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These past few days I was trying to figure out why compounds such as RU58841 typically do not result in regrowth if the androgenic activity is largely stopped - RU after all is a powerful AR antagonist, and if the AR is knocked out of commission that should effectively allow estrogen to dominate and cause regrowth. However, this typically doesn't happen.
After a while I made the conclusion that there must be more ways that DHT interacts with the hair follicle than merely through its own AR 'receptor'. If we further connect this thought with the well known fact that DHT is a strong estrogen antagonist, after a bit of searching, I discovered this study:
Thus, the antiestrogenic effect of androgen in mouse breast may be the result of effects of dihydrotestosterone on the estrogen receptor. If so, dihydrotestosterone performs one of its major actions independent of the androgen receptor.
It seems that not only does DHT kill your hair follicle by activating its androgen receptor, it also prevents estrogen from healing the follicle by modulating estrogen's receptor. When you block the AR with a compound like RU58841, you are at best only negating a part of DHT's destructive effect on the hair follicle. It will still largely inhibit the effect of estrogen by acting on the estrogen receptor thus preventing regrowth and reversal of miniaturization.
That is why, for the most part, RU58841 and other AR 'receptor' antagonists you can at best only expect maintenance.
A molecule such as S-Equol sounds like it would theoretically be superior to RU in every way.
The ideal solution is not just to block the AR, but to prevent DHT from interacting with anything in the scalp, and the best way to do that is to bind the DHT molecule like SHBG or S-Equol would do. If we achieve high enough concentration of S-Equol it will likely mop up the majority of DHT in the scalp, and you can enjoy watching your hair grow out stronger and thicker with every passing cycle.
The flipside of this question is then, why don't finasteride or dutasteride cause regrowth if they prevent the DHT from being made in the first place. I think the answer to this question is simply a matter of androgen/estrogen ratio, perhaps the problem is that both of these medications still leave a fair amount of DHT in the scalp, while removing it in the serum and other areas in far greater amounts. Perhaps the amount of estrogen a normal male has is still not enough to overcome the 30% or so of remaining scalp DHT even on Dutasteride. Certainly if we were able to disable >95% of the DHT in the scalp we would probably see regrowth in the majority of users, and maybe if that weren't enough a very low dose of estrogen to the scalp would probably be enough to tip almost everyone into regrowth territory.
After a while I made the conclusion that there must be more ways that DHT interacts with the hair follicle than merely through its own AR 'receptor'. If we further connect this thought with the well known fact that DHT is a strong estrogen antagonist, after a bit of searching, I discovered this study:
Thus, the antiestrogenic effect of androgen in mouse breast may be the result of effects of dihydrotestosterone on the estrogen receptor. If so, dihydrotestosterone performs one of its major actions independent of the androgen receptor.
It seems that not only does DHT kill your hair follicle by activating its androgen receptor, it also prevents estrogen from healing the follicle by modulating estrogen's receptor. When you block the AR with a compound like RU58841, you are at best only negating a part of DHT's destructive effect on the hair follicle. It will still largely inhibit the effect of estrogen by acting on the estrogen receptor thus preventing regrowth and reversal of miniaturization.
That is why, for the most part, RU58841 and other AR 'receptor' antagonists you can at best only expect maintenance.
A molecule such as S-Equol sounds like it would theoretically be superior to RU in every way.
The ideal solution is not just to block the AR, but to prevent DHT from interacting with anything in the scalp, and the best way to do that is to bind the DHT molecule like SHBG or S-Equol would do. If we achieve high enough concentration of S-Equol it will likely mop up the majority of DHT in the scalp, and you can enjoy watching your hair grow out stronger and thicker with every passing cycle.
The flipside of this question is then, why don't finasteride or dutasteride cause regrowth if they prevent the DHT from being made in the first place. I think the answer to this question is simply a matter of androgen/estrogen ratio, perhaps the problem is that both of these medications still leave a fair amount of DHT in the scalp, while removing it in the serum and other areas in far greater amounts. Perhaps the amount of estrogen a normal male has is still not enough to overcome the 30% or so of remaining scalp DHT even on Dutasteride. Certainly if we were able to disable >95% of the DHT in the scalp we would probably see regrowth in the majority of users, and maybe if that weren't enough a very low dose of estrogen to the scalp would probably be enough to tip almost everyone into regrowth territory.
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