Quote Originally Posted by JoeP26 View Post
Here's something interesting. Been reading a little into the hormonal and neurosteroidal pathways. So, as has been observed and experimented with here before, 5a-DHP is a 5-alpha reduced metabolite of progesterone. It is also a precursor to multiple neurosteroids in the brain that act on the GABA-a receptors and, eventually, creates neural androgens itself. But there's another metabolite in the similar line of sequence but on a different chain as 5a-DHP that comes from 17OHP (17-hydroxyprogesterone) called, 5α-Pregnan-17α-ol-3,20-dione. It can also be a metabolite of 5a-DHP itself as well, oddly enough, but not in as great of numbers as being a direct metabolite of 17OHP. Both 5a-DHP and 5a-Pregnan make 17OH-Allopregnenolone, Androsterone, Androstanediol, and then DHT. 5a-DHP is solely responsible for Allopregnenolone production as a metabolite while 5a-pregnan contributes to 17OH-Allopregnanolone production, thus increasing production of Androsterone, Androstanediol, and DHT.

Backdooor pathways of neurosteroids and sex hormones: PLOS Biology: The €œbackdoor pathway€ of androgen synthesis in human male sexual development

Info on 5a-Pregnan: 5alpha-Pregnane-3,20-dione | C21H32O2 - PubChem

However, all of these metabolites come from type 1 5-alpha reductase, whereas sufferers of finasteride damage should only have 5-alpha reductase type 2 (testosterone to DHT pathway) altered with long standing inhibited behavior, unless there is some unforeseen and unknown effect of Finasteride on type 1, directly or indirectly. Those who used Saw Palmetto would have an altered type 1 pathway (that pathway explained above via Progesterone to 5a-DHP and 17-OHP to 5α-Pregnan-17α-ol-3,20-dione). Those who used Dutasteride (like myself) would be suffering from both pathways (types 1 and 2) being altered.

It seems my specific case stems more so on the type 1 pathway, as my type 2 conversion (main androgenic pathway where most serum DHT occurs) of T to DHT appears to be intact, based on labs, but neuro androgens and precursor neurosteroids are lacking, based on the mountain of neuro symptoms (type 1) vs physical symptoms (type 2). I see the public is able to get their hands on 5α-Pregnan-17α-ol-3,20-dione without restriction from the following sources:

5alpha-Pregnan-21-ol-3,20-dione-2,2,4,4,17alpha,21,21-d7

5-ol-3,20-dione, CAS 570-59-2 | SCBT - Santa Cruz Biotechnology

(Note: this one is the most affordable so far) 5-ol-3,20-dione, CAS 570-59-2 | SCBT - Santa Cruz Biotechnology

I'm going to reach out to IdeaLabs and see if they can synthesize 5a-Pregnan as well. It in combination with 5a-DHP could be an effective treatment for stimulating 5-alpha reductase again as a result of inhibition pattern behavior in the brain caused by Saw Palmetto and Dutasteride. Maybe Finasteride as well.

For me, just as something interesting to note, anytime I use a GABA-a agonist, such as Ativan during the daytime and Ambien at nighttime, I feel loads more normal and myself. Calm throughout the day and able to sleep. When they wear off, then it's right back to PFS hell. This would obviously point more in the direction of a type 1 issue from the lack of GABA-a agonist metabolites. I'm thinking of experimenting with a cycle of pregnenolone 100mg x1 daily, 5a-DHP 5mg x2 daily (12hr), and 1mg 5a-pregnan x1 daily to start out. Thoughts?
Forgive the typical PHelp post, but If i'm not mistaken, I believe a young guy ended up committing suicide after purchasing and injecting himself with some sort of enzyme he believed he would fix him. I have read that it made his condition much worse. I'd be careful.