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Antipsychotics and magic mushrooms

The effect will be dulled significantly, if not completely.

It depends what anti-psychotic you are taking.

I have experience with both Zyprexa and Risperdal.

Risperdal, for example has a huge affinity for 5-HT2a receptors and literally creates a 100% blockage. Zyprexa is about 80%, and this effect lasts for weeks after you last take it.

You won't get high, if you do it will be extremely dulled.

They also block dopamine receptors, though to a slightly lesser extent.

These drugs, in my experience, also block the effect of things like meth and heroin.

Their action of effect of blocking your receptors is even LONGER than the drug half life.

I overdosed on meth and LSD and took a combo of these drugs and was unable to get high again for about 10-14 days (you still feel some of the drug but it is extremely dulled).

For drugs like Zyprexa and Risperdal there are a few tricks to get them out of your system faster, like inducing enzyme CYP2D6 - which can be done by smoking cigarettes oddly... there is a study where people who smoked 12 cigs/day had like 35% less of the drug in their system due to CYP2D6 induction.

I did a lot of research on them, read a lot of case studies... if you have any more questions let me know
 
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inducing enzyme CYP2D6 - which can be done by smoking cigarettes oddly... there is a study where people who smoked 12 cigs/day had like 35% less of the drug in their system due to CYP2D6 induction.

Can you show me a study on that? And it wouldn't increase the effects much would it?

I'm on zuclopenthixol 300mg depot every 2 weeks.

What about niacin or if I take shrooms just about when it's time to take my next depot....cos then most will be out of my system
 
I googled it for a sec, and I can't really find the article I remember reading...

and my facts may be a little off...
but these are close enough


I don't know anything about zuclopenthixol, but based on what I just read on the wiki it's a 1st gen anti-psychotic, which are different than the ones I took (2nd gen).

It has the same general binding sites as the ones I took, but I'm guessing it has a lower affinity, most of the older ones did.

Wait... 300mg every 2 weeks? Are you taking the long lasting injections? That's kinda bad news if you're wanting to take some shrooms. The injections lasts many many weeks.... I was referring to taking the pills which last much shorter.

Niacin doesn't do shit, that's kinda myth and I used to take it thinking it would help me pass a drug test. It's just a damn vitamin.

I would have to do some research... assuming you're taking the injections you're going to have to stop for at least a month before taking shrooms....

and I don't want to encourage you stop taking meds you actually need...

I have bottles upon bottles of anti-psychotics that I stopped taking because I was misdiagnosed. Doc said I had "drug induced schizophrenia" when in reality I just had HPPD and I'm absolutely fine now....

I have a friend who has schizophrenia and he actually needs the meds. I can tell when he doesn't take them.
 
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From my understanding the older, 1st generation antipsychotics had a lower affinity to serotonin sites like 5-HT2a, which shrooms bind to, but had a higher affinity to dopamine sites - which leads to higher incidents of the horrible side effects like tardive dyskinesia.

Affinity = how strongly a drug binds to a certain receptor (in the case of antipsychotics, they are antagonists and BLOCK the receptor). Most drugs that get you high are agonists and "excite" the receptor.

Again, I am unfamiliar with the drug you are taking so I'd have to do my research... but chances are if you just don't take it for 2-3 weeks you'll be able to get high.
 
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From my understanding the older, 1st generation antipsychotics had a lower affinity to serotonin sites like 5-HT2a, which shrooms bind to, but had a higher affinity to dopamine sites - which leads to higher incidents of the horrible side effects like tardive dyskinesia.

Affinity = how strongly a drug binds to a certain receptor (in the case of antipsychotics, they are antagonists and BLOCK the receptor). Most drugs that get you are agonists and "excite" the receptor.

Again, I am unfamiliar with the drug you are taking so I'd have to do my research... but chances are if you just don't take it for 2-3 weeks you'll be able to get high.
What about l dopa? Doesn't that increase dopamine?
 
L Dopa is a precursor to dopamine and, technically yes, it can increase dopamine levels if you are lacking in this specific area... but it's not going to help you get high.

If you're taking antipsychotics which antagonize dopamine receptors this actually upregulates the amount of dopamine in your system because you're sites are blocked so your body naturally produces more dopamine... (or less? god it's been awhile since I studied this shit - I'm no doctor)

but this has nothing to do with mushrooms, which are serotonergic and act mainly at the 5-HT2a site.
 
L Dopa is a precursor to dopamine and, technically yes, it can increase dopamine levels if you are lacking in this specific area... but it's not going to help you get high.

If you're taking antipsychotics which antagonize dopamine receptors this actually upregulates the amount of dopamine in your system because you're sites are blocked so your body naturally produces more dopamine... (or less? god it's been awhile since I studied this shit - I'm no doctor)

but this has nothing to do with mushrooms, which are serotonergic and act mainly at the 5-HT2a site.
So what's my best bet? Smoke cigarettes? Lol
 
I'm not sure man... I don't think cigarettes work for eliminating that drug.

from google - "The metabolism of zuclopenthixol is mainly by sulphoxidation, side chain N-dealkylation and glucuronic acid conjugation. The metabolites are devoid of pharmacological activity. Primarily in the feces with approximately 10% in the urine. 20 hours (range 12-28 hours) for the tablet form, 19 days for the depot form. "

that means it's going to take 19 days to get half of it out of your system... which means it's going to be in your body for months.

The In vitro study suggests zuclopenthixol is metabolised primarily by CYP2D6 and CYP3A4.


This means that cigarettes MAY help eliminate it from your body... but you need to smoke a lot of cigarettes for a period of time, and you surely don't want to pick up that habit trust me.

There are also other CYPD2D6 and CYP3A4 inducers like prilosec OTC... but you need to be careful taking things like that, because they can fuck up your stomach if abused.

I don't know how this drug blocks shrooms, I only assume that it does, compared to other anti-psychotics.

It won't HURT you to take shrooms... worst case scenario you just don't feel anything.

You've exhausted my knowledge. I just know that eventually you will be able to get high again, but again, it's probably going to be weeks if not months on the long form of that drug.
 

I've been there man...

I had a whole stash of meth, heroin, LSD, MDMA... etc... and I couldn't get high off of it because I had taken 20mg zyprexa and 4mg risperdal to calm down after overdosing....

After 2 weeks I was fine.... but you're on the long version.

I was still able to get high off things like alcohol, GABAergic drugs like xanax, weed... etc... but anything that effected dopamine or serotonin was completely dulled.

You'll get through it man.
Good luck.
 
Found this....do you have any truth do this? You may already know but keep mucuna use to 3 times a week or so, and not long term as it can downregulate dopamine, making motivation,depression etc worse off in the end.
 
The In vitro study suggests zuclopenthixol is metabolised primarily by CYP2D6 and CYP3A4.


There are also other CYPD2D6 and CYP3A4 inducers like prilosec OTC... but you need to be careful taking things like that, because they can fuck up your stomach if abused.
i read up on tagamet and it's the same thing as prilosec. I've been taking these for ages! Everyday about two years ago and I started about a month ago again. Says liver failure...but I've been eating on a full stomach.

Anyway who cares I've read that they reduce the amount of antipsychotic in your blood....but would that only be on oral use? The pills? Can you tell me more about acid reducers and antipsychotics. Fuck I love learning and being a drug nerd.
 
Wiki does, of course!

The executive summary: Cimetidine (which is not the same as omeprazole/Prilosec at all, but has a similar effect on stomach acid). It is primarily a histamine H2 antagonist, acting to reduce acid production, but also happens to be a broad spectrum CYP enzyme inhibitor
Clinically significant drug interactions with the CYP1A2, CYP2C9, CYP2D6 and CYP3A4 enzymes are noted. That is, any drugs reliant on those enzymes to be deactivated will have their duration lengthened because it is not metabolized as fast.

Prodrugs that rely on same enzymes to become 'activated' (codeine -> morphine, DXM -> DXO) will not be converted to their active metabolites and hence have much decreased effects.
 
Wiki does, of course!

The executive summary: Cimetidine (which is not the same as omeprazole/Prilosec at all, but has a similar effect on stomach acid). It is primarily a histamine H2 antagonist, acting to reduce acid production, but also happens to be a broad spectrum CYP enzyme inhibitor
Clinically significant drug interactions with the CYP1A2, CYP2C9, CYP2D6 and CYP3A4 enzymes are noted. That is, any drugs reliant on those enzymes to be deactivated will have their duration lengthened because it is not metabolized as fast.

Prodrugs that rely on same enzymes to become 'activated' (codeine -> morphine, DXM -> DXO) will not be converted to their active metabolites and hence have much decreased effects.
So will prilosec reduce the antipsychotic in my blood or the tagamet or none at all?
 
Unfortunately it's actually more likely to prolong the presence of the antipsychotic, as I understand it.

Cimetidine is a CYP2D6/3A4 inhibitor, that is, it reduces the activity of said enzymes. That means they won't work as well as they ordinarily would to convert zuclopenthixol to its inactive metabolites.

You actually want a enzyme inducer instead. Unfortunately I don't think there's an easy choice OTC. And there are not too many well known 2D6 inducers either.
3A4 inducers: apalutamide (anti-androgen), phenytoin (anticonvulsant), barbiturates e.g. butalbital, phenobarbital, carbamazepine, oxcarbamazepine, topiramate (anticonvulsants), St. Johns Wort, modafinil, rifampicin (antibiotic), efavirenz (HIV inhibitor), pioglitazone (diabetes drug), glucocorticoids (steroid horomones), capsacin.
2D6 inducers: glutethimide (sedative/barbiturate analogue) rifampicin (antibiotic), haloperidol (antipsychotic).

Glutethimide and codeine actually were sold in combination on the street because the glutethimide would both act as a potentiating sedative, but also would convert much more than the usual 10% or so of the codeine dose into morphine. So-called "doors and fours", from the brand names of the two, Doriden and Tylenol 4.

Rifampicin (or its cousin rifabutin) seem the obvious choice, but it's considered very poor form to give antibiotics with no clear infection to resolve, and without finishing a whole course, otherwise the risk of promoting antibiotic resistance is there.
And if that's not eniugh rifamp has some, er, strange side effects:
Common side effects include nausea, vomiting, diarrhea, and loss of appetite. It often turns urine, sweat, and tears a red or orange color. Liver problems or allergic reactions may occur. .

I bet I'd look like one of the guys from those old Gatorade TV ads, dripping neon red sweat.... as my liver shut off... yeah, no.
 
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