It's not? Loll
The only safe 2c is b, and that has no real research done on it either.
Oh Christ, here we go again...
Look, the vast majority of people only trot out the 'but long term effects!' argument if they're misinformed or if they're biased against an RC and want to red herring around in an effort to either scare people away from trying it or look superior to the people who do use it. I'm sure there are a few people on Bluelight that have the requisite knowledge about biochemistry to be well-informed enough to legitimately worry, or not, about long-term effects. But those people aren't the ones that make laughable, unsupported claims on a subject they don't understand, without even so much as an attempt at supporting their bold declarations. It's far too easy to read ulterior motives into posts like this one, so how about we actually objectively look for a moment at the subject of 'long-term effects' and analyze the likelihood of such risks existing in actual real life?
It's very simple really. If a compound – or one of the many metabolites of a compound – does damage to the body, then the damage has to be done while the drug is in a person's system. These research chemical psychedelics don't stick around in the body very long at all. The whole 'acid sneaks into your spine and then hides out there for years!' type of story is false, and this applies to psychedelic research chemicals as well. So if a compound has a half life of 12 hours, and I'm just throwing that out there as an example, and a drug is considered to be fully-excreted after six half lives, then you've got a period of three days.
So if the thing is going to do damage, it has three days to do that damage. The hypothetical damage is what is referred to as 'acute', meaning sudden. Considering just how little of the compound will be left even after three half lives, I would posit that the drug actually has more like a day and a half to do damage. I would also posit that the most damage is likely to be done when the drug is at its highest plasma concentration (amount in the blood), so the majority of the damage would be done very soon after administration.
Since the damage is acute, the effects of that damage will become apparent as soon as the damage is inflicted. It's not like you take a dose of a drug and then slowly start to deteriorate over the next few weeks/months/years. So the damage would be apparent pretty much immediately. It will be noticeable as a result, since the transition between normal function and reduced function due to damage happens over a short period of time, and thus isn't likely to be mistaken for natural variation.
So why haven't we heard about any cases of damage done to internal organs, perhaps the liver, or perhaps the brain, that has happened in people using a certain compound? While these compounds are relatively uncommon, they are widely-enough available that multiple cases of damage should pop up, and the longer since the discovery and subsequent appearance on the market of a compound the more cases should occur. We don't in fact see these cases.
What about effects that take time to set in? Well, I don't know of any plausible mechanisms for *continued* degradation of some system in the body or other that can occur without chronic exposure to a compound. For example, you might work in a factory with a chemical that is safe if you're exposed a few times doing only a tiny amount of harm, but over time compounds that harm, eventually doing noticeable, significant damage.
Since we are not daily exposed to psychedelic research chemicals, I don't see a mechanism for chronic exposure. And as I mentioned, for a compound to set a process of functional decline into motion as a result of a single dose or a handful of doses, it would have to set in motion some sort of cascade of harm, some sort of disruption to the natural feedback and feedforward loops in the human animal. Not only is this implausible, it would still result in noticeable cases of reduced function, and we don't see those cases.
The chemistry of PEAs and tryptamines is pretty well known. The biochemistry, less so. But nonetheless these compounds are not structurally related to any toxins or poisons that we know of. There are exceptions, like PMA for example, but I would suggest that PMA and para-chloroamphetamine are actually examples in favor of my position that the unknown nature of supposed 'long term effects' is a red herring. Those two compounds are excellent examples of compounds that do in fact do damage to the human body. And that damage is acute, and takes place while the drugs are in the system, instead of somehow setting in motion a slow decline in function.
And guess what? We are fully aware of the toxic properties of PMA and 4-chloroamphetamine. In both of these cases the dangerous nature of the drugs rapidly became apparent and that information is widely disseminated today. So I suggest that if there were any harmful effects caused by psychedelic RCs, whether that takes the form of the logically-sound acute damage scenario or the implausible slow-decline mechanism implicit in the phrase 'long term effects', we would know about those effects.
Another excellent example in favor of my argument is the NBOMe series. These chemicals definitely possess the potential to damage a person irreparably. But they've only been out on the market for a few years, and already their potential dangers have been revealed and expounded upon. And the initial cases of negative effects did indeed pop up almost immediately upon the occasion of their initial wide dispersion. So once again, we have chemicals that *do* pose some danger. In this regard the NBOMes occupy a sort of halfway-position between out and out toxins like PMA and PCA and benign drugs like the traditional PEAs. And again, the cases of damage done began to pop up pretty much as soon as human bioassays began on a wide scale.
Thus I conclude that the 'but we don't know the long term effects' argument so often brought up to back up a person's personal convictions that compound X or Y is evil, nasty shit is indeed a red herring. Historical fact shows that compounds that do immediate, acute, noticeable / significant harm are quickly identified as such. On the other side of the equation, nobody who drags this dead horse out ever seems to be able to posit a mechanism by which a compound would provoke a slow, gradual decline in the function of one or more of a human body's subsystems.
So if acute harm is quickly recognized as such judging by the history of compounds like PMA or the NBOMe series, and if we do not see such cases of harm from psychedelic research chemicals, and there isn't a plausible mechanism for a method of initiating a non-acute slow decline, then the remaining position that is logically tenable is that concerns over long-term effects are at best mistaken or overblown, and at worst are deliberate falsehoods used to bolster one's biases against a certain compound or class of compounds when debating its relative merits.
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