Part 1 : Nicotine absorption in vaping versus smoking
Some studies stated that vaping provides only about 10% of the nicotine compared to smoking - is this figure wrong?
Probably, yes. While I am quite sure that many people get less nicotine than they think they do, it is surly not 10% - e-cigs just wouldn't work at that level.
What's the likely explanation for the erroneous 10% figure?
Only about 40-45% of the nicotine in e-liquid makes it out of the atomiser and into the vapor. I cut that vaporised nicotine by 25% as an approximate figure for that unabsorbed/exhaled to give 30% absorbed. Still 3x the 10%. So something is being missed in those (not many) 10%-ish studies. One possibility is that it misses the slower rate of aborption by measuring effect of one 10 minute session of vaping at a fixed point; missing the cumulative value. That's always been my prime explanation. Alternatively, but less likely, some of the nicotine is missed in the analysis somehow - it is there but not being measured; the form may be different; and while it sounds silly to say that perhaps the nicotine recombines with glycols in the blood, perhaps 'something' like this is occuring. But the absorption rate is likely the answer.
How can e-cigs be being successful if the nicotine is much lower than what people were used to?
Somehow that 30% figure still allows e-cigs to be successful for most people (though not all - some can only stick it by increasing the nic substantially, to match what they have been used to). For that majority, what I think happens is: initially, and because of the novelty, the shortfall is compensated by increased volumes - vaping much more than used to smoke (more puffs); so the total nicotine per day (rather than per puff) is raised to near the accustomed value. This pattern of use subsides gradually, slowly enough for the body to adjust (perhaps with a need for a stronger vape in the morning).
So not only have most vapers cut the tar and soot, they have likely also cut their nicotine somewhat too.
How addictive is nicotine?
Related to this is the issue of just how addictive nicotine really is. Perhaps by itself it is not as addictive as generally believed - as evidenced by quite a few people being able to cut their nicotine use to zero in just days or weeks. The really addictive thing could be the combination of nic plus MAOIs (for which biochemistry of this double-whammy makes good sense), with perhaps other factors involved too.
More on MAOIs in part 2, below.
What about the missing buzz I used to feel when smoking an analog?
The 'buzz' that many people feel is missing with e-cigs could be the absence of the nicotine/MAOI 'double whammy', in particular. Even when the nicotine is raised, it doesn't give that special feeling - and this is not about freebase or some other nature of the nic, but the absence of the MAOIs. Alternatively, a slower absorption rate could (at least partly) account for it.
Is the nicotine from vaping really more slowly absorbed?
It is not clear yet, but it is quite likely that this is the case. In the past it had been thought that analog nicotine was faster to the bloodstream (and brain) because it had 'special' freebase (un-combined) nicotine; in fact e-liquid has more nicotine in this freebase form. The reason would be down to the carrier - with smoking, the nicotine (normally a liquid at room temperature) is carried on tiny particles of ash. With vaping the carrier is a liquid (small droplets of PG or VG in which the nicotine is disolved (the visible fog of recondensed vapor). Not only are the liquid droplets larger than the ash (smoke) particles, but it is harder for the nicotine to 'escape' the liquid that the ash (the nicotine is sitting on the outside of the ash, so to speak).
A further factor comes into play - the smaller size of the particles in analog smoke mean that (much) more of the nicotine reaches the lungs, where passage to the bloodstream is far easier (the barrier is much less here because the haemoglobin of red blood cells in the blood needs to be able to latch onto oxygen from the air; with digestion, absorption of sugars, say, needs to be slower as blood sugar levels need to be tightly controlled, so absorbtion in the mouth is much slower).
* Smoke particle size : 0.1 to 1 micron; PG mist droplet size : 1 to 5 micron
Part 2: Nicotine, addiction and MAOIs
How does smoking affect the brain?
The psychological effects of smoking are surprisingly mild considering that smoking is generally regarded as hard to stop. While there are many behavioual and sensory aspects, nicotine has been regarded as the psychoactive ingredient, providing a mix or relaxation and improvement of focus and concentration (though some of this might be down to relief of the craving that builds up between cigarettes, there is good evidence to suggest that nicotine does have some beneficial effects on brain function).
Nicotine's effect on the brain is primarily through release of dopamine, the pleasure or 'reward' neurotransmitter that gives a sense of well-being.
Is nicotine the key psychoactive in smoking?
What are MAOIs and what is their significance in smoking?
Brain chemistry is a complex of of balanced systems. Monoamine oxidase inhibitors (MAOIs) role is to inhibit the removal of monoamines, of which dopamine is one, prolonging the effect of the monoamines. As such these chemicals are sometimes used as anti-depressant drugs; predictably, some dependence is created (cessation causes withdrawal symptoms). Hence, MAOIs act in synergy with nicotine to enhance its effect by keeping dopamine levels higher for longer.
Any experimental support for the role of MAOIs?
There has been some advocacy for nicotine-free cigarettes, the idea being to make them unappealing. A much better approach might be to increase the nicotine level in cigarettes so that less are smoked (given that the dangers with smoking are not the nicotine but the smoke). The best approach of course is to replace the cigarette (tobacco) with a purified nicotine. The e-cigarette does this together with the appearance of smoke (harmless fog) and works well as a smoking alternative for most people. Whether the addition of a MAOI to e-liquid to enhance it's effectiveness further would be acceptable is open to debate; it has not received much attention so far. For practical reasons (perhaps no MAOIs are suitably vapable), it might not be possible with current e-cigarette designs that use a heating element to create vapor (but would be possible with inhaler/ultrasonic designs).
If the research continues to hold up, NRTs should also address this issue for improving their effectiveness.
~~~
* Acetaldehyde is one of a number of other smoke constituents that might help reinforce the psychoactive effects.
Other resources (related to part 2) :
Monoamine oxidase inhibitor - Wikipedia, the free encyclopedia
This is your brain on nicotine
The Good Drug Guide : new mood-brighteners and antidepressants
Best news online about cigarettes and tobacco.: Nicotine does not cause cigarette addiction
Reprinted with permission of the author from Vaping Buzzz
Some studies stated that vaping provides only about 10% of the nicotine compared to smoking - is this figure wrong?
Probably, yes. While I am quite sure that many people get less nicotine than they think they do, it is surly not 10% - e-cigs just wouldn't work at that level.
What's the likely explanation for the erroneous 10% figure?
Only about 40-45% of the nicotine in e-liquid makes it out of the atomiser and into the vapor. I cut that vaporised nicotine by 25% as an approximate figure for that unabsorbed/exhaled to give 30% absorbed. Still 3x the 10%. So something is being missed in those (not many) 10%-ish studies. One possibility is that it misses the slower rate of aborption by measuring effect of one 10 minute session of vaping at a fixed point; missing the cumulative value. That's always been my prime explanation. Alternatively, but less likely, some of the nicotine is missed in the analysis somehow - it is there but not being measured; the form may be different; and while it sounds silly to say that perhaps the nicotine recombines with glycols in the blood, perhaps 'something' like this is occuring. But the absorption rate is likely the answer.
How can e-cigs be being successful if the nicotine is much lower than what people were used to?
Somehow that 30% figure still allows e-cigs to be successful for most people (though not all - some can only stick it by increasing the nic substantially, to match what they have been used to). For that majority, what I think happens is: initially, and because of the novelty, the shortfall is compensated by increased volumes - vaping much more than used to smoke (more puffs); so the total nicotine per day (rather than per puff) is raised to near the accustomed value. This pattern of use subsides gradually, slowly enough for the body to adjust (perhaps with a need for a stronger vape in the morning).
So not only have most vapers cut the tar and soot, they have likely also cut their nicotine somewhat too.
How addictive is nicotine?
Related to this is the issue of just how addictive nicotine really is. Perhaps by itself it is not as addictive as generally believed - as evidenced by quite a few people being able to cut their nicotine use to zero in just days or weeks. The really addictive thing could be the combination of nic plus MAOIs (for which biochemistry of this double-whammy makes good sense), with perhaps other factors involved too.
More on MAOIs in part 2, below.
What about the missing buzz I used to feel when smoking an analog?
The 'buzz' that many people feel is missing with e-cigs could be the absence of the nicotine/MAOI 'double whammy', in particular. Even when the nicotine is raised, it doesn't give that special feeling - and this is not about freebase or some other nature of the nic, but the absence of the MAOIs. Alternatively, a slower absorption rate could (at least partly) account for it.
Is the nicotine from vaping really more slowly absorbed?
It is not clear yet, but it is quite likely that this is the case. In the past it had been thought that analog nicotine was faster to the bloodstream (and brain) because it had 'special' freebase (un-combined) nicotine; in fact e-liquid has more nicotine in this freebase form. The reason would be down to the carrier - with smoking, the nicotine (normally a liquid at room temperature) is carried on tiny particles of ash. With vaping the carrier is a liquid (small droplets of PG or VG in which the nicotine is disolved (the visible fog of recondensed vapor). Not only are the liquid droplets larger than the ash (smoke) particles, but it is harder for the nicotine to 'escape' the liquid that the ash (the nicotine is sitting on the outside of the ash, so to speak).
A further factor comes into play - the smaller size of the particles in analog smoke mean that (much) more of the nicotine reaches the lungs, where passage to the bloodstream is far easier (the barrier is much less here because the haemoglobin of red blood cells in the blood needs to be able to latch onto oxygen from the air; with digestion, absorption of sugars, say, needs to be slower as blood sugar levels need to be tightly controlled, so absorbtion in the mouth is much slower).
* Smoke particle size : 0.1 to 1 micron; PG mist droplet size : 1 to 5 micron
Part 2: Nicotine, addiction and MAOIs
How does smoking affect the brain?
The psychological effects of smoking are surprisingly mild considering that smoking is generally regarded as hard to stop. While there are many behavioual and sensory aspects, nicotine has been regarded as the psychoactive ingredient, providing a mix or relaxation and improvement of focus and concentration (though some of this might be down to relief of the craving that builds up between cigarettes, there is good evidence to suggest that nicotine does have some beneficial effects on brain function).
Nicotine's effect on the brain is primarily through release of dopamine, the pleasure or 'reward' neurotransmitter that gives a sense of well-being.
Is nicotine the key psychoactive in smoking?
"I question, however, whether nicotine is the active ingredient in tobacco. If it were, nicotine patches should satisfy a smoker's craving for tobacco; they don't! In prisons, where, as a part of the punishment, smoking is sometimes forbidden, the inmates take to smoking corn silk, paper, string, etc., none of which contain any nicotine. ... The authors of the widely respected "Merck Manual" say only that it is "probably" the active ingredient. ... The active ingredient in smoke is smoke."
http://www.lcolby.com/b-chap11.htm
The first point is a very good one. Then, all psychoactive chemicals aside, there are the pleasures of that smoky taste (a mild dose of the harshness of tar can be experienced as pleasurable, lie say a hot chilli or a strong spirit) and of the (blowing out of) smoke ('sensory and behavioural cues'); de-niconised cigarettes can stave off cravings to some extent.http://www.lcolby.com/b-chap11.htm
What are MAOIs and what is their significance in smoking?
Brain chemistry is a complex of of balanced systems. Monoamine oxidase inhibitors (MAOIs) role is to inhibit the removal of monoamines, of which dopamine is one, prolonging the effect of the monoamines. As such these chemicals are sometimes used as anti-depressant drugs; predictably, some dependence is created (cessation causes withdrawal symptoms). Hence, MAOIs act in synergy with nicotine to enhance its effect by keeping dopamine levels higher for longer.
"Among the different compounds contained in tobacco smoke, monoamine oxidase inhibitors (MAOI) have recently been the focus of a particular interest (Berlin and Anthenelli, 2001). Monoamines are neurotransmitters found in the central nervous system. They are involved in sending signals to the brain which regulate sleep, arousal and pleasure ("Dopamine"). The three main monoamines studied by researchers are dopamine (DA), norepinephrine and serotonin. Monoamine oxidase is one enzyme responsible for the degradation of the monoamines. MAOIs are molecules that inhibit monoamine oxidase, and as a result increase the levels of monoamines found in the brain. According to newly developed research, a synergy between nicotine and MAOIs could be of importance for tobacco addiction to set up (Berlin and Anthenelli, 2001). Then, the association between nicotine and MAOI seems to be an appropriate model to study mechanisms underlying tobacco addiction."
There might be other substances that play an active role in the brain chemistry effects of smoking*, though so far MAOIs appear to be the key factor, with a well understood mechanism.
Any experimental support for the role of MAOIs?
"Nicotine is the major neuroactive compound of tobacco, which has, by itself, 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."
Monoamine Oxidase Inhibition Dramatically Increases the Motivation to Self-Administer Nicotine in Rats -- Guillem et al. 25 (38): 8593 -- Journal of Neuroscience
Do MAOIs have any significance for vaping?Monoamine Oxidase Inhibition Dramatically Increases the Motivation to Self-Administer Nicotine in Rats -- Guillem et al. 25 (38): 8593 -- Journal of Neuroscience
There has been some advocacy for nicotine-free cigarettes, the idea being to make them unappealing. A much better approach might be to increase the nicotine level in cigarettes so that less are smoked (given that the dangers with smoking are not the nicotine but the smoke). The best approach of course is to replace the cigarette (tobacco) with a purified nicotine. The e-cigarette does this together with the appearance of smoke (harmless fog) and works well as a smoking alternative for most people. Whether the addition of a MAOI to e-liquid to enhance it's effectiveness further would be acceptable is open to debate; it has not received much attention so far. For practical reasons (perhaps no MAOIs are suitably vapable), it might not be possible with current e-cigarette designs that use a heating element to create vapor (but would be possible with inhaler/ultrasonic designs).
If the research continues to hold up, NRTs should also address this issue for improving their effectiveness.
~~~
* Acetaldehyde is one of a number of other smoke constituents that might help reinforce the psychoactive effects.
Other resources (related to part 2) :
Monoamine oxidase inhibitor - Wikipedia, the free encyclopedia
This is your brain on nicotine
The Good Drug Guide : new mood-brighteners and antidepressants
Best news online about cigarettes and tobacco.: Nicotine does not cause cigarette addiction
Reprinted with permission of the author from Vaping Buzzz
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