balder said:
Somehow, it appears that scalp hair follicles on the galea region of scalp, become "sensitive" to androgens and miniaturize, eventually becoming almost microscopic vellus hairs. Sometimes a few strands of healthy hairs exist in a region of advanced baldness then a few years later even those hairs will be gone. Don't tell me those stubborn stray hairs had a different genetic clock!
It seems that hairs are not genetically programed to fall out but instead, those hairs becomes sensitive to androgens as if they are having an allergic reaction to androgens or something associated with androgens. So if a balding follicle is transplanted to somewhere else, it will still continue to bald once the sensitivity switch has been turned on.
But, balding follicles transplanted on to the backs of immune deficient mice mysteriously regrow. So it seems that the allergic-like reaction to the association with androgens is caused by the immune system.
You raise some good points about the male pattern baldness paradox. None of this seems to have a common link. I suggest there is one however.
If as i propose, hair follicle growth is restricted in male pattern baldness by contact inhibition caused by increased pressure in the dermal tissue, this would only have its effect on new anagen follicle growth. During such an increase in pressure, existing already grown anagen follicles are not affected untill the next hair cycle. This would explain why all hair is not lost at the same time, and some follicles can show no change for years. The human scalp hair anagen period can last for years.
I think the "continue to bald" reference you make refers to Nordstroms study. This is the "follicles continue to do their thing" regardless of where they are, or the so called donor dominance Idea. This does not automaticaly mean the mechanism is locked into the follicles themselves. Nordstrom himself recognised this in this paper, when he said this could be an effect "very close to the follicle".
In my theory put simply, the follicles tend to remain in the as transplanted state because of the healing process. This produces fibrose scar tissue around the follicles, that reinforces the follicles "space". In effect the transplanted follicle is much less effected by any outside pressure, and remains in the as transplanted state (donor dominance).
What i think is happening in the immune deficient mouse study, is the healing is abnormal because of the immune status. There is no reinforced "cage" around the follicles, and follicle size can change according to the pressure around it, in this case a reduced pressure and enlargement happens.
In my opinion the normal contact inhibition of follicle growth, and its related pressure factors explain the paradox in male pattern baldness.
We also have to consider that if androgens are "locking down" follicle growth at the follicles genetic level, how can anything that does not effect androgens make any difference? Minoxidil for example.
My theory predicts that anything that reduces scalp fluid pressure in male pattern baldness, will increase hair growth.
One of the latest male pattern baldness treatment possibilities is Latanoprost and similiar drugs. What was Latanoprost developed to do? reduce tissue fluid pressure. The very well respected hairloss researcher Hideo Uno was involved in a hair growth study using Latanoprost, and it is interesting to read some background reported in this study.
http://www.google.co.uk/#hair loss=en&xhr=t&q= ... 68&bih=819
Quote:
"Latanoprost, a prostaglandin F2a analogue, is a selective
FP prostanoid receptor agonist. This drug is known to
profoundly reduce intraocular pressure and is used as
an eye drug to treat glaucoma. Although latanoprost
has no major adverse side eVects, the patients receiving
the medication have noticed an increased number,
length, thickness, and darkening of eyelashes and hair
in the medial canthal region (1–3 ). Among numerous
reports on clinical and basic pharmacological aspects of
latanoprost, the major actions related to hypertrichotic
eVects are considered to be peripheral vasorelaxation
and melanogenesis (1, 4–11). Agents that induce potent
hypertrichotic eVects are known as peripheral vasodilators
that act as potassium-channel openers, such as
minoxidil and diazoxide. Minoxidil, used originally for
hypertensive treatment, is employed topically for the
treatment of human androgenetic alopecia (malepatterned
baldness). "
I think it is important to emphasize this section quote:
" Agents that induce potent
hypertrichotic eVects are known as peripheral vasodilators
that act as potassium-channel openers, such as
minoxidil and diazoxide"
Peripheral vasodilators allow a reduction in tissue fluid pressures in surface tissue, that is around the hair follicles.
This is the common factor in these treatments for male pattern baldness.
