How Different Types Of Estrogen Promote (and Hinder) Hair Growth

[bridgeburn]

Small amounts of topical estrogen with a goal of leaving systemic hormone levels unaffected and just stimulating hair growth locally at the follicles.

you still may need to break up the fibrosis since bald scalp is thicker than non bald. and male skin is thicker but High amounts of systematic estrogen or antiandrogens does make the skin thinner.

she still has great hair but there's no doubt if you see her hair a few years ago she's lost a fair amount.

Back in the day her hair was unnaturally thick because of the initial oral minoxidil response. I think forcing too much anagen can be a bad thing, part of her problem could be minoxidil dependence and synchronized sheds.

Looks like she's starting the process of switching over to more natural estrogen therapy soon, so we will see.

it would be better for her to go on natural estrogen but an issue is that if someones been on the pill for awhile it can be difficult to stop. Because it elevates SHBG in a somewhat semi-permanent way. While SHBG is mostly good because of its preference to bind to Androgens, it still can bind to estradiol too. but EE does not bind to SHBG. Even after stopping the pill the SHBG takes a long time to go down so it can make natural E less bioavailable and cause a sorta Diane dependence. I wish I bookmarked the study If I remember correctly it basically said that Women who take the pill had the highest SHBG and women who had been off the pill for 6 months had lower but still quite higher than women who didn't take the pill at all.

 

[Georgie]

you still may need to break up the fibrosis since bald scalp is thicker than non bald. and male skin is thicker but High amounts of systematic estrogen or antiandrogens does make the skin thinner.


Back in the day her hair was unnaturally thick because of the initial oral minoxidil response. I think forcing too much anagen can be a bad thing, part of her problem could be minoxidil dependence and synchronized sheds.

it would be better for her to go on natural estrogen but an issue is that if someones been on the pill for awhile it can be difficult to stop. Because it elevates SHBG in a somewhat semi-permanent way. While SHBG is mostly good because of its preference to bind to Androgens, it still can bind to estradiol too. but EE does not bind to SHBG. Even after stopping the pill the SHBG takes a long time to go down so it can make natural E less bioavailable and cause a sorta Diane dependence. I wish I bookmarked the study If I remember correctly it basically said that Women who take the pill had the highest SHBG and women who had been off the pill for 6 months had lower but still quite higher than women who didn't take the pill at all.

He means my hair prior to any hairloss or hairloss treatments. I’ll show you. I had a lot of hair, so I’ve had a lot of hair to lose, but it’s only taken three and a half years for me to lose 70% of it. The ponytail photo is from 3 weeks ago so It’s actually a fair bit thinner now given that I lose 150+ hairs a day, but you get the idea. That little pontytail is more than what’s left, and would have been a tiny section of what I used to have.

I agree about the Diane which is why I’ve has some bad reactions when trying to
Come off it, and probably why it was what started the initial shed which kickstarted my hairloss and made my hormones flip out for good. Issue is, I need to try at least to see if switching hormones will help. If I don’t, I will always have wondered.

 

[Georgie]

Also i think @bridgeburn is correct about minoxidil and the damage it's doing. My hair shedding has never been below 80-100 hairs in a day whilst i have been on it. Shedding picks up significantly when i'm getting some regrowth (and i am albeit localised to my temples). I don't know why this has happened to me, but i have some theories. minoxidil works to increase the anagen phase of hairs, and it does - for the hairs on my body that are not affected by dht. So my body hair, facial hair grows longer and darker, i get some regrowth about my hairline, but something is really wrong about how it works also. It SHOULD NOT just "turn on" and "turn off" the way it does. I should not get terminal hair growth for a few months, then only miniaturised growth for many more months. I should NOT be constantly shedding huge amounts of hair. I have this feeling that, because my miniaturisation is so extensive, and my hair growth cycle was already so fucked up, it has had an impact upon a large portion of my hair which was already rapid cycling (and not growing back). So a lot of hair started growing all at once, maybe it means that they all stop growing at once too, although why this should happen in 9-3 month periods totally stumps me. It's like it has my hair cycles all mixed up. Catalan lasts for 9-12 months, anagen lasts for 3 months, telogen seems just to f*****g last forever.
I want to come off minoxidil, but i need a suitable replacement. Not adenosine, not stem, none of that sh*t. i mean something that causes hypertrichosis or similar effects. I wish PSI and MG were easier to source and weren't so expensive because would use them in a heartbeat. I think the only next best option i have is either cyclosporin or AGF-39/SGF-57.

 

[bridgeburn]

View attachment 83735 View attachment 83734
He means my hair prior to any hairloss or hairloss treatments. I’ll show you. I had a lot of hair, so I’ve had a lot of hair to lose, but it’s only taken three and a half years for me to lose 70% of it. The ponytail photo is from 3 weeks ago so It’s actually a fair bit thinner now given that I lose 150+ hairs a day, but you get the idea. That little pontytail is more than what’s left, and would have been a tiny section of what I used to have.

I agree about the Diane which is why I’ve has some bad reactions when trying to
Come off it, and probably why it was what started the initial shed which kickstarted my hairloss and made my hormones flip out for good. Issue is, I need to try at least to see if switching hormones will help. If I don’t, I will always have wondered.

That guy with the chopsticks, Lol.

I want to come off minoxidil, but i need a suitable replacement. Not adenosine, not stem, none of that sh*t. i mean something that causes hypertrichosis or similar effects. I wish PSI and MG were easier to source and weren't so expensive because would use them in a heartbeat. I think the only next best option i have is either cyclosporin or AGF-39/SGF-57.

maybe its possible to stop if gradually? my hair is still getting better after reducing from everyday to every other day. You could try switching to PGE2, thats part of what minoxidil does. cyclosporin is a carcinogenic immune suppressant don't take that

 

[IdealForehead]

I just read the full text of the rat study which provides the strongest suggestions for opposing roles of ER-alpha and ER-beta in hair. It's a fascinating read. Overall, I think this all provides some basis for about 50-70% of a good unified estrogen theory, which I will try to present to the best of my ability here.

I think we can conceptualize that estrogen works to affect hair growth in a few possible ways:

1) Systemic Castration Effect - Large doses of systemic estrogen in men leads to dramatic suppression of testosterone/androgen production. This is part of the intended purpose of taking estrogen in M>F transexual regimens. ie. Chemical castration. Shutting down androgens will always lead to an improvement in male pattern baldness. So any large amount of estrogen will likely be a "net positive" for male androgenic alopecia, regardless of what type is chosen, via this mechanism alone.

2) 5-alpha Reductase Inhibitor Effect - Estradiol has been shown to have an inhibitor effect on 5-alpha reductase (thus suppressing DHT production like finasteride/dutasteride). Probably it will work both locally and systemically for this effect. Interestingly enough, highlighting yet another difference between natural and synthetic estrogens (@Georgie), ethinyl estradiol does not have the same 5-AR inhibiting properties as natural estradiol. (ref)

3) Anti-Sebum Effect - Estrogen is known to downregulate sebum production in a disproportionate manner but it's not entirely known how. Sebum is known to increase hair inflammation and thus loss. Perhaps this is just a manifestation of the 5-ar inhibition effect, or maybe it is a separate behavior. To summarize the principle:

Estrogens are also powerful suppressors of androgen-stimulated sebaceous activity in doses markedly lower than those required for anti-androgens (Ebling, 1974), the mechanism of action of estradiol in the sebaceous gland was concluded to be distinct from that of an anti-androgen (Ebling, 1974) suggesting that estrogens act via a non-androgen receptor (non-AR)-dependent pathway.
​

4) Androgen Receptor Downregulation Effect - ER-beta stimulation by soy isoflavones (phytoestrogens) has been shown to downregulate androgen receptors in the prostate. If they can do the same in the hair, this can make our hair more androgen resistant.

Previous laboratories, including ours, have shown that isoflavones binding to ERβ in the prostate can down regulate the androgen receptor (AR) and thus decrease androgen hormone action.
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3032666/​

5) Direct Hair Cycle Manipulation Effect - Estrogen signalling pathways can directly manipulate the transition between telogen (shed) > catagen (rest) > anagen (growth). This is the newest and least well understood piece of the puzzle. Making this aspect more complex is that it seems there may be different mechanisms for different mammals, men vs. women, and different areas of the scalp. Science does not have all the answers here from what I can see, so we are stuck to speculate.

The rat study strongly seemed to suggest that in mice at least:

• ER-alpha promotes catagen and thus hair loss.
• ER-beta promotes an anti-oxidant and protective effect while also shutting off ER-alpha induced catagen signalling.

Here are a few pertinent excerpts from the study:

ERα expression is hair cycle dependent (with an expression maximum in telogen skin), whereas ERβ expression is more constant throughout the HF cycle (Fig. 2). Therefore, our results are consistent with the concept that stimulation of ERα, not ERβ, functions as a molecular hair cycle brake in mice.

Catagen progression is accelerated in mice lacking ERβ (Fig. 6). This supports the concept that, as in other organs, e.g. the uterus and mammary gland (43, 57), ERβ, (including ERβ ins), functions as a quencher of ERα-mediated effects.

ERβ stimulation by antiestrogens may mediate antioxidant actions on activator protein-1 sites by inducing quinone reductase (64), and the antioxidative stress enzymes glutathione S-transferase-π and γ-glutamylcysteine synthase are up-regulated by transcriptional activity of ERβ (65). Therefore, one role of ERβ may be to protect tissues from oxidative stress by inducing a battery of antioxidative enzymes (64, 65). Thus, the widespread and constant expression of ERβ within the pilosebaceous unit may also serve to protect the skin and its appendages, which are continuously more exposed to oxidative damage than most other organs.
​

Adding tangential support for ER-alpha = bad, ER-beta = good is some research I have just reviewed on prostate cancer. We know prostate problems are linked to androgenic alopecia, as those of us with hair loss are at higher risk of prostate cancer, and the same meds for enlarged prostates treat hair loss.

Here's a study summarizing some research on how ER-beta and ER-alpha connect to prostate cancer. Here's another with the final punch line that suggests overall, just like with hair, ER-alpha = bad for prostate, and ER-beta = good for prostate:

Most evidence suggests that ERA mediates the harmful effects of estrogen in the prostate, whereas ERB is tumour suppressive.​

My current biggest problem with the simplified ER-beta/ER-alpha theory is the fact that ER-alpha is not very much expressed in the human scalp as per this study. If there are no significant ER-alpha receptors in the human scalp, then it may not be so simple. However, this was just one study and it focused on occipital nonbalding scalp. It makes me wonder if we would see more ER-alpha receptors in balding areas. It would be nice if that was the case as it would really tie all this together very neatly. We can't know for sure unless someone does a study to prove it.

Advantages of the ER-Alpha vs. ER-Beta Theory
To summarize, then, overall, I like this simplified theory of ER-beta being good for hair, and ER-alpha being bad as it fits with a number of things:

• Explains why pregnant women have a dramatic improvement in skin and hair after 12 weeks pregnancy, as estriol shoots up and they shift to a more ER-beta balance, and then hair sheds after pregnancy when estriol again drops.
• Explains why topical steroids in combination with estrogens help hair growth, as steroids increase ER-beta receptor expression.
• Explains why menopausal women tend to thin all over as menopause generally represents a shift towards estrone which is the most ER-alpha predominant natural estrogen.
• May explain why some women have hair shedding on birth control pills (ie. ethinyl estradiol which is weighted to ER-alpha activity).
• Fits with findings that ER-beta is likely generally good for prostates and ER-alpha is bad for them (knowing that the underlying processes of prostate pathology tend to mirror those of hair loss).
• Explains why S-Equol was chosen as a primary ingredient for the development of Brotzu (selective ER-beta agonist).

This is nowhere near a perfect theory. But I think this in total represents the most comprehensive theory of estrogen and hair that we can currently assemble. Current studies on estrogen and hair growth are poor in general. One of them from China I reviewed with @bridgeburn a few months ago was riddled with errors that we easily picked up, so it goes to show that peer review is not perfect and we can't assume every study is perfect fact. When some studies contradict others, it may not be that estrogen is infinitely complex and beyond our potential for understanding. It may just be that some studies are crap.

Estrogen may in fact be simpler than it appears.

Final Outcomes
All this then provides more weight towards considering genistein as the cheapest, most freely available, and best suited topical estrogenic agent for hair growth, at least if growth cycle manipulation is your primary goal. Estriol would be the most ideal topical of the natural estrogens for hair.

For my own part, this is probably the absolute worst time for me to start experimenting with another agent, as I just had major scalp surgery last week. I will probably try to avoid starting genistein until at least 2-4 weeks from now to be sure my hair is stable first and not going Telogen Effluvium just from my surgery. I will continue estriol on my face and hairline unabated as I've been using that already for 2 months with good results.

I think that even if time shows there are more pieces to the estrogen puzzle, most of this general theory will be proven to be correct in time. I also think this concludes the useful extent of research that I can do on estrogen at this stage.

We'll see how the experiment goes in time.

 

[Georgie]

That guy with the chopsticks, Lol.

maybe its possible to stop if gradually? my hair is still getting better after reducing from everyday to every other day. You could try switching to PGE2, thats part of what minoxidil does. cyclosporin is a carcinogenic immune suppressant don't take that

Yeah i plan on trying pge2, but i guess there's also diazoxide. I just know that whilst i'm on minoxidil, i do not believe that my hair has a chance to grow normally.

 

[bridgeburn]

Interestingly enough, highlighting yet another difference between natural and synthetic estrogens (@Georgie), ethinyl estradiol does not have the same 5-AR inhibiting properties as natural estradiol.

I said the exact same thing earlier lol.

My current biggest problem with the simplified ER-beta/ER-alpha theory is the fact that ER-alpha is not very much expressed in the human scalp as per this study. If there are no significant ER-alpha receptors in the human scalp, then it may not be so simple

What if there are more alpha receptors in body hair?, then that could explain the negative effect on body hair and simultaneous positive effect on scalp hair.

Explains why pregnant women have a dramatic improvement in skin and hair after 12 weeks pregnancy, as estriol shoots up and they shift to a more ER-beta balance, and then hair sheds after pregnancy when estriol again drops.

could be, but estradiol also increases during pregnacy. but yeah estriol increases more than usual. It could also be that theres simply alot, The venom of cobra for example is more toxic than the venom of a king cobra however youre more likely to die from being bit by a king cobra because it injects alot more.

 

[Afro_Vacancy]

Estrogen is known to have complex effects on hair. It can both promote and inhibit hair growth depending on the type of estrogen used.

The primary factor that seems to determine the outcome of estrogen on your hair is which type of estrogen receptor you are stimulating with that type of estrogen.

Types of Estrogen Receptors
The body has two types of estrogen receptors. These two estrogen receptors have dramatically different effects on hair growth.

1) ER-alpha
ER-alpha is the type of estrogen receptor you DON'T want to stimulate.

With hair, ER-alpha stimulation promotes catagen. Catagen is the cessation of hair growth. ie. The end of anagen (growth phase). After catagen comes telogen (hair shed). Any estrogen which stimulates ER-alpha predominantly will therefore stall hair growth and lead to hair shedding. (ref)

ER-alpha stimulation also may lead to osteoarthritis and osteoporosis. (ref)

2) ER-beta
ER-beta by contrast is the estrogen receptor you DO want to stimulate.

ER-beta signalling works by silencing the ER-alpha catagen signalling pathway. By blocking this catagen signalling, hair follicles can grow longer and spend more time in anagen. This leads to longer and healthier hair. (ref)

Types of Estrogen
To evaluate the usefulness of any type of estrogen, we therefore need to know to what extent they stimulate ER-alpha vs. ER-beta receptors.

1) 17 beta-Estradiol (E2)
The primary estrogen of the natural human body is 17 beta-estradiol. Estradiol binds equally well to ER-alpha and ER-beta. (ref)

Estradiol binds most strongly to the estrogen receptors of the natural estrogens. (ref) We can therefore use estradiol as a standard to compare other estrogen binding strengths, and rate estradiol as "100" binding strength for both receptors.

Because estradiol binds equally to ER-alpha and ER-beta, I would postulate that overall this may likely be considered a "good" estrogenic agent for promoting hair growth, but not the best as we will soon see.

2) Estrone (E1)
Estrone is the primary estrogen of menopause. It has been described as the "ugly estrogen". (ref)

Estrone has a binding affinity for ER-α of 60 and for ER-ß of 37 (relative to estradiol). (ref) This means it is primarily an ER-alpha stimulator, and thus can be considered absolutely undesirable for hair growth.

Estrone will lead to premature catagen of hair follicles. It is likely the reason postmenopausal women lose hair all over their heads and bodies.

3) Estriol (E3)
Estriol binds to ER-α with an affinity of 14 and to ER-ß with an affinity of 21. (ref)

This means it is the only natural estrogen with a greater ER-beta affinity than ER-alpha.

Estriol is therefore the primary estrogen we DO want to use for hair growth.

Estriol is most famous for shooting up dramatically after about 12 weeks pregnancy (ref), and it is credited in part for the fantastic glowing skin and long thick hair that pregnant women experience from this point of pregnancy onward.

Estriol has a half life of 6-9 hours with vaginal application, which may be similar to skin application. (ref) Twice a day application thus makes the most sense. It has a low affinity relative to the other estrogens (it is the weakest to bind), so larger amounts must be used if its effects are desired.

4) Ethinyl Estradiol (EE)
This is the primary estrogen used in birth control pills. Unfortunately, EE is a mostly ER-alpha stimulator. (ref) This likely makes it less useful for hair growth promotion (unless you are using it orally for chemical castration, which will help stop male pattern hair loss by shutting down all your androgen production).

Normal women can likely get away with EE usage in birth control pills because even on high dose contraception, they will still have their natural estrogens (E1, E2, E3) to provide ER-beta stimulation and help counteract EE's ER-alpha effect. (ref, ref)

However, EE will not provide benefits for hair in this context, and should likely be minimized or avoided compared to other estrogens if hair growth is the desired outcome.

Manipulating Estrogen Receptor Expression
As @Georgie pointed out in another thread, dexamethasone (a steroid) has been shown to decrease ER-alpha receptor expression by up to 38%, while having no effect on ER-beta receptor expression. (ref)

This means that topical steroids could in theory be used to downregulate ER-alpha receptors in the scalp and promote a more ER-beta predominant effect.

Dexamethasone is used in combination with 17 alpha-estradiol (alfatradiol) in a German product called Ell-Cranell Dexa. I am unsure of the ER-alpha vs. ER-beta stimulating balance of 17 alpha-estradiol, but presuming it is similar to 17 beta-estradiol, the mechanism of action for this product would make sense. The steroid will shift receptor balance towards ER-beta predominance, and estradiol will then bind to these increased ER-beta receptors, stimulating hair growth.

The problem with this approach is that topical steroids can lead to skin atrophy over time, so they are not a good long term treatment. Additionally, the same predominantly ER-beta stimulation can be accomplished much more simply by just using estriol cream instead.

So although it is interesting to conceptualize, I do not think the alfatradiol/dexamethasone combo is the most useful approach to manipulating estrogen pathways for hair growth.

Summary
In other words:

• ER-alpha signalling stimulates catagen (stopping hair growth dead)
• ER-beta signalling blocks the ER-alpha pathway (prolonging anagen and causing hair growth)

Evaluating the different types of estrogen:

• Estradiol has a 1:1 alpha:beta binding ratio, estriol has a 3:2 beta:alpha binding ratio, and estrone has a 1.6:1 alpha:beta binding ratio (ref)
• Ethinyl estradiol has "ERα selective agonistic potency" (ref)

Therefore we can conclude that if ER-alpha stimulation is a negative factor for hair, and ER-beta stimulation is a positive one, the value of each estrogen can be ranked as:

• Estriol (best) - 3:2 beta:alpha
• Estradiol (2nd best) - 1:1 beta:alpha
• Estrone (poor) - 1.6:1 alpha:beta
• Ethinyl estradiol (poor) - primarily alpha binding

Application
For both men and women, the most useful approach to estrogen therapy in the pursuit of hair growth will therefore likely be a topical estriol cream applied directly to the areas of the hairline where stimulation is desired.

Fortunately, estriol creams are freely available most places over the counter. I have been using this one myself:
https://www.amazon.com/Bioidentical-Supplements-Micronized-Bio-Identical-Menopause/dp/B004XJIDEO

I have read a higher concentration of 0.3% estriol can be used in compounded creams for acne. This can also have an anti-aging effect. If you are brave, you can use it on your face as well for these benefits. (ref)

Primary risks of estrogen therapy in general for men will likely be sexual dysfunction. I have noticed some mild erectile dysfunction when I am using large amounts of estriol cream, but it doesn't bother me at this stage. Other risks for all estrogens are of blood clots, increased risk of breast cancer, etc. (ref)

For my own part, I will continue to use estriol for both hair growth promotion and anti-aging effect on my skin as I have been using it for about two months now and it has appeared to be quite effective for both. Dosage can easily be adjusted by using more or less cream to minimize side effects.

No treatment for hair loss or skin care is perfect or well suited for everyone. Most men will probably want to avoid estrogen therapies even just in principle alone. However, if used correctly, estrogen is likely a powerful hair growth tool to consider for those who wish to utilize it to their benefit.

Shouldn't your analysis of ER-alpha have been borne out by the testing of alfatradiol compounds? They show a modest benefit for hair.

 

[HairCook]

Melatonin inhibits it as well btw: http://www.jbc.org/content/279/37/38294.full

Dexa seems also to increase PGE2: https://www.docdroid.net/4ScJqyb/mirazi2004.pdf

 

[whatevr]

Shouldn't your analysis of ER-alpha have been borne out by the testing of alfatradiol compounds? They show a modest benefit for hair.

Why? The 'alfa' in the name of alfatradiol has nothing to do with estrogen receptor alpha.

 

[Afro_Vacancy]

Why? The 'alfa' in the name of alfatradiol has nothing to do with estrogen receptor alpha.

I thought that alphatradiol was 17-alpha estradiol.

Alfatradiol binds to the ERα and ERβ with 58% and 11% of the relative binding affinity of 17β-estradiol.[13] However, it has 100-fold lower estrogenic activity relative to estradiol

https://en.wikipedia.org/wiki/Alfatradiol

OK, you're right.

 

[HairCook]

Btw I just checked ell cranell dexa was discontinued in 2006.

 

[koolaidshade]

@IdealForehead

how long did it take you to see results from the estriol cream?

 

[IdealForehead]

@IdealForehead

how long did it take you to see results from the estriol cream?

Hard to say what I've been seeing results from at any stage as I've been overlapping many therapies. But i was on it since about two months now and after 4-5 weeks I definitely felt like there were more fine hairs coming in and the fine ones that were already there were growing longer. Nothing mindblowing but enough to make me wish I had embraced estrogenic therapies a long time ago. I try to be skeptical of everything because placebo/nocebo are both real. But the difference seemed evident. I had felt like things were slowing/stalling until I added the estriol and once I added it progress jump restarted.

 

[IdealForehead]

Holy sh*t, guys. I just read something mindblowing to me. I have been researching equol for its DHT binding capacity. I was trying to figure out if we need s-equol, r-equol, or both to bind DHT (the answer is any type of equol will work).

Along the way, I came across this in a discussion of how equol (an isoflavone) acts through ER-Beta receptors in prostates:

Previous laboratories, including ours, have shown that isoflavones binding to ERβ in the prostate can down regulate the androgen receptor (AR) and thus decrease androgen hormone action.

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3032666/​

ER-beta binding in the prostate downregulates the androgen receptor!

This is incredible and adds an entirely new dimension to managing androgenic hair loss, or at least a new dimension to our understanding of how estrogen pathways work to help with that.

Reducing androgen receptors is one of the holy grails of managing hair loss, because in principle, if we can eliminate the receptors, androgens can no longer do as much direct harm. Your hair follicles become more androgen resistant.

It looks like stimulating ER-beta is the answer to making this happen.

Again, the best ER-beta agonists are likely genistein (available here), s-equol (working on a supplier through Alibaba at the moment), and estriol.

I've updated my summary post above with this additional mechanism of action to add this as another pathway.

It really appears ER-beta agonism provides all the estrogenic benefits we want for our hair/skin.

 

[Georgie]

Holy sh*t, guys. I just read something mindblowing to me. I have been researching equol for its DHT binding capacity. I was trying to figure out if we need s-equol, r-equol, or both to bind DHT (the answer is any type of equol will work).

Along the way, I came across this in a discussion of how equol (an isoflavone) acts through ER-Beta receptors in prostates:

Previous laboratories, including ours, have shown that isoflavones binding to ERβ in the prostate can down regulate the androgen receptor (AR) and thus decrease androgen hormone action.

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3032666/​

ER-beta binding in the prostate downregulates the androgen receptor!

This is incredible and adds an entirely new dimension to managing androgenic hair loss, or at least a new dimension to our understanding of how estrogen pathways work to help with that.

Reducing androgen receptors is one of the holy grails of managing hair loss, because in principle, if we can eliminate the receptors, androgens can no longer do as much direct harm. Your hair follicles become more androgen resistant.

It looks like stimulating ER-beta is the answer to making this happen.

Again, the best ER-beta agonists are likely genistein (available here), s-equol (working on a supplier through Alibaba at the moment), and estriol.

I've updated my summary post above with this additional mechanism of action to add this as another pathway.

It really appears ER-beta agonism provides all the estrogenic benefits we want for our hair/skin.

Oh yeah i knew this about s-equol because i did a lot of my own research. I've been trying to figure out how best to use it for ages, but can't seem to find the best way to source and use it. Technically you could buy it and dump it in DMSO but i believe there's more to it than that. You could also try taking daizdin to see if you can systemically produce it yourself but it's a long shot.

 

[bridgeburn]

Holy sh*t, guys. I just read something mindblowing to me. I have been researching equol for its DHT binding capacity. I was trying to figure out if we need s-equol, r-equol, or both to bind DHT (the answer is any type of equol will work).

Along the way, I came across this in a discussion of how equol (an isoflavone) acts through ER-Beta receptors in prostates:

Previous laboratories, including ours, have shown that isoflavones binding to ERβ in the prostate can down regulate the androgen receptor (AR) and thus decrease androgen hormone action.

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3032666/​

ER-beta binding in the prostate downregulates the androgen receptor!

This is incredible and adds an entirely new dimension to managing androgenic hair loss, or at least a new dimension to our understanding of how estrogen pathways work to help with that.

Reducing androgen receptors is one of the holy grails of managing hair loss, because in principle, if we can eliminate the receptors, androgens can no longer do as much direct harm. Your hair follicles become more androgen resistant.

It looks like stimulating ER-beta is the answer to making this happen.

Again, the best ER-beta agonists are likely genistein (available here), s-equol (working on a supplier through Alibaba at the moment), and estriol.

I've updated my summary post above with this additional mechanism of action to add this as another pathway.

It really appears ER-beta agonism provides all the estrogenic benefits we want for our hair/skin.

If only there was some test we could take to see if we are equol producers. cause if we are then we can increase it by eating lots of soy

 

[IdealForehead]

Oh yeah i knew this about s-equol because i did a lot of my own research. I've been trying to figure out how best to use it for ages, but can't seem to find the best way to source and use it. Technically you could buy it and dump it in DMSO but i believe there's more to it than that. You could also try taking daizdin to see if you can systemically produce it yourself but it's a long shot.

If only there was some test we could take to see if we are equol producers. cause if we are then we can increase it by eating lots of soy

Simplest solution is just to buy some s-equol and take it orally or apply it topically. I should be able to dissolve around 1% in my usual topical solution so that is the route I will go.

My current lead for supply is this:
https://kayichem.en.alibaba.com/search/product?SearchText=equol

I am in the process of ordering from them. They have quoted 100 grams for $270 USD including shipping. It's a large quantity and the price is a bit steep, but this is basically a few year's supply for me.

At 3 mL of 1% per day, that's 30 mg per day - this will last me almost 10 years for my own use if just used topically. Realistically, I'll just throw out what remains after 2 years or so and order again to maintain a fresh batch.

Certainly much cheaper than seti or other equally experimental agents.

If I decide to start ingesting it, I'd probably want to do around 20 mg a day to start since that's what they used in this study with the following justification:

The dose of S-equol and R-equol used in this study was chosen on the basis of the dose we anticipated would be sufficient to evoke clinical effects in future trials. It was also within the estimated physiologic range for adults that produce equol when consuming soy foods (10), given that the typical average intake of total soy isoflavones is ≈25–50 mg (56–59), of which ≈50% usually represents daidzin or daidzein—the precursors to equol. Dose-response relations were not examined in this study; however, with a single 20-mg dose, perhaps not surprisingly, none of the subjects reported any significant adverse events considered related to its administration, except for one female who reported a headache after taking both enantiomers but not the racemate. Chronic administration of a supplement containing S-(−)equol, produced by incubation of soy germ with the equol-producing bacterium Lactococcus garvieae, was reported to show acceptable tolerance in a group of postmenopausal Japanese women over the dose range 10–30 mg/d.

https://academic.oup.com/ajcn/article/90/4/1029/4596986
​

Even if I'm applying it topically and ingesting it, a 100 gram supply would still last me ages. So I'm trying to see if they'll sell me 50 grams. If not I'll just take the 100 grams.

I will get it tested for confirmation and purity as this is important and I have never bought from this retailer before.

The combo of genistein + s-equol could increase the potency of my usual topical quite a bit by adding multiple new mechanisms of action, so this has been a very worthwhile discussion.

 

[kiwipilu]

Simplest solution is just to buy some s-equol and take it orally or apply it topically. I should be able to dissolve around 1% in my usual topical solution so that is the route I will go.

My current lead for supply is this:
https://kayichem.en.alibaba.com/search/product?SearchText=equol

I am in the process of ordering from them. They have quoted 100 grams for $270 USD including shipping. It's a large quantity and the price is a bit steep, but this is basically a few year's supply for me.

At 3 mL of 1% per day, that's 30 mg per day - this will last me almost 10 years for my own use if just used topically. Realistically, I'll just throw out what remains after 2 years or so and order again to maintain a fresh batch.

Certainly much cheaper than seti or other equally experimental agents.

If I decide to start ingesting it, I'd probably want to do around 20 mg a day to start since that's what they used in this study with the following justification:

The dose of S-equol and R-equol used in this study was chosen on the basis of the dose we anticipated would be sufficient to evoke clinical effects in future trials. It was also within the estimated physiologic range for adults that produce equol when consuming soy foods (10), given that the typical average intake of total soy isoflavones is ≈25–50 mg (56–59), of which ≈50% usually represents daidzin or daidzein—the precursors to equol. Dose-response relations were not examined in this study; however, with a single 20-mg dose, perhaps not surprisingly, none of the subjects reported any significant adverse events considered related to its administration, except for one female who reported a headache after taking both enantiomers but not the racemate. Chronic administration of a supplement containing S-(−)equol, produced by incubation of soy germ with the equol-producing bacterium Lactococcus garvieae, was reported to show acceptable tolerance in a group of postmenopausal Japanese women over the dose range 10–30 mg/d.

https://academic.oup.com/ajcn/article/90/4/1029/4596986
​

Even if I'm applying it topically and ingesting it, a 100 gram supply would still last me ages. So I'm trying to see if they'll sell me 50 grams. If not I'll just take the 100 grams.

I will get it tested for confirmation and purity as this is important and I have never bought from this retailer before.

The combo of genistein + s-equol could increase the potency of my usual topical quite a bit by adding multiple new mechanisms of action, so this has been a very worthwhile discussion.

you know that if you buy pharma grade sequol from legit known website , price for 1mg varies from 10 to30bucks?
with your supplier price would be 0,0027 for 1mg. there must be something wrong don't you think?
now here is the problem: storage temperature: -20°C Freezer. what about the shipping?

 

[Georgie]

Simplest solution is just to buy some s-equol and take it orally or apply it topically. I should be able to dissolve around 1% in my usual topical solution so that is the route I will go.

My current lead for supply is this:
https://kayichem.en.alibaba.com/search/product?SearchText=equol

I am in the process of ordering from them. They have quoted 100 grams for $270 USD including shipping. It's a large quantity and the price is a bit steep, but this is basically a few year's supply for me.

At 3 mL of 1% per day, that's 30 mg per day - this will last me almost 10 years for my own use if just used topically. Realistically, I'll just throw out what remains after 2 years or so and order again to maintain a fresh batch.

Certainly much cheaper than seti or other equally experimental agents.

If I decide to start ingesting it, I'd probably want to do around 20 mg a day to start since that's what they used in this study with the following justification:

The dose of S-equol and R-equol used in this study was chosen on the basis of the dose we anticipated would be sufficient to evoke clinical effects in future trials. It was also within the estimated physiologic range for adults that produce equol when consuming soy foods (10), given that the typical average intake of total soy isoflavones is ≈25–50 mg (56–59), of which ≈50% usually represents daidzin or daidzein—the precursors to equol. Dose-response relations were not examined in this study; however, with a single 20-mg dose, perhaps not surprisingly, none of the subjects reported any significant adverse events considered related to its administration, except for one female who reported a headache after taking both enantiomers but not the racemate. Chronic administration of a supplement containing S-(−)equol, produced by incubation of soy germ with the equol-producing bacterium Lactococcus garvieae, was reported to show acceptable tolerance in a group of postmenopausal Japanese women over the dose range 10–30 mg/d.

https://academic.oup.com/ajcn/article/90/4/1029/4596986
​

Even if I'm applying it topically and ingesting it, a 100 gram supply would still last me ages. So I'm trying to see if they'll sell me 50 grams. If not I'll just take the 100 grams.

I will get it tested for confirmation and purity as this is important and I have never bought from this retailer before.

The combo of genistein + s-equol could increase the potency of my usual topical quite a bit by adding multiple new mechanisms of action, so this has been a very worthwhile discussion.

You need to use a liposomal vehicle.