On this page, I will be collecting and collating all the information that I find on phenylethylamine (PEA). In my mind, I like to imagine this word as phenyl-ethyl-amine to help me remember it’s spelling, pronunciation, and organic chemical structure.
While browsing the LongeCity forum threads, I found a valuable chunk of information information about phenylethylamine by a user who goes by alpha2A. He said:
Whatever you do with phenylethylamine (PEA), don’t forget to look at the objective real world results from its use. If you plan to experiment with dosing PEA directly and concomitantly with monoamine oxidase (MAO) inhibition, yet don’t have the patience to read the rest of this admittedly long-winded article, at least take the time to read the first sentence once again. It’s not all you need in order to use PEA safely and productively, but it may save you a lot of time, for it is possible to misuse PEA without even realizing it.
When increased PEA is desired, a suitable first step is to achieve significant inhibition of the B isoform of MAO (MAO-B); this is best done with one of the selective MAO-B inhibitors selegiline or rasagiline. While non-selective MAO inhibitors can be used just as well, they are better reserved for another day, after other alternatives have failed, due to their increased risk of serious cardiovascular complications, and the requirement for dietary restrictions to avoid that risk. MAO-B inhibition on its own is sufficient to significantly elevate PEA, but the effects are not necessarily noticeable subjectively.
In the absence of MAO-B inhibition PEA is metabolised so rapidly that it’s not only questionable whether foods such as dark chocolate have any significant psychoactive effects due to their high PEA content, but it’s questionable whether even large doses of pure PEA do. I recommend looking up the monograph on PEA in Shulgin’s PIHKAL – the part in question is freely available on-line (http://www.mdma.net/pea.html).
When increased PEA production is desired, D-phenylalanine (DPA) or D,L-phenylalanine (DLPA) is superior to L-phenylalanine, because DPA is readily decarboxylated to PEA, but can’t be hydroxylated to tyrosine (Tyr). However, DPA is typically considerably more expensive than LPA and DLPA.
LPA is also safe, but its overuse may be counterproductive, as it may “distract” tyrosine hydroxylase (TH) from its more important tasks, which is to hydroxylate Tyr into L-dopa – this is the rate-limiting step in catecholamine (dopamine, noradrenaline and adrenaline) synthesis, so it is not desirable to slow down the process. If LPA is too abundant relative to Tyr, TH will increasingly be working on hydroxylating LPA to Tyr.
A peripheral inhibitor of aromatic amino acid decarboxylase (AADC) is useful to increase the percentage of the dose of LPA or DPA available to the CNS, by preventing peripheral decarboxylation, which produces little but side effects. Unfortunately, AADC inhibitors seem difficult to find, other than from chemical suppliers – the only product I’ve heard of is a prescription carbidopa drug called Lodosyn; benserazide is an alternative to carbidopa, but I’ve only seen it in fixed ratio combination products with L-dopa (Madopar, Prolopa).
Administration of pure PEA in combination with MAO inhibition is the most powerful – and most risky – way of elevating PEA. The combination of PEA with unselective MAO inhibition is particularly dangerous, but some people do engage in this practice without apparent harm. Selective inhibition of MAO-B is sufficient to render PEA into a powerful vasopressor, and if it were to be taken in excess, death seems a realistic possibility. Indeed PEA is the only drug that has given me a first hand demonstration of the function of the baroreceptors.
My first dose of PEA, under selegiline treatment, elevated blood pressure enough to give rise to reflex bradycardia – the drop in heart rate to 60 and below is impressive for someone who has rarely noted a pulse below 75 in the absence of drugs. The CNS effects were impressive as well – the first doses of PEA remain the only treatments that have ever silenced my brain enough to restore full attention – it is interesting that a stimulant could induce a silence such that I could have chosen to fall asleep.
This may be a spectacular example of the “paradoxical calming effect” that has been reported with the administration of stimulants to people with ADHD. However, the “silence” effect turned out to be temporary, and with continued use of PEA, it was lost completely, gradually being displaced by the usual effects that I’ve noticed with other stimulants, including greatly enhanced motivation and eloquence.
After prolonged use on a daily basis, the first couple of doses or so after sleep would give rise to an enthusiastic flight of ideas that resembled hypomania, whereas subsequent doses would increasingly elicit irritable and compulsive behaviour. The short half-life of PEA, even under MAO inhibition, is not compatible with productive use of stimulants, but rather promotes compulsive and binging behaviours, including the use of repetitive dosing to maintain wakefulness for as long as several days, primarily due to the drug induced zealous determination to finish one or more of the numerous tasks started as a result of the drug’s motivational effect.
Yet, despite obsessive devotion, few projects would be finished, probably due to the frequent ups and downs resulting from the short duration of the drug, and the resulting fluctuation in catecholamine innervation, which is particularly detrimental to the prefrontal cortex and working memory. […] The repetitive use of oral PEA can begin to resemble descriptions of crack cocaine binging, and although PEA may be less addictive, it is likely worse in terms of neurotoxicity, considering that its mechanism of action is more similar to that of methamphetamine than that of cocaine.
For those unfamiliar with the literature, it’s very easy to produce dopaminergic neurotoxicity with amphetamines in animal models, whereas this is not the case with cocaine and other dopamine reuptake inhibitors. Unfortunately, there is no research pertaining specifically to the possible PEA neurotoxicity, so this is purely hypothetical. It is however, consistent with my subjective experience from using kilos of 99+% pure PEA over the course of a few years in the previous decade (the 2000s), ordered directly from chemical manufacturers, since it was not otherwise available.
Subjectively, my mental health was considerably better before the experience than after it, and although I have no scientific proof as to the relative contribution of PEA to the decline, it is a prime suspect. Any positive results from the experience in terms of real world accomplishments were at best exceedingly modest, and it is particularly embarrassing to admit how long I let myself be distracted from that fact by the seductive subjective effects of the drug. After waking up from sleep, I would always feel lethargic and miserable, but there was no low from which PEA could not lift me within minutes, not only back to the baseline prior to starting the drug, but all the way up to the enthusiastic flight of ideas surpassed only by hypomania.
This is of course spectacularly impressive, and a great thing in itself, as long as one doesn’t allow oneself to be so absorbed by it that one forgets to look at the results, because it’s the results that count, and when I finally looked at them the decision to quit was easy – indeed, it was particularly easy because I was so lethargic and apathetic that I could hardly motivate myself to make the short trip into town and the office where I kept my “stash”, or, for that matter, to renew my selegiline prescription. Almost certainly, if I had had an equally abundant supply of cocaine, the results would have been considerably more impressive, and perhaps sufficient not to even bother trying to quit.
If I had used methamphetamine (or dextroamphetamine), I might have felt just as bad upon waking, and just as bad upon quitting, but I would have accomplished much more. Those who are more prone to addiction, binging, and/or obsessive-compulsive behaviour than I am should take particular care to observe the utmost caution with PEA. Of course it’s easy to say all this in retrospect, with the benefit of hindsight, but no-one seemed to have this information when I started PEA.
Dr. Hector Sabelli’s overwhelmingly positive experience and documentation was the main reading material available at the time I started PEA. If nothing else, the main point I want to make is: whatever you do with PEA, don’t forget to look at the objective real world results from its use, because in the end, that’s the only thing that counts, whereas any subjective feelings the drug may impart are, however impressive, as ethereal as ethyl ether. (OK, sure it’s important to feel better, even temporarily, especially when one is depressed, and surely PEA is better than alcohol, but the least you can do before indulging in a repetitive PEA habit, is to try and find something safer and more useful. On the other hand, PEA does have the genuine advantage of being legal, so that an addict rarely has to resort to crime to support his habit. Then again, a prescription for Ritalin is not necessarily so hard to obtain, and although not as fun as PEA when taken as prescribed, it’s so much better with regard to the results, and quite possibly sufficient to make life with depression bearable.) [Source]
My only thoughts on his detailed response is that Dark Chocolate doesn’t need to have a lot of PEA for significant psychoactive effect. You could say that the other chemicals in cocoa/cacao are responsible for psychoactivity, but I would like to add that the there is a substantial amount of MAO inhibitors in cocoa for the active effects of PEA to be felt. Additionally, Cocoa isn’t just