I'm no scientician, but my research led me to the fact that nicotine ain't the bad guy in cigarettes. It's the thousands of other compounds that are evil. You won't get the hit same as a cig, but it tastes better and you can get as much nicotine as you want.
With the right hardware, you can get really big hits. You'll know when ya done gone too far...
Rosa, I dug up this little gem about MAOIs, it may help explain how all that other stuff in analog smoke works.
It's kinda technical and edumicatedey soundin', but here 'tis:
Human monoamine oxidase is inhibited by tobacco smoke: beta-carboline alkaloids act as potent and reversible inhibitors
by
Herraiz T, Chaparro C.
Spanish Council for Scientific Research, CSIC,
Instituto de Fermentaciones Industriales,
Juan de la Cierva, 3,
28006, Madrid, Spain.
Biochem Biophys Res Commun. 2005 Jan 14;326(2):378-86
ABSTRACT
Monoamine oxidase (MAO) is a mitochondrial outer-membrane flavoenzyme involved in brain and peripheral oxidative catabolism of neurotransmitters and xenobiotic amines, including neurotoxic amines, and a well-known target for antidepressant and neuroprotective drugs. Recently, positron emission tomography imaging has shown that smokers have a much lower activity of peripheral and brain MAO-A (30%) and -B (40%) isozymes compared to non-smokers. This MAO inhibition results from a pharmacological effect of smoke, but little is known about its mechanism. Working with mainstream smoke collected from commercial cigarettes we confirmed that cigarette smoke is a potent inhibitor of human MAO-A and -B isozymes. MAO inhibition was partly reversible, competitive for MAO-A, and a mixed-type inhibition for MAO-B. Two beta-carboline alkaloids, norharman (beta-carboline) and harman (1-methyl-beta-carboline), were identified by GC-MS, quantified, and isolated from the mainstream smoke by solid phase extraction and HPLC. Kinetics analysis revealed that beta-carbolines from cigarette smoke were competitive, reversible, and potent inhibitors of MAO enzymes. Norharman was an inhibitor of MAO-A (K(i)=1.2+/-0.18muM) and MAO-B (K(i)=1.12+/-0.19muM), and harman of MAO-A (K(i)=55.54+/-5.3nM). beta-Carboline alkaloids are psychopharmacologically active compounds that may occur endogenously in human tissues, including the brain. These results suggest that beta-carboline alkaloids from cigarette smoke acting as potent reversible inhibitors of MAO enzymes may contribute to the MAO-reduced activity produced by tobacco smoke in smokers. The presence of MAO inhibitors in smoke like beta-carbolines and others may help us to understand some of the purported neuropharmacological effects associated with smoking.
Ya don't suppose that the PhDs workin' in the labs of Phillip Morris and RJ Reynolds know about this, do ya?