What Causes Hair loss?
» What Causes Hair loss?
Can anyone discuss me with this?
Aside from genetic inheritance, what would be the other causes of hair loss?
» » What Causes Hair loss?
» Can anyone discuss me with this?
» Aside from genetic inheritance, what would be the other causes of hair
A variant of the androgen-receptor gene, inherited from the mother, was correlated to be found in 98.1% of balding men in a large German study with over 1500 particpants, vs. 76.1% of men who didn’t have that variant of the androgen receptor gene. Thats ONE of the genetic factors.
Another chromosome, chromosome 20, which is autosomal (can be inherited from either the mother or the father), has also been identified in a study that had over 5000 caucasian men from different parts of the world. There are at least 11 genes on this chromosome, but probably more than that. Which gene or gene’s on this chromosome have this effect?
If you have BOTH of these genetic inhertences (the androgen-receptor variant, AND the chromosome 20 variant), then you are SEVEN TIMES MORE LIKELY TO BE BALD than another guy.
The two of them together are probably well over half (I’d say more like 80% or more) of the reasons you end up being bald like your ancestors did. There may be some other genes that exacerbate baldness or kick it into high gear “earlier” in men, but these two are almost undoubtably the “biggies” in genetic determination.
Everything else is downstream, but quickly baldness happens through the androgen receptor located in the cytoplasm on the dermal papilla of affected hairs. DHT, which is converted from Testosterone, is “made” by alpha five reductase enzymes which are located IN THE INNERMOST PORTION OF THE OUTER ROOT SHEATH OF THE HAIR FOLLICLES THEMSELVES. The DHT that miniaturizes you hair is located RIGHT THERE AT THE FOLLICLE. Serum DHT may play a “small” role, but for the most part serum DHT is bound to globulin and rendered biologically inactive by it because it can’t bind to receptors almost all of the time. Only about 2% of it normally is “free”. Believe it or not, alpha five reductase type ONE is more prevalent in hair follicles in other portions of the follicle, but Merk Pharmaceutical tested an alpha five reductase type one inhibitor and found it had very little effect in even slowing baldness, while finasteride induces much higher haircounts, especially in the first two years. Men who are born without the alpha five reductase type 2 enzyme genetically NEVER GO BALD. Its thought that stimulation from this enzyme, in your root sheaths of your hair follicles, is what gives “enough” stimulation to genetically predisposed hairs to “kick off” the baldness process. After that, other androgens like Testosterone, androstenidione, DHEA, DHEAS might be able to exacerbate the process by binding to the dermal papilla’s androgen receptors, where they then unleash androgen-inductible genes within the follicle that lead to miniaturization.
Hairs from the back and sides of your head have been shown to have LESS androgen receptors and are able to convert less DHT (those areas of the scalp have less DHT floating around anyway). When given high androgenic stimulis in tests…even hairs from the back and sides of the head miniaturize.
The variant of the androgen receptor gene than most bald men have ALONE is probably not enough. There are some “hairy” men with a lot of chest, back, leg, even arm and finger hairs…who retain full heads of hair. When combined with whatever gene (genes?) on chromosome 20 in genetic inheritance however, the two together “make” men go bald by something happening after andrognic uptake at the receptor. It may be one or two very small instructions thereafter, or something even less or more complicated than that at that point.
There is a immuno-response to the affected hairs after time that leads to inflammation around the hair follicle in these hairs. The first inflammation is seen at the infidula, which is the opening in the dermis where the hair follicle emerges onto the skin. Ive postulated, along with some others, that these might be dead keratinocytes from DKK_1, which is an androgen inductible gene secreted by the dermal papilla which has been shown to cause apoptosis in keratinocytes in experiments-----which would mean some dead cells are still “in” the body and the immune system WOULD want to kill those. That is just a guess however, and it certainly could be something going awry downstream of androgenic uptake in other parts of the follicle like the root sheath or whatever. We do know this, head hair does not need any androgens to grow at all. People with androgen isensitivity syndrome never go bald and keep all their hair all their lives because their androgen receptors dont work. Women dont go bald unless they are given testosterone injections or creams…when some of them recieve either, they go bald in a couple of years in many cases just like men do in the same patterns if they have dads or brothers or uncles that went bald—usually in the exact same pattern as their relatives. About half were shown in one study (women who were female-to-male-transesxuals) to go bald or be in the various norwood levels of baldness) after 13 years “on” testosterone.
Interestingly, the drug that usually regrows the most hair is cyclosporin, which is an immunosuppresssant. This might be indicative of showing that whatever androgens do, the immunological response that they induce against these affected hairs might be more of a detriment to these hairs than androgens alone. However in experiments, hair growth was slowed in MPB hairs by 16% in test tubes by adding testosterone, so male hormone does indeed slow the growth of these hairs by substances secreted by the dermal papilla after androgenic uptake which has been established by DP cells given testorone in many many many different experiments.
This is a good backgrounder on MPB for you that unfortunately these sites dont put up because they want you to hit the site a zillion times “getting educated” about MPB and thus up their number of hits for advertisers. It usually takes a man many visits to a site to learn all of that.