Have scientists studied the following...

[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.