Our analyses call for further studies that outline the nature of these associations – for instance, to what extent are these associations representative of causal pathways or indicative of shared predispositions? Importantly, future efforts should be targeted at understanding the role of both depression and impulsivity (Turecki, 2005), especially when considering the relationship between SA and substance involvement. For instance, studies have reported stronger associations between unplanned SA and substance involvement (Borges et al., 2010b; Delforterie et al., 2015) indicating the potential role of impulsivity but a more systematic investigation of potential mediators and modifiers is necessary. Finally, from a clinical perspective, our results suggest that in individuals at high familial risk for substance involvement, a history of SA should be viewed as a potential harbinger of escalating substance use, potentially leading to dependence. Counselling may be required to ensure that environmental alterations subsequent to SA do not result in more frequent substance use. Further, in treating mood disruptions that might be related to SA, clinicians should consider therapies that include components that address the pitfalls of self-medication or account for other shared risk factors that may lead to substance dependence in those with a history of SA.