Aromatase Induction? Feminine Penis Edition.

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Alright boyos and girls ( if there are any left).

Based on studies that @Georgie had provided in one of her threads. I'm making this thread for brainstorming and more theories.
We are only focusing on pattern of supressing DHT but our Lord and Savior Brotzu has a lotion containing S-equol which seems to be as Estrogen receptor Beta agonist.

" Estrogen receptor beta (ER-β), also known as NR3A2 (nuclear receptor subfamily 3, group A, member 2), is one of two main types of estrogen receptor, a nuclear receptor which is activated by the sex hormone estrogen.[5] In humans, ER-β is encoded by the ESR2 gene.[6]"

In layman retard terms, as mini estrogen. Which would explain it's hair stimulant properties.

Now, as studies indicate, women who have aromatase inhibited even with DHT inhibition, get their hair annihilated. Except frontal part where aromatase is more concetrated.


The idea is to find some aromatase agonist in order to increase the amount of aromatase enzyme in scalp tissue only. We could on top of that then add phytoestrogens and flavanoids to bind to estrogen scalp receptors while having 5ar2 inhibited by finasteride.

This would skew the ratio Estrogen-Androgen ( like yang and yin ) in favor of estrogen locally and cause hair growth.


Alcohol is aromatase agonist but is also a neurotoxin, so that goes out of water.



Studies:
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4252673/

https://academic.oup.com/annonc/article/24/6/1710/181282

http://www.androgeneticalopecia.com/hair-loss-biology/hair-loss-aromatase.shtml
 

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http://www.sciencedirect.com/science/article/pii/S0022202X15330396

Dexamethasone is our first suspect for overexpression of aromatase.
DHEA and Androstenedione are second bets.

1-s2.0-S0022202X15330396-gr6.gif
 

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ok boyo , so according to you SERM and AI might destroy hair and hairline ?

Yes. Even if you are on DHT inhibitiors. Theoretically yes.

Now I need some a**h** to counter my idea of using topical Dexamethasone with dermarolling. Any smart cookies?

The fact that adipose tissue( read fat) has aromatase enzyme and balding scalp has fat depletion points to aromatase deficiency in balding scalp.
 

bridgeburn

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Alright boyos and girls ( if there are any left).

Based on studies that @Georgie had provided in one of her threads. I'm making this thread for brainstorming and more theories.
We are only focusing on pattern of supressing DHT but our Lord and Savior Brotzu has a lotion containing S-equol which seems to be as Estrogen receptor Beta agonist.

" Estrogen receptor beta (ER-β), also known as NR3A2 (nuclear receptor subfamily 3, group A, member 2), is one of two main types of estrogen receptor, a nuclear receptor which is activated by the sex hormone estrogen.[5] In humans, ER-β is encoded by the ESR2 gene.[6]"

In layman retard terms, as mini estrogen. Which would explain it's hair stimulant properties.

Now, as studies indicate, women who have aromatase inhibited even with DHT inhibition, get their hair annihilated. Except frontal part where aromatase is more concetrated.


The idea is to find some aromatase agonist in order to increase the amount of aromatase enzyme in scalp tissue only. We could on top of that then add phytoestrogens and flavanoids to bind to estrogen scalp receptors while having 5ar2 inhibited by finasteride.

This would skew the ratio Estrogen-Androgen ( like yang and yin ) in favor of estrogen locally and cause hair growth.


Alcohol is aromatase agonist but is also a neurotoxin, so that goes out of water.



Studies:
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4252673/

https://academic.oup.com/annonc/article/24/6/1710/181282

http://www.androgeneticalopecia.com/hair-loss-biology/hair-loss-aromatase.shtml
How strong is equol? phtyoestrogens are usually pretty weak. better than nothing but im worried they can block the receptors and lessen the amount of real estrogen binding.
 

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It does? if this is true, it explains alot :)
https://jamanetwork.com/journals/jamadermatology/article-abstract/524193
How strong is equol? phtyoestrogens are usually pretty weak. better than nothing but im worried they can block the receptors and lessen the amount of real estrogen binding.
I have no idea. I am making a theory here. DHT is antagonist to Estrogen. But if we think about it, some people have results when inhibiting DHT. Which is inhibited around 50% in scalp and have SOME REGROWTH. But Estrogen is not even touched. I assume applying topical dutasteride/finasteride while increasing aromatase enzyme with skew the balance in favor of estrogen in scalp and induce regrowth.
 

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@ChemHead

(I've found you to be one of the most sensible and knowledgeable person on this platform, so tagging you)
 

baldingAF

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I’ve actually been looking into aromatase for a while.

Just started dexamethasone so nothing to report as of now.

The problem is a lot of phytoestrogens are oddly enough aromatase inhibitors as well

upload_2019-5-26_12-19-3.png


It’s a basic graph of how this works in our body but this coupled with an estrogen beta receptor agonist could help supposedly according to how some/most users transitioning seem to grow back a lot or all their hair.

So we need a estrogen receptor beta agonist that doesn’t inhibit synthesis of aromatase and hopefully no sides as well

and something other than or in addition to dexamethasone cause as a steroid it will kill skin if applied everyday.

Dexamethasone with
bucladesine increases aromatase.

What’s most promising is this theory has a lot of other coinciding in it
- TGF-B which is a byproduct of DHT production which will increase in puberty nulls expression of Cyp19 (aromatase)
- Increasing IGF1 will increase aromatase activity
- brown not white fat/adipose tissue has greater expression of aromatase and is reduced in balding scalp
- PGE2 is a positive regulator of aromatase
 

I'mme

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I’ve actually been looking into aromatase for a while.

Just started dexamethasone so nothing to report as of now.

The problem is a lot of phytoestrogens are oddly enough aromatase inhibitors as well

View attachment 119946

It’s a basic graph of how this works in our body but this coupled with an estrogen beta receptor agonist could help supposedly according to how some/most users transitioning seem to grow back a lot or all their hair.

So we need a estrogen receptor beta agonist that doesn’t inhibit synthesis of aromatase and hopefully no sides as well

and something other than or in addition to dexamethasone cause as a steroid it will kill skin if applied everyday.

Dexamethasone with
bucladesine increases aromatase.

What’s most promising is this theory has a lot of other coinciding in it
- TGF-B which is a byproduct of DHT production which will increase in puberty nulls expression of Cyp19 (aromatase)
- Increasing IGF1 will increase aromatase activity
- brown not white fat/adipose tissue has greater expression of aromatase and is reduced in balding scalp
- PGE2 is a positive regulator of aromatase
Thank you very much for chiming in.

Not only PGE2 but also agonists of EP1 and EP2 increase aromatase activity levels.

It's no surprise that there's been anecdotes where dexamethasone/diclofenac/indomethacin (or some other topical steroids) completely halt hair loss as well as regrew hair.
 

I'mme

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Retin-A also enhance PGE2 although no researches are there to prove it. That's why a person (Mr. Robot, if I remember correctly) has had good success with minoxidil+retinA
 

baldingAF

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Do you know if he used retinA and min in the same topical?

There are a few paradoxes in this theory I’ve found like how just in general estrogen increases as men age but typically older men lose hair.
TNFa and estrogen A receptor activation also increase aromatase but to an extent these have been seen to be bad for hair.

But I’ve attributed most of this to the body having an element within it be used for one function at one site of the body and a totally different function at a separate site. Which makes sense I suppose cause hair is it’s own organ more or less.

I haven’t been able to fit WNT into this theory through. I think estrogen Beta activation helps wnt but I’m not sure.

Cause I want to inhibit TGFb but one option I found also inhibits wnt signaling
 

I'mme

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So if we go by his theory, it is -

1. Dexa /diclofenac for selective cox 2 inhibition
2. Retin-A / diclofenac. Note: diclofenac completely inhibits prod of PGD2. While Retin-A is more of a regulator; however like minoxidil Retin-A increases PGE2.
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2673750/

3.CRTH2 - As he said, indomethacin is a weak antagonist. Ramatroban is an effective crth2 antagonist.

I guess someone need to try all these together. Who is ready to become Guinea pig? :)
 

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I'mme

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Do you know if he used retinA and min in the same topical?

There are a few paradoxes in this theory I’ve found like how just in general estrogen increases as men age but typically older men lose hair.
TNFa and estrogen A receptor activation also increase aromatase but to an extent these have been seen to be bad for hair.

But I’ve attributed most of this to the body having an element within it be used for one function at one site of the body and a totally different function at a separate site. Which makes sense I suppose cause hair is it’s own organ more or less.

I haven’t been able to fit WNT into this theory through. I think estrogen Beta activation helps wnt but I’m not sure.

Cause I want to inhibit TGFb but one option I found also inhibits wnt signaling
Yes, he mixed them after purchasing them separately. I've "Hairmax Forte solution" on my way tomorrow, which contain apart from 5% minoxidil., 0.025 Retin-A and 0.1% hydrocortisone.

Re estrogen, it is a very complex and confusing topic. If you've seen @bridgeburn success thread he allots good aprt of his success to use of estrogen and believes that estrogen causes hair regrowth. I don't have much knowledge on this topic though.
 

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Turn out TGF-beta-1 is pro fibrotic and Cox2 inhibitors inhibit tgfbeta1 as well. Gosh, can you see something here?
 

baldingAF

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For sure for tgfb. It’s dht Inducible and inhibits aromatase and is over expressed in balding scalp so it fits in with the fibrotic theory of hair loss.

I thought COX2 was too far upstream cause it also is the precursor for some positive genes/modulators for hair loss.

I think I’ll be adding a few more things to my cream from this list
 

I'mme

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For sure for tgfb. It’s dht Inducible and inhibits aromatase and is over expressed in balding scalp so it fits in with the fibrotic theory of hair loss.

I thought COX2 was too far upstream cause it also is the precursor for some positive genes/modulators for hair loss.

I think I’ll be adding a few more things to my cream from this list
Yes.

Please add Tretinoin (Retin-A) as well. From what I can understand, it is among the most overlooked as a supportive treatment in Androgenetic Alopecia. It does at least three things - 1) increases absorption of monix or anything use with it.
2)inhibits PTGS and therefore PDG2
3) is an anti fibrotic agent

Thank you! Please update how dexa works for you. I'll share my experience(s) re Hairmax forte solution as well as diclofenac.
 

I'mme

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For sure for tgfb. It’s dht Inducible and inhibits aromatase and is over expressed in balding scalp so it fits in with the fibrotic theory of hair loss.

I thought COX2 was too far upstream cause it also is the precursor for some positive genes/modulators for hair loss.

I think I’ll be adding a few more things to my cream from this list

BTW, I guess (not sure) it's COX1 which is precursor of some good modulators, not cox2
 
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