Mikazz, your theory has a few shortcomings:
1. It interprets the balding effects on the scalp solely as aging, at the same time ignoring that the programmed cell death as induced by PGD2 on the scalp is part of hair cycling. I consider it much more likely that balding is simply "hair cycling mechanisms gone out of hand", also for the following reason:
2. Minoxidil and adenosine mimic the role of NO in their environment, but are effective at treating hairloss instead of causing even more hairloss, which they should according to your theory.
3. Your theory also ignores what happens to the tissue around follicles as it only looks at the DPe/follicles themselves. In the tissue surrounding the hair follicles/DPe, there are typical inflammatory responses going on. This again supports 1. and has nothing to do with aging.
- PGD2 have been shown to inhibit hair growth, the results in mice is similar to male pattern baldness. However, this haven't been done by elevation of DHT, only by over-expression of PGD2 alone
- male pattern baldness is started when DHT supass a treshold, not by elevated PGD2. It means that DHT is causing elevation of PGD2 in male pattern baldness, but not instantaneously
- There is currently no proof that blocking PGD2 stop follicles miniaturization caused by DHT. There is only proof that PGD2 causes follicles miniaturization in mice.
- PGD2 level is varying relative to the growing phase of the follicle. DHT level do not changes according to the phase of the follicle.
- It means that elevated DHT causes accumulation of damage over time in the follicles, causing PGD2 to over-express in the long run.
- There is no proof that inhibition of PGD2 stop the damage caused by DHT in the follicles
- if elevated PGD2 in bald area of the scalp causes miniaturization of follicles, why transplanted hairs do not miniaturize in an elevated PGD2 area? Miniaturization only happens to damaged follicles from DHT locally. This means that PGD2 is only a consequence of damaged follicles locally, not a cause in male pattern baldness.
People have tried PGD2 inhibitors in hair loss forums(for exemple: topical cetirizine). At best, it helps growing vellus hairs, I haven't seen reversal of miniaturization like anti-androgens can do(finasteride, dutasteride). Ok they are not the best way to prove PGD2 effectivenes, but nothing at this moment proves that PGD2 is 100% the way to go.
IMO, the link between DHT and PGD2 is oxidation causing damages over time to the cells. What else causes cell senescence ?
2. Minoxidil and adenosine mimic the role of NO in their environment, but are effective at treating hairloss instead of causing even more hairloss, which they should according to your theory.
NO stimulate hair growth, this is why DHT is causing hair to growth all over the body (in follicles: more dht -> more NO). However, NO is causing oxidative stress over cells via peroxynitrite. Under a certain amount, cells will resists and oxidative stress won't do harm. However, in the balding scalp there is an excess of DHT, caused by low O2 leading to an excessive amount of NO. The body do not compensate instantaneously from elevation of NO, the oxidative stress will build overtime and will raise exponentially. At a certain level, the cells can't compensate from this big increase in oxidative stress and irreversable damages to the cell will start.
Minoxidil mimic NO, leading to more hair growth initially. However, oxidative damage will build over time, and the hair growth effect will be progressively inhibited by the raising oxidative stress.
3. Your theory also ignores what happens to the tissue around follicles as it only looks at the DPe/follicles themselves. In the tissue surrounding the hair follicles/DPe, there are typical inflammatory responses going on. This again supports 1. and has nothing to do with aging.
Fibrosis and inflammation is a consequence of
mitochondrial damage in cells caused by oxidative stress in aging.
Ok, if oxidative damage is not in the pathway of male pattern baldness, why superoxide dismutase makes people regrowth hair? (SOD's prevents oxidative damage from peroxynitrite)