R Andro + 4 Andro

[MungYarlon]

Sure - I'll give you my take and try to make it short.

First off androsterone is a neurosteroid. We know for a fact that finasteride lowers androsterone levels in the body and brain. Androsterone is also a GABA-A agonist just like allopregnanolone is. This means that if the brain is under some sort of stress androsterone can act as a GABA-A helper to agonize or stimulate that receptor (allopregnanolone does the same). Allopregnanolone itself isn't that important it just happens to the neurosteroid that takes the biggest hit from fin but plenty of other hormones are negatively impacted as well. All of these GABA-A agonist were being inhibited with fin which causes the GABA-A receptor to upregulate along with androgen receptor in the brain to upregulate.

What makes androsterone special though is it seems to replace a lot of the other key areas that finasteride negatively impacted - specifically in the brain and body. Androsterone increases the brain levels of androsterone, epiandrosterone, 5α-dihydrotestosterone, and androstandiol.

So we know that finasteride blocked GABA, lowered DHT in the entire body including the brain, raises serum estrogen etc.

Androsterone does the total opposite of what fin does in all areas meaning instead of blocking GABA you are agonizing it now (causing it to downregulate), instead of lowering DHT you are increasing it in the body and brain (causing the AR to downregulate), instead of raising estrogen you are lowering it etc. So whether its a receptor issue or something else you are pushing yourself in the right direction.

To pinpoint exactly which area is the root cause I don't know but in laymans terms androsterone is the best to cover all areas that fin screwed up.

References:


Psychomotor and rewarding properties of the neurosteroids dehydroepiandrosterone sulphate and androsterone: effects on monoamine and steroid metabolism - PubMed
Plasma androsterone/epiandrosterone sulfates as markers of 5 alpha-reductase activity: effect of finasteride in normal men - PubMed
PayPerView: Effects of Subchronic Finasteride Treatment and Withdrawal on Neuroactive Steroid Levels and Their Receptors in the Male Rat Brain - Karger Publishers

Ok that makes sense, so as well as boosting positive allosteric modulators of GABA, it sorts out hormones in the brain.

I was also wondering what you thought of the theory that epigenetic changes were happening in PFS patients. Surely if that were the case, the androsterone wouldn't have much of an impact on androgen receptors, not would an increase in hormones?

[Cdsnuts]

Ok that makes sense, so as well as boosting positive allosteric modulators of GABA, it sorts out hormones in the brain.

I was also wondering what you thought of the theory that epigenetic changes were happening in PFS patients. Surely if that were the case, the androsterone wouldn't have much of an impact on androgen receptors, not would an increase in hormones?

Epigenetic changes can be manipulated by the environment they're in as well. Give the body the correct inputs and (environment) live a specific way (protocol) and these epigenetic changes will take place for the better.

[TubZy]

Ok that makes sense, so as well as boosting positive allosteric modulators of GABA, it sorts out hormones in the brain.

I was also wondering what you thought of the theory that epigenetic changes were happening in PFS patients. Surely if that were the case, the androsterone wouldn't have much of an impact on androgen receptors, not would an increase in hormones?

Haven't seen any conclusive evidence on it just some speculation around some epigenetic "markers" and PFS but the studies showed nothing conclusive. It was just speculation.

I personally don't think any permanent epigenetic changes occur from finasteride since so many people have recovered and similar symptoms occur from other substances (saw palmetto, deca, minoxidil, accutane, SSRIs etc.)

To CD's point as well, you can influence gene expression by your diet anyways. Fasting and eating certain foods can trigger certain gene expressions (i.e. broccoli).