Too much Phenylethylamine (PEA)?

[mitragyna]

I've been taking PEA, continuously for about 3 months now (along with Selegiline). Due to it's incredibly short duration, I have to re-dose about every 30 minutes. I also dose so many times a day to avoid it's terrible comedown, otherwise I feel like shit for the whole day after taking it.

So I'm wondering, if I've been taking PEA about every 30 minutes (of course, not while I'm sleeping) for 3 months, am I at risk for any problems. I mean, it just seems too good to be true, it brings such a powerful euphoria and stimulation. The PEA seems to be just what I need to avoid my incredible lack of motivation.

Are there any health risks involved with administering PEA so frequently (besides a hypertensive reaction - I take a fairly low dose)? I'm worried about my Dopamine levels, and possibly a lack of endogenous PEA after cessation...

Thanks!

 

[Hammilton]

Wow, you're such a smart guy, but you've been dosing every 30 minutes for months? Seriously, do you make it through an entire night of sleep?

You're gonna end up being a case study in Addiction if you keep this up.

 

[THE EXPERIENCE]

Hey i'm new here and heard of a lot of shitbut forgive me what is pea?

 

[LuxEtVeritas]

indeed as you are a bright guy I would think you would note this is clearly abusive use of a potent stimulant substance and isfairly akin to abuse of course of the more common stimulant amphetamine and meth and has many of the same pitfalls enherent to their abuse

 

[THE EXPERIENCE]

Thank you

Now i feel stupid, another question. Has anyone figured out what is active in red dawn vector? I am on it now and it's like a mild mdma buzz, but not dxm like everyone says. I would know i used to dose on 1,600 mg. At a time. I too have also bee up on the stimulant methylphenidate, but hve not had it in 4 hrs.thank ou for your kind insight!

 

[negrogesic]

How much PEA have you been taking? What route?

How much per day?

I would imagine that PEA abuse with an MAO-B would carry risks similar to amphetamine abuse. Keep in mind that, like PEA, d-meth also binds to the TAAR...

 

[mitragyna]

How much PEA have you been taking? What route?

How much per day?

I would imagine that PEA abuse with an MAO-B would carry risks similar to amphetamine abuse. Keep in mind that, like PEA, d-meth also binds to the TAAR...

If I had to take a guess I've probably been taking up to 700 mg per day. And yes, I understand the potential for abuse, I've been trying to cut down the last few days.

I'm sorry, but what is TAAR?

 

[MurphyClox]

TAAR (Trace-amine associated receptor; see here for the term "trace amines")

 

[hamhurricane]

is 700mg/day very high? the smallest capsules i have seen used 250mg increments, what is a threshold dose for PEA when MAO-B inhibited?

 

[mitragyna]

is 700mg/day very high? the smallest capsules i have seen used 250mg increments, what is a threshold dose for PEA when MAO-B inhibited?

I don't think 700 mg/day is that high compared to the doses I've heard of other people people taking. I certainly wouldn't want to go higher though, just 25 mg makes me speed my ass off. I buy my PEA in bulk so I can cap my own doses. I am taking a fairly high dose of Selegiline though, I'm not sure if that has anything to do with it.

Well now that I've started cutting back my PEA dose substantially, I've been getting a serious case of RLS. As far as I know, RLS is usually remedied by Dopamine-enhancing drugs...so would I be getting this now because there's not enough DA to be released? Although I would think that the Selegiline would be inhibiting the breakdown of this...

Would something like DLPA be helpful for something like RLS (by contributing more Dopamine)?

 

[Hammilton]

So you don't think 28 times a strong dose is a lot? That seems like a massive dose.

What's a noticable dose? I mean, with selegiline, how does potency compare to amphetamine sans MAO inhibition?

 

[hamhurricane]

thats incredible i had no idea how strong PEA was on selegiline! back when i was on seleg i would take phenylalanine regularly but not phenethylamine, it gave a pretty decent boost but im sure nothing compared to PEA, it would seem almost equipotent to AMP.

 

[FrostyMcFailure]

Well now that I've started cutting back my PEA dose substantially, I've been getting a serious case of RLS.

IMO thats a bad sign but as stated prior this is an awesome case study. Thats a lot of PMA though i wonder if their is any side effects from taking an MAOBI for extended periods of time.

Get off that as soon as possible, if you need to wane so be it but cold turkey is usually best IMO. RLS suckksss ass during Smack withdrawal.

doesnt extended use of methamphetamine destroys dopamine receptors permanently?

 

[mitragyna]

IMO thats a bad sign but as stated prior this is an awesome case study. Thats a lot of PMA though i wonder if their is any side effects from taking an MAOBI for extended periods of time.

Get off that as soon as possible, if you need to wane so be it but cold turkey is usually best IMO. RLS suckksss ass during Smack withdrawal.

doesnt extended use of methamphetamine destroys dopamine receptors permanently?

Well if Meth does destroy dopamine receptors permanently, does that mean PEA also has the potential to do so? Since they share a lot of the same neuroactivity it seems...

UPDATE: Well, I've cut back substantially on my PEA intake thus far. It is shocking how similar PEA is to Amphetamine/Methamphetamine, like LuxEtVeritas said earlier. The 'withdrawl' is also similar, I've been sleeping a lot since I've reduced my dose. Very lethargic. Now I just need to find out what to do with the 300+ grams of PEA I have sitting here...

 

[shibireru]

^ This isn't proof of anything. I am just submitting it to give you food for thought.

Not too long ago I overdosed on phenylethylamine and selegiline: I had a hypertensive crisis and had to go to the hospital where they did fuck-all to help me because they had no idea what phenylethylamine was.

I am quite certain that I incurred significant brain damage.

I kept dosing again and again within a very short period. I knew that what I was doing was extremely stupid and risky but I couldn't stop because the euphoria I was experiencing was just so exquisite. I actually considered at the time the option of taking a huge amount of the stuff and then killing myself if and when I began to experience symptoms of overdose or began to sense the onset of a harrowing comedown. In the end, though, knowing that I couldn't bring myself to jump out the window, and fearful that the phenylethylamine would fail to kill me but not fail to cause brain damage, I called an ambulance and now I have a medical bills totaling $3300 dollars that I can not pay despite the fact that they didn't really do anything at all to help me except to give me copious amounts of benzodiazepines, upon which I am now dependent for sleep.

/It's interesting to note that while phenylethylamine induces euphoria and increased motivation in me, dextroamphetamine simply produces ergogenic, anxiogenic, and dysphoric effects. (It should be taken into account, though, that the first time I took dextroamphetamine was after my little overdose - whose silver lining was that it occasioned a more complete understanding of just how profoundly incompetent and cavalier medical "professionals" can be.)

//How fucked up is it that my doctor gave me dextroamphetamine without me even asking and despite that I showed few if any signs of ADHD but wouldn't give me any opiates when I reported to him that the dextroamphetamine he had given me had produced acute dysphoria and that opiates were the only substances I knew of that resolved my depression and made me feel normal? I even explained to the idiot that I had tried in the past fluoxetine, paroxetine, sertraline, duloxetine, desvenlafaxine, citalopram, escitalopram, bupropion, and some maoi without significant remediation of my psychiatric problems and he still wouldn't consider giving me opiates even for short-term use. I think I would prefer total physiological and psychological dependence upon opiates to feeling the way I do now; at least I would feel good for a little while. If I don't take them, I will certainly continue to experience anhedonia and despair until my death (which I may expedite if things don't change soon.)

 

[mitragyna]

^ Wow man, thanks for that post. I hope everything is well. Your experience is actually very similar to mine.

It really is quite an impulsive drug (PEA), while on an MAOI. It's induces so much euphoria, but it's duration is so short, that it's quite tough not to keep re-dosing. Not to mention the comedown is hell. I've actually never experienced a drug that brings that powerful of euphoria, to tell you the truth.

I also experienced a hypertensive crisis just lately. Luckily I'm alright...at least as far as I know. That was one absolutely terrible headache I had though, I could of sworn my head was going to explode .

Time to throw this PEA out, it's too tempting just sitting here!

EDIT: Shibireru - how much PEA were you dosing at once? How do you know you incurred brain damage? What symptoms? Why did the doctors not give you something to lower your blood pressure, not just benzodiazepines?

 

[hamhurricane]

what would the mechanism of the toxicity be with PEA if you were on selegiline? i was under the impression that (sans addiction) it was relatively safe.

 

[shibireru]

What the hell?? I thought PEA was fully inactive?

Absolutely not. It's just that first pass metabolism destroys something like 95% of it. Specifically MAO-B metabolizes it. Hence the MAO-B inhibitor, selegiline. If you don't take an MAO-B inhibitor you need to take in excess of a gram of PEA to get any effects. With the selegiline, you need to take only 100 mg or so to produce very noticeable effects.


DO NOT GIVE FUCKING SOURCES (or shit will follow)

 

[NeuronalPerception]

What the hell?? I thought PEA was fully inactive? According Shulgin at least:

http://www.erowid.org/library/books_online/pihkal/pihkal142.shtml

What is it's mechanism of action? Obviously it boosts dopamine (and perhaps norepinephrine), but how? Is it a reuptake inhibitor/releaser? Or is it merely a precursor supplement (this is what I'm leaning towards)? Or perhaps an agonist? Please elaborate on this subject I'm highly interested!

By the way also where do you guys get your PEA from? Do stores like GNC sell it by any chance or do you have to order it online? I'm going back on the MAOI phenelzine (nardil) soon and I'd really like to try it now in conjunction with the MAOI. The combination sounds lovely.

PEA works on Trace amine receptors and in higher doses may act as an dopamine reuptake inhibitor. It has quick and short acting dopamine agonist effects as well.

YOU'VE BEEN WARNED FOR POSTING SOURCES IN THE PAST, PASTING A POST WHERE SOMEONE ELSE IS WILL GET YOU ANOTHER IF YOU PERSIST

PEA does not get destroyed so much as it gets converted into active metabolites. However it gets converted quickly so it usually requires 1.5-2 grams to notice an effect or predosing with MAO-B inhibitors and taking a lower dose.

Here's a massive thread discussing it.

NO HERE'S A SOURCE WHERE THEY DISCUSS IT, WHICH ISN'T ACCEPTABLE

 

[macropsia]

Mitrgyna: Have you considered trying to switch to D,L-PA or L-PA to sort of 'detox' off of the PEA? D,L-PA should increase endogenous PEA as well (+ l-dep, that is), plus L-PA is a decent dopamine precursor. Either of these + deprenyl should be active and provide a significant boost, and are probably not significantly harmful. I'd recommend trying this over the considerably more dangerous deprenyl+PEA. (I've tried both and they just seemed to, quite paradoxically, worsen my persistent idiopathic akathisia for about four hours in the middle of the day. However, I'm well aware my neurochemistry is in no way normal, so I'm not going to try to generalize from my experience)

Also, it would seem that the risk of neurotoxicity would be somewhat lower here than with AMP, since the l-deprenyl is obviously 'narrowing' the metabolic pathway that typically leads to the production of free radicals and such (which I figure is the primary mechanism of dopamine neurotoxicity?).. that, is, unless there's another toxic mechanism at play here.

Would it thus seem likely (assuming that the regular pathways for neurotoxicity are not active in any substantial amount) that any lingering effects are more liable to be from compensatory upregulation of dopamine receptors, plus compensatory decreases in transmission and (possibly) production? These would explain any hypersomnolence, amotivation, anhedonia etc. This could also explain the RLS as well. Just a thought.

Also, I'd be interested to see if atomoxetine would work to mitigate the RLS, as it's done good things for my akathisia. That's not something that's fun to live with for any period of time.

IMO thats a bad sign but as stated prior this is an awesome case study. Thats a lot of PMA though i wonder if their is any side effects from taking an MAOBI for extended periods of time.

Err, I hope you mean PEA. And the inventor of selegiline, Jozsef Knoll, recommended daily low-dose deprenyl for everyone over 40 as a protection against natural oxidative stress. It's really a pretty neat and safe drug, actually. By itself, I don't think it should have any negative long-term consequences.