Hi I wanted to see if I could continue this old thread.
<LINKS to cigarettes and MAO inhibition being critical in tobacco dependence is listed at bottom of post >
I am using whole tobacco alkaloid 3mg nicotine e juice at the moment and wondered if anyone else does. Also wanted to see if we can continue the discussion.
Here is a link to old thread : Beta Carboline MAOIs - towards a more effective e-liquid
All I see is it is closed to replies and haven’t found any other recent threads/posts for it.
But I have been vaping nicotine and find it ineffective in quitting cigs. Smoking and vaping felt totally different, nicotine alone (even 3mg per ml juice) gives me quite a bit of anxiety. I tried to increase to 6mg and so on, and the anxiety gets even worse the higher I go. I still vape anyways but hate the anxiety. Cigs don’t give me anxiety, in fact they often calm me while also being stimulating. Many times after a cigarette I have no anxiety left, so it reduces anxiety. Yet vaping literally gives me anxiety. Also I noticed increased depression when trying vape only (due to lack of MAOIs and other tobacco alkaloids) So yeah I knew something was missing/wrong and I researched WTA.
I bought some WTA 3mg liquid a while ago, but am just truly trying them out daily starting today. They aren’t even close to expired and juice taste fine. I am going to try to vape ONLY WTA e liquid stating today, and try not to smoke any cigarettes at all.
Here is what my juice contains:
Nicotine (3mg per ML) , Nornicotine, Anabasine, Anatabine
Unfortunately I cannot find any liquid that contains harman and norharman, which are known to be sufficiently potent MAO inhibitors. I believe those are the only two things missing to make this nicotine juice work perfectly to get me fully off cigarettes.
Does anyone know if Nornicotine, Anabasine, Anatabine has MAO inhibitor actions? Google doesn’t seem to help. I read a couple of patents (or applied for patents) that mention them working as MAO inhibitors, but that’s all. I can add link later if anyone interested.
I would post more details but want to make sure it’s okay to continue that old topic first so I don’t waste anymore time typing lol.
“Nicotine is the major neuroactive compound of tobacco, which has, by itself has WEAK reinforcing properties. It is known that levels of the enzymes monoamine oxidase A (MAO-A) and MAO-B are reduced in the platelets and brains of smokers and that substances, other than nicotine, present in tobacco smoke have MAO-inhibitory activities. Here, we report that inhibition of MAO dramatically and specifically increases the motivation to self-administer nicotine in rats”
Link:
https://www.jneurosci.org/content/25/38/8593
“Several studies have documented a strong association between smoking and depression. Because cigarette smoke has been reported to inhibit monoamine oxidase (MAO) A in vitroand in animals and because MAO A inhibitors are effective antidepressants, we tested the hypothesis that MAO A would be reduced in the brain of cigarette smokers”
Link:
https://www.pnas.org/doi/abs/10.1073/pnas.93.24.14065
“Effects of Monoamine Oxidase Inhibition on the Reinforcing Properties of Low-Dose Nicotine”
Link: Effects of Monoamine Oxidase Inhibition on the Reinforcing Properties of Low-Dose Nicotine | Neuropsychopharmacology
There is a hypothesis that substances present in, or derived from, tobacco smoke inhibit monoamine oxidase (MAO) in the brains of smokers, reducing the degradation of catecholamine neurotransmitters involved in central reward pathways and acting synergistically with nicotine to increase its addictive effects.
Link:
https://academic.oup.com/ntr/article-abstract/18/5/509/2511632?redirectedFrom=fulltext
“Interestingly, cigarette smoking produces inhibition of brain MAO activity in humans. Since monoamines are involved in the reinforcing and rewarding effects of tobacco smoking, MAO inhibitors have been proposed as a treatment for tobacco dependence
in vitro studies have identified several components, namely the alkaloids harman (a specific competitive MAO-A inhibitor; IC50=0.34 μM) and norharman (non-specific competitive MAO-A and B inhibitor, with IC50's of 6.5 and 4.7 μM respectively) as contributing to the inhibitory effects of tobacco smoke on MAO isoforms [21]. Besides harman alkaloids, other components of tobacco smoke may also inhibit MAO-A and –B [22, 23].
Since it has been observed that: 1) MAO inhibition leads to increases in synaptic monoamines which are also increased by nAChR activation; 2) cigarette smoke possesses components which inhibit MAO isoforms, we (and others) have reasoned that MAO inhibitors may be promising candidates for developing medications to aid smokers with tobacco cessation.“
link: Monoamine Oxidase Inhibition for Tobacco Pharmacotherapy
“Smoking inhibits the enzyme monoamine oxidase B (MAO–B), which is responsible for the catabolism of several brain neurotransmitters, including dopamine, serotonin and noradrenaline (Reference Haustein, Haffner and WoodcockHaustein et al, 2002). Smokers therefore have lower brain MAO–B levels than non-smokers, although levels return to normal on quitting (Reference Khalil, Steyn and CastagnoliKhalil et al, 2000). Inhibition of MAO–B causes dopamine levels to increase, thereby making smoking potentially rewarding. Long-term smokers have been found to have neurochemical abnormalities in the locus cerulus similar to those seen in animals treated with antidepressant drugs and opposite to those observed in people with major depression (Reference Klimek, Zhu and DilleyKlimek et al, 2001). Since MAO inhibitors are effective antidepressants, these findings suggest that smoking might have some antidepressant effects (Reference HughesHughes, 1999)”
I could go on and on with the links and sources, as the evidence is overwhelming. Does this mean everyone who smokes cigs becomes dependent on the MAO inhibition of cigarettes? No. Everyone’s brain chemistry is unique. For most simply replacing the nicotine is enough. However for some simply replacing the nicotine alone it is not enough (need the MAOIS and other alkaloids), and the links above explain why.
<LINKS to cigarettes and MAO inhibition being critical in tobacco dependence is listed at bottom of post >
I am using whole tobacco alkaloid 3mg nicotine e juice at the moment and wondered if anyone else does. Also wanted to see if we can continue the discussion.
Here is a link to old thread : Beta Carboline MAOIs - towards a more effective e-liquid
All I see is it is closed to replies and haven’t found any other recent threads/posts for it.
But I have been vaping nicotine and find it ineffective in quitting cigs. Smoking and vaping felt totally different, nicotine alone (even 3mg per ml juice) gives me quite a bit of anxiety. I tried to increase to 6mg and so on, and the anxiety gets even worse the higher I go. I still vape anyways but hate the anxiety. Cigs don’t give me anxiety, in fact they often calm me while also being stimulating. Many times after a cigarette I have no anxiety left, so it reduces anxiety. Yet vaping literally gives me anxiety. Also I noticed increased depression when trying vape only (due to lack of MAOIs and other tobacco alkaloids) So yeah I knew something was missing/wrong and I researched WTA.
I bought some WTA 3mg liquid a while ago, but am just truly trying them out daily starting today. They aren’t even close to expired and juice taste fine. I am going to try to vape ONLY WTA e liquid stating today, and try not to smoke any cigarettes at all.
Here is what my juice contains:
Nicotine (3mg per ML) , Nornicotine, Anabasine, Anatabine
Unfortunately I cannot find any liquid that contains harman and norharman, which are known to be sufficiently potent MAO inhibitors. I believe those are the only two things missing to make this nicotine juice work perfectly to get me fully off cigarettes.
Does anyone know if Nornicotine, Anabasine, Anatabine has MAO inhibitor actions? Google doesn’t seem to help. I read a couple of patents (or applied for patents) that mention them working as MAO inhibitors, but that’s all. I can add link later if anyone interested.
I would post more details but want to make sure it’s okay to continue that old topic first so I don’t waste anymore time typing lol.
“Nicotine is the major neuroactive compound of tobacco, which has, by itself has WEAK reinforcing properties. It is known that levels of the enzymes monoamine oxidase A (MAO-A) and MAO-B are reduced in the platelets and brains of smokers and that substances, other than nicotine, present in tobacco smoke have MAO-inhibitory activities. Here, we report that inhibition of MAO dramatically and specifically increases the motivation to self-administer nicotine in rats”
Link:
https://www.jneurosci.org/content/25/38/8593
“Several studies have documented a strong association between smoking and depression. Because cigarette smoke has been reported to inhibit monoamine oxidase (MAO) A in vitroand in animals and because MAO A inhibitors are effective antidepressants, we tested the hypothesis that MAO A would be reduced in the brain of cigarette smokers”
Link:
https://www.pnas.org/doi/abs/10.1073/pnas.93.24.14065
“Effects of Monoamine Oxidase Inhibition on the Reinforcing Properties of Low-Dose Nicotine”
Link: Effects of Monoamine Oxidase Inhibition on the Reinforcing Properties of Low-Dose Nicotine | Neuropsychopharmacology
There is a hypothesis that substances present in, or derived from, tobacco smoke inhibit monoamine oxidase (MAO) in the brains of smokers, reducing the degradation of catecholamine neurotransmitters involved in central reward pathways and acting synergistically with nicotine to increase its addictive effects.
Link:
https://academic.oup.com/ntr/article-abstract/18/5/509/2511632?redirectedFrom=fulltext
“Interestingly, cigarette smoking produces inhibition of brain MAO activity in humans. Since monoamines are involved in the reinforcing and rewarding effects of tobacco smoking, MAO inhibitors have been proposed as a treatment for tobacco dependence
in vitro studies have identified several components, namely the alkaloids harman (a specific competitive MAO-A inhibitor; IC50=0.34 μM) and norharman (non-specific competitive MAO-A and B inhibitor, with IC50's of 6.5 and 4.7 μM respectively) as contributing to the inhibitory effects of tobacco smoke on MAO isoforms [21]. Besides harman alkaloids, other components of tobacco smoke may also inhibit MAO-A and –B [22, 23].
Since it has been observed that: 1) MAO inhibition leads to increases in synaptic monoamines which are also increased by nAChR activation; 2) cigarette smoke possesses components which inhibit MAO isoforms, we (and others) have reasoned that MAO inhibitors may be promising candidates for developing medications to aid smokers with tobacco cessation.“
link: Monoamine Oxidase Inhibition for Tobacco Pharmacotherapy
“Smoking inhibits the enzyme monoamine oxidase B (MAO–B), which is responsible for the catabolism of several brain neurotransmitters, including dopamine, serotonin and noradrenaline (Reference Haustein, Haffner and WoodcockHaustein et al, 2002). Smokers therefore have lower brain MAO–B levels than non-smokers, although levels return to normal on quitting (Reference Khalil, Steyn and CastagnoliKhalil et al, 2000). Inhibition of MAO–B causes dopamine levels to increase, thereby making smoking potentially rewarding. Long-term smokers have been found to have neurochemical abnormalities in the locus cerulus similar to those seen in animals treated with antidepressant drugs and opposite to those observed in people with major depression (Reference Klimek, Zhu and DilleyKlimek et al, 2001). Since MAO inhibitors are effective antidepressants, these findings suggest that smoking might have some antidepressant effects (Reference HughesHughes, 1999)”
I could go on and on with the links and sources, as the evidence is overwhelming. Does this mean everyone who smokes cigs becomes dependent on the MAO inhibition of cigarettes? No. Everyone’s brain chemistry is unique. For most simply replacing the nicotine is enough. However for some simply replacing the nicotine alone it is not enough (need the MAOIS and other alkaloids), and the links above explain why.
Last edited:
, I agree with 
