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Opiates (Buprenorphine) and MAOIs

mitragyna

mitragyna

Bluelighter
Joined
Dec 7, 2006
Messages
242
I have been Suboxone (Buprenorphine) for about 6 months now. Just about 2.5 months ago, I was put on Nardil (Phenelzine). Before I was put on the Bupe, I was also taking Emsam (Selegiline) for about 2 years.

Before I started taking Nardil, I was at the point where I didn't really feel anything from the Bupe, it just kept me from withdrawling. After I started taking the Nardil though, I noticed a dramatic increase in the effects of the Bupe.

I'm wondering exactly how Nardil (or any MAOI for that matter), increases the effects of Opiates/Opioids. I mean, I understand how an MAOI can increase the effects of a drug such as Amphetamine...basically because it prevents the breakdown and degradation of DA and NE (there's more but I'm being blunt). I understand that MAO-A is responsible for the breakdown of SER/NE, etc., and MAO-B is responsible for DA/trace amines. But what is the Nardil preventing the breakdown of, when it comes to Opiates...and what is responsible for the increase in effects? Is it the DA?

Also, is there something an MAO-A/MAO-B Inhibitor does different to an Opiate than just an MAO-B Inhibitor? I'm asking because I'm curious why I felt such an increase in the Suboxone's effects with the Nardil, but not the Selegiline...

I apologize if this is confusing...I just didn't know how else to put it. Thanks for the help!
 
You know, since I've started on selegiline (7-8mg orally) I've noticed greatly increased effects. Not sedation-wise. That's not much different. However, if I lay down to take a nap when it's effects are strongest (2.5-3 hours after first putting it under my tongue) I experience substantial "rushes" like I'd have from nodding on a 'real' opiate.

No idea why, but no complaints either.
 
^
That's odd you say that, because I get the same thing. I've been nodding like mad since I've started the Nardil. The weird thing is, when I'm nodding on a full agonist, I have extreme euphoria. On Suboxone and Nardil, I nod...but I'm really not that euphoric. It's quite odd!

I really get noddy when I'm tired now. Even just a little bit and I can't even keep my eyes open!
 
The rushes? I used to notice them when I was first on methadone (if I'd take the drug and then go to bed) or when I'd nod from whatever. Now, though, this has been rather interesting.

I also take 125mg of diphenhydramine each day (tommorow it'll be doxylamine) and since I've added the selegiline when the diphen kicks in, it is a really uncomfortable feeling. Something of a blend between akathasia and general dizziness, like something is just a bit off. Only lasts about 30-45 minutes, though.

First time it happened I had a panic attack, thought "Oh fuck, serotonin syndrome"
 
Hammilton said:
The rushes? I used to notice them when I was first on methadone (if I'd take the drug and then go to bed) or when I'd nod from whatever. Now, though, this has been rather interesting.

I also take 125mg of diphenhydramine each day (tommorow it'll be doxylamine) and since I've added the selegiline when the diphen kicks in, it is a really uncomfortable feeling. Something of a blend between akathasia and general dizziness, like something is just a bit off. Only lasts about 30-45 minutes, though.

First time it happened I had a panic attack, thought "Oh fuck, serotonin syndrome"
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Whoops sorry, I read your post wrong. I missed the "rushes" part, I though you just said "nodding".

How long have you been on Suboxone, Hammilton? And what dose? If you don't mind me asking...
 
3 years, 8mg daily. I use a bit of whatever 40% ethanol I have on hand to increase bioavailability. Tequila lately. Never drink any of it though. I forget if it increase the 30% to 50% or increases the 30% by 50% to 45%. Something like this though.
 
Hammilton said:
3 years, 8mg daily. I use a bit of whatever 40% ethanol I have on hand to increase bioavailability. Tequila lately. Never drink any of it though. I forget if it increase the 30% to 50% or increases the 30% by 50% to 45%. Something like this though.
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Ethanol increases bioavailability?? How so? How do you do this?
 
hold a cap's worth of tequila (I prefer whiskey) under yer tongue. you get used to the burning pain after a few minutes and the tears stop
 
Opiates stimulate dopamine release, that might have something to do with why an MAOI would enhance the opiate effect. Also Subuxone contains nalaxone which antagonizes the mu-opioid receptor which might be the reason for no euphoria on subuxone. Subutex doesn't contain nalaxone, just bupe.
 
Also Subuxone contains nalaxone which antagonizes the mu-opioid receptor which might be the reason for no euphoria on subuxone.
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What a load of bullshit.

The reason you don't get euphoria from buprenorphine is that it isn't a very euphoric substance to begin with. Naloxone has nothing to do with it since naloxone's binding affinity is lower than buprenorphine's thus the two cannot bind simultaneously.
 
Illuminateur said:
Opiates stimulate dopamine release, that might have something to do with why an MAOI would enhance the opiate effect. Also Subuxone contains nalaxone which antagonizes the mu-opioid receptor which might be the reason for no euphoria on subuxone. Subutex doesn't contain nalaxone, just bupe.
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Bluelight should start imposing some sort of monetary penalty on people who continue to disseminate this incorrect information regarding the whole suboxone/naloxone issue.
I dont think there has been a myth that has been MORE completely dispelled, and yet every single day people still come on here and rant on about how the naloxone in suboxone acts as an antagonist.
For the last time... (I wish)- the naloxone is essentially not active because buprenorphine has such higher affinity. The manufacturers of suboxone pulled a fast one on the medical community. It's almost admirable how effectively they pulled the wool over the medical communities eyes. -DG
 
Bluelight should start imposing some sort of monetary penalty on people who continue to disseminate this incorrect information regarding the whole suboxone/naloxone issue.
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Hear hear, and pay the money to me! =D

Let's put it this way... I just IV:d a suboxone today. Works just fine.
 
I could be wrong but isnt the antagonist effect supposed to kick in after the bupe wears off? Maybe that action somehow avoids chem dependence from forming
 
I think the nalaxone isn't for the bupe, they want the bupe working so the heroin addicts don't go into withdrawal, although that still can happen. But the nalaxone does have a stronger binding affinity that many of the other opiates, it's a backup to prevent the person abusing other drugs. Also, nalaxone's primarily a mu-antagonist with lower affinity at delta and sigma, and I think buprenorphine affects all?

Maybe the selegiline also presents a danger because it's metabolised by similar enzymes? Though iI think it's more 3A4 based that 2D6, which is what does opiates. But there's crossover...
 
Illuminateur said:
I think the nalaxone isn't for the bupe, they want the bupe working so the heroin addicts don't go into withdrawal, although that still can happen. But the nalaxone does have a stronger binding affinity that many of the other opiates, it's a backup to prevent the person abusing other drugs. Also, nalaxone's primarily a mu-antagonist with lower affinity at delta and sigma, and I think buprenorphine affects all?
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That doesn't make any sense. A backup? There's no need for a backup. Bupe itself blocks other opioids due to its very high binding affinity. This topic has been discussed over and over in this forum from what I've seen... and I've only been posting a few months! Also, the sigma receptor is not an opioid receptor - the endogenous ligand for sigma receptors has yet to be discovered.

You are right that Bupe has effects at other opioid receptors though. It acts as a weak partial agonist at Delta receptors and as a potent antagonist at kappa receptors. It's also an agonist of the ORL-1 receptor.

Oh, and as for the OP... I know its an old post, but a possible mechanism here is Nardil's inhibition of GABA-Transaminase. That could, theoretically, add to the sedating effects of opiates. That would only apply to Nardil though, not all MAOIs.

I myself was on Bupe and Nardil for a time many years ago... it was a pretty sedating combo.
 
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Sigma was considered an opioid receptor for many years (decades?). Many opioids bind to it, though it's usually one optical isomer and not the other, but why exactly it isn't considered an opioid receptor isn't entirely clear to me. It seems to be a meaningless distinction. It doesn't make much sense to name receptors based upon which exogenous compounds bind to them, anyway. The only reason to continue is tradition and simplicity, in my mind. Naming them based on endogenous ligands isn't usually the way to go either, though, since they usually need names long before the endogenous ligand is discovered.

Sigma has at least one known endogenous ligand (DMT), and for some reason I think that DHEA is a sigma ligand, but that's probably wrong.
 
Yeah I knew about DHEA and DMT. I should have said is there is no endogenous ligand that's considered to be the "primary" ligand, if that makes any sense... that may be an erroneous concept on my part anyway.
 
Let me clarify what I meant: Pretty much any drug you take is not going to bind to 100% of receptors, that's a large part of the reason why taking more has a stronger effect. The nalaxone isn't to get between the buprenorphine and the receptor, it's a line of defense not only against heroin/oxy etc, but also to counteract any that gets through. Assuming it sends negative signal, not just blocks. Someone?
 
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