The Cause?

[wookster]

Hair follicle miniaturization is associated with inflammation at the follicular level, it seems. Certain types of immunosuppressive drugs don't block DHT, but they somehow cause hair regrowth.

So the inflammatory reaction is caused by the DHT and becomes somewhat irreversible as time progresses. DHT appears to be the main culprit in the male pattern baldness scenario.

Of course that leads one to the question: if DHT causes an inflammation of the hair follicle then why does body hair grow due to DHT?

There seems to be an inverse relationship where body hair grows due to DHT and head hair dies due to DHT. This could be controlled by genetics within the hair follicle itself? If that is the case then male pattern baldness would not require an immune response. Follicles would simply miniaturize according to pre programmed instructions within the genes themselves without the inflammatory reaction.

Superoxide causes any hair to miniaturize be it body hair or scalp hair.

http://www.hairlosshelp.com/hair_loss_r ... _a_SOD.cfm

Nitric oxide is a vasodilator that appears to be important for hair growth, while superoxide is a vasoconstrictor that may be part of the signaling mechanism that tells hair to stop growing. Superoxide can also interact with nitric oxide to form a highly destructive free radical called peroxynitrite, which causes protein and lipid oxidation.

Nitric oxide causes hair growth but when nitric oxide combines with superoxide, it forms peroxynitrite allowing further hair loss and an immuno response. Minoxidil allows for an exogenous supply of a nitric oxide "agonist" to restore offset hair growth, if only temporarily. The body must eventually up its production of superoxide to match the extra NO of minoxidil? The regrowth will wither and die, statistically speaking.

DHT actually increases nitric oxide production:

http://www.ncbi.nlm.nih.gov/entrez/quer ... uery_hl=31

Remarkably, basal NO level was enhanced threefold by stimulating dermal papilla cells with 5alpha-dihydrotestosterone (DHT) but not with testosterone.

But for scalp hair, there is the superoxide which appears to mitigate the effect of the DHT produced NO in the scalp. Ergo, DHT is possibly not the main culprit but actually the more elemental hair loss factors would be free radicals like superoxide.

What causes the excess superoxide to be produced in the Norwood horeshoe region of scalp?

Would exogenous sources of equal amounts of superoxide dismutase and catalase? neutralize the superoxide free radical, and regenerate the damged tissues, enabling hair regrowth?

http://whyfiles.org/057aging/radical.html

To test the second prediction, Orr and associates manipulated the genes of some fruit flies to make transgenic animals that produced more SOD or more catalase. These animals did not live longer than the average fruit fly. But when transgenic lines were created that simultaneously over-expressed both enzymes, the average life span jumped from 45 to 75 days.