Lower monoamine oxidase (MAO) activity (Whitfield et al. 2000) and serotonin function (Malone et al. 2003) in smokers compared to non-smokers has been proposed as a biological mechanism for the role of smoking in suicide. Deficits in serotonergic function have been associated with an increased hostility, impulsive/aggressive behaviors and suicide (Kamali et al. 2001). A deficiency of central monoamines is one of the features of depression, (Belmaker and Agam 2008) and several antidepressant drugs are designed to increase monoaminergic transmission. However, it has also been suggested that smoking might have antidepressant properties, (Balfour and Ridley 2000) a hypothesis that could explain reduced symptoms of depression noted with the use of nicotine patches among non-smoking depressed patients (Salin-Pascual et al. 1996). Malone et al. (2003) suggested that lower serotonergic function predisposes to smoking habit and psychiatric disorders, and a further depletion of serotonin by smoking after the onset of a depressive disorder, may enhance the risk of aggressive and suicidal behaviors.
