S-equol (or Similar) Will Likely Be Better Than Ru. Poor Performance Of Ar Antagonists Explained

[IdealForehead]

If general consensus among those who are currently trialling ODM-201 remains positive I'll hopefully switch out the oral AA's I'm currently on for it sometime in early 2018.

From what you have written above are you implying S-equol has a half-life similar to RU? S-equol as far as I can tell should be quite an effective weapon against Androgenetic Alopecia, it binds to DHT, and is an agonist of the β-oestrogen receptor.

I don't know anything about s-equol. I've quit researching hair treatments because I'm done. I was just commenting on RU.

 

[HairCook]

I don't know anything about s-equol. I've quit researching hair treatments because I'm done. I was just commenting on RU.

Yeah, I hope topical finasteride as good (safe) as the claim, then maybe we get some research on the hard anti-androgens like odm...

JK

 

[Zoro]

and is an agonist of the β-oestrogen receptor.

This is one of the main reasons I've been interested in equol, seems like it could be good to try for regrowth, with possibly less risk than using topical estradiol. Too bad the stuff is so expensive and hard to find, you can find equol easily but I believe it's mostly R-Equol

 

[HairCook]

This is one of the main reasons I've been interested in equol, seems like it could be good to try for regrowth, with possibly less risk than using topical estradiol. Too bad the stuff is so expensive and hard to find, you can find equol easily but I believe it's mostly R-Equol

Isnt Equol in Brotzu included?

I remember that was supposed to be missing but arriving this month for our internal tests on ger forums. (we are gonna use gla instead of dgla though)

 

[ElTioLaBota]

Isnt Equol in Brotzu included?

I remember that was supposed to be missing but arriving this month for our internal tests on ger forums. (we are gonna use gla instead of dgla though)

Yes

 

[ElTioLaBota]

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.

Long time back i heard of a theory in this se forum of a used that said RU works better for ppl with high estrogen levels, so what you are saying might be true

 

[ElTioLaBota]

I could get it tested. Interestingly enough when I used to do alternate-day fasting 2-3x a week, several years ago, I developed a serious case of hyperandrogenicity. Drastic surge in libido, painful cystic acne out of nowhere, oily face and scalp, hair loss started right about that time as well.
That would suggest lower SHBG i.e. much more free androgens. It took me some months of 'normal' eating for that to subside.

U did fastings for 24h 2 to 3 days a week?

 

[whatevr]

U did fastings for 24h 2 to 3 days a week?

Yes.