The association between smoking and subsequent suicide-related outcomes in the National Comorbidity Survey panel sample
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CitationKessler, R C, G Borges, N Sampson, M Miller, and M K Nock. 2008. “The Association Between Smoking and Subsequent Suicide-Related Outcomes in the National Comorbidity Survey Panel Sample.” Molecular Psychiatry 14 (12) (July 22): 1132–1142. doi:10.1038/mp.2008.78.
AbstractControversy exists about whether the repeatedly-documented associations between smoking and subsequent suicide-related outcomes (SROs; ideation, plans, gestures, and attempts) are due to unmeasured common causes or to causal effects of smoking on SROs. We address this issue by examining associations of smoking with subsequent SROs with and without controls for potential explanatory variables in the National Comorbidity Survey (NCS) panel. The latter consists of 5001 people who participated in both the 199002 NCS and the 2001–03 NCS Follow-up Survey. Explanatory variables include socio-demographics, potential common causes (parental history of mental-substance disorders; other respondent childhood adversities) and potential mediators (respondent history of DSM-III-R mental-substance disorders). Small gross (i.e., without controls) prospective associations are found between history of early-onset nicotine dependence and both subsequent suicide ideation and, among ideators, subsequent suicide plans. None of the baseline smoking measures, though, predicts subsequent suicide gestures or attempts among ideators. The smoking-ideation association largely disappear, but the association of early-onset nicotine dependence with subsequent suicide plans persists (Odds-ratio = 3.0), after adjustment for control variables. However, the latter association is as strong with remitted as active nicotine dependence, arguing against a direct causal effect of nicotine dependence on suicide plans. Decomposition of the control variable effects, furthermore, suggests that these effects are due to common causes more than to mediators. These results refine our understanding of the ways in which smoking is associated with later SROs and for the most part argue against the view that these associations are due to causal effects of smoking.
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