Can we try to use artificial allo?
Hej! Please allow me to step in, but I am also a vortioxetine user: do you believe long-term use can make it harder to recover overall? I been on it for only 2 months because according to psychiatrist it would help me get rid of the benzo control the panic, but that I managed instantenously with CBD, and now I am wondering whether I should leave this medication in order to find my new baseline before starting the goose-chase, or is it too dangerous dropping it too soon? Hard to say if my sleep recovery and partial cognitive gains I have had since crashing in April are a product of the medicine… would it be a problem coming back to it if I don’t like my new baseline?
We have studies where most of the pfs patients had borderline 0 levels of allo in their csf though
Hey man I’m not a doctor I can only offer my advice. I had to stop the vortioxetine because I felt it was making me more anxious/overly stimulated (perhaps as a result of increased glutamate activity) and I was feeling nauseous everyday. I switched over to fluoxetine and it’s been a week. I’m not quite sure how us with PFS will be affected my ssris long term, I just got to the point where I had to take it to function and it has completely changed my life for the better anxiety wise. If you’re able to get by with CBD then I say that’s probably safer although you should never stop medicine without talking to your doctor first
1 Like
Does it help with other symptoms asides from anxiety?
Good luck bro hope you get better
Not really everything else has been the same so far. I mentioned in other threads that after about a month of lexapro I started feeling somewhat better sexually but not recovered. So far the positives have outweighed the negatives with these meds. But my anxiety was so bad that I could not function at work or enjoy what life I still have with pfs
1 Like
How are you going now man? I too am running 2.5mg prozac. Seems to be working for me, but interested to hear your experience thus far since I have only started recently.
1 Like
I was dealing with extreme hypersenstivity to stimulation, I just felt wired, fried & overstimulated. It was like my GABA was not working at all. The only thing that helped previously were bendodiazapines. Interestingly, allopregnanlone acts on the GABAa receptor similarly to how benzodiazapines do. I would rather take low dose prozac than benzos… Anyway, triggers included being on the computer or socialising. For example, I would be on the computer late at night, get stuck in that wired overstimulated state, and it would lead to severe insomnia. I now have no issues being on the computer or socialising, and my sleep has been great. My testosterone also recently came back at 1091 ng/dl. I’ve been taking 2.5mg for just over 3 weeks now.
1 Like
What I think needs to be looked into further is the question “is this for a reason”?
I have highish Allopregnanolone in my urine. What’s in urine is what “the body does not want”…,
Obviously this means I’m still producing ample amount of Allopregnanolone. My theory is that maybe the body “does not want the Allopregnanolone” because the GABA receptors are messed up. Thisisarealbummer had high Allopregnanolone in his urine and in his CNS he claims. The neurosteriod study showed low Allopregnanolone in the CNS of PFS patients. So what I really want to know is if these PFS patients in that study had high or low Allopregnanolone in their urine.
We need to know if others are peeing out high amounts of Allopregnanolone. I’m talking to a functional health company about making the urine test easily accessible to as many people on this site who are interested in having theirs tested. I’ll know more this week.
Allopregnanolone is a positive allosteric modulator of the GABA receptors like benzodiazepines are. Pregnenolone sulfate is a negative allosteric modulator of the GABA receptors and I’m low in saliva pregnenolone sulfate. I’m doing massive amounts of research on this and in order for the GABA receptors to function properly they need even amounts of negative and positive allosteric modulation. Now if I’m low in pregnenolone sulfate production and I’m peeing out most of my Allopregnanolone then it makes sense to theorize that my GABA receptors are not able to function properly
If we can replicate my abnormal high urine Allopregnanolone and my abnormal low saliva pregnenolone sulfate in others we could send this to Melcangi because as of right now it sounds like he’s currently under the impression that PFS patients are simply not producing enough Allopregnanolone. And I’m not sure if this the case… It may be the case that it’s low in the CNS of PFS patients because we are peeing it all out so that it stays low in the CNS so that it does not hit the GABA receptors in the CNS
1 Like
I also agree melcangi are off target as a number of us have not responded well via increasing Allo. However I did once upon a time when I first had the symptom on set 2 decades ago overtime that fell away as Pfs became more pronounced.