Monoamine oxidases and tobacco smoking

Although nicotine has been identified as the main ingredient in tobacco res ponsible for aspects of the tobacco dependence syndrome, not all of the psy chopharmacological effects of smoking can be explained by nicotine alone. A ccumulating preclinical and clinical evidence has demonstrated that smoking also leads to potent inhibition of both types (A and B) of monoamine oxida se (MAO). Smokers have 30-40 % lower MAOB and 20-30% lower MAOA activity th an non-smokers. Reduced MAO activity in smokers has been shown by direct me asures (platelets, positron emission tomographic studies) or by indirect me asures (concentration of monoamine catabolites in plasma or CSF). We examin e the hypothesis that chronic habitual smoking can be better understood in the context of two pharmacological factors: nicotine and reduced MAO activi ty. We speculate that MAO inhibition by compounds found in either tobacco o r tobacco smoke can potentiate nicotine's effects. Based on this concept, m ore effective anti-smoking drug strategies may be developed. As a practical consequence of tobacco smoke's MAO-inhibitory properties, comparative psyc hiatric research studies need to screen and control for tobacco use.