Im not going to look up links for any of you, but I’ll tell you what past experiments have revealed.
The hair in the front and top of your head has more androgen receptors.
The skin in the front and top of your head has more DHT.
When HIGH androgen stimulis is added to ex vivo cultured hair follicles from the back and sides of the scalp, it will indeed respond negatively to those androgens, just like balding follicles from frontal scalp.
Transplanted hair maintains its characteristics (color and curl) when moved to another area of the scalp. Dark hair will stay dark even if moved to an area that is surrounded by grey hair and vice versa.
A small slice of skin is indeed moved with the grafts, so the “very close surround” is moved with grafts. It has to be. To trim a graft down to the bare follicle would remove the sebaceous gland and arrector pilli muscle that comes with it. The arrector pilli muscle is where some of the stem cells come from down to the dermal papilla when its time to start a new anagen phase.
Your body is covered with vellus hairs (look close at your shoulders when out in the sun, but they usually dont get to be large terminal hairs because they lack the genetic instructions to do so or they have less androgen receptors on them.
Experiments have shown that the dermal papilla releases substances that control the growth of the rest of the follicle. The dermal papilla’s cell walls have androgen receptors, and after uptaking these androgens (DHT), they release chemicals like TGF-beta 1, TGF beta 2, throbospondin, PKC, and others to the rest of the follicle. Balding hairs release more negative growth factors like TGF-beta instead of positive growth factors like Fiberblast growth factor 7.
If baldness is not in the follicles themselves, it would have to be in the VERY close surrounding skin, perhaps upstream of alpha-five redcutase like an overabundance of NADPH in this skin that gets more alpha five synthesized.
WE KNOW FOR A FACT, via a South Korean study, that they seven genes that are associated with alpha five reductase expression show that there is no differnce between balding and non-balding men in regards to this enzyme. However balding men have more DHT in their balding areas…so thats a bit of a quandry. There are a couple of pathways upstream of alpha five reductase that might get more of the enzyme synthesized in the scalp.
98.6% of all balding men have a particular variant of the androgen-receptor gene, but 76.1% of all NON-balding men have the same variant of the androgen-receptor gene. There is another gene strongly correllated with baldness on chromosome 20. When men have both these genes, they are 7 times more likely to be bald statistically. You need to have them both. The one on chromosome 20 is probably the biggest genetic factor, but there are a couple of more genes supposedly statistically correllated with baldness also. Perhaps having these genes in fetal development somehow “design” the follicle in such a way as to make it susceptible to androgens in later life.
When androgen is uptaken in the cells, several different androgen-inducible genes are activated. One of these genes overexpressing itself might be the reason for baldness upon androgenic uptake also.
Its probably in the papilla (genetics), but could be (although unlikely) just be a result of too much alpha five reductase getting synthesized in the very close surround.
We will have a method of ‘creating hair’ via HM or wounding before they figure out how to make it regrow in my opinion. Like Ive written before, miniaturized hairs lose CD200 immuno-marker cells, and thus their immune-status, so the immune system probably just keeps on attacking them if they have the tiniest bit of androgenic uptake.
One final note----------------dutasteride inhibits 51% of type 1 ALPHA five reductase and over 90% of type two alpha five reductase. It definitely inhibits most of your DHT, almost all of one kind if you take .5mgs a day.
