3α-Hydroxysteroid dehydrogenase (3α-HSD) -- levonorgestrel?

[Ciprofloxacin]

Cipro, excessive daytime hypersomnolence has (had?) been a hallmark of my PSSD. Extremely flattened affect, too. In fact, one of the few only windows I got to feeling emotions pre-Donepezil was during a Clomiphene trial without an aromatase inhibitor (raising estrogen), but after a couple of weeks I lost my emotions again (probably through estrogen receptor mediated progesterone induction.)

I really do believe that at least Venlafaxine's main chemical castrating effect is mediated through progesterone via its 3-hydroxysteroid dehydrogenase upregulation, raising progesterone and allopregnanolone (positive GABA receptor modulator).

That aside, I read that Finasteride alters alpha-5 reductase expression/function, causing permanent:
1- Decreased testosterone -> DHT conversion.
2- Decreased progesterone metabolism.

It must be a really vile drug. But wouldn't that mean 5-alpha reductase induction would help me and those suffering from post finasteride syndrome?

Hypersomnia was the first side effect I noticed while using antidepressant. This made me think that this disease is not caused by a crash or a sudden change but instead a slow detrimantal effect.

This guy tried 2.5 mg fluoxetine to balance his allopregnanolone levels and became successful at improving some of his symptoms.

https://forum.propeciahelp.com/t/ssri-t ... ay/5053/26

I started taking a micro-dose of Prozac (fluoxetine) about 5 or 6 weeks ago, based on similar research I had seen. I take 2.5mg daily (normal dose is 20-40mg). So far, I’ve been happy with the results. My main issues were brain fog and anxiety. I have definitely noticed an improvement in both.

Many people on here stated that they felt ssri’s are a bad idea - most notably because of potential sexual dysfunction. 2.5mg has been shown to increase allopregnanolone significantly, but it’s not high enough to even touch serotonin. I haven’t noticed any sides, at all.

If you are experiencing brain fog symptoms several months after quitting, I would recommend trying low dose Prozac. I personally feel it can’t hurt anything, and in my case, I would say my mental issues have improved 50-75%.

Though, I don't suggest you to take 5a-reductase inhibitor. It may end up with normal Allo but low 5a-DHP, as your 3a-hsd will still be functioning over excessive but your 5a-reductase will synthesis less substance. Just a guess tho. I don't know what can be happen.

I've researched 3beta-HSD inhibitors a little, to find easily accessible ones, and there are 4 good ones: daidzein, genistein, biochanin A and formononetin (all found in soybeans).

If an issue is largely progestronic in nature, without the involvement of low testosterone, then a phytoestrogen like soybean should be okay.

https://www.ncbi.nlm.nih.gov/pubmed/7488041

Dietary estrogenic isoflavones are potent inhibitors of beta-hydroxysteroid dehydrogenase. The isoflavones daidzein, genistein, biochanin A and formononetin selectively inhibit the gamma-isozymes of mammalian alcohol dehydrogenase (ADH). Since gamma-ADH is the only ADH isoform that catalyzes 3 beta-hydroxysteroid oxidation, it was conjectured that these isoflavones might also inhibit other enzymes involved in 3 beta-hydroxysteroid metabolism.

I saw that study but never thought eating soybeans. I'm freaking out from the further estrogenic side effects like gynecomastia and also I couldn't find any soybean here.
My Estradiol (42) is in the range but it pretty close to the upper limit (20-47). I wonder if it because of the desensitized estrogen receptors as you said. Maybe lack of negative feedback causing that elevation.
And my progesterone is in the middle of the range (0.52).

[taarn]

Cipro, excessive daytime hypersomnolence has (had?) been a hallmark of my PSSD. Extremely flattened affect, too. In fact, one of the few only windows I got to feeling emotions pre-Donepezil was during a Clomiphene trial without an aromatase inhibitor (raising estrogen), but after a couple of weeks I lost my emotions again (probably through estrogen receptor mediated progesterone induction.)

I really do believe that at least Venlafaxine's main chemical castrating effect is mediated through progesterone via its 3-hydroxysteroid dehydrogenase upregulation, raising progesterone and allopregnanolone (positive GABA receptor modulator).

That aside, I read that Finasteride alters alpha-5 reductase expression/function, causing permanent:
1- Decreased testosterone -> DHT conversion.
2- Decreased progesterone metabolism.

It must be a really vile drug. But wouldn't that mean 5-alpha reductase induction would help me and those suffering from post finasteride syndrome?

Hypersomnia was the first side effect I noticed while using antidepressant. This made me think that this disease is not caused by a crash or a sudden change but instead a slow detrimantal effect.

This guy tried 2.5 mg fluoxetine to balance his allopregnanolone levels and became successful at improving some of his symptoms.

https://forum.propeciahelp.com/t/ssri-t ... ay/5053/26

I started taking a micro-dose of Prozac (fluoxetine) about 5 or 6 weeks ago, based on similar research I had seen. I take 2.5mg daily (normal dose is 20-40mg). So far, I’ve been happy with the results. My main issues were brain fog and anxiety. I have definitely noticed an improvement in both.

Many people on here stated that they felt ssri’s are a bad idea - most notably because of potential sexual dysfunction. 2.5mg has been shown to increase allopregnanolone significantly, but it’s not high enough to even touch serotonin. I haven’t noticed any sides, at all.

If you are experiencing brain fog symptoms several months after quitting, I would recommend trying low dose Prozac. I personally feel it can’t hurt anything, and in my case, I would say my mental issues have improved 50-75%.

Though, I don't suggest you to take 5a-reductase inhibitor. It may end up with normal Allo but low 5a-DHP, as your 3a-hsd will still be functioning over excessive but your 5a-reductase will synthesis less substance. Just a guess tho. I don't know what can be happen.

I've researched 3beta-HSD inhibitors a little, to find easily accessible ones, and there are 4 good ones: daidzein, genistein, biochanin A and formononetin (all found in soybeans).

If an issue is largely progestronic in nature, without the involvement of low testosterone, then a phytoestrogen like soybean should be okay.

https://www.ncbi.nlm.nih.gov/pubmed/7488041

Dietary estrogenic isoflavones are potent inhibitors of beta-hydroxysteroid dehydrogenase. The isoflavones daidzein, genistein, biochanin A and formononetin selectively inhibit the gamma-isozymes of mammalian alcohol dehydrogenase (ADH). Since gamma-ADH is the only ADH isoform that catalyzes 3 beta-hydroxysteroid oxidation, it was conjectured that these isoflavones might also inhibit other enzymes involved in 3 beta-hydroxysteroid metabolism.

I saw that study but never thought eating soybeans. I'm freaking out from the further estrogenic side effects like gynecomastia and also I couldn't find any soybean here.
My Estradiol (42) is in the range but it pretty close to the upper limit (20-47). I wonder if it because of the desensitized estrogen receptors as you said. Maybe lack of negative feedback causing that elevation.
And my progesterone is in the middle of the range (0.52).

My progesterone is also at the middle of the range and I have high estradiol. I also wonder what's the relationship between decreased SERT and elevated estradiol, as estradiol was shown to increase SERT expression. Could be a reaction to chronically decreased SERT?

Also, is that possible increased 3α-HSD expression is somewhat responsible for my low DHT levels? Mirtazapine was also shown to inrease 3α-HSD just like Venlafaxine.