This Paper Has Some Interesting Data About Estrogen In Androgenetic Alopecia

[Gone]

http://www.sciencedirect.com/science/article/pii/S0022202X15529497

It's been known for a while that estrogen receptor activation can influence androgen receptor activity/quantity, but not until reading this paper did the connection really become clear to me. The most interesting part of this was the data that showed that Estrogen receptor beta (ER-b) is found in more parts of the pilosebacious unit than the androgen receptor is.

(paraphrasing) ER-b was found in the outer root sheathe, epithelial matrix, keratinocytes of the stratum basale and stratum spinosum, bulge, and the dermal papilla, whereas AR was only found in the dermal papilla.

So if it's clear that estrogen receptor modulation can affect androgen receptors, I wonder if it's also possible that androgen receptor modulation can in turn affect estrogen receptors; or if this is the actual effect that takes place when men use anti-androgens.

I was originally trying to find data showing which body tissues in men are found to possess the ER-b receptor, the primary (16x selectivity) receptor to S-equol. Interestingly, while this article is not that thorough at delivering on the subject of its title, it elaborates extensively on estrogen's receptor activity in the scalp and pilosebacious units. I'd still like to know which tissues would be affected by ER-b activation/S-equol, so if you have any good sources please share them.

I have to wonder if S-equol would be a better option for treating Androgenetic Alopecia than anti-androgens.

 

[Grasshüpfer]

This makes sense. The estrogen receptor modulates the ar. Low testo causes low estrogen as well as a higher dht conversion rate. So low testosterone leads to both ar upregulation as well as stronger ar binding through dht.

Which would be a disbalance, harming dp cells.

Well, maybe.

 

[Afro_Vacancy]

http://www.sciencedirect.com/science/article/pii/S0022202X15529497

It's been known for a while that estrogen receptor activation can influence androgen receptor activity/quantity, but not until reading this paper did the connection really become clear to me. The most interesting part of this was the data that showed that Estrogen receptor beta (ER-b) is found in more parts of the pilosebacious unit than the androgen receptor is.

(paraphrasing) ER-b was found in the outer root sheathe, epithelial matrix, keratinocytes of the stratum basale and stratum spinosum, bulge, and the dermal papilla, whereas AR was only found in the dermal papilla.

So if it's clear that estrogen receptor modulation can affect androgen receptors, I wonder if it's also possible that androgen receptor modulation can in turn affect estrogen receptors; or if this is the actual effect that takes place when men use anti-androgens.

I was originally trying to find data showing which body tissues in men are found to possess the ER-b receptor, the primary (16x selectivity) receptor to S-equol. Interestingly, while this article is not that thorough at delivering on the subject of its title, it elaborates extensively on estrogen's receptor activity in the scalp and pilosebacious units. I'd still like to know which tissues would be affected by ER-b activation/S-equol, so if you have any good sources please share them.

I have to wonder if S-equol would be a better option for treating Androgenetic Alopecia than anti-androgens.

We'll find out when Fidia releases their trial data later this year.

 

[Gone]

^ I think there's plenty of reason to think it works, but I'd like to know all the tissues it might affect. You can buy S-equol right now, lotion or not. Clearly you can be an S-equol producer and not grow breasts, but an estrogen receptor agonist sounds risky to me.

Also, you can get fantastic results on anti-androgens alone, with no estrogen receptor agonist needed. So I guess it might not matter which you try, except that perhaps if anti-androgens don't work for you, you could try s-equol. And if AR affects ER and vice versa, then again it doesn't matter which you use, only which you think is safer.

 

[Gone]

I couldn't believe how much more extensive Estrogen receptor beta was found to be in the hair follicle when compared to AR, just reading that makes you question that androgen regulates the hair follicle. Luckily we already have approaches to deal with either.

 

[Grasshüpfer]

Children have very low hormone levels, yet great hair. I think it's more about the ratio.

 

[Armando Jose]

Children have very low hormone levels, yet great hair. I think it's more about the ratio.

IMHO, children have exactly the same hormone levels as adults inside pilosebaceous unit in scalp. Did you noticed that they have an operative sebaceous gland? Sebaceous gland needs DHT to be functional, and PSU have all enzymes to make its hormones, even in childrens....

 

[GiveMeAccessToMyAccount]

I'm out of my league here, I don't follow the technicalities of all these things but here we go: my question is, does the ratio really matter when people who go bald are actually predisposed to go bald?

To be more clear, if two people, one affected by male pattern baldness and the other will never have male pattern baldness, have the same estrogen and androgen levels on the scalp then how does one really know to treat male pattern baldness by messing around with estrogen levels on the scalp without some horrible side effect?

 

[Gone]

I'm still looking for a good source that explains all known roles of Esteogen receptor beta in males. A lot of the ones I'm finding are in rats, and while there could be some overlap, so far it's proven to be highly variable, to the point where rat data is probably not helpful.

I'm out of my league here, I don't follow the technicalities of all these things but here we go: my question is, does the ratio really matter when people who go bald are actually predisposed to go bald?

To be more clear, if two people, one affected by male pattern baldness and the other will never have male pattern baldness, have the same estrogen and androgen levels on the scalp then how does one really know to treat male pattern baldness by messing around with estrogen levels on the scalp without some horrible side effect?

The people who are predisposed to go bald end up with a higher/lower number of androgen/estrogen receptors; the amount of testosterone, DHT, and estrogen, the actual hormones, is not affected.

Inhibiting the androgen receptor locally and without side effects has not been accomplished, except maybe in CB though that's a different discussion. And from what I've read, S-equol, despite inactivating DHT and having a strong effect on one of two estrogen receptors, doesn't seem to cause any problems for some people. Hard to believe, but if it's as safe as it seems, that's a good thing. I'd really like to know the details before I buy into it though.

 

[MrJolly16]

So, does the onagra or borraja work? What can we take to improve our hair? We just wait for Fidia to release the S-equol lotion or what? Thanks!

 

[Cody1212]

Are we talking about using something like this? I have no idea?
https://www.amazon.com/gp/aw/d/B00J...d=1488675692&sr=8-1&keywords=equol+supplement

 

[rupture]

http://www.sciencedirect.com/science/article/pii/S0022202X15529497

It's been known for a while that estrogen receptor activation can influence androgen receptor activity/quantity, but not until reading this paper did the connection really become clear to me. The most interesting part of this was the data that showed that Estrogen receptor beta (ER-b) is found in more parts of the pilosebacious unit than the androgen receptor is.

Is this true across the board or is it different in a bald, non balding scalp. Men or Women ?

 

[LusciousLadyLocks]

Watch out for estrogen receptor a. It induces apoptosis in the hair follicle.

Phytoestrogens are receptor b selective. In vitro, they seem to slow hair growth while preventing telogen phase, but in vivo, they seem to just increase hair growth across the board.

I use this as an adjunct: https://www.amazon.com/Source-Naturals-Phyto-Estrogen-Advanced-Liposomal/dp/B000GFJJHE/


Liposomal delivery is necessary for it to penetrate the skin at all.

Also, no boobs in guys--it's the a receptor that's responsible for that, too.

 

[LusciousLadyLocks]

IMHO, children have exactly the same hormone levels as adults inside pilosebaceous unit in scalp. Did you noticed that they have an operative sebaceous gland? Sebaceous gland needs DHT to be functional, and PSU have all enzymes to make its hormones, even in childrens....

Not true at all. Sebaceous gland upregulation is a normal part of childhood.

Actually, children's hair generally thickens through age 30, on average, in men and 40, on average, in women, after which it thins. Of course, lucky folks like me get severe premature thinning. Thanks, genetics!

 

[whatevr]

This is why AR antagonist like RU and CB have such poor real world results.

AR is only a small angle through which DHT causes hair loss. It does far more damage by modulating estrogen receptor and preventing its proper induction of hair follicle growth.

When you combine the OP with this study you will see why AR antagonism will always lead to very poor result of slowing down hair loss or maintenance at best. The key is not just to protect against AR damage but to bind or remove the majority of scalp and HF DHT to prevent it from interfering on the estrogen receptor. This will produce regrowth.

Theoretically S-Equol can potentially be the best hair loss treatment ever if it works topically and if we can get it in sufficient amounts. The ERb agonism doesn't even matter (so even the opposite isomer can work), your HF make estradiol themselves and it is a more potent agonist than S-Equol, so just bind all the DHT and let E2 do its work.

 

[Armando Jose]

Actually, children's hair generally thickens through age 30, on average, in men and 40, on average, in women, after which it thins

Have you any data? Your assert seem erroneous because normally we have the better hair under the 20.

 

[Seuxin]

I would like to add Estriol as powder in my minoxidil !

 

[plisk]

This is why AR antagonist like RU and CB have such poor real world results.

AR is only a small angle through which DHT causes hair loss. It does far more damage by modulating estrogen receptor and preventing its proper induction of hair follicle growth.

When you combine the OP with this study you will see why AR antagonism will always lead to very poor result of slowing down hair loss or maintenance at best. The key is not just to protect against AR damage but to bind or remove the majority of scalp and HF DHT to prevent it from interfering on the estrogen receptor. This will produce regrowth.

Theoretically S-Equol can potentially be the best hair loss treatment ever if it works topically and if we can get it in sufficient amounts. The ERb agonism doesn't even matter (so even the opposite isomer can work), your HF make estradiol themselves and it is a more potent agonist than S-Equol, so just bind all the DHT and let E2 do its work.

if what I'm reading about s-equol isnt a gross oversimplification, then it sounds like it could be as good as finasteride without the side effects as it would only bind DHT, not 5AR which has other biological actions we need.

 

[Afro_Vacancy]

if what I'm reading about s-equol isnt a gross oversimplification, then it sounds like it could be as good as finasteride without the side effects as it would only bind DHT, not 5AR which has other biological actions we need.

Yes, maybe, a few issues though ...

1) We know finasteride acts in each of the skin, the blood, the cerebrospinal fluid, etc. Where does s-equol act?
2) finasteride has a dose-independent response. What's the dose response curve of s-equol?
3) finasteride has a long half-life and its effects last a few weeks. How long do the effects of s-equol last?

 

[tylerduren]

Weird thing is. I seem to be getting good results with miconazole which is a potent anti estrogen