Have scientists studied the following...

[WillhasWill]

People may be able to put me straight quite quickly, but these are just some of my thoughts out loud. Questions that haven't been clarified during my research into baldness. On the face of it the answers seem quite obvious, but are they with the latest findings and lack of scientific evidence?

Are there actually differences between "permanent" and "non-permanent" hair follicles?

The general consensus is that there are both permanent and non-permanent hair follicles on the head. On men the sides of the head are permanent and do not seem to be affected by baldness through the life of the sufferer. Where as the entire top of the head from the vertex to the frontal line is susceptible to baldness.

This would lead me to assume that these hair follicles on the sides of the head are different in some way to the hair follicles on the top of the head. They are resistant to baldness.

However, if this is the case, I have not seen this being scientifically proven. To prove this the most obvious thing to do would be to compare the two different follicles to find the differences. Has this been done and has a study been conducted to prove whether this is the case or not?

If the two follicles are different I'd imagine there would be one of two scenarios. Either:

a) Non-permanent hair follicles contain differences which make them susceptible to baldness
OR
B) Permanent hair follicles contain differences which make them resistant to baldness.

If (a) is true then the answer to baldness could be removing/destroying the differences in the non-permanent hair follicles so they become identical to permanent hair follicles.

If (b) is true then the answer to baldness could be adding the differences seen in permanent hair follicles to the non-permanent hair follicles, so they become identical to permanent hair follicles.

If the two follicles are actually identical...

If in fact it has been found, or is to be found, that all hair follicles on the head are identical then it could mean that the processes going on inside the body (such as the conversion of testosterone to DHT) are creating the balding environment on only specific areas of the head. On men, this would be the pattern at the top of the head.

With recent findings that PGD2 has been found to inhibit hair growth (and could be a major cause of baldness) and is found in large amounts in balding areas of the scalp then this scenario could be possible. That is, all follicles are actually identical and it's the body processes causing the hair inhibiting environment at the top of a mans head only. It just so happens to be the top. And if in fact the body processes were to cause the hair inhibiting environment over the entire head then men would go completely bald.

I don't mean to regress.

I don't mean to go back to the drawing board in the cure for baldness but to me this seems like the most obvious place to start from when trying to actually cure baldness. But I can't find any research into these areas.

Going back to my first assumption, that (what we call) non-permanent and permanent hair follicles are different, then this would suggest the body process cause the balding environment over the entire head already and that the follicles on the sides of the hair are already resistant. Therefore, instead of trying to grow new hair, or transplant this hair, then why aren't scientists trying to find the differences?

If on the other hand hair follicles are identical and it's the body processes causing the balding environment only on the specific area of the head on the top, then surely this finding would be very crucial in the search for a cure for baldness.

Are there any studies that prove or disprove any of the above?

[Pate]

You honestly think scientists haven't considered that they should probably try and figure out what makes balding and non-balding follicles different? Well yes, they have. Research continues into the exact mechanism of hair loss but broadly speaking it's understood to involve androgen receptors in the hair follicles.

Susceptible follicles have large numbers of androgen receptors that are bound to by DHT and to a lesser extent T, which sets off the chain of events (involving prostaglandins and apparently cortisol) that leads to the body's immune system attacking and destroying its follicles.

Resistant follicles, which includes the back and sides of nearly everybody, plus the full scalp of those who don't go bald, have a much smaller number of androgen receptors so DHT can't bind to them as much and the balding mechanism isn't activated.

The follicles aren't identical, and that has been known since the 1950s in the west and I think in Japan since the 1930s. This was proven with the concept of donor dominance - if you transfer follicles from the back of the head to the top, those follicles continue to grow and aren't affected by DHT. If they were the same follicles and baldness was caused by something different in the scalp, the transplanted follicles would undergo balding just the same. But they don't, which means they must be fundamentally different from the other follicles.

Specifically, they don't have high levels of androgen receptors. This is why there are drugs in development that either compete for the androgen receptors to block them (androgen antagonists like RU or CB-03-01), or destroy the androgen receptors temporarily like ASC-J9.

Unfortunately nobody has been terribly eager to develop these drugs up to now, possibly because their opportunity to actually regrow hair is limited. Their real value is in stopping further loss. So instead we face the difficult decision of taking finasteride with its attendent systemic effects, or letting ourselves go bald.

[WillhasWill]

Hi Pate,

Thanks very much. No I never necessarily thought they hadn't considered this. Quite the opposite. But I was wondering on specific studies into this and if hair follicles are different then why isn't their more work into treatments specifically tackling these differences in hair follicles. The androgen antagonist drugs sounds very interesting.

Cheers for the bite size lesson :-)

[gutted]

the conept that dht binds to the androgen receptor and causes minitarisation is flawed and outdated and needs to be looked at again.

the only differnces between the donor ares and the balding areas is the genetically determined sensitivity and possibly the number/distribution/size of the sebcaceous glands in these areas with a higher number of these glands in the balding areas.

Not the individual follicles, the follicles are the same.

[WillhasWill]

the only differnces between the donor ares and the balding areas is the genetically determined sensitivity and possibly the number/distribution/size of the sebcaceous glands in these areas with a higher number of these glands in the balding areas.

So follicles are the same? This is very different to Pate's point about androgen receptors in the follicles

If this is true and sebcaceous glands were a factor then transplants would not necessarily be immune from baldness.

Regardless of sebcaceous glands, this is the first time I have heard that they play a role, but has it been proven that hair transplants are immune from balding?

Pate, you mention the concept of donor dominance. Has this been proved? You mention that if hair follicles were the same follicles and baldness was caused by something different in the scalp, the transplanted follicles would undergo balding just the same. But they don't, which means they must be fundamentally different from the other follicles. But on it's own this would not prove hair follicles are different.

Baldness could still be caused by something different localised in specific areas on the scalp and simply takes years to destroy the follicle. Therefore a fresh follicle transplanted into the balding area would not be affected for many years. If a person underwent surgery at 40 years old and only went balding in the few years leading up to have the transplant, then it took many years for the hair follicles to be affected. So the new follicle may not be affected again for many years, but it is still susceptible. We just do not see it in the patients life time.

[gutted]

So follicles are the same? This is very different to Pate's point about androgen receptors in the follicles

If this is true and sebcaceous glands were a factor then transplants would not necessarily be immune from baldness.

Regardless of sebcaceous glands, this is the first time I have heard that they play a role, but has it been proven that hair transplants are immune from balding?

Pate, you mention the concept of donor dominance. Has this been proved? You mention that if hair follicles were the same follicles and baldness was caused by something different in the scalp, the transplanted follicles would undergo balding just the same. But they don't, which means they must be fundamentally different from the other follicles. But on it's own this would not prove hair follicles are different.

Baldness could still be caused by something different localised in specific areas on the scalp and simply takes years to destroy the follicle. Therefore a fresh follicle transplanted into the balding area would not be affected for many years. If a person underwent surgery at 40 years old and only went balding in the few years leading up to have the transplant, then it took many years for the hair follicles to be affected. So the new follicle may not be affected again for many years, but it is still susceptible. We just do not see it in the patients life time.

i should say however, all of the previous science states that follicles in the sides/back and the balding areas are different due to the sensitivity between the follicles...in my opinion the genetically determined androgen sensitivity between the areas applies true but not to the follicles but the sebcaceous glands.

so a hair transplanted from the donor region to the balding area will not be susceptible to balding because th sebcaceous glands androgen sensitivity is genetically, not high, so its likley thoose hairs will not be destroyed, ever.

here is some research that was done -

http://www.ncbi.nlm.nih.gov/pubmed/2909628

[25 going on 65]

Sorry if someone already mentioned this, but it seems relevant to the discussion:

From what I understand, hairs on the back and sides of the head aren't immune to the miniaturization process, just extremely resistant. There are some MPB sufferers who experience considerable thinning in the "horse shoe region" (not sure if it's just miniaturization or if it includes actual shedding).

[NotBelievingIt]

Its entirely possible the donor hair is more or less exactly the same.

If it takes 30 years for regular hair to finally start falling/thinning...it stands to reason that if indeed something is 'different' about the scalp, it would take another 30 years to "break down" transplants.

Have they been doing high quality FUE and FUT for 30 years? Hell no, barely 10 maybe 15. So if you've got some 25 or 30 year old who got it done in 2000...lets revisit them in 15-20 years and see if that transplant hair is still around.


Just recenly they did show that the scalp areas that lose hair have a higher PDG2 level. Why? Is it a byproduct of balding or part of the reason? If its part of the reason, it stands that any other hair should fall victim eventually.

[Pate]

Pate, you mention the concept of donor dominance. Has this been proved? You mention that if hair follicles were the same follicles and baldness was caused by something different in the scalp, the transplanted follicles would undergo balding just the same. But they don't, which means they must be fundamentally different from the other follicles. But on it's own this would not prove hair follicles are different.

It doesn't prove that follicles from the back contain fewer androgen receptors, no. But it does prove that they are different SOMEHOW, because donor dominance is fact.

Don't listen to gutted, he has it a bit twisted. The mechanism has not been fully worked out but what is known for sure is that androgens are implicated. Furthermore estrogen seems to have a protective effect on the follicle, which is why women usually don't suffer severe AGA until after menopause (though of course some do earlier).

What's NOT known is the exact sequence of events that lead from androgen receptors getting attached to by androgens, to follicle miniaturisation. This is what gutted is getting at. We know it seems to involve prostaglandins and cortisol and probably an autoimmune reaction where the body attacks its own follicles but gutted is right that it still needs to be looked at.

But to imply, as he did, that androgens aren't responsible is downright nonsense. It's been known for centuries that eunuchs (castrated men) don't go bald. The reason is because androgens are the first step in what's turning out to be an increasingly complicated chain of events. We're not entirely sure what the other steps are, but if you stop the androgens the chain is never started in the first place.

Its entirely possible the donor hair is more or less exactly the same.

No it's not. For a couple of big reasons.

First, it doesn't take 30 years to break down regular hair. If you take Propecia for 20 years, your hair will be protected from DHT, but if you then stop taking it, you experience 'catch-up balding' where you quickly return to the point your hair loss would have been at had you never taken Propecia at all.

So even though your hair has been protected for 20 years, it will go through 20 years of balding in about six months. This shows that it's nothing to do with cumulative effects of DHT. There is something else going on - and that something is related to AGE, but not TIME exposed to DHT.

Second, why would it matter if they have been doing HIGH QUALITY FUT or FUE for 30 years? The point is, they have been doing hair transplants for much longer than that - the old plugs, then minigrafts. The fact there are STILL guys going in to HT doctors for repairs shows that those plugs can easily last 30 years. And what happens? The original hair continues to fall out, which is why their plugs look so dreadful these days - all the original hair fell out around it over those 30 years, even if they got the plugs done in their 20s (ie less than 10 years since the onset of puberty).

So imagine a 60 year old guy who got a transplant 30 years ago (1982).
The front hair has been there subject to androgens for 40 years.
The transplanted hair has been there subject to androgens for 30 years.

The front hair is 100% gone. The transplanted hair is 100% still present (which is why it looks so bad).

Face it - donor dominance is reality. In fact the entire HT industry is based off the fact.

Just recenly they did show that the scalp areas that lose hair have a higher PDG2 level. Why? Is it a byproduct of balding or part of the reason? If its part of the reason, it stands that any other hair should fall victim eventually.

Not necessarily. As I said above, it could be that PDG2 is an active part of the process, but that it's not an ISOLATED part. In other words, it has to be activated by the chain of events that starts with DHT and ends with miniaturisation.

Think of it this way. What if DHT binds to a receptor, which does something, which releases PDG2, which does something, which results in the hair miniaturising. Then you would lots of PDG2 in bald scalp because it's getting lots of activation by DHT. But it doesn't stand that any transplanted hair should fall victim eventually, because the transplanted hair won't get attacked by DHT in the first place, so it won't produce any PGD2.

[gutted]

But to imply, as he did, that androgens aren't responsible is downright nonsense. It's been known for centuries that eunuchs (castrated men) don't go bald. The reason is because androgens are the first step in what's turning out to be an increasingly complicated chain of events. We're not entirely sure what the other steps are, but if you stop the androgens the chain is never started in the first place.

castration does not lead to a total, 0 redcution of tesosterone, it only minimizes the levels,(to levels that do not cause any damage), this implies hair growth is still being maintained by androgens. I wonder if castration leads to a loss of hair in body hair grwoth too?

No it's not. For a couple of big reasons.

First, it doesn't take 30 years to break down regular hair. If you take Propecia for 20 years, your hair will be protected from DHT, but if you then stop taking it, you experience 'catch-up balding' where you quickly return to the point your hair loss would have been at had you never taken Propecia at all.

So even though your hair has been protected for 20 years, it will go through 20 years of balding in about six months. This shows that it's nothing to do with cumulative effects of DHT. There is something else going on - and that something is related to AGE, but not TIME exposed to DHT.

this is another common myth sparked by HT surgeons and merck and spread by these forums, there is no such thing as catchup balding. People who get off of propecia, induce a very very big spike in androgen levels once they are off it, hence this percieved "catchup balding happens"
they will continue to "minituarise" at a normal rate...you will not instantyl lose all the hairs that were being maintained by propecia...mintarising will take its course.

Not necessarily. As I said above, it could be that PDG2 is an active part of the process, but that it's not an ISOLATED part. In other words, it has to be activated by the chain of events that starts with DHT and ends with miniaturisation.

Think of it this way. What if DHT binds to a receptor, which does something, which releases PDG2, which does something, which results in the hair miniaturising. Then you would lots of PDG2 in bald scalp because it's getting lots of activation by DHT. But it doesn't stand that any transplanted hair should fall victim eventually, because the transplanted hair won't get attacked by DHT in the first place, so it won't produce any PGD2.

[/QUOTE]

this is flawed and needs to be re-researched.

pgd2 is upregulated anywhere where there is inflamation present, it can also be found upregulated in wounds, scars...

this can easily state the obvious, that the body is attacking something and itself, which it is, the traditional theory may state its dht, which it probably is not and i believe it not to be.
there probably is an infection going on in follicular cells.

transplanted follciles/sebcaceous glands are genetically immune in the sense they dont have a high sensitivity to androgens and so dont take androgens up as much as balding susceptible follciles/glands... when hair from donor regions is trasplanted its sebcaceous gland is also taken with the follicle.

[Aston]

pgd2 is upregulated anywhere where there is inflamation present, it can also be found upregulated in wounds, scars...

this can easily state the obvious, that the body is attacking something and itself, which it is, the traditional theory may state its dht, which it probably is not and i believe it not to be.
there probably is an infection going on in follicular cells.

transplanted follciles/sebcaceous glands are genetically immune in the sense they dont have a high sensitivity to androgens and so dont take androgens up as much as balding susceptible follciles/glands... when hair from donor regions is trasplanted its sebcaceous gland is also taken with the follicle.

Mice treated with PGD2 lost their fur in the treated area. There is little doubt PGD2 is part of an active chain of events following the androgen receptor. Nothing's flawed about the research. Prostaglandins are simply molecules which act as "local" signals and don't necessarily produce inflamation. In fact, they have a multitude of roles which have nothing to do with inflamation at all.

Research: http://stm.sciencemag.org/content/4/...6ra34.abstract
Prostaglandin info: http://en.wikipedia.org/wiki/Prostaglandin

[gutted]

Mice treated with PGD2 lost their fur in the treated area. There is little doubt PGD2 is part of an active chain of events following the androgen receptor. Nothing's flawed about the research. Prostaglandins are simply molecules which act as "local" signals and don't necessarily produce inflamation. In fact, they have a multitude of roles which have nothing to do with inflamation at all.

Research: http://stm.sciencemag.org/content/4/...6ra34.abstract
Prostaglandin info: http://en.wikipedia.org/wiki/Prostaglandin

i said they are upregulated in inflamed areas.

your link to wikipedia -
"prostaglandin levels are increased by COX-2 in scenarios of inflammation."

prostglandins are involved with inflamation.

pgd2 and its role in inflammation.

http://www.caymanchem.com/app/template/Article.vm/article/2140;jsessionid=EEAEFB409423347FDE326280AABDD091

[gutted]

Mice treated with PGD2 lost their fur in the treated area. There is little doubt PGD2 is part of an active chain of events following the androgen receptor. Nothing's flawed about the research. Prostaglandins are simply molecules which act as "local" signals and don't necessarily produce inflamation. In fact, they have a multitude of roles which have nothing to do with inflamation at all.

Research: http://stm.sciencemag.org/content/4/...6ra34.abstract
Prostaglandin info: http://en.wikipedia.org/wiki/Prostaglandin

i said the theory that dht targeting the androgen receptor on the hair follicle causing minituarisation is flawed.