You have the right to decide for yourself, but I recommend against taking dangerous SSRI. It’s too risky for what it could potentially do to you.
I have a history with depression and took Bupropion (not an ssri) for a while to help alleviate it, but in retrospect I don’t think it played a major role in my battle against depression.
For me, the best thing I ever did was getting a coach, who helped me with correctly pacing out all the shit I wanted to do, practising self-care and caring for my environment, making sure I was able to get on top of things, resulting in huge reduction of negative factors and so much more headspace to focus on positive and new things.
I promise you that lifestyle changes do a lot more than medication ever could. Which sounds difficult, I know, but that’s why you don’t have to do it alone.
You can’t fix PFS until research finds what it is, but until then you can improve your life and it can certainly be done without SSRI.
I pee out high amounts of Allopregnanolone. With this being said I don’t think I’m producing low amounts of Allopregnanolone. In fact I think my body is getting rid of it for a reason. I believe that this is a strong indication that I don’t want to do anything that increases Allopregnanolone
Allopregnanolone is a positive Allosteric modulator of the GABAa receptors similar to benzodiazepines. Pregnenolone sulfate is a negative allosteric modulator of the GABAa receptors which I’m low in production of
I think my body is getting rid of Allopregnanolone due to being low in Pregnenolone sulfate
Interestingly the only thing that would help me before Fluoxetine were Benzodiazapines.
Solid affective feedback. Great words.
5htp made me permanently worse too
as for anxiety, id stay away from all SSRI’s
last year i couldnt look at screens without getting shocks all over and getting anxiety attacks until i went extremely low carb in diet and stayed in ketosis
obviously im not giving you medical advice here, just sharing my opinion
Sorry if I already asked. I have been posting on a lot of different threads and can’t remember
I googled fluoxetine and this is what I get:
“Fluoxetine sold under the brand names Prozac and Sarafem among others, is an [antidepressant] selective serotonin reuptake inhibitor”
I think someone else here also mentioned that fluoxetine increases Allopregnanolone…
When I googled it I see that it’s a selective serotonin reuptake inhibitors. An easy google search does not show this drug having any impact on Allopregnanolone.
Did you read anywhere that low dose of fluoxetine impacts Allopregnanolone? I’m just curious I would like to read the study or where ever you got this info
I recently ended up in severe relapse insomnia. Benzodiazepines provided instant relief for me on the insomnia but did not help me with any of the sexual sides.
As much will power as it takes because they do work for the insomnia I stopped taking the benzodiazepines because I’m worried that even though they help my insomnia temporarily while on them that maybe they are further down regulating the GABAa receptors if this is a part of my problem. I know I’m kinda rambling but I think there is something to my body peeing out high amounts of Allopregnanolone and both benzodiazepines and Allopregnanolone are doing the same thing to the GABAa receptors.
I almost want to find a way to temporarily inhibit Allopregnanolone and see what happened’s. But obviously I don’t want to do this experiment with a 5AR inhibitor.
Which specific sides of yours did benzodiazepines help ?
How did it make you worse and how much did you take?
You are correct that Fluoxetine / Prozac is primarily trademarked as an SSRI. However, there are studies which show that microdosing Fluoxetine have positive effects on neurosteroids and allopregnanlone. At the doses required to act as a Selective Brain Steroidgenic Stimulant, Fluoxetine does not act as an SSRI and has little to no effect on serotonin. I have linked some references below that I found via google search.
My symptoms were hypersensitivity to stimulation and stress. The best way to describe it was a severe sensation of feeling wired, fried and overstimulated in the brain whenever I engaged in anything stimulating or stressful. Some examples include using the computer, watching TV, socialising, etc. I couldn’t even look at a computer screen for more than 10 minutes without feeling severely wired. It was like my GABA was not working at all. It felt like the accelerator was stuck ON with no break is the best analogy I can describe. After starting the fluoxetine I have no issues when socialising and when using the computer, the change has been quite incredible actually. Prior the only thing that would work for me were benzodiazapines. I would much prefer to microdose Fluoxetine than take benzos. At the doses I plan to take Fluoxetine does not have an effect on serotonin.
low non-serotonergic doses of fluoxetine and congeners increase allopregnanolone levels as their primary mechanism of action
SSRIs act as selective brain steroidogenic stimulants (SBSSs) at low doses that are inactive on 5-HT reuptake
Treatment with fluoxetine and other SSRIs can increase the concentration of allopregnanolone in rat and mouse brains, a response which can be seen within an hour and at doses lower than those required to inhibit the re-uptake of serotonin. Low doses of SSRIs can also increase allopregnanolone in human brains.
Increase in the cerebrospinal fluid content of neurosteroids in patients with unipolar major depression who are receiving fluoxetine or fluvoxamine. We hypothesized that the increase of ALLO brain content induced by treatment with SSRIs could contribute to alleviating the anxiety.
Certain antidepressant drugs such as fluoxetine and fluvoxamine, which are generally thought to affect depression by acting as selective serotonin reuptake inhibitors (SSRIs), have also been found to normalize the levels of certain neurosteroids (which are frequently deficient in depressed patients) at doses that are inactive in affecting the reuptake.
i took 1 pill cant remember the amount
it made me worse because its an ar inhibitor just like finasteride and other SSRI’s
Alex50 posted studies explaining how SSRI’s such as fluoxetine increase allopregnanolone with out inhibiting the reuptake of serotonin at low doses. So knowing the dose of the SSRI is key. And then I think the other thing that should be considered is the question as to “if you want to increase allopregnanolone”. I say this because the Melchangi study showed low allopregnanolone in the CNS of PFS patients. Assuming spinal fluid is accurately reflecting the brain allopregnanolone levels in the PFS group in Melcangi’s study the PFS group has low Allopregnanolone levels in the brain. The thing is though “thisisarealbummer” claims to have had his spinal fluid tested which showed high amounts of allopregnanolone. Thisisarealbummer also said he has high amounts of allopregnanolone in urine. I have high amounts of allopregnanolone in the urine. So maybe there are different variants of PFS and that some have high allopregnanolone and some have low allopregnanolone while the symptoms of both are similar. This theory is further evidenced by the variety of different responses we get from different treatments. Kinda of like how some have low and some have high DHT production while in a “PFS like state”
im aware of that we have low allopregnanolone
i have my eyes kept on Zuranolone aka sage 217 which is basically synthetic allopregnanolone
but i wont be trying it first. its too much of a risk since allo isn’t the root problem for us
it might help some people A LOT
and it might help others A LOT
as for SSRI’s, you couldnt pay me to take them either in regular, high, or low doses
the risks associated are not worth anything for me. id rather bear the pain currently
Thisisarealbummer claims to have high allopregnanolone confirmed by spinal fluid and urine testing
so what? we will never know for sure
Never know what for sure ?
How many have high allopreg and how many people have low allopreg? I think it’s important that we find out if it’s possible
If my high allopreg in my urine is telling me that my body wants to get rid of allopreg I think this is huge. At the very minimum this probable means that I don’t want to increase allopreg.
I also have low preg sulfate which does the exact opposite to the GABAa receptors that allopreg does. So it’s providing me with a path to explore further and making me feel more comfortable about trying bacopa like realbummer did
A couple guys numbness got worse from bacopa. So maybe there is a correlation with those who have high allopreg feeling better on bacopa and those who have low allopreg getting worse on bacopa. If we could make this correlation this would be huge
Very interesting. Thank you for posting those studies. It’s good that low dose fluoxetine helped you with the hypersensitivity to stimulation. I definitely learned a lot from these studies.
So what dosage of fluoxetine are you on and how long have you been taking it? Did you get any other PFS sides other then hypersensitivity to stimulation and stress such as any of the sexual sides? and if so does the low dose fluoxetine help the other sides?
It would interesting to see if you are peeing out high or low amounts of Allopregnanolone. I don’t think I’m low in allopregnanolone. But I do believe the sleep issues I had during PFS and the relapse sleep issues I’m experiencing now are related to an issue with the GABAa receptors. I also think that because my bodies main inhibitory system is not working correctly the bodies main excitatory system (glutamate) gets thrown off as well. I wonder if the excitatory neurotransmitters such as glutamate, norepinephrine and Epinephrine are responsible for or involved in sexual function. On another forum I’m on it’s believed that issues with the norepinephrine receptors are responsible for poor orgasm in PFS.
All of our symptoms are different
Some of us overlap others don’t
Because the origins of the issue is at a gene and cellular level most likely according to the hypothesis of the foundation
I suspect this is occurring with me as well. It’s like my GABA / Glutamate system is not working properly.
I have been taking the Fluoxetine for 2 weeks. From my research its effects on neurosteroids are pretty much instant and that resembles my experience and relief of symptoms. I started at 10mg and am slowly dropping it to find the minimum effective dose required to achieve the effects I’m after. Today’s my first day at 2.5mg so hopefully my reduced sensitivity to stimulation & stress will remain.
From what I understand, the mechanisim of action is Fluoxetine stops Allopregnanalone from metabolising into downstream products. Therefore you actually need to have good levels of Allopregnanlone first for Fluoxetine to have this desired effect. For this reason I plan to experiment in a few weeks with Progesterone to raise Allopregnanlone further and see how I feel and see if this has any positive effect on my libido.
Finasteride destroyed my sex drive, gave me chronic fatigue, severe sensitivity to stimulation, hyperarousal, low stress tolerance, testicular atrophy.
I’m not claiming to have any answers. I am just experimenting on myself to see what works for my body, my situation and my symptoms, and want to share my thoughts & results.
@MatchaTea Please do not take them. Ever. There is a syndrome just like PFS from taking SSRIs.
It is much better to do psychotherapy on your own or with a therapist who is willing to accept the existence of PFS.
The most effective forms of psychotherapy are CBT, DBT, ACT, REBT. These types involve you doing WORK on your mind, thoughts, beliefs, negativity.
Just simply talking to a therapist is not enough if you want to end your depression.
Physical therapy would not be effective if you just sat down with the PT and talked about the problem with your back or knee. In the same way, psycho or mental health therapy must actually be effective–you actually have to do the exercises to get better.
I know from experience. I am alive because of good psychotherapy (done with trained therapists and on my own). I have had PIS/PFS/PCS since 1996. PM me.
I can assure you that our gaba neurotransmitters are out of wack.