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There is little doubt that stress plays a role in the etiology of depression, but a relative minority of people who face negative life events, even severe events, develop depression (Hammen, 2005). As such, considerable research has focused on better understanding individual differences in sensitivity to depression following stress exposure. Central to this work is the stress sensitization model, which proposes that exposure to life stress during a developmentally sensitive period can increase sensitivity to future stress, thereby increasing depression risk (e.g., Post, 2016). In essence, the stress sensitization model suggests that early stress exposure alters the effects of later stress exposure on depression, in what could be described as an “environment-by-environment” (E × E) interaction.
Consistent with the stress sensitization model, research suggests that childhood adversity (CA; e.g., maltreatment, parental loss, parental separation) increases individuals’ sensitivity to later proximal stress, thereby increasing risk for depressive symptoms and major depressive disorder (for a review, see Stroud, 2019). For example, prior work suggests that the link between proximal major stress and depression is stronger among those with a history of CA, as compared to those without such history (McLaughlin, Conron, Koenen, & Gilman, 2010). Further, adolescents who have experienced CA are more likely to develop depression in the face of lower levels of recent stress (vs. those without CA exposure; e.g., Harkness, Bruce, & Lumley, 2006; La Rocque, Harkness, & Bagby, 2014; Rudolph & Flynn, 2007), suggesting that CA increases stress sensitivity. Notably, among adolescents, the sensitizing effect of CA has been supported across different types of CA, including childhood maltreatment (e.g., Harkness et al., 2006; La Rocque et al., 2014), parental separation and divorce, marital conflict, and caregiver chronic illness (Espejo et al., 2007; Rudolph & Flynn, 2007; Starr et al., 2017), suggesting that even relatively less severe forms of CA have the capacity to shape sensitivity to future stress. In contrast, some evidence suggests that exposure to mild CAs may produce a protective “stress inoculation” or “steeling” effect (Seery, Holman, & Silver, 2010), reducing the association between proximal stressors and depression (although evidence for this effect in youth has been somewhat mixed; Rudolph & Flynn, 2007; Shapero et al., 2014). These contrasting findings suggest there may be individual differences in how CA influences...