Why is the thinning area in male pattern baldness exactly the galea area ?

[cyberprimate]

it can apparently take a lot of TIME (decades) for scalp hair follicles to slowly increase their sensitivity to androgens in some cases, which explains why balding isn't always in full force immediately after puberty. Furthermore, I suspect that the negative effect from androgens can be cumulative, which could further explain a considerable time-lag.

It's possibly true.

But then how does one explain the sudden shed that happens to some women after menopause (and first and mostly on the galea area btw)? Does that mean the sensitivity of their hair follicles to hormones is already in full development when it starts suddenly? Or the cumulative effect of hormones happens that fast for them?

 

[Alcatel]

Yes, but that is based on observation and on the assumption that no other factor is involved. Is that right?

It's based on simplicity, common sense, and the results of published scientific studies.

Not ever scientific studies are right.

In medical journals and in the popular media, one of the most infamous cigarette advertising slogans was associated with the Camel brand: "More doctors smoke Camels than any other cigarette." The campaign began in 1946 and ran for eight years in magazines and on the radio. The ads included this message:

"Family physicians, surgeons, diagnosticians, nose and throat specialists, doctors in every branch of medicine... a total of 113,597 doctors... were asked the question: 'What cigarette do you smoke?' And more of them named Camel as their smoke than any other cigarette! Three independent research groups found this to be a fact. You see, doctors too smoke for pleasure. That full Camel flavor is just as appealing to a doctor's taste as to yours... that marvelous Camel mildness means just as much to his throat as to yours."

 

[cyberprimate]

A "Doctors report" is not a scientific study.

 

[freakout]

It's based on simplicity, common sense, and the results of published scientific studies.

Thanks. So the current understanding is that the level of sensitivity lies in the hair follicles themselves.

It does not make sense from a biological perspective that hair follicles will dangle androgen receptors and slowly kill themselves.

I tend to think that the correlation between the topography of the galea/skull and the pattern of progression indicates an unknown variable that has influence over those sensitivities.

That Japanese study on low blood supply is on top of my list. Intermittent and low blood supply can cause sensitivities and death to any organ or cell.

It took Einstein to break down the "laws" of three-dimensional physics which were based on published scientific studies which we believed for centuries. It turned out that those 'laws' were based on pure observations

Just to think that physics is an exact science. It gets one to rethink how simplistic models can be applied to in-exact sciences with complex variables and no established blueprints.

 

[cyberprimate]

Another reason i tend to think the galea may be a major factor in the systemic process of male pattern baldness, is the hypothesis of increase oxygen supply to the follicles by vasodilation with minoxidil. If one accepts this possibility of action by minoxidil on follicles, one should logically accept the idea of blood supply level (and oxygen) as influential factor on male pattern baldness, and therefore the possible influence of the galea on blood supply (and therefore on follicular health), given the immediate presence of the galea in the follicular region.

 

[freakout]

EXACTLY!

And that's why the makers of that drug said it was discovered by 'accident' so they don't have to reason out the mechanism.

 

[cyberprimate]

Since you have brought up the subject of "time" I will ask your opinion on some thoughts I have been trying to develope.

This is a pretty different topic. Maybe you could create a new thread on it.

 

[elliotramsey]

Yea, i think it would def be best to create another thread for that, anything is definitely worth considering though.

Im personally convinced though that skull expansion (skull remodeling) is the direct cause, with the resulting tight galea being the second cause.

It has been proven that DHT is associated with bone growth. And theres a study that confirms that the bones in the human skull move as we age.. it just seems plausible that the tight galea is a result of this growth/movement.

I apologize for me inability to get into scientific (biology) talk, i'm a physics major so im studying the way things move and forces and stuff, im not well versed in human biology.

I am keeping a photo log of my using the techniques. Some of them are posted in my hair loss blog. Since my hairloss was limited to temple recession (and possibly SLIGHT back thinning), maintenance (with possible slight regrowth) is the evidence im looking for as to whether these methods work. If i can maintain what i have for a year, i will conclude that the methods work. Since i started loosing my hair so early (prob round early 17), i can only assume that my hairloss is aggressive, so halting for a year and possibly regrowing would mean that they work for me.

What i'm doing..

Tom Hagerty Scalp Exercise
Skull expansion techniques (which includes massage)
Nizoral Shampoo (maybe once a week at most)

Most of these are geared to physically altering the skull/galea.

Tom's scalp exercise works out the muscles that attach the galea to the scalp. The skull expansion exercises attempt to counteract the skull expansion process. The nizoral, while it has an inhibiting effect on dht, is used so sparingly that i dont think it has much of an effect at all. I pretty much use it cus i like how it smells .

It'll be 1 year april since ive started the skull expansion exercises.

 

[cyberprimate]

It has been proven that DHT is associated with bone growth. it just seems plausible that the tight galea is a result of this growth/movement.

If dht is responsible for bone growth, which is responsible for tight galea, which is responsible for hair loss on it, how come you're not using finasteride?

Tom's scalp exercise works out the muscles that attach the galea to the scalp.

I thought developping a muscle through exercise reduced its flexibility, unless you stretch them after the exercise (that's what people do at the gym). If that's the case, working out the muscles holding the galea would worsen its tightness, wouldn't it?

 

[Bryan]

It's based on simplicity, common sense, and the results of published scientific studies.

Thanks. So the current understanding is that the level of sensitivity lies in the hair follicles themselves.

Yes. The biological design and structure of the hair follicle.

It does not make sense from a biological perspective that hair follicles will dangle androgen receptors and slowly kill themselves.

It does, if one believes the "brain-cooling" theory for the evolutionary development of balding. I've discussed that theory a number of times over the years.

 

[elliotramsey]

I don't use finasteride for a number of reasons. I'm not going to risk the side effects, and I don't have the money for a prescription.

The author of the skull expansion theory theorized that finasteride doesn't always revert hairloss because even if you do inhibit dht, the skull growth doesn't just reverse itself.

One reason why it seems to be more effective when started when male pattern baldness has just begun is because the skull growth is being stopped early, where some natural recovery may still be possible.

That's the simple explaination.

At any rate, I don't want to take finasteride, hence the reason why these theories are being discussed

 

[freakout]

It does not make sense from a biological perspective that hair follicles will dangle androgen receptors and slowly kill themselves.

It does, if one believes the "brain-cooling" theory for the evolutionary development of balding. I've discussed that theory a number of times over the years.

I was kind of expecting a response on 'brain cooling'.

cyberprimate, read this

Blood vessels anastomose throughout the scalp. These blood vessels allow blood to circulate the scalp but do not feed any scalp tissue or follicle and merely return blood back into circulation.

These blood vesels function as 'heat exchangers' to cool the brain.

When low blood flow occurs at the scalp, anastomotic blood vessels will compete and win over hair follicles in terms of blood flow because it has far less resistance – leaving the hair follicles with little blood flow or none at all.

 

[cyberprimate]

Blood vessels anastomose throughout the scalp. These blood vessels allow blood to circulate the scalp but do not feed any scalp tissue or follicle and merely return blood back into circulation.

These blood vesels function as 'heat exchangers' to cool the brain.

When low blood flow occurs at the scalp, anastomotic blood vessels will compete and win over hair follicles in terms of blood flow because it has far less resistance – leaving the hair follicles with little blood flow or none at all.

Where did you get that? How does the original author know about that?

 

[freakout]

everything im posting here is from the book except the putin thingey and except the Einstein thing.

I talked to the author. he gave me permission to post excerpts limited to the ones he approved.

How does the author know about that

He's a physiologist.

 

[S Foote.]

My opinion on the effect of the galea in male pattern baldness, is that it can be a contributing factor, but certainly not causal. The galea membrane acts as a barrier to tissue fluid drainage from the male pattern baldness area, and is another factor that can magnify the poor drainage that is primarily responsable for male pattern baldness in my opinion.

To recap for the newbies.

According to my theory hair follicles have evolved to adjust their size and therefore hair production, depending on the pressure of the tissue around them. During anagen follicle enlargement, increased tissue pressure will resist the enlarging follicle, and enlargement will be cut short by the normal contact inhibition of cell multiplication that effects all non cancerous cells. The resisting pressure of the tissue being controlled by the local tissue fluid pressures.

In this way hair production is very simply linked to a mammals basic temperature control of moving fluid to or from the surface tissue in response to climate.

So hot climate= increased fluid in the surface tissue to disapate heat = increased pressure around follicles = smaller anagen follicles = less hair growth to aid in heat disapation. In cold climates the opposite happens and the mammal gets increased hair growth and a nice warm "winter coat".

I think that the same mechanism of fluid pressure changes, this time induced by androgens, is the actual mechanism responsable for male pattern baldness. This increased tissue fluid pressure explains "ALL" the recognised conditions in the male pattern baldness scalp in the simplist possible way. The pressure and stagnation of tissue fluid (edema) is known to cause hypoxia, poor circulation and oxidative stress, fibrosis and inflamation, and tightness in the effected tissue.

All these factors are recognised in the male pattern baldness scalp, and the increased tissue fluid pressure also explains the much increased sweating capacity of the bald scalp (sweat is basicaly tissue fluid).

I think this is why any treatment that helps, affects the tissue fluid pressure ie tissue "hydraulics" Think about it?


As has been referenced in this thread, the survival of transplanted follicles has to be explained by any valid theory. If the galea is a factor, why do transplants work?

Bryan has refered to the study by Nordstrom. In this Nordstrom himself states that the observations made could be explained by some action *very close" to the follicle, that is external. I think such an external action makes far more sense of the information we have, against any internal "difference" in follicles.


In my personal experience, there are experiments that could answer the genetic "difference" assumption once and for all.

Years ago i had a series of scalp reductions and the old large plug grafts (4mm) diameter. Over about the same period of my original balding, the hair moved upwards by scalp reduction receeded back to its starting position, and the plug grafts lost hair from the center outwards, untill all that was left was around the edges of the grafts.

Modern transplantation has evolved towards very small grafts without reductions or flaps, and i think this is very significant.

The transplantation industry accepts that large grafts lose hair from the center, and refer to this as "doughnutting" The claim is that this is due to a lack of oxygen because of impaired circulation. However, the period of bad circulation exists early on before the cappilarys have healed restoring a blood supply in the grafts.


Bryan has studies that prove hair growth remains throughout these larger grafts for at least two years, and this is also my personal experience. This loss follows the same time period as the original follicles in the area, generaly longer than has been studied, and as such cannot be related to any notion of hypoxia or oxygen starvation.

If the effects of scalp reductions and large grafts had been studied over longer periods of time, it would have been clear that the balding process has continued in this kind of transplantation.

The only follicles that survive are those very close to the healing area at the edge of grafts. This in my opinion is why small grafts are better, and current procedures are based on these. So why is this?

According to my theory, it is external pressure that causes male pattern baldness. The respected researcher Hideo Uno has stated that the fibrose tissue that forms around male pattern baldness follicles, is a physical barrier to their enlargement. I think such a physical barrier can also protect existing "large" follicle from miniaturisation by external pressure.

When large anagen follicles are transplanted in small grafts, or near the edge of large grafts, the healing process creates fibrose scaring in the area. This "toughens" the tissue around the large follicles, and protects them from external forces. This preserves this "space" for future hair cycles, and the continued growth of large follicles.

Such a concept of an extra-cellular matrix has been refered too in the research into hair multiplication.


I also think that such a factor would explain the results of the immune deficient mouse transplant study where male pattern baldness follicles regrew. The healing process here lacked fibrose tissue because of the immune status. The follicles where not restricted by fibrosis, and could enlarge in line with the local tissue pressures.

I dont intend getting involved in the usual drawn out debates on these forums, i just offer my opinion and suggest experiments that would support this. We can all argue for ever more, but i think we should concentrate, and lobby for novel experiments that would really get to the truth behind male pattern baldness.

S Foote.

 

[cyberprimate]

My opinion on the effect of the galea in male pattern baldness, is that it can be a contributing factor, but certainly not causal.

I'm not sure there's a single cause to male pattern baldness. I'd see it more as a systemic process that involves the galea, androgens, and other factors.

 

[Bryan]

I am going to assume your theory of hairloss is 100% true. Assuming this, what is your opinion on the difference between my (one who suffers from male pattern baldness) and non-balding man's (one who doesn't suffer male pattern baldness regardless of age) follicles?.... Androgen receptor numbers can vary depending on whats going on in the body....do I have more receptors?...or could it be mine are more sensitive to androgens then non-balding man? What is the difference between the functioning of his follicle and mine? I know if you had an absolute answer you would have "the cure", but surely you (or those you have studied more than I)are leaning toward something? How does the non-effected follicle act or react to androgens?

From everything I've read, I think there are two overall factors which determine the rate of balding or non-balding in a given individual:

1) The total rate of androgenic stimulation in the individual. That covers a considerable number of individual factors, of course! It would include how much testosterone he makes; how much of various steroidogenic enzymes he makes like 5a-reductase, aromatase, steroid sulfatase, and many others; how many androgen receptors he normally makes; and the specific androgen receptor gene polymorphism that he has seems to be one of the most important factors in how much androgenic stimulation he puts out.

2) The sensitivity of his scalp hair follicles to androgenic stimulation. Because scientists haven't figured out yet what accounts for the paradoxical response of body hair follicles to androgens versus that of scalp hair follicles, I can't be any more specific than that.

I believe #2 is more important than #1, although I have no idea what percentage of relative importance to assign to them. Is it 90% 2 and 10% 1? Or is it only 60% 2 and 40% 1? The apparent importance of the androgen receptor gene polymorphism (see #1) in determining the likelihood of balding in an individual makes this a difficult thing for me to estimate.

 

[cyberprimate]

a) Isn't the existence of #2 purely speculative when it's about the hair on our head? Why would nature genetically organize this huge variation of androgenic sensitivity between on galea/off galea hair follicles? Why would nature choose the galea boundaries to give that difference?

b) Why not put the "specific androgen receptor gene polymorphism" in the #2 category?

 

[S Foote.]

To recap for the newbies.

According to my theory hair follicles have evolved to adjust their size and therefore hair production, depending on the pressure of the tissue around them.....
I think that the same mechanism of fluid pressure changes, this time induced by androgens, is the actual mechanism responsable for male pattern baldness. This increased tissue fluid pressure explains "ALL" the recognised conditions in the male pattern baldness scalp in the simplist possible way. The pressure and stagnation of tissue fluid (edema) is known to cause hypoxia, poor circulation and oxidative stress, fibrosis and inflamation, and tightness in the effected tissue.

All these factors are recognised in the male pattern baldness scalp, and the increased tissue fluid pressure also explains the much increased sweating capacity of the bald scalp (sweat is basicaly tissue fluid).

I think this is why any treatment that helps, affects the tissue fluid pressure ie tissue "hydraulics" Think about it?

S Foote.

Thank you for explaining not only your theory but Bryan's as well! I know you have debated many people many times about the same things both here and other places. I am going to assume your theory is 100% correct. With that assumption in mind I would like your opinion on how the non-balding (who does not have male pattern baldness regardless of age) man's scalp copes with these topics. Do they not loose their hair because their follicles react differently to androgen exposure or because their scalp somehow handles the symptomes of edema more effeciently or in a different manner? What is the difference between me (one who suffers from male pattern baldness) and nonbalding guy's scalp?

Good point that again any valid theory has to explain.

Androgens grow hair over the larger part of the body in close to a dose related manner. It is male pattern baldness in "some" men that is the inconsistancy.

According to my theory, anything that effects the local tissue fluid pressures will effect the local hair growth. The areas where androgens significantly grow hair (beard, armpits, pubic area) are also areas rich in lymphatic drainage vessels close to the local hair follicles. The lymphatic system plays a central role in the control of tissue fluid pressures.

The conclusion according to my theory is that DHT must be increasing lymphatic drainage, so reducing local tisue fluid pressures and increasing local hair growth.

If you think about it, this would be very beneficial from an evolutionary view of male "performance" Increasing lymphatic drainage increases the turnover rate of the supply of nutrients to tissues, and removal of waste products from tissues. This supports the role of androgens in building "high performance" tissues.

I think the problem in male pattern baldness can be best thought off in terms of Hydraulic effects in plumbing systems.

We all know about what happens in some households if you are in the shower upstairs, and someone turns the water on downstairs? Depending on the plumbing, increasing the flow in one area can reduce flow in another area.

The human head has evolved a very complex "plumbing" system to service our large brains, this involves connections with the surface tissue. The lymphatic system of the scalp is not as concentrated as in the face and neck. and lies at the end of the system (upstairs). The same increased drainage that increases beard growth can reduce scalp drainage through simple fluid dynamic princibles of back pressure.

This may or may not create enough scalp fluid pressure to create male pattern baldness, depending on other factors. These are an individuals plumbing characteristics that determine the back pressure factor, and the individuals blood "feed" pressure. If the feed pressure is higher than the drainage systems can handle, scalp edema and male pattern baldness will develope.

This is what makes the difference in individuals in my opinion, as to if a particular level of androgens will lead to male pattern baldness in the individual. You may be aware of the known link with male pattern baldness and increased risk of heart problems? I think the common factor here is a higher core blood pressure.

This mechanism of male pattern baldness also explains why there seems to be no direct link with rising androgen levels, and the onset of male pattern baldness. You get a slow build up of scalp edema, and this only effects follicles as they try to enlarge during anagen. The human hair cycle can last for years, so these factors readily explain the time factor and the loss patterns.

In this thread as in others that talk about different theorys like the influence of the galea, we always get someone claiming that the old in-vitro studies rule out other ideas about male pattern baldness.

So i think this claim needs to be examined closely, and i will post something on this tommorow.

S Foote.

 

[Bryan]

a) Isn't the existence of #2 purely speculative when it's about the hair on our head?

Because at the very least in stumptailed macaques, it was proved by very serious scientists to be a fact! Levels of sensitivity to androgens increased in the scalp hair follicles of older macaques, compared to younger macaques. There's no doubt in my mind that the vary same thing happens in humans, too.

Why would nature genetically organize this huge variation of androgenic sensitivity between on galea/off galea hair follicles? Why would nature choose the galea boundaries to give that difference?

If you believe the "brain cooling" theory for the evolutionary development of balding (and I think it's as good a theory as any other I've seen), it's to get rid of scalp hair, to help cool the brain. The galea just coincidentally happens to be in about the same area in which Evolution wants to get rid of hair for that purpose.

b) Why not put the "specific androgen receptor gene polymorphism" in the #2 category?

Because the androgen receptor gene polymorphism that an individual has is in ALL of his androgen receptors, not just the ones in his scalp hair follicles. It affects the level of androgenic stimulation in his entire body, not just his scalp hair, so it's more appropriately in the same category as how much testosterone he makes, how much DHT he makes, how many estrogen he makes, etc.