PSSD Research - YOUR INPUT IS NEEDED.

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guacamo
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PSSD Research - YOUR INPUT IS NEEDED.

Unread post by guacamo »

Hi, u can remember me from last thread about pssd etiology. I do research on my own reading every paper (full one, not the shortcut that is often time available for free) that i think might relate to pssd in one way or another. I stated that 5-HT2B receptor play important role in genesis of PSSD, but to be fair with you i have several other ideas alongside 5-HT2B. To rule them out or not your input is needed. If you took anything that made difference, good or bad on your PSSD symptom, please state which substance it was and what difference did it made. Be as specific and detailed as possible, describe every sensation you encountered on every pssd symptom - anhedonia, sexuality, emotionality, cognitive functioning, etc. Describe every change, not only those that relate to PSSD. Please contribute, it will help me a lot in my research.

Thank you,
Guacamo
finities infinities
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Re: PSSD Research - YOUR INPUT IS NEEDED.

Unread post by finities infinities »

I have mianserin induced PSSD and CBZ post acute withdrawal syndrome. Here you are.
Concise and specific:
- 5ht2a antagonist (antipsychotics, metergoline) when sharply administered reduces the symptoms of PSSD significantly, in the long run antipsychotic very aggravate the condition (eventually suffering from 5ht2a antagonist induced PSSD). Acute strong 5ht2 antagonist is able to remove virtually all symptoms of PSSD
- serotonin depletion: mimics my 5ht2 antagonism, seems even stronger. Reduction of all PSSD symptoms.
- 5ht1a agonist: even stronger effect, 100% PSSD reduction after the first dose, very strong crash.
- psilocybin: mimics the 5ht1a agonist with a slight dark shade of the 5ht2 agonist that reduces the 5ht1a euphoria and "sexy feeling". I would describe it as inferior buspirone. It has horrible withdrawal similar to buspirone.
5htp - like psilocybin but stronger on the 5ht2 side.
-Propranolol (weak 5ht1a + 5ht1b antagonist + beta antagonist). Acute exacerbates the symptoms very much, makes me into extreme dysphoria after just 1 dose, I noticed a slight improvement after withdrawal (a step in the right direction).
-Rimonabant- it greatly aggravates all my symptoms (carbamazepine withdrawal + PSSD, after withdrawal there is a strong reduction of all symptoms (one month after taking). The effect was ruined by lipoic acid, which made me take another dose of rimonabant.
- alpha 1 adrenergic blocker - increases the symptoms of carbamazepine PAWS (anhedonia, depersonalization) after discontinuation, the symptoms decrease, it does not affect PSSD.
- alpha 1 agonist and strong NRI: they mimic to a large extent carbamazepine and cause a similar withdrawal.
- drug with D2 antagonist: also worsen symptoms, seem to block the effect of 5ht2a antagonism on libido. That is, the D2 antagonist, if strong enough, blocks the 5ht2 antagonist effect.
- muscarinic agonist: improve state similar to 5ht1a agonist but weaker and less vivid.
- anticholinergic: mimic 5htp and serotonin enhancement, dellirium and torturing anxiety in higher dose.
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