This Paper Has Some Interesting Data About Estrogen In Androgenetic Alopecia

[TNTS]

I have low testosterone levels and three years ago i was on clomid only therapy for almost 18 months.
In this period my testo goes up to 750 from 190 and dht as estradiol was above upper limits.
My hair was in the best shape ever, no shedding and after three months on clomid starting to looks thicker also.

Anyway, i had some libido issues so i had to stop clomid and i am on HCG shots for almost a year now.
I keep my testo level at 700-750 and dht as estradiol still are above normal levels.
The thing is that my hair are very thin now and i have lost a lot of ground. More sebum also...

Clomid is an estrogen agonist in some tissues and estrogen antagonist in some others.
Never manage to find clear info regarding estrogen receptors (alpha-beta) but i am still looking.

Estrogen receptors is not innocents and surely has something to do with Androgenetic Alopecia, but it's not easy to found out the exactly mechanism as it's not the same with the females...

 

[Swiss_Tampons]

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

Are you referring to this? https://www.ncbi.nlm.nih.gov/pubmed/2591441

 

[growssj3]

Sorry if its a stupid question.

So higher Estrogenlevels are good? Doesnt finasteride raise testo and estrgo by about 10%?

Whats with an estrogen dominance?

 

[tylerduren]

Are you referring to this? https://www.ncbi.nlm.nih.gov/pubmed/2591441

Yeh and found another study showing that it affected it quite drastically

 

[mr_robot]

Regarding S-Equol, if you look at the brotzu patent and accept that the amount of S-Equol is correct it looks like the dose is only 0.2mg per 1ml daily dose.

I've been extracting S-Equol from four crushed Equelle tablets for nearly a year now at 1.42mg (assuming 100% extraction) and recently upped the dosage to what would be 3.57mg a day topically. I can't say that it has had a magical effect athough I can't even be certain that my extraction S-Equol is working.

 

[Gone]

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.

AR Antagonists such as CB have proven to be effective, on their own, in clinical trials. Whether this method affects Estrogen receptor alpha or beta in the same way that estrogen seems to modulate AR remains to be confirmed. Regardless, they do work, no S-equol needed. It's only needed if it provides better results or is safer, and at this point it's hard to make a 1:1 comparison of the two.

 

[whatevr]

AR Antagonists such as CB have proven to be effective, on their own, in clinical trials. Whether this method affects Estrogen receptor alpha or beta in the same way that estrogen seems to modulate AR remains to be confirmed. Regardless, they do work, no S-equol needed. It's only needed if it provides better results or is safer, and at this point it's hard to make a 1:1 comparison of the two.

Clinical trials also suggest a very low incidence of side effects for drugs like Finasteride and Dutasteride, yet here we are, the forums are full of them.

I'm asking where are the real world results with people using drugs like RU? I understand that CB is expensive and no one has trialed it properly, but I have yet to see a single long term success story of someone maintaining using just RU which is also a stronger AR antagonist than CB will be.

Finasteride with its reduction of total and scalp DHT has far more of a proven track record simply because by removing DHT it prevents hair interruption through both the AR and the ER. S-Equol could potentially allow us to do this topically.

 

[Gone]

My original post is pretty much just bringing together information regarding ER-beta's distribution in the pilosebacious unit, I didn't and still don't have strong claims to make about whether upping ER-b activity or inhibiting AR is more effective, I think they both could be effective if ER-B indeed affects AR prevalence.

The fact remains that regular hair growth is uninterrupted in children who have barely any 17-b-estradiol in their blood (https://www.ncbi.nlm.nih.gov/m/pubmed/16995570/?i=2&from=/15379966/related) which would result in almost no ER-b activation. I honestly don't know why ER-b is so prevalent in hair follicle structures, it could be vestigial for all I know.

But it really seems like good hair is not dependent on estrogen, the hormone balance only becomes relevant when you have estrogen competing with androgens in hormone sensitive hair cells.

I would consider CB's results to be legitimate despite the drug not being available for personal testing, and I've read lots of good things about RUsers, although it's true it's hard to find people using it in isolation and reporting consistently. I think Swoop did or still does cycle using RU in isolation, maybe ask him about this.