WTA and potentiation

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Drael

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Hi all, you may know that tobacco produces potentiation. The most obvious example of this is while drinking. I believe this is due to the MAO inihibitors.

I have noticed that WTA e-liquids tend to have a slightly different profile regarding this, probably due to more reliance on the native MAOI in WTA e-liquids, and less on combustion MAOI's, like harmine in combustion tobacco. What I noticed was a slight but noticable increase in general potentiation. Since this experience, I started mixing down my WTA a little, and have noticed nothing since, but its not something you get to notice a lot.

Ive had an injury for which I was prescribed codiene, and noticed nothing there, but have not tried anything stronger. It is however known, and makes sense, that painkillers can be potentiated by tobacco.

I just want to know, of all you WTA users out there, have you noticed a slightly different interaction of your vape, with drinking, painkillers, or any mild herbs?

It would be very interesting to get feedback from others regarding this.
 

snork

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Interesting question, though I have nothing to add. In my life there's basically nothing for WTA to potentiate on/with/of. Which is also a word I don't think I've seen in print before and had to work out in my head what it means.
So you've come to believe that WTA potentiates stuff differently than nic-only? For the good or bad?
 

Drael

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What the heck is potentiation

It means one thing makes another stronger. Like with smoking and drinking.

Its essentially what makes WTAs work in the first place, the mao inhibitors potentiate the beat endorphin effects of nicotine, shifting the profile from plain stimulant to pleasurable relaxant. Tolerance of course working in the other direction.

So you've come to believe that WTA potentiates stuff differently than nic-only? For the good or bad?

I don't think nicotine by itself really potentiates at all. But yes, I think WTA does potentiate differently from smoked tobacco, a little more strongly - at least for certain things. According to my research on the mao profiles of tobacco WTA, versus combustion MAOI, this might seem to have something to do with the balance of mao-a verus mao-b inhibition, which would be slightly different (I believe more "b" from memory) in wta e-liquids versus tobacco smoke. In theory, this effect would be selective for certain things.

Unfortunately like yourself I don't have a lot going on in my life to where I would notice, I don't even really drink these days. I did have 30mg codiene without noticable effect however, but thats not a particularly large dose of opiates.

But I did notice some stronger than tobacco potentiation at one point, and have heard some people on heavy painkillers get sleepy (usually converting from nic only, so they could basically be consider WTA niave - meaning no tolerance, which is bound to be a factor too).

It would be interesting and also useful to chart out what peoples experience is here.
 
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olderthandirt

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Hullo Drael, a pleasure.
Your question is an interesting one for sure.

When DVap first embarked on isolating the various alkaloids along with the nicotine in 2009 there were many threads regarding the effects of harmine and such in the body. For the most part I got lost in those threads as the level of discussion was waaay over my head!
I am a simple sort (-;

I currently use nothing other than Welbutrin and a lot of Naproxin Sodium.
I stopped drinking about a month ago because having a couple of fingers of bourbon would immediately lead to grabbing one of the wife's rollies. Now after several days using the current run of WTA I'm very tempted to stop and pick up a pint of Makers Mark and see what's what (-:
 

Drael

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Oh, i aim for about 2/3 wta e-liquid to 1/3 nic only but its kinda rough sometimes it ends up more like 60/40 or 50/50. Not dripping either, just a clearo, smaller battery, no VV (although it is 2.0 ohms ish, so little warmer).

Id guess the stuff I had with my last little tipple was probably what 60/40? Definately nicer than nic only w/ drinking, some pleasure in the puffing with drinks, but little less than combustion tobacco I would guess, but thats at the mix and method I used.

Because the difference would be, in theory, partly in the mao-a, mao-b balance, in theory diff stuff could work differently, so ideally it would be nice to hear back from someone who a)drinks and b)has been on heavy painkillers, or some such...but..

I would say however from my experience, if anyone is avoiding drinking, to avoid smoking, well, you may have less reason to if you've got some good wta around. Seems to stratch a similar itch at least. Although that's not entirely the point in this thread, lol, i guess its still worth noting.

and of course, booze does mess with your judgement, so it might be worth keeping that in mind anyway....
 
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olderthandirt

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Ah, I see homepro. Lucky fella that your wife will self administer.
Can't get my wife to vape at all..... wonder if mine would let me "shotgun" some WTA to her occasionally (-;

ETA: Simultaneous posting there drael, Hullo!

As it is the DIY is covering all the bases for me with regards to tobacco cravings.
For the now I'm strictly dripping the 24mg DIY. With the scarcity of the stuff I'm hesitant to dilute what I have at all.
I've yet to try having a drink again to see about any potentiation effects.
 
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radiokaos

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I'm going to think about this and do a little research before I come up with a hypothesis.

However, wouldn't most drugs that work on the CNS might have some play with potentiation?

I was wondering if the term "potentiation" might be mistaken for "synergy" and wanted to see what you guys think?
 

Drael

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No, not really from my understanding.

What a mao inhibitor does is it stops a certain enzyme in the brain from preventing precursor's for neurotransmitors cross the blood brain barrier. This means there's basically more of everything. There are two types, a and b, that effect different NT's. This extra flood of NT's into the brain, should be what converts nicotines relatively strong acetylcholine stimulation, and weak beta endorphin stimulation, into a stronger beta endorphin effect, which produces pleasure and relaxation (versus mainly alertness and stimulation).

Tolerance with regular use does lower the impact, however smokers have been shown to have lower levels of mao-a and mao-b at all times, and we know there is both actions in WTA.

Mao's have been used to enhance everything from psychedelics to opiates to stimulants. Tobacco as it is, is anecdotally reported to enhance alcohol, opiates, a certain green herb, etc. The profile, from memory of the beta-carbolines in combustion tobacco, is slightly different to those mao inhibitors present in tobacco itself (from memory, the former is more "a" and the latter more "b")- and I think the half life of the former is shorter.

Now I don't know if this makes a lot of difference in smoked tobacco versus wta, but it might make a difference. Certainly WTA is thusly chemically more like snus, but with a quicker onset. We do know that some people on very heavy painkillers reported sleepiness on trying WTA, and they stopped using it for that reason. Keeping in mind they were essentially tobacco niave, because they weren't consuming WTA prior. In theory, if they started smoking it could be the same. We don't know.

I am 99.9% sure that the mao is the reason why WTA works like it does, by enhancing the beta endorphin effect of nicotine, based on both studies, and my own pretty intense knowledge of the brains chemistry. I am, to a very limited degree guessing, but based on a heck of a lot of known facts, such as the beta endorphin effect of nicotine, mao-b's ability to enhance any similar action, and studies on wta and nicotine, versus nicotine alone. So even though this is not what science currently says, it is "this close" to the same conclusion already (and I used to be a major drug geek, and I have a degree in psychology too) - so I am pretty damn sure this is how wta does its magic (and the longer half lives of WTA's also help of course, with the nicotinic receptor action)

But I don't know if this has implications for medications, or drinking, or not versus smoking which does definately enhance some things, but its theoretically possible. I am not sure the implication would be huge, though, but it might be there.

From what I can tell drinking is about the same as smoking versus vaping WTA, which is a huge plus, because you don't feel like smoking so much. But I can't speak for the other chemicals except for my paltry 30mg codiene dose when I was temporarily ill.
 

Drael

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Here's some related science:

Monoamine Oxidase Inhibition Dramatically Increases the Motivation to Self-Administer Nicotine in Rats (Monoamine Oxidase Inhibition Dramatically Increases the Motivation to Self-Administer Nicotine in Rats)

Human monoamine oxidase is inhibited by tobacco smoke: beta-carboline alkaloids act as potent and reversible inhibitors.(Human monoamine oxidase is inhibi... [Biochem Biophys Res Commun. 2005] - PubMed - NCBI)

Brain monoamine oxidase A inhibition in cigarette smokers (Brain monoamine oxidase A inhibition in cigarette)

Parkinson's Inhibitor Fingered in Tobacco (Parkinson's Inhibitor Fingered in Tobacco | Science/AAAS | News)

Anatabine, one of the major WTAs, as a mao inihibitor (Anatabine - Wikipedia, the free encyclopedia)

Other WTA's and mao (actually most of the minor WTAs seem to be mao. Some of them are just like nicotine though)
http://www.tandfonline.com/doi/abs/10.1080/10298420290015854#.UnbJ_uWHN3E


And just so everyone knows what I am talking about better:

Minor alkaloids in tobacco are - cotinine, beta nicotyrine, nornicotine, myosmine, anasabine, n-methylanasabine and anatabine

(A good portion of these are mao-i, and both of the below combustion products are also, this is why e-liquid WTA is different, different nicotine levels are absorbed - usually this is less than smoking per puff, probably same with the minor parts - different absorbption, and WTA relies more on this list, because the combustion ones are absent -this _may or may_ not create a slightly different level of mao-a or mao-b inhibition, and potentially an altered duration of said inhibition, slightly altering the mao profile versus smoking)

Present only in combustion tobacco; harman and norharman.
 
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