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The Big & Dandy 1P-LSD Thread, Volume 1

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I'm not sure what you're trying to say. *I* am saying that these are some of the differences that I have experienced between the 2 drugs, but by all means not all of the differences. I respectfully disagree; to me the time course of effects is a quantitative difference.

By definition, time course cannot be a qualitative difference -- it is a quantitative difference, just like intensity. If you take a lower dose of a drug, or inject it, that will also change the time course. But that doesn't necessarily mean you are having a qualitatively different experience.


And of course mushrooms are not the same as Psilocybin; I never said otherwise. And respectfully, yes I am doing this comparison with mushrooms because (wait for it) I am comparing mushrooms; I didn't mention Psilocin, Psilocybin, 4-AcO-DMT or any other specific chemical. The effect I get from mushrooms is different than the effect I get from 1P-LSD, I could tell them apart easily.

I think you are completely missing the point of what I am saying. I'm not saying that it isn't possible to perceive differences between different hallucinogens. Clearly people perceive differences. What I am saying is that (1) the differences that people perceive are not due to specific, pharmacological differences between the drugs. And (2) that the differences that you may perceive are subjective, meaning that they are not inherent properties of the drugs.

Psilocybin mushrooms contain all kinds of alkaloids in addition to psilocybin and psilocin that produce GI side-effects, so of course you may be getting somewhat different effects from mushrooms vs. 1P-LSD. But along those lines, if you had mushrooms that contained 1P-LSD, they very possibly might produce different effects then 1P-LSD on blotter paper.

You can't disprove that.

It isn't necessary for me to prove it. You are the one making the claim that you can do something that you have never actually tried to do. Because when people have tried to do what you are claiming you can do, they have found it very difficult, so it's up to you to to prove that those published studies are wrong.

Yes, I've seen things on mushrooms that I haven't on 1P-LSD. Again, not sure what you're trying to say.

I'm trying to say that the effects of hallucinogens cannot be separated from set and setting. So if you eat a mushroom, it is going to markedly influence how you perceive the experience. Some people will have different experiences depending pn whether they ingest 15 mg of psilocybin in the form of mushrooms vs. as pure psilocybin in a pill.

Maybe you misinterpreted my saying 'they just feel different' ? I'm saying that in the same sense that I would say 'I just don't like pancakes' because I don't.

Tom

Not liking pancakes is an opinion, and of course you can feel any way you want about pancakes. I can't say you are wrong for not liking pancakes or saying they taste bad. But people here are claiming that 1P-LSD and LSD consistently cause qualitatively different experiences across all people ingesting them. Those claims are a statement of fact, not of opinion.
 
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First, these comparisons are done in a way so that the time-course doesn't influence differentiation. Of course, you could distinguish a drug that lasts 4 hours from one that lasts 8-10. That doesn't mean that you can tell the difference between their effects.

Second, mushrooms are not the same thing as psilocybin. Mushrooms are not exactly pleasant things to eat and they can produce nausea independent of the effect of psilocybin. The nausea has nothing to do with the hallucinogenic effects. You can't effectively do this type of comparison with mushrooms, it has to be pure psilocybin. What you are claiming is effectively like saying that the ethanol in vodka and wine is different because wine always gives you a headache and vodka doesn't.

Third, the fact that you are ingesting a hallucinogen in the form of a natural product (mushrooms) is going to markedly color your experience. People often report seeing mushroom-specific visual hallucinations.

Firstly , Ive read that in the early days of psychedelic reseacrh they believed that mescaline, LSD and psilocin are identical in effects....Sure...tracers, CEVs/OEVs, profound thoughts etc etc... This in and of itself was a suggestibility issue...from an outside perspective they ARE the same....it isnt until further examination and experience that these differences become apparent. They later discovered that each the assumption that they (psychedelics) are identical in effects was wrong... all of the psychedelcs bind to different 5ht receptor groups and at differnent affinities just for starters....(5htxx). We now know that all the classical psychedelics are also useful for therapeutically , however each tend to be therapeutic for different issues...

Your assumption that pure psychedelic chemical alone does not cuase nausea is just flat out wrong. We have serotnin receptors in our gut and psychedelics are known to cause gas and nausea....its not the fungi itself.
 
Under blind dosing conditions, people experienced with LSD can't effectively differentiate between psilocybin, LSD, and mescaline. They fail utterly. And those people had been given doses of pure Sandoz LSD on numerous occasions over a period of years. If people can't actually tell the difference between LSD and mescaline then do you honestly think you have any hope of differentiating between LSD and 1P-LSD?

I'm aware that many people think that they can make these distinctions, but there is no way for a person to know whether they can or not until they try, under blind conditions.

I'd really like to see a link to that blind study you are talking about all the time, please. Honestly, it sounds like serious bullshit to me. As long as you are only talking about the study, it's just as much a wild claim as anything else.

I do agree though, that 1-P-LSD and LSD are so close in effects, that any perceived differences are probably mostly due to other factors.
 
In the early days of psychedelic research, it was believed that mescaline, LSD and psilocin were [essentially] identical in effects. This, in and of itself, was a suggestibility issue [with tested subjects].

Precisely. Those early studies, in hindsight, are highly suspect. As I said earlier, I'm certain that I and many other observant, mature and well-traveled psychonauts can perform very well on such tests.
 
I do recall this being mentioned in older books and documentaries on psychedelics (that effects are identical) but you have to understand how flawed this is... I mean the duration is a dead giveaway so the subjects had to have been asked while they were under the psychedelics....we already know that its a highly suggestible state. Any sort of thoughts such as "I bet I got psilocin...I just know it..." will color the experience.

Its hard to argue with science....

qIfhwMG.png

As far as 1p is concerned....I dont know what it is exactly thats causing it but its different enough for me to be an entirely different chemical altogether....I would certainly be upset if I was sold one instead of the other...1p cuts off without residual stimulation for me...thats a big deal...Ill be up all night on classic L25 ....Maybe this ones more versitile than L25 because...well.. wouldnt it be a more complex molecule by having the propionyl add on? Meaning more "things"(reactions) can happen through metabolism? This is just a guess.
 
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Not only the residual stimulation and Zero hAngover....but the fact it takes me 200-300 to have hardcore visuals where classic LSD-25 I trip hard off 100-150?
 
I think you are completely missing the point of what I am saying. I'm not saying that it isn't possible to perceive differences between different hallucinogens. Clearly people perceive differences. What I am saying is that (1) the differences that people perceive are not due to specific, pharmacological differences between the drugs. And (2) that the differences that you may perceive are subjective, meaning that they are not inherent properties of the drugs.

So your belief is that despite different receptor binding profiles and affinities, all psychedelics produce the same effects, that there's nothing possible to objectively differentiate between different ones, and that perceived differences are only due to individual response?

I mean of course the range of possible effects from any given substances covers a huge span of possibilities, and every individual trip is unique, but that doesn't mean there aren't objectively unique effects that are experienced by most. For example, LSD hits dopamine receptor sites whereas psilocybin does not... how could they possibly have the same effects? Considerable overlap, sure, but identical? It doesn't even make sense that they would be, pharmacologically.

You can't take all studies as gospel, especially old ones about psychedelics.
 
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I do recall this being mentioned in older books and documentaries on psychedelics (that effects are identical) but you have to understand how flawed this is... I mean the duration is a dead giveaway so the subjects had to have been asked while they were under the psychedelics....we already know that its a highly suggestible state. Any sort of thoughts such as "I bet I got psilocin...I just know it..." will color the experience.

Its hard to argue with science....

qIfhwMG.png
Are these the numbers from this Ray paper?
 
Another thing that is worth pointing out is that virtually every time that the media mentions a psychedelic -- any psychedelic -- they say that the drug is similar to LSD. Is that ignorance? Deliberate misinformation? Deliberate conditioning? All of the above?

Be that as it may, that's just as ridiculous as saying that a beer -- any beer -- is similar to Westvleteren, or Samichlaus, or whatever brew replaces LSD in your mind. Will beer connoisseurs consistently and miserably fail blind tests involving just a handful of major brews? How about wine connoisseurs? I doubt it, yet such tests would involve aroma and taste (very tough), and optionally, appearance (less tough). Psychedelics are easy in comparison with that.
 
There was a study where blindfolded people couldn't distinguish between red and white wine if they were served at the "wrong" temperature.

I think you answered your own question there lamanoguacha, the media doesn't write for psychedelic connoisseurs like ourselves. To the outside world, any 5ht psychedelic is similar to LSD.
 
Firstly , Ive read that in the early days of psychedelic reseacrh they believed that mescaline, LSD and psilocin are identical in effects....Sure...tracers, CEVs/OEVs, profound thoughts etc etc... This in and of itself was a suggestibility issue...from an outside perspective they ARE the same....it isnt until further examination and experience that these differences become apparent. They later discovered that each the assumption that they (psychedelics) are identical in effects was wrong... all of the psychedelcs bind to different 5ht receptor groups and at differnent affinities just for starters....(5htxx). We now know that all the classical psychedelics are also useful for therapeutically , however each tend to be therapeutic for different issues...

Your assumption that pure psychedelic chemical alone does not cuase nausea is just flat out wrong. We have serotonin receptors in our gut and psychedelics are known to cause gas and nausea....its not the fungi itself.
Please re-read my post. I never said that psychedelics do not produce nausea. What I said is that secondary compounds in mushrooms can also produce nausea on their own, independent of psilocybin and psilocin. So mushrooms have the potential to produce substantially MORE nausea than pure psilocybin.

I am well aware of the affinity and selectivity issues that surround hallucinogens and serotinin receptors. This issue was addressed by Franz Vollenweider's studies where he was able to block ALL of the hallucinogenic effects of psilocybin with the selective 5-HT2 antagonist ketanserin. That means that although psilocybin activates several types of serotonin receptors, only the 5-HT2 subtypes are responsible for mediating the hallucinogenic effects. Those findings mean that the other serotonin receptors do not appear to appreciably contribute to the subjective experience produced by psilocybin.

I'm not trying to say that some people may not perceive subtle differences in the effects of different hallucinogens. Some people may have that experience. The problem is that people also tend to perceive exactly those same differences when they use one substance at different dosages. Are you certain that if I gave you 50 mcg LSD on one occasion and 500 mcg on another, without telling you what you had received, that you would absolutely be able to tell that you had received the same drug? What about if I gave you LSD iv? It certainly might have a different "feel" -- it would act more quickly, peak a bit faster, and be more potent.

PharmChem used to analyze LSD samples in the '70s. They found that the only difference between what submitters were calling "clean" vs "speedy" LSD was the clean LSD tended to be dosed lower. It is probably that people are more aware of the physical side-effects of LSD when they take lower doses.

So the point I am trying to make is that people are notoriously bad at assessing the effects of hallucinogens. People get qualitatively different responses when they take the same drug in different colored pills, or at slightly different doses. So if you think there are slightly different effects from LSD vs 1P-LSD, that is pretty meaningless for determining whether 1P is a prodrug. Just the pharmacokinetic differences alone, or dose differences, or expectation could be responsible for 1P having a different feel.
 
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I agree with the last post you made, more or less. The "clean vs dirty" acid thing I am sure can be chalked up to expectation. I mean, people report effects from placebo pills when they think it might be something else. However I still think I would have no problem telling mescaline, LSD and psilocybin apart in a blind test, especially psilocybin from the other two. Could I tell 4-HO-MiPT and psilocybin apart? I'd like to think so but I admit to the possibility I wouldn't be able to in a truly blind test. Nor do I feel confident someone could give me any tryptamine I've tried and I would be able to identify it over the others (other than AMT). But a lysergamide vs a tryptamine vs a phenethylamine, that I could do with confidence. But someone who isn't into and experienced with psychedelics might not be able to do the same.
 
I'd really like to see a link to that blind study you are talking about all the time, please. Honestly, it sounds like serious bullshit to me. As long as you are only talkin
g about the study, it's just as much a wild claim as anything else.

I do agree though, that 1-P-LSD and LSD are so close in effects, that any perceived differences are probably mostly due to other factors.

I'm not saying there are NO differences between hallucinogens -- they are different drugs. I am saying that it is pointless to try to figure out if 1P is a prodrug based on any perceived subjective differences because of how variable the effects of hallucinogens can be, and because people are notoriously bad at objectively evaluating those differences. People can mistake one drug for another, and they may get qualitatively different effects from different doses or even from factors such as the color of a pill. If the placebo effect works when someone is sober, can you imagine how much it will be amplified in someone after taking 100 mcg LSD?

There were several studies that looked at the differences between individual hallucinations. Here is the one that I was specifically talking about. Again, I'm not claiming that there are no differences, just that they are not apparently useful if you want to try to identify which drug you have taken:
http://eywa.maps.org/w3pb/new/1967/1967_Abramson_1999_1.pdf
 
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@ Perpetual - Serving wine at the wrong temperature will alter its aroma and taste! Did that study include a second group that was given the wines at their correct temperature?

@ Everyone - Here's an idea for a study: Two subject groups are informed that they will eat. Both groups are blindfolded. The first group is given a grossly overcooked (but not burnt) piece of filet mignon, a piece of slightly undercooked pork, and a piece of raw horse (the latter is fairly common in Japan, btw). The second group receives a perfectly cooked piece of filet mignon (medium-rare or nearly rare), a perfectly cooked piece of pork, and a piece of raw horse. The goal of the study is to see which group can more accurately identify the broad type of food that they ate (i.e. meat) and what kind (i.e. beef, pork and horse).

It's reasonable to assume that most of the subjects in the first group will be able to tell that what they ate was meat, but not at all which kind. However, most of those in the second group will not only be able to tell that what they ate was meat, but also readily identify the first two kinds. In both groups, few subjects, if any, will succeed in identifying the horse.

Do you guys get my drift?

Incidentally, for those that aren't aware, blind studies typically don't require blindfolds!
 
Precisely. Those early studies, in hindsight, are highly suspect. As I said earlier, I'm certain that I and many other observant, mature and well-traveled psychonauts can perform very well on such tests.
Any bias on the part of the scientists would have no bearing on whether a test subject given psilocybin or LSD would be able to correctly identify which drug they had taken. If it actually as easy to differentiate between the effects as you are saying, then the subjects should have had no trouble with such a task.

Serving wine at the wrong temperature will alter its aroma and taste! Did that study include a second group that was given the wines at their correct temperature?

It isn't necessary to manipulate wine by serving it at the wrong temperature to show that some aspects of wine tasting are subjective. You can do that by adding food coloring so that white wine looks red, or even by putting an expensive wine into a cheap bottle:

http://scienceblogs.com/cortex/2007/11/02/the-subjectivity-of-wine/

They added food coloring to wine and it changed how people described the flavor. It just shows how much our perceptions are colored by subjective factors.
 
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Is it explained whether these people are those who enjoy/are partial to psychedelics? Are they experienced? Having been given several doses of sandoz LSD in the past does not equate to the level of experience of many people in this forum, who have taken different psychedelics many times in an attempt to analyze and understand the effects. I'm sure if I did a blind study with a group of people who had taken each of the 3 drugs at some point(s) in college or something but hadn't thought about psychedelics since then and never really got to know any of the substances, that I'd find they couldn't distinguish most of the time. But if I did a study with selected people from here, I would expect the results to be totally different.
 
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I am well aware of the affinity and selectivity issues that surround hallucinogens and serotinin receptors. This issue was addressed by Franz Vollenweider's studies where he was able to block ALL of the hallucinogenic effects of psilocybin with the selective 5-HT2 antagonist ketanserin. That means that although psilocybin activates several types of serotonin receptors, only the 5-HT2 subtypes are responsible for mediating the hallucinogenic effects. Those findings mean that the other serotonin receptors do not appear to appreciably contribute to the subjective experience produced by psilocybin.

yes, I also believe that people overestimate the importance of other receptors like sigma and the other serotonin receptors in the experience, which probably wouldn't have a noticeable psychoactive effect on their own. the fact that ketanserin blocks all hallucinogenic effects of psilocybin points towards that, at least.

let's not forget though that LSD does have affinity for D2r which probably accounts for some inherent difference in effects. I think I remember of a paper from Nichols were ketanserin did not block all of the behavioural effects of LSD in mice, while haloperidol did.

but may be there still is space for some differences in how each psychedelic interacts with the 5-HT2Ar that could make the effects inherently different. different rates of activation of phospholipase C vs. A2 vs. D perhaps? as far as I know, it's not as simple as '5HT2A agonism causes psychedelia', and some psychedelics are so different from others I don't think one would have to be a very experienced psychonaut to tell them from the others. I'm thinking mescaline here.

who knows though...
 
@ Serotonin - You're talking about methodology that is very different from what we're talking about. Things like taking near-threshold and heroic (or even crazy doses) isn't what true psychonauts do on a normal basis. Of course it would be virtually impossible to tell the difference between LSD, mescaline, et al. if one is tested with doses at the upper and (particularly) lower extremes of their activity! C'mon... That's just common sense! We're talking here about *standard* doses. You give me standard doses of AL-LAD, 2C-E and 4-AcO-DMT, and I will tell them apart and name them in a heartbeat! Give me standard doses of 4-AcO-DiPT, 4-AcO-DMT and 4-AcO-MiPT, and voila! No problem! Ditto with 2C-P, aMT and DOC. Ditto with 2C-T-2, 2C-T-4 and 2C-T-7. DPT, DiPT and LSZ? Pft! And so on...
 
So your belief is that despite different receptor binding profiles and affinities, all psychedelics produce the same effects, that there's nothing possible to objectively differentiate between different ones, and that perceived differences are only due to individual response?

I mean of course the range of possible effects from any given substances covers a huge span of possibilities, and every individual trip is unique, but that doesn't mean there aren't objectively unique effects that are experienced by most. For example, LSD hits dopamine receptor sites whereas psilocybin does not... how could they possibly have the same effects? Considerable overlap, sure, but identical? It doesn't even make sense that they would be, pharmacologically.

You can't take all studies as gospel, especially old ones about psychedelics.

Again, please re-read what I posted. I said "I'm not saying that it isn't possible to perceive differences between different hallucinogens. Clearly people perceive differences."

But it is one thing to perceive differences, and quite another to say that those differences are characteristic effects of the drugs that prove that 1P-LSD is not a pro-drug for LSD.

I posted about the PharmChem data above and I'll bring that up again here:

https://www.erowid.org/chemicals/lsd/lsd_article1.shtml

The relevant passage from that page on erowid is as follows:
Interestingly, people who submitted samples to PharmChem also often submitted comments about whether they believed that the acid contained "speed" or "strychnine". Although no strychnine was ever detected in any of the submitted samples--and only a few tested positive for methamphetamine--PharmChem reported that the more LSD that was present in a dose unit, the more likely the submitter was to think it contained strychnine.

So here is evidence that people are detecting qualitative differences between the effects of LSD when it is taken at different dosage levels. If that is the case, then how much faith should we put in people's perception about differences in the effects of LSD and 1P-LSD at different doses? How do we know that the differences people are picking up between LSD and 1P-LSD really reflect pharmacological differences between the two drugs, as opposed to subjective differences like those that lead people to think their LSD is contaminated with strychnine?
 
@ Serotonin - You're talking about methodology that is very different from what we're talking about. Things like taking near-threshold and heroic (or even crazy doses) isn't what true psychonauts do on a normal basis. Of course it would be virtually impossible to tell the difference between LSD, mescaline, et al. if one is tested with doses at the upper and (particularly) lower extremes of their activity! C'mon... That's just common sense! We're talking here about *standard* doses. You give me standard doses of AL-LAD, 2C-E and 4-AcO-DMT, and I will tell them apart and name them in a heartbeat! Give me standard doses of 4-AcO-DiPT, 4-AcO-DMT and 4-AcO-MiPT, and voila! No problem! Ditto with 2C-P, aMT and DOC. Ditto with 2C-T-2, 2C-T-4 and 2C-T-7. DPT, DiPT and LSZ? Pft! And so on...

They did use standard doses -- the most common dose of LSD in those studies was 50 mcg and that is approximately equivalent to what a square of blotter paper contains. It is certainly not a threshold dose (25-30 mcg) nor a very high dose.

https://www.erowid.org/chemicals/lsd/lsd_article1.shtml

According to the DEA, the average dose of LSD on street blotter is between 20 and 80 micrograms (µg). Based on this, they now consider a "standard dose" of LSD to be around 50 µg. They also report that crystal LSD they have seized averages about 62% d-LSD

So if LSD crystal is typically 62% pure, then when people aim for 100 mcg blotter squares, you are effectively going to only get 62 mcg LSD. But most people who lay sheets probably aim for lower then 100 mcg/dose to conserve LSD, so the DEA's estimate of 50 ug/dose may not be too far off. In any event, the studies were using what is effectively a standard dose of LSD.
 
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