indicators of psychiatric illness in this sample, and adjustment for these factors attenuated but did not abolish the relationship between smoking and subsequent suicide risk over 35 years. The association between smoking and suicide observed in this study may be elevated by psychiatric illness not captured, but it is not plausible that an unexplained psychiatric variable associated with tobacco smoking could be responsible entirely for a dose-related, 2.5-fold increase in suicide rates. Residual confounding due to imperfect information on the known and measured confounders would need to be more substantial than is plausible to account for the observed strong association, given our use of multiple sources of data. The observed effect was so persistent that to negate the finding, an unanticipated confounder would have to have both a very strong effect and a very biased distribution within the sample, making the likelihood of such a confounder highly implausible (Kotz et al. 2015; Leone & Schnoll, 2015). Further, in the within-pair analysis controlling for unmeasured genetic and environmental factors, in 24 of the 28 twin pairs discordant for both smoking and suicide, the twin that died from suicide was the smoker. An experimental design in which some smokers were assigned to
