Story of 5 Alpha

[5-alpha-victim]

The first time was in 2017. I took once 50 MG tablet for three days in a row. After this all within a three month period I tried it 2 more times and it did not work. I stopped trying at this point because I could not source more

Once I was able to source more from approximately mid 2019 to mid 2020 I tried it approximately 7 more times in dosages ranging from 10MG-200MG for 3-10 days at a time. It never worked. Never once did I feel anything close to how I felt when I was on that first trial in 2017. At the time I called it “RU surges” going through my brain. While on it. It was not intense but at the same time very noticeable and it felt good. I speculate that the reason it worked the first time was because how I felt on it the first time.

Also please be aware that I’m on several forums, have been at this for ten years and I’m not aware of one person who was permanently cured from it. But I am aware of a handful of near temporary recoveries. So please factor this into your potential risk/reward calculation. In my opinion I think it will take learning more about what exactly the RU did to give us these temporary recoveries and what other drugs or supplements one would need to take to not let these changes “become undone”. This will require lots of experimentation in my opinion

[surviveplz]

Interestingly Mifepristone leads to a Glucocorticoid rebound, because its a GR antagonist… If found a study documenting this. So after coming off, you might have gotten a surge of glucorticoids, and that made you feel better.

Ive been thinking about why it wasnt replicable, maybe you crashed your HPA axis with it?

[5-alpha-victim]

Good point about mifepristone potentially causing some type of cortisol rebound seeing that like you said it can block or at least partially block the GR receptors. I would have to go back to my notes so we could see what is known about the required mifepristone dosages needed to antagonize the GR receptors.

But based on my experiences through other experimentation I know that my sexual sides don’t respond to increasing total T, free T or LH past any standard labs reference range. I also know through other experimentation that increasing the amount of cortisol available to bind to the GR receptors makes me worse.

I did not run before during and after labs for any of my mifepristone experiments. So it’s impossible for me to know for sure how RU impacted my hormone levels. But based on everything I have tried and everything that I know about my own imbalance I can make the best educated guesses. I speculate that the mifepristone helped the first time because it did something at the receptor level tilting things in favor of estrogen in some way.

Additional evidence of this in my case is as follows:

1. I get worse when I inhibit estrogen even when my T is above any standard labs reference range

2. my plasma DHT is high

3. my saliva DHT likely showing free unbound levels of DHT is low. I speculate that this means my endocrine system is binding as much of my high plasma DHT as possibly in order to “protect the AR receptors”.

4. When I agonize my estrogen receptor alpha receptor (Era) with hops extract some of my sexual sides improve to a noticeable degree. When I discontinue the Hops extract I lose the improvements in sexual sides. The only sexual side this particular experiment helped is erections. No others

5. I’m flagged low in the metabolite 3b-Diol which is a potent estrogen receptor beta (Erb) agonist. I have not tried agonizing Erb yet because so far I have not been able to source a substance capable. In fact I’m trying to source 3b-diol so that I can try experimenting with it.

I speculate that in my case if I could fix what ever issue I have going on with the estrogen receptors (Era and Erb) that I would see some of my blood DHT start to unbind leading to an increase in saliva DHT and improvements or possible a complete cure of all my sexual sides. This is all speculation of course.

[Forwardsnotbackwards]

The only thing I through into the mix was I started using 10mg Amitriptyline about 6-7 weeks ago for pain .
I felt really good with it at first though and Amitriptyline is supposed to be a medicine for insomnia so I’m not sure that it specifically is that.
I think it’s so easy to start saying this has caused this , or this has triggered this by X, y , z though and sometimes we can’t be sure it could be a number of things .
I have stopped it for the time being though and I’m gonna switch to pregabalin for my pain instead .

[5-alpha-victim]

Interesting

So your insomnia started while already being in a PFS state after taking amitriptyline. It appears amitriptyline works in a similar way
as trazodone which is a drug people develop PFS like disorders from

Did you get PFS from fin?
Prior to taking amitriptyline did you have insomnia as part of your “regular PFS”
What have you had done for labs ?

I find it very suspicious that it’s common for us to have these issues from both 5AR inhibitors and drugs that impact neurotransmitters. In fact as previously mentioned I just gave my self “PFS type insomnia” from increasing several neurotransmitters.

“Amitriptyline is classified as a tricyclic antidepressant (TCA), with strong actions on the serotonin transporter(SERT)”

“Amitriptyline inhibits neuronal reuptake of serotonin and noradrenaline from the synapse in the central nervous system; this increases their availability in the synapse to cause neurotransmission on the post-synaptic neurone.[84] Amitriptyline is metabolised by cytochrome P450 enzymes in the liver to nortriptyline, which also acts as a noradrenaline reuptake inhibitor; this potentiates the antidepressant effects of amitriptyline”

Amitriptyline

Trazodone is a phenylpiperazine compound of the serotonin antagonist and reuptake inhibitor (SARI) class.[15][16]

Trazodone