also suggested that shared genetic influences may be responsible for the comorbidity across MDD and alcohol (Kendler et al., 1993) and nicotine dependence (Edwards et al., 2011;Thornton et al., 2016). However, adjustment for MDD did not abolish our association suggesting that this shared liability may be more general than MDD (e.g. Ellingson et al., 2016). Third, increased likelihood of substance use disorders in those with a prior history of SA may reflect a general predisposition towards impulsive and aggressive behaviors (Turecki, 2005). It is noteworthy that despite all individuals who reported SA also reporting SI (i.e., no attempts without ideation), results differed for the two outcomes. This finding might indicate that SA represents an escalation in severity of suicidal thoughts and behaviors and that new risk and protective influences might come into play at this more severe stage. Also, that significant effects in our data might relate to ascertainment and individuals being at higher familial liability for substance use and misuse cannot be discounted as such internalizing pathways are commonly noted in offspring of individuals with alcoholism (e.g.,(Hussong, Jones, Stein, Baucom, and Boeding, 2011).
