It is often assumed that the association between mental health and smoking can be explained by a self-medication model – that is, symptoms of mental illness, or side effects of psychiatric medications, are alleviated by the chemical properties of tobacco (Desai, Seabolt, & Jann, 2001; Khantzian, 1997; Lerman et al., 1996; Levin, Wilson, Rose, & McEvoy, 1996). However, observational evidence cannot determine whether the association between smoking and mental health is causal or the result of confounding (Lawlor, Harbord, Sterne, Timpson, & Davey Smith, 2008). Furthermore, traditional observational evidence cannot robustly identify the direction of causation (Lawlor et al., 2008), and there is growing evidence to suggest that smoking may be a causal risk factor for poor mental health. The genome-wide association study (GWAS) of schizophrenia conducted by the Psychiatric Genomics Consortium (PGC) found that variants in the gene cluster CHRNA5-A3-B4 were associated with increased schizophrenia risk (Ripke et al., 2014). These variants are known to be strongly associated with heaviness of smoking (Munafò et al., 2012; Thorgeirsson et al., 2008; Tobacco Consortium, 2010; Ware, van den Bree, & Munafò,
