The title says it, actually.
More specifically, regarding oral consumption - what are the effects of these two and are there any differences in results?
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Phenylalanine vs Phenylethylamine
Started by
steelsky
, Apr 04 2010 02:48 PM
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#2
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Posted 04 April 2010 - 03:43 PM
The title says it, actually.
More specifically, regarding oral consumption - what are the effects of these two and are there any differences in results?
Phenylalanine: dietary amino acid; converted into Tyrosine by PAH. It's also converted by AACD into phenyethylamine (PEA). Phenylalanine only has direct biologic effects if you can't metabolize it. Any effects from phenylalanine come from its metabolites, tyrosine and PEA. I'm not sure what controls the ratio of tyrosine to PEA; possibly the amount of tyrosine present, and possibly the availability of P5P (the active form of vitamin B6).
What complicates things is that tyrosine, in turn, can be converted into tyramine, which has effects similar to PEA.
Phenylethylamine/phenethylamine/PEA: Easily crosses blood-brain barrier, but rapidly broken down in the body (half-life of about 10 minutes). Effects similar to amphetamines, although those with more experience with PEA can give you more details. It's broken down by MAO-B so it's often combined with selegeline (deprenyl) to extend its half-life.
Tyramine and PEA are both agonists of TAAR1 (Trace Amino-Acid Receptor). This receptor was only discovered recently but it has a lot of significance for us.
Aspartame, the artificial sweetener, is about 50% phenylalanine (hence the warning on diet sodas for people who have trouble metabolizing phenylalanine). I have a few friends who crave Diet Coke, and could easily drink a 2L bottle in a sitting. This provides about 500g of phenylalanine. I used to drink a lot of Diet Coke before I started Adderall; my cravings disappeared when I started. My theory is that I was self-medicating with aspartame.
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Posted 04 April 2010 - 03:59 PM
The combination of either of these substances with selegeline (deprenyl) interests me. Does selegeline has the same effect on PEA converted from Phenylalanine (by inhibiting its breakdown), or does it just allow more PEA to be absorbed in the body?
If one is interested in boosting one's Dopamine/Nurepinephrin levels, which combination should one try, and in what dosage?
If one is interested in boosting one's Dopamine/Nurepinephrin levels, which combination should one try, and in what dosage?
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Posted 04 April 2010 - 04:10 PM
The combination of either of these substances with selegeline (deprenyl) interests me. Does selegeline has the same effect on PEA converted from Phenylalanine (by inhibiting its breakdown), or does it just allow more PEA to be absorbed in the body?
If one is interested in boosting one's Dopamine/Nurepinephrin levels, which combination should one try, and in what dosage?
Selegeline should have the same effect on PEA no matter where the PEA comes from. As you've learned, PEA will increase dopamine and NE levels.
You can search the forum for info about combos. I take selegeline every other day but not with PEA. I recommend seeing what PEA does without selegeline first; it'll be much safer that way. Then titrate your selegeline dosage upwards. But bear in mind that selegeline is an irreversible MAO-B inhibitor, so it takes a week or two to reach prior MAO-B levels after selegeline. If you take it in small doses periodically, you will progressively knock down your MAO-B capacity.
As with all stimulants, you will probably develop tolerance, so be careful.
Edited by LabRat84, 04 April 2010 - 04:13 PM.
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Posted 06 April 2010 - 11:16 PM
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 realising 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. Indeed, i would go as far as to assume that even the relatively short-lasting cocaine would be a better choice than PEA for the purposes of productivity enhancement, at least in the case of oral or intranasal cocaine. 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.)
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. Indeed, i would go as far as to assume that even the relatively short-lasting cocaine would be a better choice than PEA for the purposes of productivity enhancement, at least in the case of oral or intranasal cocaine. 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.)
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Posted 08 April 2010 - 07:22 AM
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.
This is why you should stay somewhat active when you feel the rush. Sitting down doing nothing my blood pressure went from 130/70 to 180/112. My heart rate was a little lower than I would have thought from feeling so great so I wondered if I got my heart rate up, will my blood pressure compensate. And it did. 40 pushups later (pea must help with stamina as usually I couldn't be bothered anymore after 20), my blood pressure dropped to 80/50 and my heart rate went skyward to 144 which is higher than what I would normally get from doing some pushups.
I think PEA must also help with memory. I remember almost each instance, each night I took PEA I would have just forgotten and slipped my mind. Years later I still remember the readings on the blood pressure monitor without having to look it up
(another reason I think PEA should be used rarely and not to get through a boring day of work or motivation for some boring house chores.
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Posted 14 April 2010 - 08:33 PM
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.
This is why you should stay somewhat active when you feel the rush. Sitting down doing nothing my blood pressure went from 130/70 to 180/112. My heart rate was a little lower than I would have thought from feeling so great so I wondered if I got my heart rate up, will my blood pressure compensate. And it did. 40 pushups later (pea must help with stamina as usually I couldn't be bothered anymore after 20), my blood pressure dropped to 80/50 and my heart rate went skyward to 144 which is higher than what I would normally get from doing some pushups.
Adrenaline, released in response to exercise (or agitation) normally dilates blood vessels, especially those supplying the muscles, and this causes a drop in especially the diastolic blood pressure. However, pulse pressure isn't supposed to drop drastically, but in your example it went from 68 (180 minus 112) to 30, and the drop down to 80 systolic is not a healthy response either. If it had dropped much further, it's likely that you would have passed out. The high heart rate was simply required in order to maintain sufficient pressure. Taken together, these facts would seem to indicate a depletion of sympathetic nervous system catecholamines, which is hardly surprising considering PEA's mechanism of action. I had this kind of effects from PEA too. Although it boosts determination, and hence facilitates sustained effort, it seems to actually reduce exercise tolerance.
I think PEA must also help with memory. I remember almost each instance, each night I took PEA I would have just forgotten and slipped my mind. Years later I still remember the readings on the blood pressure monitor without having to look it up
PEA does boost attention and memory, much like other stimulants. The vivid memories of the intense high is a major mechanism underlying the psychological addiction to crack cocaine and crystal meth.
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