might shed some light on it...
from two posts located here -
Snus Forum Post
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Nicotine has a half-life of only about 2 hours, so within one day (24h = 12 half-lives) you only have 0.5 ^ 12 = 0.000244 times as much in your system as you did 24h prior. By two days you have only 60 billionths the amount - it goes away quickly. What doesn't go away quickly is your brain's sensitivity to it. Nicotine stimulates production of several neurotransmitters which, present in excess, reduce the sensitivity of your brain and body to them.
I quote from a 2001 study :
(...) (R)eversal of tolerance appears to be very limited, or very slow, following extended abstinence from smoking and presumed elimination of dependence. Tolerance to subjective effects of nicotine was moderate in exsmokers, who had been abstinent an average of nearly 7 years, because dose-response curves generally were shifted to the right, relative to those for nonsmokers, but usually not as far right as those for currently dependent and nondependent smokers. These results are consistent with one study (Hughes et al., 1989), but not another (Hughes et al., 2000), of tolerance to nicotine in long-time exsmokers, both of which examined the subjective effects of nicotine gum in exsmokers versus current smokers and nonsmokers. Preclinical research suggests that lengthy nicotine exposure can produce a "persistent inactivation" of nicotinic receptors that may be irreversible (Reitstetter et al., 1999). Thus, mechanisms responsible for at least some of these subjective effects may never fully regain the same degree of sensitivity to nicotine as that exhibited during initial exposure (e.g., teens experimenting with tobacco). Such incomplete tolerance reversal may help explain why many exsmokers who relapse can rapidly resume smoking at a high rate, often within days or weeks, after even extended abstinence (Norregaard et al., 1992), whereas those initially naïve to smoking invariably require at least a few years to escalate to high-rate smoking (McNeill et al., 1989).
The finding of substantial chronic tolerance to most subjective effects of nicotine but little or none to cardiovascular and performance responses (except hand steadiness) supports the notion that tolerance is response-specific (Arcavi et al., 1994; Perkins et al., 1994). Although the timing of the performance tasks later in the battery could have reduced the chances of observing tolerance to those measures, this seems unlikely given that the hand steadiness task, which did show tolerance, was performed after finger-tapping, which did not. Moreover, we observed a similar lack of tolerance to cardiovascular measures, which were obtained concurrently with subjective measures that did show tolerance. Underlying mechanisms responsible for subjective effects of nicotine must show substantial chronic adaptation with repeated exposure, whereas mechanisms responsible for cardiovascular and most performance effects do not. Notably, we saw little evidence of sensitization, or increased sensitivity to nicotine due to past exposure, which would result in a shift to the left in dose-response curves of smokers compared with nonsmokers (Kalant and Khanna, 1990), although memory recognition was improved by nicotine in dependent smokers only.
from :
Dissociation of Nicotine Tolerance from Tobacco Dependence in Humans
Kenneth A. Perkins, Debra Gerlach, Michelle Broge, James E. Grobe1 , Mark Sanders, Carolyn Fonte, Josh Vender, Christine Cherry and Annette Wilson
Department of Psychiatry, University of Pittsburgh Medical Center, Pittsburgh, Pennsylvania (K.A.P., D.G., M.B., J.E.G., M.S., C.F., J.V., C.C.); and Department of Anesthesiology, Children's Hospital of Pittsburgh, Pittsburgh, Pennsylvania (A.W.)
THE JOURNAL OF PHARMACOLOGY AND EXPERIMENTAL THERAPEUTICS - Vol. 296, Issue 3, 849-856, March 2001
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In terms of the tolerance associated with cigarettes - I've just dug up a study which notes that cigarette smoke contains monoamine-oxidase inhibitors (MAOIs) (clicky link (http://www.biopsychiatry.com/nicotine-mao.htm)) : chemicals which retard the effectiveness of this chemical in breaking down neurotransmitters. It could well be that these are not present in snus and are a product of the heat of combustion in the cigarette. MAOIs extend the life of all of the neurochemicals it is ordinarily responsible for destroying, so things like dopamine, serotonin, etc, are all extended in lifetime in the synapse.
Basically, what happens is that, in normal operation, a neuron discharges neurotransmitters into the narrow space between itself and its neighbour. The neurotransmitters bind to receptors in the neighbouring neuron and cause it to react by firing neurotransmitters itself. After firing, monoamine-oxidase does the work of destroying the messenger chemicals in the synapse. If, however, you have monoamine-oxidase inhibitors in your bloodstream, these will slow the destruction of these and extend the duration of the synaptic firing - making the sensory message more "intense".
So it could be the case that the MAOI effect of the cigarette smoke is what causes the heigtened response rather than the nicotine. MAOIs are notoriously non-specific, so they wlll heighten the sensations of many neurochemical pathways in addition to those stimulated by nicotine. The study I quoted was testing people only on nicotine response and not on cigarette response - maybe that's an explanation
