To adapt the “stress-diathesis” model to explain adolescent suicidal behaviors and substance use, we propose that a developmental-transactional model is required that includes not only precursors and salient risk factors (Bridge et al. 2006; Windle, 2004), but also plausible mechanisms that explain how, when, and to what extent interactions among these risk factors occurs. Precursors include familial factors, such as parental mood disorders and parental impulsive aggression; exposure to these familial factors can lead to neuroticism, hopelessness, and mood symptoms in pre-pubertal offspring, and depression later in adolescence. Other precursors include parental impulsive-aggressive traits and parental suicide attempts, producing altered serotonin function, and deficits in executive functioning, leading to impulsive-aggressive traits in pre-pubertal and pubertal offspring. At least three causal pathways are hypothesized to underlie the vulnerabilities that lead to adolescent suicidal behaviors. These pathways (identified by ①, ②, and ③ in Fig. 2) address the possibilities of bidirectional interactions between (1) stressful life events, genetic markers of serotonin dysregulation, and suicide attempts; (2) substance use and impulsivity; and (3) substance use and suicide attempts.
