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Esoteric Who here has used acetylcholinesterase inhibitors?

Esperighanto

Esperighanto

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I just wanted to ask if anybody here has ever had mystical experiences off of acetylcholinesterase inhibitors, specifically I've used sinicuichi and galantamine+CDP-Choline (I've been referring to it as GCC). Sinicuichi felt a lot more mystical and mushroom-y/ayahuasca-y in a very spiritual, natural way, eliciting very mushroom like visuals and euphoria, a deeply empathogenic emotional openness that was upbeat but somewhat neutral in a peculiar way. I could remember so many things I forgot I had even forgotten, it was very peculiar, and lasted about 4 hours after smoking 6 bowls of the shit, stems and all.

Galantamine felt more sharp, colorful, energetic, euphoric, and it reminded me much more of a highly unique variant of LSD if that makes sense. It has that sharpness of DOXs, 2C-B, and N-benzylated phenethylamines, but much like those aforementioned compounds the headspace was outweighed by the euphoric pins and needles, the code I was writing was clicking like figurative gears in a well oiled machine, I got an insane amount of work done as a software engineer at that time. I didn't expect this combo to cause a trip so I took it before work, foolishly as I now know in retrospect. The visuals at many points were akin to 25I-NBOMe, my boss' finger moving through the air as she traced the paths of database connections for a query I was writing looked like a goddamn psychedelic sparkler, and both of the AcEH inhibitors caused size warping effects visually with a huge intensity, as well as general color saturation. The closest I've ever got the body feeling with other drugs is eating a lot of 2C-B and Etizolam with ~60mg of MDA, but a little less rolly yet with that same velvet-y vibe to it.

I'm shocked that I haven't heard more people talk about experiences from these substances, ancient Media American people treated sinicuichi on par with psilocybin containing mushrooms, LSA containing seeds, and mescaline containing cacti.

The compounds in Sinicuichi are incredibly understudied, and I have no idea if any of these are safe, but between that and the galantamine paired with CDP-Choline, I'm just surprised nobody else has really gone in on these.

Edit: I cannot tell how a low dose of blue lotus and a moderate dose of b caapi tea leads to a trip either, does anybody here know about that yet? Apomorphine, nuciferine, harmine, harmaline and tetrahydroharmine seemed to be the five way chemical synergy as far as I'm aware but maybe there's more going on? Idk.
 
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I take a low dose of galantamine (2mg) daily to offset the anticholinergic side-effects of another med I take. What dosages of galantamine and CDP-choline do you use?
 
I think I took a single capsule of CDP-Choline as it was marketed for supplement use, and that day was 16mg of galantamine. I usually use 8 or 16 to potentiate lucid dreaming but I was heading into work to code so I figured it would help.
 
Esperighanto said:
I just wanted to ask if anybody here has ever had mystical experiences off of acetylcholinesterase inhibitors, specifically I've used sinicuichi and galantamine+CDP-Choline (I've been referring to it as GCC). Sinicuichi felt a lot more mystical and mushroom-y/ayahuasca-y in a very spiritual, natural way, eliciting very mushroom like visuals and euphoria, a deeply empathogenic emotional openness that was upbeat but somewhat neutral in a peculiar way. I could remember so many things I forgot I had even forgotten, it was very peculiar, and lasted about 4 hours after smoking 6 bowls of the shit, stems and all.

Galantamine felt more sharp, colorful, energetic, euphoric, and it reminded me much more of a highly unique variant of LSD if that makes sense. It has that sharpness of DOXs, 2C-B, and N-benzylated phenethylamines, but much like those aforementioned compounds the headspace was outweighed by the euphoric pins and needles, the code I was writing was clicking like figurative gears in a well oiled machine, I got an insane amount of work done as a software engineer at that time. I didn't expect this combo to cause a trip so I took it before work, foolishly as I now know in retrospect. The visuals at many points were akin to 25I-NBOMe, my boss' finger moving through the air as she traced the paths of database connections for a query I was writing looked like a goddamn psychedelic sparkler, and both of the AcEH inhibitors caused size warping effects visually with a huge intensity, as well as general color saturation. The closest I've ever got the body feeling with other drugs is eating a lot of 2C-B and Etizolam with ~60mg of MDA, but a little less rolly yet with that same velvet-y vibe to it.

I'm shocked that I haven't heard more people talk about experiences from these substances, ancient Media American people treated sinicuichi on par with psilocybin containing mushrooms, LSA containing seeds, and mescaline containing cacti.

The compounds in Sinicuichi are incredibly understudied, and I have no idea if any of these are safe, but between that and the galantamine paired with CDP-Choline, I'm just surprised nobody else has really gone in on these.

Edit: I cannot tell how a low dose of blue lotus and a moderate dose of b caapi tea leads to a trip either, does anybody here know about that yet? Apomorphine, nuciferine, harmine, harmaline and tetrahydroharmine seemed to be the five way chemical synergy as far as I'm aware but maybe there's more going on? Idk.
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I have been using Huperzine A regularly, almost daily, for over 5 years.
About 200ucg per day, I basically never redose.

It's just a slight cognitive boost but I hear that a large dose without a tolerance can be psychedelic/mystical.

It is also a NMDA antagonist so I think that will come into play at high dosages.
 
Phobos said:
I have been using Huperzine A regularly, almost daily, for over 5 years.
About 200ucg per day, I basically never redose.

It's just a slight cognitive boost but I hear that a large dose without a tolerance can be psychedelic/mystical.

It is also a NMDA antagonist so I think that will come into play at high dosages.
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I've taken Huperzine A up to some pretty reckless doses I don't want to mention out of the sake of harm reduction, but the feeling could be easily replicated with a fistful of galantamine tablets (25-30mg perhaps) and a bump or two of ketamine.
 
Esperighanto said:
I've taken Huperzine A up to some pretty reckless doses I don't want to mention out of the sake of harm reduction, but the feeling could be easily replicated with a fistful of galantamine tablets (25-30mg perhaps) and a bump or two of ketamine.
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There definitely is a potential for reaching lethal levels of acetylcholinesterase inhibition.
You would die of cardiac or respiratory arrest while your whole body cramps I guess?
 
Deliriants have a similar mechanism of action (antagonism instead of indirect agonism of acetylcholine receptors) and are notorious for their hallucinogenic activity.
...maybe there's a connection? It's a stretch... :doh:
 
Phobos said:
There definitely is a potential for reaching lethal levels of acetylcholinesterase inhibition.
You would die of cardiac or respiratory arrest while your whole body cramps I guess?
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For example, zyclon B and other nerve gases, act on the acetylcholine pathway...
for that reason, taking some strong AChe inhibitor like huperzine A can protect you somewhat against that shit as it competes with the terrible gases.
 
Huperzine A I've taken a couple of times at therapeutic doses. Nothing to remark on. Sinicuichi was unbelievably mild, and even more unbelievably bitter. Calea zac was far worse, and did even less.
 
Neuroborean said:
For example, zyclon B and other nerve gases, act on the acetylcholine
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That’s hydrogen cyanide gas. Sarin, tabun, soman (the G series), the V series, and a number of pesticides are all organophosphate/organothiophosphate acetylcholinesterase inhibitors.

However, they covalently bind the active site in the enzyme, so their action lasts until new enzymes are produced and trafficked to where they need to go. Even weak organophosphates like tri-ortho cresyl phosphate are associated with disturbing nerve damage such as Jake leg, and a pretty largely increased risk of neurodegenerative protein aggregation diseases from sublethal exposures.

I have always avoided AChE inhibitors due to fears of similar symptoms, but just as RIMAs seem to lack the hazards of covalent MAO inhibitors, competitive AChE inhibitors are probably quite a bit safer. This guess is also corroborated by the fact that these drugs have been used for a long enough time that extremely penetrant and severe side effects are unlikely.

Edit: I looked up a review, and it cites a study that looked at Alzheimer's patient’s acetylcholinesterase enzyme activity levels measured from their CSF. They had been treated with different types of acetylcholinesterase inhibitors, finding competitive inhibitors including galantamine resulted in increases in AChE enzyme activity, but a covalent inhibitor decreased the activity. This probably is a reason for the difference in toxicity between the two classes.

The review also cited a nature paper, which compared amyloid beta and phosphorylated tau in post morten brains of Alzheimer’s patients either treated with AChE inhibitors or not. Now it is known for sure that those proteins, and their respective aggregates are certainly somehow involved in the disease. It is hotly contested whether they are a causative factor in pathology or an example of the wreckage of the disease. Anyway, AChE inhibitors did not really change amyloid beta, but did slightly increase the amount of phospho-tau (from around 3 to 6 percent area of the brain). The discussion mentioned that this p-tau increase is seen in previous studies. They used cell lines and transgenic mice to measure the effects of AChE inhibitors and nicotinic agonists.

This change in phospho tau likely doesn’t result in an even noticeable difference in the disease progression. These drugs improve cognition enough that doctors only advocate taking a patient off them once the are too demented to benefit.
:End edit





Neuroborean said:
for that reason, taking some strong AChe inhibitor like huperzine A can protect you somewhat against that shit as it competes with the terrible gases.
Click to expand...

Can you point to something that recommends this? The only way it would make sense to me is if the huperzine A was blocking the binding of the nerve gas. The antidote is a drug called pralidoxime (or an analog of it), which binds to the affected receptors, kicking off the nerve gas molecules (though some like sarin, undergo a second chemical reaction, known as maturation, where the bound bits re-arrange, making it unable to be treated with oximes). This treatment briefly causes the same symptoms as nerve gas poisoning, but the pralidoxime hydrolyzes off fairly quickly. Due to the treatment being super unpleasant symptomatic drugs like atropine, which at least deals with the muscarinic toxidrome, and diazepam, which relaxes the muscles some.
 
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Skorpio said:
Can you point to something that recommends this? The only way it would make sense to me is if the huperzine A was blocking the binding of the nerve gas. The antidote is a drug called pralidoxime (or an analog of it), which binds to the affected receptors, kicking off the nerve gas molecules (though some like sarin, undergo a second chemical reaction, known as maturation, where the bound bits re-arrange, making it unable to be treated with oximes). This treatment briefly causes the same symptoms as nerve gas poisoning, but the pralidoxime hydrolyzes off fairly quickly. Due to the treatment being super unpleasant symptomatic drugs like atropine, which at least deals with the muscarinic toxidrome, and diazepam, which relaxes the muscles some.
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I've read several publications like this one,
makes sense to me honestly: https://pubmed.ncbi.nlm.nih.gov/8139389/
 
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