Okay, so to the heart of the matter. I have tried to make this as unambiguous but yet as unbiased as I can. I think it's a good summary of what a contaminant would require as far as activity levels etc, because the evidence does seem to me to point to the improbability of a contaminant, but at the same time I included speculation on sub-active doses at the end because I think it's a valid rebuttal to that argument, albeit one that is itself somewhat unlikely and would require more research as to whether there are any analogous situations in medicine.
What do you guys think? Especially folks on the pro-dirty acid side?
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What properties would a potential contaminant require?
Whether one wishes to illuminate the subject of dirty acid to prove that it is a real phenomenon, or instead prefers to explain the symptom set of dirty acid syndrome as a natural result of LSD itself, the question of contamination must be raised. If dirty acid is real then a contaminant will be the culprit. If it is not real, supporting evidence would have to include the absence of a contaminant. However, as amateur drug enthusiasts instead of professional researchers, it is difficult to unambiguously prove the presence or absence of a contaminant for lack of proper equipment – such as gas chromatography / mass spectrometers and nuclear magnetic resonance spectrometers – that would be necessary to unambiguously prove the presence and then identity of any contaminants.
Due to the inability to easily settle this problem using advanced equipment, we will apply our curiosity about the veracity of any claims that dirty acid syndrome is a real phenomenon to examining what characteristics a contaminant would need to possess. These characteristics include an intrinsic activity at incredibly low dose levels and a symptom set that is unpleasant but not harmful or fatal.
The first such characteristic as mentioned is the required potency of any contaminant. A piece of blotter, frequently found to be the delivery method for 'dirty' acid, will be dosed with a given amount of drug. Depending on the chemical, the required dose will vary, from potentially several milligrams in the case of 2C-B blotter that is meant to be used several blotters at a time, to 0.5 to 1 mg for NBOMes, to 100 micrograms for a piece of acid blotter that is well-dosed.
Acid however possesses four different isomers, the (+)- and (-)- versions of LSD and iso-LSD respectively. These four stereoisomers are the result of LSD possessing two chiral centers: one at the 5-carbon and one at the 8-carbon. In practice however, a large amount of the acid on the market is derived ultimately from precursors such as ergotamine that are extracted from fungal or less-commonly plant matter, and (-)-LSD and (-)-iso-LSD are not actually found in nature. Therefor the product of a synthesis that begins with only (+)-ergotamine and (+)-iso-ergotamine will yield only (+)-LSD and (+)-iso-LSD, so only two of the isomers have to be taken into account when determining the amount of the racemate formed from both of those isomers that is applied to blotter.
Since LSD and iso-LSD interconvert – keeping their respective optical isomerism of (+) or (-) – we may assume that for each molecule of LSD that becomes iso-LSD, a molecule of iso-LSD makes the opposite transition. So ultimately the ratio of 1:1 between these two isomers will be preserved, and we can therefor assert that any blotter that contains 100 micrograms of *active* material will actually contain 200 micrograms – half of which will be the active isomer and half of which will be the inactive isomer. This is relevant because taking a hypothetical purity figure of 80% for example will result in very different values depending on whether the total amount of alkaloids is 100 or 200 micrograms total.
Taking that 80% figure as an example, and understanding that there is actually 200 micrograms of alkaloids present in a well-dosed blotter, we see that at most there could be 40 micrograms of contaminant. The rest of the alkaloid content would be 80 micrograms of each of the (+) isomers of LSD and iso-LSD. This quantity, 40 micrograms, is very small. In fact, this is barely even the lower bound for the dose of (+)-LSD necessary for a threshold experience, and LSD is one of the strongest known psychedelics that is known to exist.
This dose of 40 micrograms is the absolute highest possible dose of contaminant in this scenario, but the compound may have to be active at an even smaller dose. This is because it is reasonable to assume that if there is contamination, there is likely more than one contaminant. Additionally, there are other forms of LSD like the inactive lumi-LSD that may partially make up the 20% of our total alkaloid content that is neither (+)-LSD nor (+)-iso-LSD. However, for the purposes of this examination we will take 40 micrograms to be the quantity of contaminant and disregard these complicating factors, since this entire analysis is to one extent or another an abstraction.
Moving on to the next requirement for the hypothetical contaminant, it must produce a symptom set that is unpleasant but not truly harmful and certainly not fatal at this very low concentration. The number of known poisons and toxins that are active at concentrations this low is small, but very real. Unfortunately, identifying other substances that are indeed active at this level yet do not show terribly dangerous activity is much harder, as compounds that have an adverse effect on the human body such as neurotoxins like Sarin or VX often have their incredible potencies tied up with their immensely toxic properties. That is to say that the mechanisms that produce the incredibly dangerous effects are the same as the mechanisms that produce their high potencies; organophosphorous compounds such as the aforementioned sarin and VX are good examples of this, should the reader wish to learn further about the subject of their modes of action.
Another interesting angle to the possible effects of any contaminant reflects the symptom set that is common to lysergamides, and ergoloids in general. The effects that constitute dirty acid syndrome are often exactly those negative side effects that can be associated with having taken an ergoloids in the first place. So naturally our search for potential candidate contaminants is drawn towards ergoloids. This would have another benefit: the fourth criterion for a contaminant is not completely necessary, but the contaminant should be the result of an improper or partially incomplete acid synthesis, as it is difficult to imagine where else the contaminant would come from or how it could be introduced into the blotter. So searching amongst the ergoloids is a natural extension of both the side effects that are reported as being a result of dirty acid as well as the need for a plausible mechanism for the introduction of this contaminant into the dosing medium.
Alas, there are not any known ergoloids that for these four requirements. A list of ergoloids and their relative potencies follows, as assembled by Bluelighter Anon0631:
Ergine - Also known as LSA, this molecule is similar to LSD except that in lieu of two ethyl groups on the amide moiety, there are instead two hydrogens, creating a primary amine. The dosages for LSA are notoriously ambiguous, due mainly to the administration of this chemical in botanical form. However, Hoffman determined that an effective intramuscular dosage was 500 micrograms circa 1947. As such it is not a likely candidate since the potency is an order of magnitude too low, not even counting the difference in bioavailability between intramuscular and sublingual dosing.
Ergotamine - This is often used as raw material for the synthesis of LSD, so on that count it strongly fulfills the requirement. Additionally, it also produces strong cardiovascular effects and delirium, as in the condition of ergotism. Unfortunately, the doses required are much larger; it is used as an anti-migraine medication in the United States, at a dosage of 2 milligrams, and the dosage necessary to bring on unpleasant side effects is necessarily larger than the 2 milligram therapeutic dosage.
Lysergic acid - Lysergic acid is often one of the intermediate steps between ergotamine and LSD. It is apparently totally inactive, though what dosages it has been assayed at are unknown. It will suffice to say that it is unlikely that it is an even more potent or perhaps equally potent ergoloid than LSD, as someone somewhere would likely have discovered this effect. Even if it was a nearly poisonous compound, any activity would still be occasionally exploited by the risk-taking drug adventurer, as with datura, but we do not see this phenomenon.
Ergoline - Apparently without action, this compound is missing entirely the side chain that contains the diethylamide group in LSD. this side chain also exists in ergotamine and lysergic acid, though the amine has been replaced by an alcohol in lysergic acid, and thus it's presence would be very unlikely even as a product of poor synthesis.
Ergometrine - This compound is used medically to aid in the process of childbirth, apparently through its action upon the smooth muscles of the uterus. It is mentioned in TIHKaL that it may possess psychoactive properties between 2 and 10 milligrams, but it's use as such should be discouraged since it can exert such a powerful response within the autonomic nervous system. It is also unlikely to be produced by faulty synthetic method since the functional group that sprouts from the nitrogen of the amide side chain is dissimilar to an ethyl group, and there is only one such group instead of two, yielding a secondary amine instead of a tertiary amine such as LSD.
Taking these chemicals' properties into account, it is apparent that LSD is quite unique amongst the ergoloids. Recently there have been developed various potent lysergamides such as LSZ, where 2,4-dimethylazetidide replaces diethylamine within the structure of the overarching amide function. Additionally there have been some less recent developments where the side chain that chemists label R6 has been modified, such as ETH-LAD and AL-LAD. But out of all of the active analogues LSD appears to still reign as the most potent, possibly tied with LSZ, and in any case there is no mechanism for altering the group at R6 or inducing the formation of a dimethylazetidide without very specifically aiming for such compounds. Further, these compounds would fail as contaminant candidates on the basis of their lack of intrinsically negative physiological activity. It is possible, however unlikely, that there may be an ergoloid that is not known to science that can produce the necessary symptom set for dirty acid syndrome.
The presence of a non-ergoloid contaminant is even less tenable than that of a possibly unknown lysergamide or other ergoloid, because of both the necessity for a mechanism of introducing such an impurity as well as the paucity of potential choices. There simply aren't really candidates that have that level of activity. All things considered, the presence of a contaminant within blotter is doubtful, and experts in the field of organic chemistry categorically deny the presence of such a contaminant, preferring to ascribe the symptoms of dirty acid syndrome to the variable nature of the drug LSD itself.
However, recently several users that are proponents of dirty acid as a real phenomenon have suggested that it may not be necessary for a contaminant to have full activity at such a low concentration. They suggest that a sub-active dose may modulate the LSD experience in some way, much as the phenethylamine drug TOMSO is inactive until combined with another psychoactive, alcohol specifically. This mode of action may not be likely, but it is impossible to say at the moment, since it is possible that a contaminant could in fact be an as-yet unknown lysergamide, or another form of ergoloid, which would have unknown properties. It has additionally been suggested that the contaminant, should it exist, may in some way alter the metabolic fate of LSD, somehow creating the conditions for dirty acid syndrome to occur. This is much less likely than a sub-active dose of an unknown chemical, as there are no real analogous examples of an enzyme inhibitor shutting down or modifying an enzyme's activity at low double-digit microgram quantities. For readers interested in alterations of enzymatic metabolism, a google search on cytochrome P450 and its inhibitors should provide an easy entry into the topic.
