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

[Ollie]

The studies I have seen are pretty clear on the sexual role of estrogen in men:

* Estrogen in the penis will cause erectile dysfunction. There is no real replacement for DHT as an erectile function stimulant, followed by testosterone.

* Estrogen in the brain will increase libido

So this is a Goldilocks problem, where you do not want too little, and you do not want too much. Too little and you will lose libido and interest in sex. Too much and you will get erectile dysfunction.

Too high Estrogen will kill your libido as well - not increase.

 

[persistentone]

Too high Estrogen will kill your libido as well - not increase.

Do you have any studies showing that? The only studies I have found say high estrogen will lower erection quality, not libido.

 

[Ollie]

Do you have any studies showing that? The only studies I have found say high estrogen will lower erection quality, not libido.

No studies unfortunately only anecdotal evidence. finasteride soars my E through the roof however if i use some Adex to control it then my libido comes back quite significantly. Also ive spoken to a fair few users here who have trialed topical E and that killed their libido as well. However if you tank your E then you'll actually get similar sides (low libido, ED etc..) .

 

[persistentone]

No studies unfortunately only anecdotal evidence. finasteride soars my E through the roof however if i use some Adex to control it then my libido comes back quite significantly. Also ive spoken to a fair few users here who have trialed topical E and that killed their libido as well. However if you tank your E then you'll actually get similar sides (low libido, ED etc..) .

I just wonder how many people make valid distinctions between erectile function and libido. Many might mistakenly call erectile function a libido problem, which it is not.

Your test with Adex seems valid and that is interesting evidence. An alternate hypothesis to explain that might be that the finasteride is blocking the DHT receptors in the penis, which allows more estrogen to bind into their receptor and creates erectile function problems. But how these things all interplay is very complex.

 

[DavidsDome]

So far 4,5 months doing topical oestrogel.
The gyno development disappeared when I lowered the dose
Im very slowly building it up. Its difficult to say exactly how much the dose is now.
Im guessing its around 0.25mg daily now.
I did a blood check and my estradiol blood level was within the normal range, suggesting it doesnt go systemic at this dose.
So far no visible effect.
Im gonna raise the dose since my blood results were good. Hoping to at least notice something around the 6 month mark.
Doing temples only.
Side info: 6 months of topical Estriol didnt have any result on me.

 

[DavidsDome]

https://onlinelibrary.wiley.com/doi/pdf/10.1111/j.1600-0625.2005.00377.x
page 86

The ER-a and ER-b proteins bind 17b-estradiol (E2) with nearly equal affinity and exhibit a very similar binding profile for a large number of natural and synthetic ligands (63). Isoflavone phytoestrogens daidzein and genistein are wellknown ER-b-selective compounds (64). They bind and activate human ER-a and ER-b with an up to 100-fold stronger activation of ER-b

Not sure if this contributes but thought it was worth sharing...

 

[xaragedom]

https://onlinelibrary.wiley.com/doi/pdf/10.1111/j.1600-0625.2005.00377.x
page 86

The ER-a and ER-b proteins bind 17b-estradiol (E2) with nearly equal affinity and exhibit a very similar binding profile for a large number of natural and synthetic ligands (63). Isoflavone phytoestrogens daidzein and genistein are wellknown ER-b-selective compounds (64). They bind and activate human ER-a and ER-b with an up to 100-fold stronger activation of ER-b

Not sure if this contributes but thought it was worth sharing...

I used topical genistein and it give me no change in hairloss/hair growth and genistein also is inhibitor for EGFR(which is unknown if its good or bad for hair). S-equol is almost similar to genistein in terms of prefering ER-beta over ER-alpha and S-equol activate ER-beta with same affinity(or even stronger) as genistein but without inhibition of some tyrosine kinase (like EGFR). S-equol is used in trinov/brotzu lotion and that product doesnt provide almost any regrowth in peoples who use it(maybe it's use not enough of S-equol??). Even using estradiol on scalp is giving no effect

 

[whatevr]

This is a fool's errand. Basically, any estrogen strong enough to do something against Androgenetic Alopecia (when used in a sufficient quantity) will likely cause strong systemic side effects. If it doesn't cause side effects (like estriol) then it won't really do anything for hair anyway.

However, there are different types of plant estrogens with different affinities for the two types of estrogen receptors - alpha and beta. Alpha seems useless or harmful for hair and greatly promotes gyno. Beta will not promote gyno or even mildly reduce it, but in my experience can still tank androgens by negative feedback on gonadotropin in the brain.

More promising than any estrogen was my trial of racemic equol - binds to DHT and reasonable agonist of estrogen receptor when used in 30-60 mg daily dose, which is a huge dose, but again, gyno (I'm very prone).

S-Equol would probably be even more promising (only estrogen-beta agonist) but again, you need doses in the range of 20-30 mg per day or higher, and not that lame amount that was in Brotzu (something like 0.2 mg per day). I would still expect some sides at that dose as well though.

 

[whatevr]

S-equol is used in trinov/brotzu lotion and that product doesnt provide almost any regrowth

The dosage in that product was at least an order of magnitude too low to do anything meaningful. I would argue that 30 mg of S-equol daily in a topical form would definitely give some results, but it would be insanely expensive, so no wonder Brotzu used a pathetic dose.

 

[pegasus2]

This is an interesting old patent for estriol. I can't understand why no researcher out there has bothered to even try a potent and selective ERβ agonist for Androgenetic Alopecia. If it wasn't around $100,000 for a year's supply of erteberel I would try it. As far as estriol goes, they say 7-14mg/day directly applied to the scalp is the useful limit. Up to 70mg can be used, but they say it's not economical. This is why people don't get results with estriol, they are only using around 1mg. I didn't get any results from it except when I used gobs of it twice a day. Then I believe it made a big difference. I thought it was slow, but looking at the people who used estradiol I think it was just as fast-acting as some of those results when I used it in large doses. You have to use an AA with it though for maximum results.

"Active ingredient" refers to estriol:

it is possible to treat the target organ in question, namely, the scalp, topically with sufficient and extremely high concentrations of the hormone, actually relatively great quantities thereof, without the risk of unwanted systemic side elfects upon resorption of the active material from the sites of topical application.

A pathologically-increased hair shedding can be decreased even down to normal values, according to the impression of the patient, and according to hair samples collected over a lengthy time span.

(B) The status of the hair roots by microscopic evaluation in some cases can be shown to have improved as to the percentage of actively growing (anagen) roots in relation to dormant (telogen) roots in an extracted hair tuft.

Estradiol, the most studied human estrogen, has about three hundred to five hundred times greater estrogenic effect than its metabolic end product, estriol, when studied by the commonly employed Allen-Doisy test which measures vaginal cornification in spayed mice or rats. Estriol also has a very weak eifect on the endometrium (inner layer of the uterus). Therefore, until recently, this hormone has been considered mainly as an unimportant by-product of estradiol metabolism

The finding of the present applicant that the active ingredient of the invention exerts local action upon the scalp and hair but no measurable systemic effect was unpredictable and contra-indicated by the results of earlier workers

Topical application of the active ingredient of this invention has definitely produced observable, even measurable, effects on the hair

Whatever the reason or scientific explanation may be, topical application of the active ingredient and compositions of the present invention has produced remarkably good elfects in female patients with diffuse hairfall or thinning out of the female pattern alopecia type (alopecia androgenetica)
In men with male pattern alopecia, results have been much less spectacular, but still sufficiently successful to warrant continuation of the treatment over a period of several years.

As already noted, the various side effects which commonly appear in patients treated with estrogens did not appear when using the active ingredient and compositions of the invention in the manner of the present invention. It thus appears that one can actually speak of a separated hormonal activity in the sense that the active ingredient is active at the site of topical application for purposes of the present invention, but produces, as far as has been observed to date, no systemic effects on the internal sexual organs upon resorption.

in persons with a strong hereditary trend to abnormal sensitivity or reactivity of the hair follicles in certain areas of the scalp to androgen, particularly to testosterone, must be expected to respond much more slightly if at all to any treatment, and such is the observed fact when employing the treatment and compositions of the present invention. Thus, only in men with a weaker trend to baldness can any observable reduction in hairfall and/or the resulting thinning out of the hair be expected. In women, where the trend toward baldness because of the female hormone balance is much less, the observable effect is much greater and occurs more frequently.

The activity of estrogen in evoking a marked increase in the activity of several amino acid-activating enzymes, which are involved in the biosynthesis of protein, and thus also with hair growth phenomenon, may be a factor.

The active ingredient of the invention, as previously stated, is estriol. The compositions of the invention involve the active ingredient in a pharmaceutically and cosmetically acceptable solvent, which comprises at least mainly if not entirely volatile components, such as lower alcohols, preferably ethyl or isopropyl alcohol or a mixture thereof, preferably diluted with water. In such composition, the water is a less volatile, but still slowly evaporating component.

The concentration of the active ingredient in the solution or suspension should be at least 0.02 percent, is preferably at least 0.05 percent, and has a maximum useful upper limit of approximately 0.2 percent. Higher percentages up to about 1 percent may be used if desired but are not economically attractive. Striking results have been obtained at about 0.1 percent or slightly above, but treatment effects can sometimes be increased by increasing the concentration of the active ingredient in the compositions of the invention.

METHOD OF TREATING The treatment of the invention is carried out by applying the active ingredient in any acceptable form, advantageously in a pharmaceutically and cosmetically acceptable topical solvent, and preferably in the form of a composition according to the present invention, to the scalp subject to the undesirable condition, preferably once a day. The recommended period of treatment is at least six months before a preliminary assessment of the results can be made. If no obvious hairfall is present, most male patients will require from eight to twelve months of treatment or even more before satisfactory observable results are obtained. The minimum period of treatment before favorable results have been positively effected has been approximately twelve weeks.

In any event, the recommended treatment is application to the parts of the hair and/or scalp having the undesirable condition, preferably at least once daily, and the recommended period of treatment before definite assessment of positive effect is at least six months. For

maximum efiicacy a year or more is usually recommended, particularly for men.

Example 1 The composition most commonly used in the clinical experiments reported herein is designated Composition 0L and has the following formula:

Estriol 0.1 gram. Benzalkonium chloride (antibacterial surface-active agent) 0.05 gram.

Ethyl alcohol 39.0 grams.

Corrigentia odor As desired.

Distilled water To make 100ml.

of solution.

Use of such a composition has been found entirely satisfactory. In many cases, application of approximately 50 ml. of the composition per week

the solubility of estriol in m1. of solvent is as follows: In 95% ethanol 1.2%

If an effective treatment can be given, it will, obviously, have to continue for several months, before the poorly functioning follicles will be restored to a degree, where thicker hairs with a close-to-normal life span can again be produced, and the telogen count (if increased) can reverse towards normal values. Therefore, when the possible efiicacy of a new treatment is studied, no definite evaluation can be undertaken until the lapse of a considerable time span.
Even patients who ultimately obtained an obvious improvement could sometimes see little effect in the first three or four months.

Summary of clinical results: Upon a recent survey of the clinical material, 122. patients had been treated and observed for a sufficiently long period (6 months or more) to allow estimation of the results.

In some cases, the total assessment was made only on the basis of such subjective estimation by the patient, his or her family and the hairdresser. In most cases, to this information was added a direct observation of the amount of hair in samples taken at regular intervals in connection with shampooing procedures, comparisons of photographs taken before and after the treatment, and different- Females Males Total Obviously very good, well verified improvement. 16 2 18 Good, but less obvious and less impressive improvement 21 22 43 Clearly positive 37 24 61 +1 Improvement observed, but not sufficiently clear or well documented to be classed as may get improved grade 12 7 19 after longer observation 7 Improvement so far questionable, but some of these cases may be classed as after longer observation 5 9 14 Negative or nearly negative result, or possibly slight improvement 13 28 Doubtful or negative 5 On this basis, the percentage improved was 50%.

Side effects: A boy of 1'8 observed swelling and slight tenderness of the mamillary area after three weeks treatment, disappearing again two weeks after stopping the treatment. When this had happened twice, further experiments were abstained from.

With this exception, during the trial period of five years no systemic side eflfects have been observed, that could reasonably be considered to have been caused by the treatment.

In men, the results have necessarily been less spectacular. However, a continuing hairfall has often decreased and a recently started thinning out of the hair has stopped in some cases. In several patients, the process appears to proceed more slowly under treatment. Also in On the basis, the percentage improved was 61/132: 46.21%.

 

[Sanchez1234]

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.

This is an interesting old patent for estriol. I can't understand why no researcher out there has bothered to even try a potent and selective ERβ agonist for Androgenetic Alopecia. If it wasn't around $100,000 for a year's supply of erteberel I would try it. As far as estriol goes, they say 7-14mg/day directly applied to the scalp is the useful limit. Up to 70mg can be used, but they say it's not economical. This is why people don't get results with estriol, they are only using around 1mg. I didn't get any results from it except when I used gobs of it twice a day. Then I believe it made a big difference. I thought it was slow, but looking at the people who used estradiol I think it was just as fast-acting as some of those results when I used it in large doses. You have to use an AA with it though for maximum results.

"Active ingredient" refers to estriol:

So to summarize. The theory is that because estriol is the only natural estrogen with a greater ER-beta (good for hair) affinity than ER-alpha (bad for hair) we should trial that instead of estradiol.

If we get the right dose we get the same benefits as estradiol without all the bad sides from ER-alpha which Estradiol give.

So couple of questions;

1. This is not new information. A lot of sh*t has been trialed on HairLossTalk.com. Really nobody tried high dose of estriol? Why not? Anybody knows highest dose that has been tested?

2. Anybody got information how much more potent 1mg of estradiol is compared to 1mg of estriol?

 

[John Difool]

Wikipedia: Given by subcutaneous injection in mice, estradiol is about 10-fold more potent than estrone and about 100-fold more potent than estriol. In most tissues, such as the liver and endometrium, estriol is weakly estrogenic, but in the vaginal epithelium, it produces pronounced and full estrogenic responses.

 

[Sanchez1234]

Wikipedia: Given by subcutaneous injection in mice, estradiol is about 10-fold more potent than estrone and about 100-fold more potent than estriol. In most tissues, such as the liver and endometrium, estriol is weakly estrogenic, but in the vaginal epithelium, it produces pronounced and full estrogenic responses.

And in hair?

So estradiol is 100 times more potent and people here say that 1mg estriol doesnt work... well that explains a lot

 

[pegasus2]

So to summarize. The theory is that because estriol is the only natural estrogen with a greater ER-beta (good for hair) affinity than ER-alpha (bad for hair) we should trial that instead of estradiol.

If we get the right dose we get the same benefits as estradiol without all the bad sides from ER-alpha which Estradiol give.

So couple of questions;

1. This is not new information. A lot of sh*t has been trialed on HairLossTalk.com. Really nobody tried high dose of estriol? Why not? Anybody knows highest dose that has been tested?

2. Anybody got information how much more potent 1mg of estradiol is compared to 1mg of estriol?

As far as I'm aware nobody has ever tried it. The patent for it states up to 70mg/day. I think this is the most recent data on general potency.

"The estrogenic potency of β-Estradiol is 12 times that of estrone and 80 times that of estriol."

And in hair?

So estradiol is 100 times more potent and people here say that 1mg estriol doesnt work... well that explains a lot

You'll find that a lot of the things people have tried on here "didn't work" because the dosage was far too low, or they didn't dissolve it properly, or it was degraded. I think a lot of useful things have gotten a bad name around here because of improper experimentation. Darolutamide is another, people using 0.1mg when the oral dose is 1200mg/day, and then saying it doesn't work. Or PTD-DBM where they used micrograms when the trial used 6mg.

Then you have people using one thing by itself, and expecting it to regrow their hair in three months. It doesn't work like that. Even minoxidil won't give you a noticeable difference in 3 months if you're not also on finasteride. You aren't going to replace the big 3, you are trying to complement them. Start out with the big 3, and see what it does for you. Then start adding stuff to see what improves your results.

 

[DavidsDome]

So estradiol is 100 times more potent and people here say that 1mg estriol doesnt work... well that explains a lot

Problem is that the pharmacy only has 1mg/g creme or gel.
So it's pretty impossible to get a high dose out of this, unless if you are applying the creme every hour of the bloody day haha
If one would source bulk powder from a supplier, creating your own high dosed lotion would be possible of course.

 

[John Difool]

Problem is that the pharmacy only has 1mg/g creme or gel.
So it's pretty impossible to get a high dose out of this, unless if you are applying the creme every hour of the bloody day haha
If one would source bulk powder from a supplier, creating your own high dosed lotion would be possible of course.

That's the way to go financially and conveniently. If we know that dosage is 70-100mg daily then get 10g and carry your bottle around to apply frequently (e.g. each time you go pee which could be often enough if you are on Spironolactone

 

[Sanchez1234]

That's the way to go financially and conveniently. If we know that dosage is 70-100mg daily then get 10g and carry your bottle around to apply frequently (e.g. each time you go pee which could be often enough if you are on Spironolactone

Thinks is any use to apply once a day with the short half life? I would be applying 4ml x 12mg/ml...
Still a lot more than 1mg/ml some trialed.

 

[whatevr]

You'll find that a lot of the things people have tried on here "didn't work" because the dosage was far too low, or they didn't dissolve it properly, or it was degraded.

Brotzu lotion.

Dump 30+ mg of S-Equol on your head every day and tell me it doesn't work.

(Brotzu had ~0.3 mg per daily dose IIRC)

 

[pegasus2]

https://www.tocris.com/products/g-15_3678

This could be big. I've been doing some research on GPER, and I am leaning strongly towards it being a negative regulator of hair growth. Spironolactone can block the effects of GPER, which could be one reason why estradiol works better when paired with spironolactone. Estriol is a GPER antagonist, so there's another reason it could be better than estradiol at the right dose. Conversely, Equol is a GPER agonist. Interest in GPER is starting to pick up, so hopefully we will get a study on its actions in hair follicles before too long.

eplerenone and spironolactone partially inhibit G1-mediated responses, suggesting that both can serve as partial antagonists of GPR30.

Edit: Eplerenone is a more potent inhibitor of aldosterone than spironolactone, and has been shown to stimulate human hair regrowth ex-vivo

RU + estriol + eplerenone may be the right combination for people looking for a simple solution without side effects. Risk of gyno with eplerenone is only .5% compared with 10% for spironolactone.

 

[inmyhead]

https://www.tocris.com/products/g-15_3678

This could be big. I've been doing some research on GPER, and I am leaning strongly towards it being a negative regulator of hair growth. Spironolactone can block the effects of GPER, which could be one reason why estradiol works better when paired with spironolactone. Estriol is a GPER antagonist, so there's another reason it could be better than estradiol at the right dose. Conversely, Equol is a GPER agonist. Interest in GPER is starting to pick up, so hopefully we will get a study on its actions in hair follicles before too long.



Edit: Eplerenone is a more potent inhibitor of aldosterone than spironolactone, and has been shown to stimulate human hair regrowth ex-vivo

RU + estriol + eplerenone may be the right combination for people looking for a simple solution without side effects. Risk of gyno with eplerenone is only .5% compared with 10% for spironolactone.

Is it really such a simple solution? I'm not sure how you would even obtain correct does of estriol and eplerenone