Why does only the hair on the top of our heads succumb to bad diet/ DHT/ MPB?assfrus

LawOfThelema wrote:if they werent the answers to some of his specific questions i wouldnt have brought them up.

what surprises me is how j887 can go on so many probabilities and maybes and completely ignore the things which have numerous lines of empirical support. it is not only hair transplant doctors or doctors with vested interests in the HT industry who have done the research on the things that i mentioned.

i would agree with him, if antiandrogens didnt get results at regrowing hair. how do you reason that away. just because propecia and avodart cause unwanted effects in the body, you cant wish away their efficacy.

also if they werent developed precisely on the observation of males with 5ar deficiency (they had no BHP and no MPB) and the desire to deal with those conditions by clinically duplicating 5ar deficiency with chemical intervention.

that is experimental support that there is some correctness to the hypothesis that balding in the male pattern is highly mediated by androgen effects on scalp tissue.

what part of this do you disagree with specifically?

of course inhibiting 5ar systemically has numerous effects on the body. mercks downplaying of these was highly premature. it was their irresponsible error or willful ignorance for the sake of profit to not realize that inhibiting 5ar through the whole body has more effects than shriking the prostate, and maintaining hair. but the fact that it does regrow hair despite the negative effect lends support to the androgenetic hypothesis despite whatever negative result that 5ar inhibition also has. and this is just one line of support. some of the others are the findings of associated genes, scalp biopsies showing the androgen receptor concentrations, testing the concentration of 5ar enzymes in the scalp, and the fact that other non inhibiting androgen approaches also work, such as degrading the receptor or antagonizing the receptor also show results. These would not work if there was no strong causal role for androgen binding the receptor. Surely you see this? i believe there should be safe ways to do this without systemic side effects. ru5841-myristate which antagonize the receptor with prodrug action is one possibility, and things like s-equol which don't inhibit 5ar and thus dont bring about a systemic side effect associated with inhibition (no changed T-E ration, hence no gyno, no change in neurosteroid due to inhibition, etc). id recommend looking at the review of the sides of finasteride and dutasteride in the journal of sexual medicine. reduced dht itself isnt the full account of the side effects. the irreversable inhibition of 5ar account for many of them, namely the change in neurosteroids and the changed estrogen to testosterone ratio.

it really is starting to look like these beliefs that circulation and such are more important and androgens are minimally important arise from the desire to avoid propecia and avodart for fear of their side effects. it is completely fine to not be comfortable using such potent endocrine system modulators, but one shouldnt allow that to color their appraisal or understanding of the rest of the theory.

did you know that researches like Elsevier who have published on the correlations of insulin resistance and the cardio vascular risk factors still endorse the core theory despite these recent findings?

do you know that the researcher who proposed the AGA is mircroinflammatory process of the scalp, has not disavowed the earlier found androgenetic basis of the conditions.

these are not mutually exclusive things.

a

SlowMoe wrote:Why do you keep avoiding my question? Doesn't it make sense that an environment devoid of 60% of it's nutritional supply, and with a similar lack of waste removal, would cause the hair cells to be succeptible to attack?

Do you think the poor circulation/ lack of fatty tissue in only the MPB area is a huge coincidence?