I don’t claim to fully understand all the details and potential implications of this find, but in laymen’s terms, smoking tobacco while under the influence of other psychoactive substances may increase and/or prolong their effect. This would be relevant to both certain entheogens and mood altering prescription medications. The study also suggests that smoking may play a role in reduced MAO activity in the brain, which might tell us more about its neuropharmacological effects. Many indigenous shamans who use tobacco as a healing plant, which they often smoke themselves and blow over the sick. However, the tobacco shamans smoke is very different from the commercial cigarettes used in this study.

Note: This study is from January 2005.

Human monoamine oxidase is inhibited by tobacco smoke: beta-carboline alkaloids act as potent and reversible inhibitors
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


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.