• Psychedelic Drugs Welcome Guest
    View threads about
    Posting RulesBluelight Rules
    PD's Best Threads Index
    Social ThreadSupport Bluelight
    Psychedelic Beginner's FAQ
  • PD Moderators: Esperighanto | JackARoe |

Miscellaneous What Psychedelics Do You All Wish Were More Accessible?

We also know that the NBOH series is less potent than the NBOMe series, so that alone qualifies it for being potentially safer.

Without knowing what pharmacological action is causing the NBOMes (and very presumably other NBXX) to be toxic, this statement cannot be made with any confidence. In fact, if the toxicity arises due to interaction with some other receptor type, then NBOHs could be more toxic than NBOMes after accounting for the dosage requirement.

It is unfortunate that so little is known about the mechanisms in the various psychedelic-caused deaths that have occurred. There may not be a simple answer in so far as certain people have certain weaknesses that they may succumb to when the body is under certain kinds of high stress. Fortunately most commonly available psychedelics appear to be quite safe in mostly healthy people (who thus far have been far more likely to use them than people with serious health problems), especially if dosages are not pushed very high. Other than the few NOMBes with wide distribution, the psychedelic that comes to my mind that killed a few people even when taken at fairly reasonable doses was 2C-T-7. People have died from things like 2C-E, 2C-P, AMT, 5-Meo-DIPT, but these involved either very high doses or combination with known contradicated things in light of the MAOI activity of AMT at least. Some would argue that the 2C-T-7 deaths were complicated by use of MDMA in combo. However, MDMA is frequently used with many other psychedelics without serious problems and one of the 2C-T-7 deaths did not involve MDMA.
 
Idk about that. I can't see where making that moiety attached to the n-benzene ring a hydroxy instead of a methoxy group would somehow make it more potent and/or more dangerous. That doesn't really make sense.
I haven't looked at the postulated in silico binding, so this is just some baseless speculation - just like your comment is - but 2,4,6 is a different substitution pattern than 2,4,5. For instance for the Ganeshas it is postulated that the additional 3-alkyl moiety forces the 2-methoxy into steric clash with the a-methyl group, hence why their potency may be similar in amphetamine and phenethylamine. Similarly, it wouldn't be impossible that the additional 6-methoxy group of the 246-NBx compounds makes the difference and forces the NBOMe into an unfavourable binding mode, whereas the NBOH is less affected. But who knows how credible this statement is, especially all in the analytical vacuum that is clandestine pharmacology. Also I did not say anything about potency at all, I talked about toxicity, but I think it was truly said that the NBOH is indeed more potent too. It was also said it was seemingly "tryptaminergic" in terms of its qualitative effects.

Also I'm not sure where I put any comment about the general toxicity of NBOMe/NBOH. After being traumatised by a (misguided) 25E-NBOH at a much too high first dose (I was let astray by dosing information on blotter, but had pure material and 1.2 mg were much too high!), I'm actually very skeptical of that class. Even if it turned out that some NBOx are perfectly safe (for everyone or for people lacking certain genes etc which may be involved in their toxicity), they are heavily stigmatised by now and that baggage alone is enough to drag a trip down. I'm aware that the misguided dosing was my mistake, but due to the traumatising nature I had problems even with psychedelics afterwards that I believe to be very safe. Fortunately I can now trip again and this trauma will now at most haunt me for a couple minutes, not the entire trip. But I was really worried I may have to give up psychedelics and aside from a small experiment with 25D-NBOH (which I quickly realised I'm too biased to bioassay properly) decided to give up on that class, as attractive as some of their properties may seem like. To this day, 25E-NBOH was the most euphoric and colourful psychedelic I have ever taken, but also the scariest one.

That being said, I'd love to know the exact mechanisms of toxicity with these compounds. I don't think it is impossible to use them as lead compounds for psychedelics with less (real or perceived) danger.
 
so this is just some baseless speculation - just like your comment is
Relax. There's no need to be defensive. Personally, I wouldn't qualify either of our speculation as "baseless". I'm quick to point out and admit when something is my own conjecture based on making an educated guess, which is little different than "baseless." Also, the few vendors I've seen selling these compounds have a higher quantity per hit with the NBOH drugs, consistently. Also, everyone I've talked with who has done both NBOMes and NBOH drugs agrees regarding potency. And yes, this is still a small group of people's anecdotal evidence, and it's possible we're all wrong, and that 25x-NBOH drugs are more toxic than 25x-NBOMe drugs, but I doubt it. Of course, this is my conjecture—an educated guess—and I'm freely admitting this. Feel free to prove me wrong. Sure, something like steric hinderance could be possible; I wasn't ruling any of that out.

Moreover, I'm basing my statement about the NBOH class versus the NBOMe class on the anecdotal reports I've encountered and on my own personal experiences. Some of this is summed on the psychonautwiki. IME, the NBOH class is less potent, mg for mg, or µg for µg, as it were, than their NBOMe counterparts, and they have less body load. I've taken a couple of them over the years and quite a few of the NBOMes… dozens of times, bc I had a pretty decent personal cache of 25I- and 25B-NBOMe ~10 yrs ago and later tried a few other NBOMes , then 25I- and 25B-NBOH. But that's just me.

Without knowing what pharmacological action is causing the NBOMes (and very presumably other NBXX) to be toxic, this statement cannot be made with any confidence.
Anecdotal reports all point to NBOMe drugs being more potent mg for mg than NBOH drugs. Generally if a drug is less potent, then it's probably a bit more forgiving with exact dosing, thus making it slightly to significantly safer to dose properly when administering said drug. So, no I can't 100% for sure tell you this is true, but I can still state that generality with much confidence, particularly with the qualifier "being potentially safer." Nothing is ironclad, you know. All paths lead home. One hand shakes the other. The rooster is in the hen house. The fox is in the coop. The bishop is in the convent. And Robert is your mother's brother. Selah.

People have died from things like 2C-E, 2C-P, AMT, 5-Meo-DIPT
That doesn't mean much when you think about it. People have died from things like H₂O, ethanol, a Nitrogen leak, countless opioids and fentanyl analogues, suicidal ideation due to antidepressants, taking two contraindicated drugs both of which were your legit ℞'s, combining bleach and ammonia cleaning products in the bath tub and breathing in the deadly chlorine gas this produces, and either the doctor or the pharmacist giving someone the wrong meds on accident. Do you know about the Bhopal Disaster of 1986 with Union Carbide in Bhopal India where over 500,000 people were exposed to the highly toxic gas, methyl isocyanate overnight due to a storage tank leak. The gas descended on a nearby shanty town. The immediate death toll was 2,259. It's estimated another 8,000 died within two weeks of exposure, and another 8,000 from gas-related diseases. But I digress.

My point is: people overdose—withdraw violently from, and continue to poison themselves with—ethyl alcohol. The U.S., and many other countries subsequently, tried prohibiting alcohol, but after 12 long years, prohibition's detrimental effects on society were obvious and worse than it was prior to prohibition. What makes anyone think drug prohibition is any different? Sure, good intentioned, but very poorly though out and ultimately not just inefficient and ineffective, but crippling to wide swaths of society as well.
 
Relax. There's no need to be defensive. Personally, I wouldn't qualify either of our speculation as "baseless". I'm quick to point out and admit when something is my own conjecture based on making an educated guess, which is little different than "baseless." Also, the few vendors I've seen selling these compounds have a higher quantity per hit with the NBOH drugs, consistently. Also, everyone I've talked with who has done both NBOMes and NBOH drugs agrees regarding potency. And yes, this is still a small group of people's anecdotal evidence, and it's possible we're all wrong, and that 25x-NBOH drugs are more toxic than 25x-NBOMe drugs, but I doubt it. Of course, this is my conjecture—an educated guess—and I'm freely admitting this. Feel free to prove me wrong. Sure, something like steric hinderance could be possible; I wasn't ruling any of that out.

This is just my way of speaking, I'm neither aggressive nor defensive. Sorry if it came across wrongly, I tend to be rather direct and English is not my native language either. There is not much useful in vivo data of these compounds, hardly any comparisons - you admit it yourself that it is just conjecture and thus baseless is a reasonable attribute in my view. Given that NBOMe/NBOH dosing on the clandestine market is anything but precise, I'm very skeptical of any data derived from random online posts. In vitro data is limited in its usefulness for obvious reasons.

By the way, here is a comment of a competent chemist from 2012 comparing 25E-NBOH and 25E-NBOMe:

Thank you very much for sharing this experience. I must admit that I never gave this compound [25E-NBOMe] a second chance at a higher dose even though I wrote above that I probably will. The main reason was in that meanwhile I found that BOH-2C-E [25E-NBOH] was exactly what I was looking for. It is at least twice more potent than its BOMe counterpart and is one of the most beautiful psychedelics ever (in my opinion). It gives me experiences that reach beyond my subjectivity. If you (or anybody else) still have enough 2C-E, make it into the BOH derivative. I would truly like to hear what others think of it.

Even with the limited data, I think someone actually making the 246-NBOMe/246-NBOH and tasting them is a better datapoint than conjecture based on forum posts of lay person buying random unanalysed powders from the internet. Especially as there are only few people who have run the NBOHs and NBOMes side by side, and much less with pure material and known dosages (tabs, especially so of NBOx, are anything but pure or known). Given the data I have heard from people (who I trust) who had pure (non-commercial) 25B-NBOH and 25B-NBOMe, I'd agree to say that 25B-NBOMe is probably more potent (and has a worse side effect profile). But unfortunately 25E-NBOMe was never much around, and neither 25C-NBOH and 25I-NBOH of the compounds which were popular in their NBOMe version. So I'm not even sure what you base your data on. I seem to recall a Reddit post of 25C-NBOH which talked about some nasty side effects, but I don't want to dig it out currently.

I think in the end every compound has to be addressed individually. Sure, there may be some trends, but in pharmacology there can absolutely be unforeseen consequences even from small molecular changes. But of course you know that.

PS: And of course the problem with the validity of experience reports could be fixed by some independent analysis :)
 
Shugun said Myristicin in the presence of Ammonium yields MMDA so does that mean eating something like chocolate 🍫 could make MMDA if you also have Myristicin in your body right, or am I incorrect?
 
Generally if a drug is less potent, then it's probably a bit more forgiving with exact dosing, thus making it slightly to significantly safer to dose properly when administering said drug.

Again I must push back because in reality the opposite is true. You need to give this careful thought in light of what is actually known versus not known. Chemicals can be toxic via all kinds of different mechanisms: activity at a wide variety of receptors (not all necessarily even yet known to science), blocking or tying up of enzymes, becoming metabolized into other toxic things. The possibilities are very long, and in general, almost everything is more toxic in higher dose. Therefore, in the absence of other information, high potency is generally desired because there is actually less likelihood of toxic side-effects occurring at fully active doses.

Now it's possible that most toxic reactions to NBOMe are mediated through 5-HT2A, but even if this is the case, the toxicity is clearly independent from the psychedelic effect, and in the absence of additional information, the more potent compound (in terms of psychedelic effect) is perhaps a little more likely to be less toxic. Because of the overall lack of information, however, this distinction isn't really useful. The bottom line is that no one really knows.

That doesn't mean much when you think about it. People have died from things like H₂O, ethanol, a Nitrogen leak, countless opioids and fentanyl analogues, [...]

To be clear, the difference is that with all the things you named, the mechanisms of toxicity and margins of safety are quite well understood. We all breathe nitrogen all the time, and it's only toxic when it causes displacement of oxygen. I can't really tell you why people died from 2C-E, 2C-P, and/or 5-Meo-DiPT. I do know that these cases all seemed to involve doses which were well above what would normally be needed for a full experience. Unfortunately with 2C-T-7 and the NBOMes, deaths appear to have occurred at doses that weren't much higher than required to be effective. Note I didn't mention AMT because it is actually better studied, and deaths could possibly be attributed to known mechanisms like MAOI-type interactions.
 
Given that NBOMe/NBOH dosing on the clandestine market is anything but precise, I'm very skeptical of any data derived from random online posts.
You should be. Anything not published in a respected peer-reviewed science journal has value limited at being anecdotal evidence at best. Kinda like your entertaining story about an alliterative "competent chemist" along with your expectation that we take your word for their legitimacy and agree. Regardless none of this is the same as published repeatable test result from reputable groups & journals w/peer review

Sorry if it came across wrongly, I tend to be rather direct
It's fine. At times I think tact is a lost art/skill.

By the way, here is a comment of a competent chemist from 2012 comparing 25E-NBOH and 25E-NBOMe:
So… a recounting from a third party account no one can verify, from over a decade ago, talking about their own anecdotal trips? Chemistry competency, which, whatever that mean, aside, has no bearing on this person's opinion or what I should make of it.

Given the data I have heard from people (who I trust)
In other words, more anecdotal evidence, only it's from just one person's undocumented oral report. Whom you trust doesn't mean anything to me, no more than whom I trust means jack shit to you. And "heard"? Like that matters to the rest of us. And anyways why would your loquacious friend bother to have anything printed, peer reviewed, or published? Those kinda standards don't matter. Let's just argue back & forth for no goddamn good reason without any real evidence to present, you and me, champ champ… Oh but then let's suddenly fold after senselessly trying to dispute something of dying relevance anyway… like this:

I'd agree to say that 25B-NBOMe is probably more potent
Then why are we… … what? What is the point of … you know what? It's cool. Don't even sweat it. Have a great weekend and Happy Halloween!
 
Oh but then let's suddenly fold after senselessly trying to dispute something of dying relevance anyway…
The only thing I'm saying is as follows: based on the information I personally know and somewhat trust (btw in the case of the 25E-NBOMe/NBOH these compounds were actually verified by NMR, if we can trust the writings of the person not to be falsified, which we can't even in some actual journals :P ), I only know of the pairs 25E-NBOH/Me, 246-NBOH/Me and 25B-NBOH/Me being taken by the same people and potencies assigned.

In two of these three cases the people associated the NBOHs with higher potency than the NBOMes. This is not a lot of data, but I think it is enough to say that it does not seem wise to always associate the NBOMes with higher potency than the NBOHs.

Man, I really feel like I'm stepping on your toes. I don't mean to do that. I'm just debating generalisations which I personally think go too far, I don't mean to insult you or get on your nerves. It's just that I think these generalisations based on limited data can be harmful. Yes, this is a "me" problem, but that 25E-NBOH experience I talked about was in part because I a) trusted online dosages of 25E-NBOH tabs and b) I wasn't skeptical of 1.2 mg being too much because a lot of NBOMes were sold with claims of those dosages and c) thinking that NBOHs are less potent than NBOMes due to many people saying so (who in hindsight probably only had 1-2 examples, all without knowing the exact dosages and likely even without verification of their compounds). So I just think it is important to be careful with such sweeping generalisations, and I was providing (to you understandably untrustworthy, to me pretty believable) counterpoints.

Again, I don't mean to harm or annoy you, I actually think you are a pretty cool person with probably some pretty interesting stories over the years. I do know a lot of people find my tone a bit harsh or I am really too confrontational going about things. I am trying to improve. Probably I'm indeed sometimes a bit confrontational especially about things that I really care and that's those pesky little phenethylamines.

Have a great Halloween! :)
 
LSD.
Because it was LSD that kept me from shooting myself 10 years ago.
It literally saved my life.
And had I not been tripping that night, I would haven ever had the epiphany about my life that I did, and I very likely would not be alive and here today.
 
I just wish it weren't so goddamn nauseating. I have a hard time enjoying it because of this and much prefer n,n-DMT to 5-MeO-DMT…
Do you get any nausea from regular n,n-DMT? The first few times I did it I was hugging the toilet spitting or hugging a bucket waiting to throw up but never did. After that the nausea effect never came back though
 
Do you get any nausea from regular n,n-DMT? The first few times I did it I was hugging the toilet spitting or hugging a bucket waiting to throw up but never did. After that the nausea effect never came back though
No, for me, it's very rare that n,n-DMT gives me any nausea. I've noticed that it happens to me if I try to wake and bake DMT. My body does not like that, and I have to be up and have something in my stomach before I vaporize the Deems or I'm risking ~6 min. of nausea. Whereas 5-MeO-DMT triggers this response damn near every time. My mouth salivates and I'm careful to place myself in a "recovery position" type of pose just in case I actually vomit, but I never have. People have died from asphyxiating on their own vomit because they were on 5-MeO-DMT which nauseated them to the point of sickness but also rendered the person unconscious.
 
Never tried&wanna try LSD,dmt,Aya,...no interest about ket at all..idk why...no interest at designer drugs at all.....mostly prefer something from nature....found or grown by me.....but being hooked on painkillers or tranquillezers/gaba spoiled the things.....must be free to embrace those gifts-enteheogens.that's how I feel these things...pure body,pure mind...be prepared and take some when the moment comes...beautiful memories I got....is there something ahead?
 
Last edited:
You asked specifically about mescaline. That suffers from both its low potency (making it comparatively expensive to produce by any means)
Mescaline is extremely potent if you know what you're doing. A dose of 150-200mg could be plenty if you have access to the right tools.

Just phenethylamines in general.
This post details a novel endogenous tek for accessing phenethylamine and tryptamine experiences. If DMT isn't available for whatever reason then this tek is the next best thing.

Nutmeg ... does contain myristicin and elemicin, which unless youre a rabbit will NOT turn into the fun kind of phenethylamines...
It's a common misconception that allylbenzenes form phenethylamines. It's more likely that they form ß-aminoketones which are based on phenylpropylamine, as I mentioned in your thread on psychedelics. The researchers discovered these ß-aminoketone metabolites for several allylbenzenes including safrole, elemicin, myrstricin, estragole, eugenol etc.

...and instead just gives you a long lasting stoning deliriant high.
This is easily avoided by removing the stoning pro-endocannabinoid compounds and the toxic anxiogenic trimyristin fat. Conveniently these are not present in the essential oil; it also helps to check the CoA before buying to ensure it's the right chemotype. If you prefer to avoid the psychoactive essential oil terpenes then acquire the pure allylbenzenes instead.

I'll admit that the allylbenzene protocol is either too obscure or appears confusing to most people but from what I recall at least 2 standardised approaches were established.
 
Last edited:
Firstly, taking ALDH inhibitors with Mescaline does not change the fact that Mescaline is not potent in the mg for mg sense when compared to virtually any other psychedelic drug. Sure, the ALDHI will potentiate it some, but that's not the same as it being potent on its own, and it still is only a marginal improvement when you stop to consider the active range of, idk say,: 2C-B. Secondly, what you're implying with "if you know what you're doing" is that anyone not potentiating their mescaline in this manner does not know what they are doing. I've read your posts in other threads and I trust that's not how you intended to come across. Thirdly, this is not a common practice, so I'm not sure why you were attempting to refute the fact that Mescaline is powerful in its effects, but is otherwise not potent. To call it "extremely potent" is ridiculous.

A dose of 150-200mg could be plenty if you have access to the right tools.
And that's extremely potent to you? Come on, now… Allylescaline is ~30 mg dose, 2C-B is ~20 mg, and 2C-B-FLY is ~8 - 11mg dose. DOB is like 0.8 mg while LSD is 0.1 mg as the standard dose. These are potent, to extremely potent drugs. Mescaline is not among their ranks in that department, no matter how much you want them to be. Enzyme suppression techniques are a separate thing and don't count here. Regardless, enzyme suppression doesn't increase the drug's potency sufficiently to call it "extremely potent."

This post details a novel endogenous tek for accessing phenethylamine and tryptamine experiences. If DMT isn't available for whatever reason then this tek is the next best thing.
What? What does DMT have to do with this?


It's a common misconception that allylbenzenes form phenethylamines.
"Common"? Also, while there is virtually no direct route – nothing endogenous and maybe a handful of low-yielding one-pot "teks" – an intermediate ketone is formed first and then reduced to the target molecule in the lab, as you know. That's worth mentioning.

It's more likely that they form ß-aminoketones
Bingo.

The researchers discovered these ß-aminoketone metabolites for several allylbenzenes including safrole, elemicin, myrstricin, estragole, eugenol etc. … If you prefer to avoid the psychoactive essential oil terpenes then acquire the pure allylbenzenes instead.
NOTE: Some of these are definitely watched and reportable, particularly safrole (aka: 3,4-methylenedioxyallylbenzene) which is a List I precursor with the DEA (and it's similarly watched in virtually every other country, too) and ordering it will very likely attract unwanted attention. Look into your local laws and do not just go ordering essential oils all willy nilly.

I'll admit that the allylbenzene protocol is either too obscure or appears confusing to most people but from what I recall at least 2 standardised approaches were established.
Things that fall outside the scope and capabilities of the average user have severely limited utility.

Don't get me wrong, @Allylbenzene – I applaud the work you've done in sharing all this info with everyone backed up with very real science. I'm not trying to be argumentative, and I generally agree with you. I'm just saying that Mescaline is not a potent drug, period, and most people aren't going to get into playing the whole "oilhuasca" game, but thinking about personal enzymology is a worthwhile endeavor all the same! So, thank you, is what I'm saying and I hope you're not offended by any of this pushback. Not the intention. One love.
 
It's a common misconception that allylbenzenes form phenethylamines. It's more likely that they form ß-aminoketones which are based on phenylpropylamine, as I mentioned in your thread on psychedelics. The researchers discovered these ß-aminoketone metabolites for several allylbenzenes including safrole, elemicin, myrstricin, estragole, eugenol etc.
This is true but with the rabbit thing I was referring to the wikipedia statement that rats and rabbits turn myristicin into MMDA endogenously. Altough I admit I was only able to find a study showing that rats do…

”One study, using isolated perfused rat liver, found that the liver is also capable of biotransforming myristicin into 3-methoxy-4,5-methylenedioxyamphetamine”
This is easily avoided by removing the stoning pro-endocannabinoid compounds and the toxic anxiogenic trimyristin fat. Conveniently these are not present in the essential oil; it also helps to check the CoA before buying to ensure it's the right chemotype. If you prefer to avoid the psychoactive essential oil terpenes then acquire the pure allylbenzenes instead.
As far as Im aware the majority of the psychoactive effects from raw nutmeg are simply due to the anticholinergic effects of myristicin and elemicin. I know that trimyristicin is anxiogenic and has some achr activity but Im not aware of any cannabinoid compounds in nutmeg
 
This is true but with the rabbit thing I was referring to the wikipedia statement that rats and rabbits turn myristicin into MMDA endogenously. Altough I admit I was only able to find a study showing that rats do…

”One study, using isolated perfused rat liver, found that the liver is also capable of biotransforming myristicin into 3-methoxy-4,5-methylenedioxyamphetamine”

As far as Im aware the majority of the psychoactive effects from raw nutmeg are simply due to the anticholinergic effects of myristicin and elemicin. I know that trimyristicin is anxiogenic and has some achr activity but Im not aware of any cannabinoid compounds in nutmeg
Eat some Nutmeg, get your urine in a distillation apparatus then check to see if either MMDA or MMDA metabolites are found. :)
 
This is true but with the rabbit thing I was referring to the wikipedia statement that rats and rabbits turn myristicin into MMDA endogenously. Altough I admit I was only able to find a study showing that rats do…
This might very well be possible but the ß-aminoketone metabolite explanation seems more viable.

This is easily avoided by removing the stoning pro-endocannabinoid compounds and the toxic anxiogenic trimyristin fat. Conveniently these are not present in the essential oil; it also helps to check the CoA before buying to ensure it's the right chemotype. If you prefer to avoid the psychoactive essential oil terpenes then acquire the pure allylbenzenes instead.
As far as Im aware the majority of the psychoactive effects from raw nutmeg are simply due to the anticholinergic effects of myristicin and elemicin.
There are many theories about this. IMO the main candidate responsible for the apparent anticholinergic effects is the toxic trimyristin fat causing anxiogenic effects - combined with stoning cannabinoid effects (FAAH inhibitors) and several psychoactive terpenoids (eg limonene, α/ß-pinene, sabinene, terpineol, y-terpinene) which are all biologically active.

Assuming that someone has acquired nutmeg that actually contains allylbenzenes (eg myrstricin, elemicin, safrole) it's possible for these to be metabolised into active ß-aminoketones that appear to produce psychedelic effects.

Taken together it's easy to see why anyone would conclude that they experienced "anticholinergic" effects. All the elements are there. It seems more sensible to acquire purified allylbenzene extracts or use other less "toxic" botanical sources.

Ironically nutmeg contains many pro-cholinergic compounds including these, trimyristin, myrstricin, limonene, eugenol, terpineol and α-pinene. I assumed that trimyristin was anticholinergic when I started writing this post.

An old study looked at the response to pure myrstricin, concluding that the characteristic psychoactive effects of nutmeg are due to the volatile oils.
Myristicin's psychoactive properties were confirmed by a study on ten human participants in 1961 (Hallstrom & Thuvander 1997, citing Truitt et al. 1961). Each of the participants was administered 400mg of myristicin, or approximately 6-7 mg/kg by body weight, with some given placebos. Only four of the participants experienced psychoactive effects, including euphoria, anxiety, and trouble concentrating. That only four participants experienced psychoactive effects at this level suggests that 400mg or (6-7mg/kg) is a threshold effective dose for nearly half of the population. Time of onset was between two and three hours after ingestion. Interestingly, 400mg of myristicin is around twice the amount of myristicin that would be present in a moderate-high psychoactive dose of nutmeg. Myristicin generally makes up 4-8% of nutmeg's volatile oil and has been found in concentrations as high as 1.3% of nutmeg by weight (C.E.F.S. 2005). the myristicin content of mace is generally double that of nutmeg, making it potentially more potent than nutmeg.
On the presence of toxic/sedating non-volatile compounds in nutmeg:
Since the quantity of myristicin ingested by the previous subjects did not reproduce the character or intensity of response elicited by ground nutmeg, the question arose as to whether or not the response is dependent upon myristicin. Accordingly, two of us ingested 10 grams of nutmeg which had been previously deprived of all its volatile constituents. The characteristic psychopharmacologic effects of whole ground nutmeg were eliminated but some undesirable side effects remained. These consisted of occasional flushing, lower intestinal discomfort and unusually heavy sleep in one case; and lower intestinal discomfort and insomnia in the other case. This suggest that the other volatile constituents (safrol, eugenol, etc.) in nutmeg contribute markedly to its psychopharmacologic effect in man.

I know that trimyristicin is anxiogenic and has some achr activity but Im not aware of any cannabinoid compounds in nutmeg
Nutmeg contains a few FAAH inhibitors which increase endocannabinoid levels.
 
Last edited:
Top