htownballa said:
docj077 said:
Perfectionist said:
So male hairloss is passed on through females ? ! Why and WTF ? !
Why does evolution hate head hair so much anyway ? !
Surely it is body hair that is not required anymore and should be slowly breeding out .....
God damn DNA !!
The androgen receptor is on the X chromosome that you get from your mom. The 5alpha reductase type II enzyme gene is on chromosome 2, so you get that from both parents.
After testosterone is converted to DHT, binds to the receptor, and is internalized into a cell to move on into the nucleus, the result is pretty much based upon your immune response and your body's ability to handle the downstream chemical mediators that seem to cause perifollicular fibrosis, collagen deposition, and in some people possible venous stasis or lymphedema.
Doctor are you sure the DHT receptor is only the X chromosome? Also can you explain what you mean by perifollicular fibrosis, collagen deposition, and lymphedema and how exactly this miniturizes hair.
PS The androgen receptor is in the cell and not on the surface so the DHT diffuses in. Then I'm guessing the complex leads to fibrosis etc...?
The androgen receptor gene is on only the X chromosome. I have not seen a study that says otherwise. Everytime I read a study involving triplet repeat mutations in the androgen receptor, it's always localized to the X chromosome.
As you said, the androgen receptor is cytoplasmic as it is indeed a nuclear receptor protein. DHT is lipid soluble, so it moves across, binds the receptor, induces a conformational change, and the whole complex becomes a transcription factor. In the scalp, it appears that in vitro studies seem to show that the target is the TGF-beta gene. In the prostate, one of the targets is the prostate specific antigen promoter.
Lastly, when I say perifollicular fibrosis and collagen deposition, that's actually what is observed at the microscopic level when a lab tech. or pathologist examines someone with androgenic alopecia. I've had this pathology confirmed with a dermatopathologist. In some cases, the histology can demonstrate an inflammatory response with increased immune cell infiltrates. Once this process occurs, the nutritional framework of the follicle is compromised and the area surrounding the follicle is filled with fibrosis and incredible amounts of collagen.
Foote's theory says that androgen binding on striated muscle and the corresponding hypertrophy causes venous stasis and lymphedema. I don't buy it, because the lymphatics run too close to the skin and even muscle hypertrophy would not cause lymphedema. He also states that androgens may bind to the valves and endothelial cells within lymphatics. Again, something I don't think happens as androgen receptor carcinomas from the prostate will stain positive, but the surrounding lymph node and lymphatics will not when being investigated for prostate cancer metastasis.
Personally, I think the fibrosis and collagen deposition narrow blood flow to and from the dermal papilla of the hair follicle basically cutting off all nutrition. Not only that, but TGF-beta is a paracrine factor that can induce cell death in cells within the hair apparatus, so hair growth slows and finally remains at a very low level which is recognized as miniturization.
