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PEA + reboxetine

wreckhead

Bluelighter
Joined
Dec 22, 2008
Messages
58
I've been interested in phenylethylamine for a long time and tried some a few days ago with selegiline. It gave massive euphoria, but effects on heart rate and BP were too great for regular use. I've been looking into ways to isolate the dopaminergic effects and came across this study:

http://ajpheart.physiology.org/cgi/content/abstract/236/4/H592

beta-Phenylethylamine increased mean aortic blood pressure, total peripheral vascular resistance, left ventricular dP/dt, and (dP/dt)/P in chloralose-anesthetized dogs. Pretreatment with phentolamine reduced the increases in aortic blood pressure and total peripheral vascular resistance produced by beta-phenylethylamine, whereas, the effects of beta-phenylethylamine on left ventricular dP/dt and (dP/dt)/P were abolished by propranolol. beta-Phenylethylamine pretreatment, but increased both after phentolamine pretreatment. Furthermore, both the cardiac and vascular effects of beta-phenylethylamine were abolished by desipramine. These results indicate that beta-phenylethylamine exerts both positive inotropic and vasoconstrictory effects, probably by releasing endogenous norepinephrine from the adrenergic nerve endings.

This proves that PEA's adrenergic effects can be completely negated by the use of NRIs such as reboxetine, or even SNRIs which many people are on. It appears similar to the way reboxetine prevents MAOI tyramine reactions.

I'm not sure about dose, but doesn't this mean the main problem with PEA use can be overcome?

I've also considered carvedilol for mixed alpha and beta blocking, but this seems like a cleaner approach. Maybe I could use some to block the effect of reboxetine itself.

Comments?
 
Using these RIs with an MAOI is a really bad idea, a good way to end up with serotonin syndrome.
 
I am using selegiline, which is selective for MAO-B at lower doses, thus does not increase noradrenaline levels. Serotonin is not involved anywhere in this combination so I don't know where you came up with that idea.

Any serious replies?
 
Actually Hammilton's reply is as serious as they come.

Remember that this is first and foremost a Harm Reduction forum.

Perhaps not serotonin syndrome, but you could just as easily end up with hypertensive crisis. You are simply taking far too many chances mixing up three contra-indicated drugs altogether.

Also while doing that, you are playing with not just your brain, but your brain AND your enzymes all at once, as you already know. Do you know EVERYTHING that goes on between those three? Do you realize that, with every drug you add to the mix, you add a multitude of complications simply to remove one.
 
^ Although PEA has some pressor activity, the real thing to watch for is probably hyperthermia (core temp increasing to dangerous levels). This is the main swrious complication to occur with a conbo of amphetamine & deprenyl/selegeline.

It's not serotonin syndrome, but it has a fair few symptoms in common with it (like death)
 
i've read that PEA's effects are really short lived, even with MAOb inhibitors. Unless you use it regularly, I don't think that increase in heart rate and BP would be a problem. Think of how weed makes your heart go a million miles per hour (which also can increases PEA by 4-fold), and it doesn't cause any problems with occasional use, unless you already have heart problems. You could also look into ginkgo biloba, which will cause vasodilation that will decrease heart rate and BP. Gingko is also a mild MAOI which can increase PEA's effects.
 
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I am using selegiline, which is selective for MAO-B at lower doses, thus does not increase noradrenaline levels. Serotonin is not involved anywhere in this combination so I don't know where you came up with that idea.

Any serious replies?

1. Doses aren't given, and selegiline is commonly used at doses where serotonin and NA are effected.

2. I was thinking of Femoxetine, not Reboxetine, which has significant SRI effects. My mistake here.

perhaps by providing enough information you could get a few more "serious" replies?
 
Dear Wreckhead,

I'm curious as to what you'll find out, BUT.......

PEA is dangerous in other ways too. Others have mentioned some of them, and I'll add that it also inhibits the enzyme that breaks down histamine. I had my first asthma attack ever very soon after starting to use it.

PLEASE BE CAREFUL.....merely exceeding the dose accidentally by losing track of times you take it can really harm you.

That being said, I use it because it's the only thing that helps me with neurological complications from long term high dose Effexor use, and if anyone finds a safe way to use it I'm all ears.

Jim
 
^ Interesting about the Histamine. Do you happen to have more info on the matter?

---

It seems to me that these day, playing with enzymes has become a sort of pastime for some people. It seems they do not realize just how thin a line they are walking.
 
1. Doses aren't given, and selegiline is commonly used at doses where serotonin and NA are effected.

perhaps by providing enough information you could get a few more "serious" replies?

Most people use selegiline at MAO-B selective doses and in this context you're being a bit pedantic. There are plenty of unselective MAOIs that are much cheaper for that purpose.

Dear Wreckhead,

I'm curious as to what you'll find out, BUT.......

PEA is dangerous in other ways too. Others have mentioned some of them, and I'll add that it also inhibits the enzyme that breaks down histamine. I had my first asthma attack ever very soon after starting to use it.

Source? I experienced the same coughing on a high(ish) dose, but assumed it was due to pulmonary hypertension (something reboxetine would prevent). Shortness of breath and dizziness also occurred, which are other signs of pulmonary hypertension.

PLEASE BE CAREFUL.....merely exceeding the dose accidentally by losing track of times you take it can really harm you.

I found out how dangerous PEA + selegiline is (especially with alcohol and other drugs), but when my next batch arrives I will have a nice pile of benzos and opiates for the case of hypertensive crises. The reboxetine should stop this happening, but my point is, I'm perfectly safe.

Taken on its own PEA is way too dangerous, but this combination should be incredibly selective to dopamine and highly euphoric.
 
Source? I experienced the same coughing on a high(ish) dose, but assumed it was due to pulmonary hypertension (something reboxetine would prevent). Shortness of breath and dizziness also occurred, which are other signs of pulmonary hypertension.

Reboxetine does not prevent hypertension, it actually causes it http://www.ingentaconnect.com/content/adis/cns/1999/00000012/00000001/art00006, though the opposite is sometimes also seen.

Lots of them:
Voigt et al. 1974 Summer and Taylor 1979 Taylor and Lieber 1979 Lyons et al. 1983 Hui and Taylor 1985 Taylor 1986

Most people use selegiline at MAO-B selective doses and in this context you're being a bit pedantic. There are plenty of unselective MAOIs that are much cheaper for that purpose.

Is it fashionable now to use the word pedantic as an insult incorrectly? Reread #4&5 in this thread.
 
Reboxetine does not prevent hypertension, it actually causes it http://www.ingentaconnect.com/content/adis/cns/1999/00000012/00000001/art00006, though the opposite is sometimes also seen.

That's true, but we can assume the PEA-induced hypertension is due to its release of noradrenaline, and a low dose of reboxetine would prevent this release theoretically. The dose of reboxetine would slightly raise BP, but probably to an even lesser extent than SNRIs which people don't tend to worry about.
 
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