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Miscellaneous Most atypical psychedelic experiences?

That's shadow people...

mainly paranoia while in a super altered state.

Can happen on many different substances.

I've only experienced it on stimulant benders.
Yeah I know it can happen on lots of different chems.... shadow people on stims are more scary/alarming and peripheral for me though. This was different, somehow less malevolent
 
Last time I did a high-ish DXM dose (around 450 or 500mg) with around 100mg of benadryl as a potentiator and nausea killer with my friend, I kept getting a feeling that there was another person in the room, maybe like a ghost? I don't know. A few times during the trip I could've sworn they were talking to me or maybe I even started mumbling to them. Strange stuff, I don't remember too much of it.
Totally did the same combo with same doses lol. Coolest part was sitting on my bed and weed seeds rolled a few inches towards me and they turned into cute spiders. Benadryl can make people appear on its own at high doses. Even medium/ low doses can make you hear whispers.
 
5-MeO AMT is one of the few psychedelics I declined. I had such terrible experiences with 5MeO DMT & already knew that the stuff had killed people so even if it was free, I didn't want it,

Erowid even has a vault of 'fatalities/deaths' for the stuff and a HUGE one for 'health problems' related to it's use.

Go to Google Scholar and search for deaths related to it's use.

If I had to guess, I think it's because it has significant MAOI activity ALONE so mixing with an MAOI inhibitor isn't a smart move. It's orally active alone. It has also been demonstrated to produce hypertensive crisis.

It does appear to me that some people treat the consumption of known hazardous compounds like a danger sport. I'm very, very conservative about what I take. Too often our 'monkey logic' kicks in. Someone says 'I took it and was FINE' and others think 'oh, so it's safe'. No, one persons experience has no statistical value.

Arthur Conan Doyle (author of Sherlock Holmes) used to consume poisons to see how much he could survive! He did systematically work up the doses but his letters show that he did this many times and with some of the most toxic compounds known at the time.
I declined 5-MeO-aMT as well as DOB and 2C-P. TMA-2 is on the fence. I only sniffed 5-MeO-DMT but didn't like it until after the peak. The comeup was pure dysphoria and panic while I chugged water straight from the kitchen faucet.
 
5meo-amt is so much better than 5meo-dmt imo.. i guess if people dyed from it which i didn't know about when i took it maybe it's not for everyone... but if it were legal and i could get proper estimated doses, i'd definitely go for it again. my friend did a really bad job putting the sugar cubes together and each cube had dramatically different doses, so i ended up having a few different type trips.. i have to say that it has less body load than any of the lsd anologues that i've taken and i've done 1p-lsd, eth-lad, ald-52, and al lad... i probably got stronger visuals than any of the lsd anologues too maybe because of dosing so high. but i had a really good time with that drug and not a lot of body load or weird sensations, just a lot of visual hallucinations and if i took the time to close my eyes i'd get lost in the visuals and pretty much get ego loss. i took this before any types of lsd so maybe that's why it was so strong to me, but it lasts like 18 hours or more so that might make it not for some people, but i had really good results from the length of it, maybe it was a good time in my life too... 5meo dmt when taken orally for me just was like weirder feeling mushrooms that made me feel like i had the flu with out the stuffy nose when coming down from higher doses,

maybe my 5meo-amt responses were atypical, so i'd probably read some more about it before trying if anybody gets the chance, but i wouldn't rule it out. i hear of people taking stuff that i think is a lot worse on this site.
 
(R)-7,a-DMT is an entactogen rather than a psychedelic.

I don't know why their is a HUGE blind spot when it comes to all of the alpha alkyl tryptamines. They are ALL chiral and after I resolved AMT, I quickly discovered that in every single case, the action of the (S) enantiomer is responsible for all of the 5HT2a activity.

So even with 5-MeO AMT, why has nobody researched (S) 5-MeO AMT? It could be that the toxicity is due to the (R) enantiomer.
 
Intriguingly, the same study linked above shows that NBOMes are generally also more potent than LSD at 5-HT2A receptors, with 25I-NBOMe for instance having seven times higher affinity there than LSD, and LSD actually having similar activation efficacy to the NBOMes at 28%. However, despite this, a “standard dosage” of LSD is 100 micrograms and blotters of 25I-NBOMe would usually contain something like 1000 micrograms or more. I’m not saying the comparison is going to be exact - drug science is more complicated than that - but based on these numbers alone, one might be left with no choice but to point out that that “standard dosage” of 25I-NBOMe could be as much as like seventy times stronger than the “standard dosage” of LSD, given that it’s seven times more potent at the receptor with similar levels of activity there and yet you take ten times as much by weight. So, here’s an interesting question for anyone still reading this post at this point: are the NBOMes actually genuinely more active than other psychedelics like LSD visually and energetically and stuff like they’re often claimed to be, or do people simply take them at ridiculously, hilariously high dosages in comparison to other psychedelics, without even realizing what they’re doing? Also, is it really that crazy that people have died from dosages like 2-4 mg of 25I-NBOMe when that’s theoretically equivalent to like 140-280 doses of LSD?

I know this is a semi-old post already, and my reply to it totally off-topic, but I wanted to say that I really like your post. I always find your contributions valuable, well thought-out and insightful.

Anyway, I wanted to chime in that, as you already know, LSD is supposed to interact in a very specific way (compared to other psychedelics) with a specific loop in the 5Ht2A receptor, which augments it's "occupancy time" on the ligand binding site, which is thought to explain why it's so uniquely potent and long-lasting. So yeah, binding affinity may be lower than compared to NBOMes, but it activates the receptor for longer and more persistently, which might mean that in practice it is still more potent.

I like your hypothesis, though, that NBOMes were actually being taken in huge overdoses. I mean, specially for a drug that is so selective for a specific subtype of serotonin receptor, it makes sense for me to think that you could push the dose higher and higher, and some effects will be getting stronger without having a huge amount of general "psychedelia", like the sum overall effects can still manageable while only some of the effects are getting stronger. Makes sense then that people would be pushing the dose to absurd levels.

I bought a sizeable amount of 25i just a few weeks before coming across the first report of an NBOMe death I encountered. I was scared to take it for years, but I still kept the solution I had prepared stored away. Recently I diluted it 100x and then flushed it, it was the first time ever I did something like that. But I still stashed away a couple of doses for my personal drug museum lol.
 
Their are not NBOMe derivatives of tryptamines. It's still far too early to know if they are any safer but they MAY be more active orally. It's my understanding that people were snorting the PEA NBOMes and that seemed to be the most hazardous ROA.
 
Looking at IP3 mobilisation isn't a holistic measure of receptor activation because it neglects the contribution of beta arrestin biased signaling. IP3 signaling is downstream of Gq activation.

There's a recent paper (shoutout @Psychestim for showing me! ) that measures the signaling bias at the 5HT2a receptors, and 25I-NBOMe has higher efficacy than LSD at beta arrestin signaling.

They also make pure beta arrestin agonists, which are analogs of 25I where the NBOMe is expanded to a biphenyl or napthyl, and these do not produce a head twitch in rodents (but have antidepressant effects apparently).

A likely reason why 25I is so harmful is that it is quite a strong beta arrestin pathway agonist, but weaker at the Gq pathway, so an equipsychadelic dose will have much more beta arrestin signaling, which based on the pathology of 25I overdose, causes seizures somehow.

I didn't mean to imply that inositol phosphate provided the whole picture of 5-HT2A receptor agonist activity. This is essentially what I was getting at: if NBOMes are weaker psychedelics that require larger dosages, then that increases the potential for other undesirable effects that are unrelated to the direct presentation of those psychedelic effects, which people may be underestimating because they assume they're more potent at these receptors in those pathways than they actually are. Beta-arrestin could be part of that, but I couldn't speak to that. I'll read the paper some time (I'm coming off of a cold right now so I don't want to get into it right now but I've saved it because it's interesting).

I know this is a semi-old post already, and my reply to it totally off-topic, but I wanted to say that I really like your post. I always find your contributions valuable, well thought-out and insightful.

Anyway, I wanted to chime in that, as you already know, LSD is supposed to interact in a very specific way (compared to other psychedelics) with a specific loop in the 5Ht2A receptor, which augments it's "occupancy time" on the ligand binding site, which is thought to explain why it's so uniquely potent and long-lasting. So yeah, binding affinity may be lower than compared to NBOMes, but it activates the receptor for longer and more persistently, which might mean that in practice it is still more potent.

I like your hypothesis, though, that NBOMes were actually being taken in huge overdoses. I mean, specially for a drug that is so selective for a specific subtype of serotonin receptor, it makes sense for me to think that you could push the dose higher and higher, and some effects will be getting stronger without having a huge amount of general "psychedelia", like the sum overall effects can still manageable while only some of the effects are getting stronger. Makes sense then that people would be pushing the dose to absurd levels.

I bought a sizeable amount of 25i just a few weeks before coming across the first report of an NBOMe death I encountered. I was scared to take it for years, but I still kept the solution I had prepared stored away. Recently I diluted it 100x and then flushed it, it was the first time ever I did something like that. But I still stashed away a couple of doses for my personal drug museum lol.

Thanks, @Img_9999. :) I appreciate you saying that.

Yeah, I know that about LSD as well, and it may be playing some role in this as well. There are certainly a lot of different factors to consider, I'm just still suspicious about the whole thing. In the same vein, I feel like there's probably more to understanding why the NBOMes do what they do than just what we think we see at first glance.

I ended up trashing the 25I-NBOMe and 25C-NBOMe I had too. It's painful but it's for the best I think, lol. I find it's one of those things that gets easier. I recently trashed literally multiple lifetimes worth of some synthetic cannabinoids I had stashed up because I didn't feel like transporting them anymore (I moved recently) and also didn't feel safe in just giving them away to someone else. I've had so many drugs in my life, I barely even care anymore, but I'm incredibly lucky in that way. I've given away more drugs than I've ever taken at this point.

This is tangential, but that's part of why I just don't see the point in taking a risk with NBOMes too. It's been many years at this point since I'd already taken enough psychedelics that I gave up my old dreams of "trying them all". It's a fun dream when you're young and new to drugs but there is no "trying them all" if you actually understand drug science nor any need to if you ask me. I've gotten more than I needed or than most people at least who live in this time period ever will.

I try not to shove it in people's faces, though. But I still think people are probably more likely to be better off just using different psychedelic in general.
 
Well, about 2 months ago me and my friend bought some LSD from a dealer we hadn't bought from before. The guy was really nice and he offered to give me trip killers for free "just in case" (which in hindsight makes it seem like he knew that it wasn't LSD). But I declined since I had some benzos collecting dust anyways. They were supposed to be 150ug tabs, a very comfortable dose for both of us. When we ate the tabs my friend said he tasted something a tiny bit off, a mild bitter taste, but I didn't notice anything myself so we chalked it up to him being paranoid. About 45 minutes in we definitely were feeling *something*, it was comparable to an LSD come-up, and we know perfectly well how much experiences can vary, so we were both fully calm, and we decide to smoke our first joint, we had about a gram of bud. After the joint things started getting weird, maybe 1h 15min in we came to the conclusion that it propably wasn't LSD, the visuals/external hallucinations were hazy and blurry, pretty easy to ignore and just plain weird. But internal hallucinations on the other hand were insane, completely absurd shit. But it was all fine and well we were enjoying the novelty of the experience of not knowing what's gonna happen, trying a new drug accidentally, very exciting. About 4 hours in, the weed started wearing off, and now we were both experiening whatever it was on its own, very different than LSD, but someone who hasn't done LSD before would propably believe it. A very weird and heavy body high combined with a mental state I could only compare to the few hours after a MDMA peak, before the come down, except it was way more confusing and psychedelic. We smoked more and just kinda paced around the house talking, mostly wondering what the fuck was in the tabs. I can't really tell when the effects started wearing off since we smoked more, but I feel like the peak lasted about 3 hours, and the come down maybe 6, so about 10 hours in total.

So in conclusion, bought fake LSD with a friend, but still had fun, still don't know what the fuck it was. I've never done any "rare" psychedelics, only psilocybin and LSD and whatever this was, so I'm completely clueless. If anyone has any guesses as to what it could've been please do tell, propably just some random research chem. It reminded me a bit of ketamine also now that I think about it.
 
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