Mesolimbo wrote:So, short of Jaxx, it doesn't seem like anyone has tried a serotonergic that is not an SSRI/SNRI before trying SSRI reinstatement for the sake of experimentation.
Truskawa wrote:I got PSSD from six months on 50mg sertraline.
Will be trying fluoxetine soon. I will be reporting the results.
Can you try a MAO-A inhibitor or even a tricyclic before SSRI reinstatement?
Actually, I think I'll try this myself.
I’ve tried MDMA,LSD, and hordenine with PEA if that counts. Also 5HTP.
All give immediate resolving of most symptoms followed by a decrease in baseline (besides hordenine on it’s own)
Mesolimbo wrote:So, short of Jaxx, it doesn't seem like anyone has tried a serotonergic that is not an SSRI/SNRI before trying SSRI reinstatement for the sake of experimentation.
Truskawa wrote:I got PSSD from six months on 50mg sertraline.
Will be trying fluoxetine soon. I will be reporting the results.
Can you try a MAO-A inhibitor or even a tricyclic before SSRI reinstatement?
Actually, I think I'll try this myself.
I’ve tried MDMA,LSD, and hordenine with PEA if that counts. Also 5HTP.
All give immediate resolving of most symptoms followed by a decrease in baseline (besides hordenine on it’s own)
many say l-tryptophan makes them worse, have you tried it?
The idea here is as follows:
-- If SSRI reinstatement helped you, does other serotonergics (MAOIs, etc) make your symptoms better or worse?
---> If other serotonergics make you much worse, then SSRI helped you through non-serotonergic action(s), which play a big role in PSSD.
---> If other serotonergics make you much better, then SSRI helped you through serotonergic actions, which means your PSSD would be resolved (cured) upon serotonin receptor upregulation.
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I just read a paper about RG108 in that was stated in low dose it increased methylation in the promoter region of the Bdnf1 gene. In higher doses it decreased methylation.
As far as my knowledge goes, my take on the topic is that SSRIs either differ in effect based on dose, or taking them is completely non-deterministic when it comes to effects, or depends on a combination of a genetic predisposition and enviromental peculiarities that makes it at least pseudo-random. The well-known Citalopram paper also showed that some of the genes were overmethylated and some of them were undermethylated. So what decides in which direction which genes will be methylated? Some people get better after switching to another AD that may cause new changes in methylation of certain genes.
Great found taarn! And also lets don't forget that ssri at low doses stimulate the neurosteroidogenesis of allopregnanolone in the brain,as we can see from many studies from Graziano Pinna.
SSRIs act as selective brain steroidogenic stimulants (SBSSs) at low doses that are inactive on 5-HT reuptake
I have try low dose SSRI in past and it's worsen my PSSD even Ayurvedic Med Like Aswagandha, Macca worsen my PSSD.
So for me it' s not working.
I do believe PSSD is connected with emotions or feelings ...... cuz what i have notice everyone who is here they are emotionless and feeling less , And we are some where fucked up in our brains.
taarn wrote:I just read a paper about RG108 in that was stated in low dose it increased methylation in the promoter region of the Bdnf1 gene. In higher doses it decreased methylation.
As far as my knowledge goes, my take on the topic is that SSRIs either differ in effect based on dose, or taking them is completely non-deterministic when it comes to effects, or depends on a combination of a genetic predisposition and enviromental peculiarities that makes it at least pseudo-random. The well-known Citalopram paper also showed that some of the genes were overmethylated and some of them were undermethylated. So what decides in which direction which genes will be methylated? Some people get better after switching to another AD that may cause new changes in methylation of certain genes.
Dryed wrote:Great found taarn! And also lets don't forget that ssri at low doses stimulate the neurosteroidogenesis of allopregnanolone in the brain,as we can see from many studies from Graziano Pinna.
SSRIs act as selective brain steroidogenic stimulants (SBSSs) at low doses that are inactive on 5-HT reuptake
Exactly, guys. I'm looking deeper into actions other than their SERT inhibition. I want to completely rule out that improvements from SSRI reinstatement is mediated through the increase in serotonin. Unfortunately, there isn't a 'clean' SERT inhibitor other than SSRIs, so I'll end up using either a MAO-A inhibitor or a tricyclic antidepressant.
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In case of mine fluoxetine gave me pssd.After stopping fluoxetine for 10 months there was no sign of improvement of sexual dysfunction.Then anxiety nd depression returned nd I start taking fluvoxmine.I took it for 2 months starting from 50 mg per day to 200 mg a day.At first it gave me anhedonia and worsen pssd.After 1 week of stopage I felt brutal withdrawal effects.But after 2-3 weeks my pssd improved significantly to 70-80 percent nd was improving gradually.But the withdrawal effects nd anxiety was unbearable nd I hv started taking fluvoxamine again from last 2 months.I want to add that before I hv taken escitalopram , paroxetine but they had no effect on fluoxetine induced pssd.Hope it helps.Beware of emotional numbness of fluvoxamine..it can cause.
Last edited by Adweit saha on Fri Sep 13, 2019 8:52 am, edited 1 time in total.
you can put me on the very worse symptomes list, i give it a try again and ended very suicidal, i would deffently warn about repeating lowdose this stuff, it seems work our bodys reverse its "goal"....
I had every SERT blocking drug at the beginning causes an increase in libido and well-being which lasts about 3 weeks, then the action disappears and even begins to deepen sexual dysfunction and increase my overempathy, irritability, dysphoria and depression (like mianserin). Long therm SERT blocking drug work similar in me to serotonin antagonist- mianserin, metergoline etc. At the beginning, the opposite action gets insomnia stimulation and an increase in libido but temporary erectile disfunction and analgesic effect, then it disappears and libido along with it.
Summarizing:
First acute effect SERT blockade ( first 3 week)
-increase libido
-stimulation+insomnia
-analgesia effect+erectile disfunction
-decreased empathy and negative emotion states, increase emotional numbness ( good for me)
Effect similar to nicotine agonist.
Chronic effect:
-no erectile disfunction and no analgesia.
-no insomnia.
-increase negative emotion, depressive state, irritability, agression, empathy.
-lowered libido.
-feeling tired.
-slighty reduced my overconsciouness.
SERT blockade drug discontinuation/lowered doses:
-suicidal attack.
-crying attack.
-,,horror movie" feeling attack, very strong anxiety.
-hypersalivation.
-strong nausea and temples, eye headache ( like flu and migraine)
-hyperalgesia.
-very very strong empathy.
-libido changes from high to zero, very fast changes.
-incraase my overconsiouness, dissociation.