To reiterate, and in case you forgot;
OK I have read quite a bit of your material and certainly enough to get the gist of your proposition. You are quite correct on one point androgenic alopecia should not be considered a 'desease' nor should it be considered a disease.
As to the rest of your material I would say this is a perfect example of dicto simpliciter (look it up) and a healthy infusion of misinformation.
Your initial preamble (ramblings) are full of inaccuracies, here are a few examples to correct you.
* Not all androgenic alopecia (AA) starts at the temples or crown.
* Not all AA progresses to a full crown (bald head) loss.
* Contrary to 'your' belief science actually knows only a small fraction of the complex mechanism that results in AA.
* We don't know for certain that DHT is the main cause of hair loss, we do know that it appears that DHT is part of the mechanism involved. However even if DHT is integral it could for example be more to do with receptor site rather than DHT.
* We don't know if DHT is excessive in both the scalp and the blood stream in the majority of cases of AA and in fact there is no hard evidence to draw a cause and effect relationship as DHT levels can be identical in those with and those without AA, in fact it could be that the enzyme 5α-reductase is the culprit rather than DHT.
* Other mammals do have plenty of incidences of AA, notably the male Tsavo lions, dogs, macaques, and even our closest primate species the chimpanzee.
* Both the big cats, domesticated cats and host of other species will suffer from alopecia and a host of other health issues related to a nutrient deficient diet.
* We do not know that AA is caused by a hormonal 'in balance' (imbalance) in fact there is very little to support that those with men with AA have significantly different hormonal levels to those without AA.
* Some women do suffer with AA this appears to occur as oestrogen levels decline with age which has lead to the hypothesis that oestrogen has a protective role and as it declines women hair follicles are exposed to DHT leading to AA in a similar way to men. Though I stress this is unproven.
* Logically women and men are not exposed to the same gene pool, as a result of the 'XY' chromosomes vs 'XX', hence the reason we have sex linked diseases.
* There is absolutely no evidence that the prostate is the 'single cause for hair loss' nor have I seen any credible evidence to make such an assumption, the prostate is however regulated by DHT which is synthesized in the prostate, testes, hair follicles, and adrenal glands by the enzyme 5α-reductase.
* There is no credible evidence to suggest that ejaculation has anything other than a transitory effect on DHT, in fact if we take your own results on face value your DHT level actually fell below the pre ejaculation level a short time after. And once again I stress that there is no credible evidence that those with AA have significantly different serum DHT levels to those without it.
* There is evidence of a potential increase in both benign prostatic hyperplasia and cancer of the prostate in those with low levels of sexual activity (ejaculation), you may like to think of this as clearing the pipes if you like.
Overwhelmingly the evidence is that AA is a genetically determined outcome, we can see evidence of this all around us in our groups of family and friends. The mere fact that such a high percentage of men will experience AA is sufficient to conclude that it is a natural process that most will experience to a greater or lesser degree.
Whilst we all may like to delay the loss of a youthful appearance lets not lose perspective and engage in silly and potentially unhealthy self abuse.
As to the rest of your material I would say this is a perfect example of dicto simpliciter (look it up) and a healthy infusion of misinformation.
Your initial preamble (ramblings) are full of inaccuracies, here are a few examples to correct you.
* Not all androgenic alopecia (AA) starts at the temples or crown.
* Not all AA progresses to a full crown (bald head) loss.
* Contrary to 'your' belief science actually knows only a small fraction of the complex mechanism that results in AA.
* We don't know for certain that DHT is the main cause of hair loss, we do know that it appears that DHT is part of the mechanism involved. However even if DHT is integral it could for example be more to do with receptor site rather than DHT.
* We don't know if DHT is excessive in both the scalp and the blood stream in the majority of cases of AA and in fact there is no hard evidence to draw a cause and effect relationship as DHT levels can be identical in those with and those without AA, in fact it could be that the enzyme 5α-reductase is the culprit rather than DHT.
* Other mammals do have plenty of incidences of AA, notably the male Tsavo lions, dogs, macaques, and even our closest primate species the chimpanzee.
* Both the big cats, domesticated cats and host of other species will suffer from alopecia and a host of other health issues related to a nutrient deficient diet.
* We do not know that AA is caused by a hormonal 'in balance' (imbalance) in fact there is very little to support that those with men with AA have significantly different hormonal levels to those without AA.
* Some women do suffer with AA this appears to occur as oestrogen levels decline with age which has lead to the hypothesis that oestrogen has a protective role and as it declines women hair follicles are exposed to DHT leading to AA in a similar way to men. Though I stress this is unproven.
* Logically women and men are not exposed to the same gene pool, as a result of the 'XY' chromosomes vs 'XX', hence the reason we have sex linked diseases.
* There is absolutely no evidence that the prostate is the 'single cause for hair loss' nor have I seen any credible evidence to make such an assumption, the prostate is however regulated by DHT which is synthesized in the prostate, testes, hair follicles, and adrenal glands by the enzyme 5α-reductase.
* There is no credible evidence to suggest that ejaculation has anything other than a transitory effect on DHT, in fact if we take your own results on face value your DHT level actually fell below the pre ejaculation level a short time after. And once again I stress that there is no credible evidence that those with AA have significantly different serum DHT levels to those without it.
* There is evidence of a potential increase in both benign prostatic hyperplasia and cancer of the prostate in those with low levels of sexual activity (ejaculation), you may like to think of this as clearing the pipes if you like.
Overwhelmingly the evidence is that AA is a genetically determined outcome, we can see evidence of this all around us in our groups of family and friends. The mere fact that such a high percentage of men will experience AA is sufficient to conclude that it is a natural process that most will experience to a greater or lesser degree.
Whilst we all may like to delay the loss of a youthful appearance lets not lose perspective and engage in silly and potentially unhealthy self abuse.
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