armando.

Are you talking purely about Androgenetic Alopecia here Armando?

S Foote.

 

[Footy]

Stephen, are you suffering from male pattern baldness? If so, have you had any success growing hair back?

I'm just curious to know that but the main reason for my post is the following:

I understand a great deal of your theory and I think it makes a lot of sense. I don't have the time to be reading all the links and also I'm pretty new in this forum, therefore I don't yet have the scientific knowledge about male pattern baldness yet to talk with all these big words, but I would like to voice my opinion and observation which may relate to your theory.

I got the following ideas from a free booklet I recieved by mail years ago from a person named Oleda Baker, which she's a hair stylist and she makes her own hair products. I'm relying just on memory so these are not exact quotes from the booklet. In a nut shell, she states that the cause of male pattern baldness is that in men, the galea (a protective sheet that covers the skull) thickens and causes deprivation of blood supply to the follicles. This supposedly explains why the part of the scalp where male pattern baldness occurs is tighter than the sides and back that is not effected by male pattern baldness. Her remedy is just to massage your head on a daily basis to increase circulation.

MY OPINION:

I can relate to the above because the scalp on the sides and back of MY scalp is loose enough that I can even pinch it, whereas the top is so tight I can barely move it. Is this just a COINCIDENCE? Now my wife's scalp is a lot more loose on the top.

Why that peculiar pattern that starts on the temples and crown?
Well, it probably comes from birth. Haven't you noticed the pattern in which babies grow their hair after their shed as newborns? It resembles that of male pattern baldness don't it? Only in reverse, right? Maybe the follicles on the temples are just genetically weaker or have a naturally shorter anagen phase. As far as the crown is concerned, that is probably the tightest section of the scalp isn't it?

Another important point I have observed is that everywhere else in the body where hair grows, the skin is loose, but on the top of the head, the scalp is tight. Does that scalp tightness have any relation to your theory Stephen? Do you think it's the cause or the effect of male pattern baldness?

Hi.

Yes have male pattern baldness. I am 52 now, and i started with male pattern baldness at 28. In the early 80's i had a number of scalp reductions with frontal grafts.

Over the 20 odd years since, all the hair moved up by the scalp reductions recceded back just like the original, and the 4mm grafts all lost most of the central hair or `doughnutted', as described here.

It was my personal experience of transplantation that first made me question the current theory of male pattern baldness.

I think the scalp tightness you refer to is because of the edema or higher fluid pressure in the male pattern baldness area. When people talk about a shiny bald head, i think this shine is because the skin is stretched smooth by the pressure.

I do think the galea membrane does play a part. as it restricts the drainage of the fluid to deeper levels. It is a natural tendancy for higher pressure fluid to spread into the tissue around, so reducing the local pressure. I think the galea prevents this action to a degree in the male pattern baldness area.

But i do think that a build up of fluid pressure is the primary cause of male pattern baldness through normal contact inhibition of follicle enlargement.

It seems we are cursed with characteristics in the scalp that conspire to add to the problem!

S Foote.

 

[Footy]

Stephen, are you suffering from male pattern baldness? If so, have you had any success growing hair back?

I'm just curious to know that but the main reason for my post is the following:

I understand a great deal of your theory and I think it makes a lot of sense. I don't have the time to be reading all the links and also I'm pretty new in this forum, therefore I don't yet have the scientific knowledge about male pattern baldness yet to talk with all these big words, but I would like to voice my opinion and observation which may relate to your theory.

I got the following ideas from a free booklet I recieved by mail years ago from a person named Oleda Baker, which she's a hair stylist and she makes her own hair products. I'm relying just on memory so these are not exact quotes from the booklet. In a nut shell, she states that the cause of male pattern baldness is that in men, the galea (a protective sheet that covers the skull) thickens and causes deprivation of blood supply to the follicles. This supposedly explains why the part of the scalp where male pattern baldness occurs is tighter than the sides and back that is not effected by male pattern baldness. Her remedy is just to massage your head on a daily basis to increase circulation.

MY OPINION:

I can relate to the above because the scalp on the sides and back of MY scalp is loose enough that I can even pinch it, whereas the top is so tight I can barely move it. Is this just a COINCIDENCE? Now my wife's scalp is a lot more loose on the top.

Why that peculiar pattern that starts on the temples and crown?
Well, it probably comes from birth. Haven't you noticed the pattern in which babies grow their hair after their shed as newborns? It resembles that of male pattern baldness don't it? Only in reverse, right? Maybe the follicles on the temples are just genetically weaker or have a naturally shorter anagen phase. As far as the crown is concerned, that is probably the tightest section of the scalp isn't it?

Another important point I have observed is that everywhere else in the body where hair grows, the skin is loose, but on the top of the head, the scalp is tight. Does that scalp tightness have any relation to your theory Stephen? Do you think it's the cause or the effect of male pattern baldness?

I believe that scalp exercises are necessary in conjunction with dutasteride or finasteride minoxidil etc. I have kept my scalp from getting tight (and stopped my chin from going double or my face getting wrinkled) with the scalp and face exercises over the past twenty years. I just needed the finasteride and to develop new methods of microcapillary stimulation, and my hair wanted to grow again.
I was doing this long before Tom Hagerty published his book five years ago. The question is, will young men want to go to the bother of these exercises every day? It only takes a few minutes every now and then, and you get into the habit.
I don't have fewer capillaries, I just have to work harder than non male pattern baldness prone men to keep them healthy. At male pattern baldness is to some degree linked with heart disease, it seems logical to me to conclude that there is a tendency for capillaries to athropy in the male pattern baldness prone area. It is a symptom which should alert us to keep our hearts healthy. Worshiping good fruit and veg is my new religion. No red meat, fenugreek (fed to horses to give them glossy coats) and anything else I can get to look after my heart. Get your arteries unclogged as well. If the efficiency of the main blood supply is put at risk, the capillaries will suffer first.
Boru

Hi Boru.

I hope i answered your previous question in my explaination of my theory.

Thanks for your input.

S Foote.

 

[Bryan]

Bryan. In response to the two points being discussed.

The first point about the `oddball' terminal follicles, that can exist in the heart of the male pattern baldness area for long periods. I suspect that there hasn't been any specific research following on from that study you quoted, aimed at answering this question?

From the viewpoint of my theory, this would propose that what is actually `oddball' about these particular follicles, is that they have an exeptionally long anagen phase. This is why they do not miniaturise, as this requires a `re-cycling' as i have explained.

But you are right in thinking Bryan that my theory would be wrong, if it could be shown that these follicles are surviving in the male pattern baldness area through `normal' cycling. So the real question here is are there studies that can `PROVE' that these `odd' follicles are cycling at the same average rate as the male pattern baldness follicles next door?

Stephen, I just dug-out that study again and re-read it, and I misremembered the details of those 'oddball' follicles. Their comments are a little bit vague, but what they seem to be saying is that they found both androgen-sensitive and androgen INsensitive follicles in the occipital region of the scalp, not in the vertex. Sorry I screwed-up on that particular detail!

However, that still doesn't let your theory off the hook. You still have no really good way of explaining why some follicles in a particular geographic region of the scalp show the effects of contact inhibition, while others do not. The only tentative explanation you have is (once again) that the alleged "edema" sets in at some midpoint between cycles of those follicles. That hypothesis obviously doesn't work for someone who's been balding for a long period of time.

As far as the current theory you support goes Bryan, this particular study `again' shows that androgens do not `DIRECTLY' convert non male pattern baldness follicles into male pattern baldness follicles, which is the very heart of this theory!!

How does it show that? Please explain.

You ask me to provide evidence for the time line i claim rules out hypoxia, as the cause of this hair loss. Here it is!

There is one other factor that occours in transplanted grafts, this was even noted by Nordstrom in the study you posted Bryan! It is this factor that proves a timeline that rules out hypoxia as the cause of the `doughnutting' hair loss.

This is a quote from that Nordstrom study out of the results section.

"The hairs in the hair-bearing grafts gradually fell off over a couple of weeks and started to grow again after about 3 months as is normally seen in punch hair grafting.

5, 10 and 21 months after transplantation the numbers of hairs in the transplants were counted. The grafts were then excised for histological examination. In the graft taken from the occipital region the number and macroscopical quality of the hairs remained unchanged"

The initial `shock' hair loss in grafts is a fact, and normally seen as Nordstrom said.

Nordstrom also confirms the common observation that there is around a 3 month period before hair in these grafts starts growing again.

Any conditions of oxygen starvation (hypoxia) in these grafts will be well established before 3 months, so the regrowing hair should reflect this by growing back with this `doughnutting' pattern of loss in the centre.

But as Nordstrom noted, this didn't happen! In fact he reports above that even after 21 months the terminal hair bearing occipital graft, showed `NO' loss!

You are very subtly MISINTERPRETING what Nordstrom said, and I'm going to explain this to you once and for all so that we can get past this point of confusion! :wink:

Nordstrom only did haircounts at months 5, 10, and 21, and he reported the EXACT numbers for those haircounts. But the only thing those numbers demonstrate is that THERE WAS NO FURTHER LOSS AFTER THE FIFTH MONTH in the graft that came from the non-balding donor area. I'm trying to get you to understand that in my opinion, doughnutting DID occur (and quite possibly caused by hypoxia, just like the medical establishment claims), and it occurred DURING THE FIRST 5 MONTHS. The results of Nordstrom's careful little experiment are perfectly consistent with both the standard medical theory of male pattern baldness, and the real-world observations of "doughnutting".

Do you understand my position, now?

I would say this Bryan.

I wish Nordstrom had also transplanted occipital 4mm grafts to the male pattern baldness area in this individual, and followed this up for a few years!

I am willing to bet that the 4mm occipital grafts to the forearm, would `NOT' doughnut over time, but the same grafts to the male pattern baldness area `WOULD'!

This is because i think it is the conditions in the surrounding tissue that determine the fate of large anagen follicles, in the absense of a protective `scaffold'.

Well, at the very least Orentreich did something fairly CLOSE to that. Even though he didn't report specific haircount numbers like Nordstom did, I think he would have noticed if there were a differential effect of the growth rates of the grafts, depending on the recipient site. But his conclusion at the end was unequivocal: "hair to hair" grew hair; "hair to bald" grew hair; "bald to bald" remained bald; and "bald to hair" remained bald.

Bryan

 

[Dave001]

Dave, listen up.

The problem is, you have yet to raise any specific points regarding my theory you have a problem with?

The problem is that you don't have a theory. It is readily dispensed of by Occam's razor.

Your "Hydraulic Dermal Model" is a complete joke. Your entire "theory" is presented in descriptive lay terminology, and demonstrates no fundamental understanding or knowledge of fluid or hydrodynamics, subjects which cannot be discussed meaningfully in nonmathematical language.

If you want your theory to be taken seriously, tell me where it is presented.

 

[michael barry]

BRYAN,
Not interfereing with your and Stephen's debate, but I did remeber something that I'd read on a "Surgical Alternatives" thread on HairLossTalk.com. A guy who was shiny bald on top (forget his handle) got transplants in San Fransisco and they were not growing many months later. His Doctor said that it was the fibrosis that had taken place on that scalp (it had hardened into forehead skin that we see in male pattern baldness).
Im not claiming that it supports Stephen's theory or anything like that (if I had male pattern baldness figured out, Id be one rich guy who would get free drinks from grateful men at every bar I walked into for the rest of my life), but the "bald to bald" ending up bald in the study you quote could have been attributed to that couldnt it? The skin fibrosis may have "just went too far" to support follicle growth perhaps.

You make a great point however. The simplest way to try Stephen's theory would be to just transplant 1 hair in a male pattern baldness temple that was gonna go in the next few years to the other temple and mark it with a very small tatoo. If it was there and grew to full size 3-4 years later, then his tissue fibrose scaffold hypothesis would at least be proved right. This would be a huge boon for the transplant business as a matter of fact because docs could then tell patients "If I can just move that hair before it dies where it is, you'll save it". Therefore they could radically enlarge the amount of viable follicles for young men just starting to male pattern baldness.

Maybe it isnt true though, but it would only take one follicle and on Doctor to find out.

 

[Bryan]

BRYAN,
Not interfereing with your and Stephen's debate, but I did remeber something that I'd read on a "Surgical Alternatives" thread on HairLossTalk.com. A guy who was shiny bald on top (forget his handle) got transplants in San Fransisco and they were not growing many months later. His Doctor said that it was the fibrosis that had taken place on that scalp (it had hardened into forehead skin that we see in male pattern baldness).
Im not claiming that it supports Stephen's theory or anything like that..., but the "bald to bald" ending up bald in the study you quote could have been attributed to that couldnt it? The skin fibrosis may have "just went too far" to support follicle growth perhaps.

Isn't it ironic that Stephen's theory actually DEPENDS on the existence of fibrosis to try to explain the SUCCESS of (most) hair transplants?? It's even more ironic that the Doctor above blamed the FAILURE of that guy's transplants on fibrosis! :wink:

I think what we have here is some fairly blatant ad hoc excuse-making. If I were forced to choose one side or the other, though (Stephen's theory or what the Doctor said above), I'd go with the Doctor: I think it's FAR more likely that fibrosis intereferes with hair follicle growth, rather than supporting or enhancing it.

You make a great point however. The simplest way to try Stephen's theory would be to just transplant 1 hair in a male pattern baldness temple that was gonna go in the next few years to the other temple and mark it with a very small tatoo. If it was there and grew to full size 3-4 years later, then his tissue fibrose scaffold hypothesis would at least be proved right.

Yep, it seems like that would be fairly convincing evidence, if that actually happened. On the other hand, if it DIDN'T regrow to full size and continued balding, I'm sure Stephen would think up some NEW reason to explain it that would fit in with his theory! :wink:

In Nordstrom's experiment, the graft from the balding site declined sharply from 12 hairs to only 4 hairs over a period of 16 months, whereas the graft from the non-balding site actually INCREASED slightly (from 13 hairs to 14 hairs) over the same period of time. Stephen simply has no credible way to account for that with his theory. It's screamingly obvious. Do you agree with that, Michael? Doesn't THAT disprove his fibrosis scaffold hypothesis? How else could you explain a -66% decline, versus a +7.6% increase?

Maybe it isnt true though, but it would only take one follicle and on Doctor to find out.

Yeah. I wonder if some intrepid soul who is going in for a "follicular-unit" transplant anyway would volunteer to test that for us?? All they'd have to do is have two or three BALDING follicles moved slightly to a new position in the same balding area, and see what happens over the next couple years or so! That wouldn't interfere in any way with the regular transplants being done, and wouldn't add significantly to the cost at all! Any volunteers out there who are about to have transplants done??

Bryan

 

[Dave001]

Isn't it ironic that Stephen's theory actually DEPENDS on the existence of fibrosis to try to explain the SUCCESS of (most) hair transplants?? It's even more ironic that the Doctor above blamed the FAILURE of that guy's transplants on fibrosis! :wink:

I think what we have here is some fairly blatant ad hoc excuse-making. If I were forced to choose one side or the other, though (Stephen's theory or what the Doctor said above), I'd go with the Doctor: I think it's FAR more likely that fibrosis intereferes with hair follicle growth, rather than supporting or enhancing it.

Bryan,

Do you think premonitions of Stephen's theory may have been what drove Pascal nuts?
:wink:

 

[Old Baldy]

Bryan wrote:

Yeah. I wonder if some intrepid soul who is going in for a "follicular-unit" transplant anyway would volunteer to test that for us?? All they'd have to do is have two or three BALDING follicles moved slightly to a new position in the same balding area, and see what happens over the next couple years or so! That wouldn't interfere in any way with the regular transplants being done, and wouldn't add significantly to the cost at all! Any volunteers out there who are about to have transplants done??

Why waste a few grafts?! :wink:

 

[Boru]

BRYAN,
Not interfereing with your and Stephen's debate, but I did remeber something that I'd read on a "Surgical Alternatives" thread on HairLossTalk.com. A guy who was shiny bald on top (forget his handle) got transplants in San Fransisco and they were not growing many months later. His Doctor said that it was the fibrosis that had taken place on that scalp (it had hardened into forehead skin that we see in male pattern baldness).
Im not claiming that it supports Stephen's theory or anything like that..., but the "bald to bald" ending up bald in the study you quote could have been attributed to that couldnt it? The skin fibrosis may have "just went too far" to support follicle growth perhaps.

Isn't it ironic that Stephen's theory actually DEPENDS on the existence of fibrosis to try to explain the SUCCESS of (most) hair transplants?? It's even more ironic that the Doctor above blamed the FAILURE of that guy's transplants on fibrosis! :wink:

I think what we have here is some fairly blatant ad hoc excuse-making. If I were forced to choose one side or the other, though (Stephen's theory or what the Doctor said above), I'd go with the Doctor: I think it's FAR more likely that fibrosis intereferes with hair follicle growth, rather than supporting or enhancing it.

[quote="michael barry":ae79a]You make a great point however. The simplest way to try Stephen's theory would be to just transplant 1 hair in a male pattern baldness temple that was gonna go in the next few years to the other temple and mark it with a very small tatoo. If it was there and grew to full size 3-4 years later, then his tissue fibrose scaffold hypothesis would at least be proved right.

Yep, it seems like that would be fairly convincing evidence, if that actually happened. On the other hand, if it DIDN'T regrow to full size and continued balding, I'm sure Stephen would think up some NEW reason to explain it that would fit in with his theory! :wink:

In Nordstrom's experiment, the graft from the balding site declined sharply from 12 hairs to only 4 hairs over a period of 16 months, whereas the graft from the non-balding site actually INCREASED slightly (from 13 hairs to 14 hairs) over the same period of time. Stephen simply has no credible way to account for that with his theory. It's screamingly obvious. Do you agree with that, Michael? Doesn't THAT disprove his fibrosis scaffold hypothesis? How else could you explain a -66% decline, versus a +7.6% increase?

Maybe it isnt true though, but it would only take one follicle and on Doctor to find out.

Yeah. I wonder if some intrepid soul who is going in for a "follicular-unit" transplant anyway would volunteer to test that for us?? All they'd have to do is have two or three BALDING follicles moved slightly to a new position in the same balding area, and see what happens over the next couple years or so! That wouldn't interfere in any way with the regular transplants being done, and wouldn't add significantly to the cost at all! Any volunteers out there who are about to have transplants done??

Bryan[/quote:ae79a]

I thought finasteride was suppressing the effects of DHT, and this is part of the reason why my hair is growing back quite nicely. So my follicles must be sensitive to DHT, unless the finasteride is accidentally doing something mysterious. When I used minoxidil on its own many years ago it did nothing. Note, I used used only my device and saw palmetto (which obvioulsy has some affect on dht) to bring back vellus hair, then I began adding supporting agents gradually.
Today my wonderful doctor agreed to give me a regular prescription for Nizoral, and to continue my prescription for proscar.
Despite all of the opposing theories here, which exercise the mind, the only theory that makes great sense to me is mobility, exercising the whole system, from within and without, to improve microcapillary circulation. That is what my device does, with saw palmetto, minoxidil or any of the other topicals, it improves the penetration of anything that can assimilate with the follicle, and improve overall circulation.
The disfunction of the follicle has been misunderstood in so many ways, these theories are confusing the issue. Keeping it simple. It is partly down to the type and quality of muscles that you have inherited, and what you or don't do to keep them mobile. Once you stop using part of your body, it withers.
I have seemingly done the impossible. Hair in a bald scalp can regrow with many kinds of treatments, as long as the conditions are right. It involves some hard work, dedication and patience. Put your theories aside for a while, I am proof of my pudding. If it turns out that I have the answer, admin owes it to you all to contact me in some way to confirm my discovery. But admin has not replied to me recently, having promised to put me in touch with an expert researcher. I am mystified, why is my good news being ever so slightly sidetracked?
Boru