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  • TDS Moderators: AlphaMethylPhenyl | paranoid android

Mental Health Coming off Invega/Xeplion (paliperidone) injections v. 10

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herbertadams said:
Am I correct to interpret that as THC works as a pgp substrate but CBD acts as an inhibitor?
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I don’t think CBD is an inhibitor. While I was going through the forums too many people recommended CBD for it to be not of use against invega.

THC does the same thing SJW does. We don’t know to what degree relative to SJW although.
 
herbertadams said:
Your probably targeting the wrong area. General public's interpretation of dopamine is largely incorrect and your thesis is likely based on bad information. These drugs do much more than mess with your dopamine, and perhaps after cessation if anything would increase dopamine sensitivity.

Other areas of more interest would likely be Alpha a adregenic system, histamine system, seretonin system perhaps particularly 5HT2A, choline, aswell as hormones.

Then the downstream effect of chemically imbalancing these for an extended period of time.
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That's a lot. Please tell me how I can fix this. Do I need a powerful agonist for each receptor?
 
herbertadams said:
I really don't have the background knowledge to interpret it
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Direct quote from one of the studies

“Furthermore, we demonstrated that THC exposure increased P-gp expression in various brain regions important to risperidone’s antipsychotic action.”

p-gp to my knowledge pushes some of the crap out of the blood brain barrier. Smoking weed will increase your brains ability to express or otherwise demonstrate pushing toxic crap like Invega out the brain
 
This microsphere technology of the Invega depot makes this drug last sooo much longer than they claim. Half lives only apply to oral meds. It doesn’t apply to the depot injections because it has to take into account an absorption rate. It’s more complicated and there isn’t any research or data
 
herbertadams said:
I would doubt that even if you found an agonist with higher affinity for the receptor sites than the antagonist that it would have the desired effect.
And even if it did dislodge the antagonist (which likely is no longer even in your blood or brain or bound to the receptor in your case) where would the antagonist go? Wouldn't it just bind back into the receptors when the agonist wears off?
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At least it would give me a moment of relief. Please tell there are drugs that help with this
 
rawbanana said:
This microsphere technology of the Invega depot makes this drug last sooo much longer than they claim. Half lives only apply to oral meds. It doesn’t apply to the depot injections because it has to take into account an absorption rate. It’s more complicated and there isn’t any research or data
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i'm absolutely fucked, 10 invega injections + 3 haldol. Yup 8 years minimum recovery for me
 
Abilify2mg said:
i'm absolutely fucked, 10 invega injections + 3 haldol. Yup 8 years minimum recovery for me
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I’m sorry man. I know paranoid android had a lot of abilify shots and recovered but that’s probably because the abilify shot is more soluble.
  • Abilify depot: Made with an extended-release suspension (polymer microspheres for Maintena; prodrug salts for Aristada). Absorption is still slow, but the depot is less “sticky” than Invega’s ester.
  • Invega depot: Paliperidone palmitate is a very insoluble ester, which dissolves extremely slowly in muscle tissue. That’s why its apparent half-life is so long (25–90+ days).
The Invega suspension is a lot more insoluble than the abilify one so yes. It takes a long long time.
 
rawbanana said:
I’m sorry man. I know paranoid android had a lot of abilify shots and recovered but that’s probably because the abilify shot is more soluble.
  • Abilify depot: Made with an extended-release suspension (polymer microspheres for Maintena; prodrug salts for Aristada). Absorption is still slow, but the depot is less “sticky” than Invega’s ester.
  • Invega depot: Paliperidone palmitate is a very insoluble ester, which dissolves extremely slowly in muscle tissue. That’s why its apparent half-life is so long (25–90+ days).
The Invega suspension is a lot more insoluble than the abilify one so yes. It takes a long long time.
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I had 3 months worth of invega injections and 18 plus months of abilify and recovered
 
Matthew01 said:
I keep wondering how it was possible for you to recover from all that. You sure you didn't take anything?
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I was on a fair few meds including clonazepam, zopiclone, morphine and latuda. The latuda was fucking awful though and gave me the worst akathisia. I think i would have recovered much much sooner if not for latuda. I think i would have been recovered in 4 months or so not a year if not for latuda because my attension span was the last thing to come back.

I also smoke alot of weed but i dont know if that helps everyone. Helps with my ptsd anyway
 
herbertadams said:
It probably wouldn't. Your receptors are almost certainly unbinded by now.

Some nootropics MIGHT help provide some relief from cognitive symptoms perhaps you could try piracetam, noopept or low dose phenibut.

Perhaps you could try choline supplementation. Perhaps dopamine choline balance is more important than dopamine agonists.
"Citicoline (CDP-choline) is a form of choline that has been studied as an add-on therapy with risperidone to target negative symptoms and improve cognitive function in patients with stable schizophrenia."

I really don't know.
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Id it's unbinded then why do I still feel like this. Aren't I supposed to pop back to normal?
 
paranoid android said:
I was on a fair few meds including clonazepam, zopiclone, morphine and latuda. The latuda was fucking awful though and gave me the worst akathisia. I think i would have recovered much much sooner if not for latuda. I think i would have been recovered in 4 months or so not a year if not for latuda because my attension span was the last thing to come back.

I also smoke alot of weed but i dont know if that helps everyone. Helps with my ptsd anyway
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When some people recover they leave. Why do you stay?
 
herbertadams said:
"P-glycoprotein (P-gp) inhibitors increase the concentration of P-gp substrate drugs by blocking their transport, while P-gp inducers decrease it by enhancing the transporter's activity.

P-gp inhibitors include clarithromycin and verapamil, and inducers include rifampicin and St John's wort.

P-gp substrates are drugs that are transported by the P-gp efflux pump, such as digoxin, cyclosporine, and tacrolimus. "

Cross referencing this to the study you posted earlier it seems to me that CBD inhibits p-pg transport and THC being a p-pg substrate would possibly compete with the paliperidone for removal. Don't have the background knowledge to interpret it though.
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What nootropic do u think enhances dopamine the most. Not allowed stimulants , what are good alternatives?
 
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