Stress Reactivity and Cognitive Vulnerability for Depression in Adolescence

Abstract

Major Depressive Disorder (MDD) is the most common mental illness, with estimated lifetime prevalence of 25% (Kessler, Avenevoli, & Merikangas, 2001). Importantly, research suggests that the one-year prevalence rates of depression are relatively low in childhood, but dramatically increase, as much as six-fold, from early to late adolescence (Hankin et al., 1998; Kessler et al., 2003). These trends have led researchers to examine the developmental antecedents of depression in hopes of identifying risk factors associated with the first onset of disorder. This study examined the relationship between two empirically supported risk factors for depression: stress reactivity and cognitive vulnerabilities (CV). To varying degrees, these factors have been examined throughout development; yet, these bodies of literature have been surprisingly separate, which may contribute to the disappointing performance of selective intervention strategies to identify and treat youth at risk (Kovacs & Lopez-Duran, 2010). The current study examined the developmental antecedents and combined effects of two risk factors for depression. A sample of 127 adolescents and their mothers from the greater Philadelphia area completed questionnaires and interviews. In addition, adolescents participated in a social stress task to elicit a stress response. Measures of biological stress reactivity were measured through the endocrine system (e.g., cortisol) and the autonomic nervous system (e.g., heart rate). Findings suggest that a number of proximal stressors predict higher levels of both CV and stress reactivity components. We did not find evidence for more distal antecedents (e.g., early life stress, maternal depression, parenting styles) in the prediction of these risk factors, however. Importantly, this study highlights the combined risk factors of CVs and biological stress reactivity. Specifically, adolescents with higher levels of CV and a poorer ability to regulate after a stressor are at increased risk for depressive symptoms. Findings did not support the hypothesis that the mechanism through which CVs lead to depression is biological reactivity. The current study presents an important methodological and theoretical advancement in the body of literature examining risk factors for depression and stress reactivity. From the evidence obtained, it appears that in many cases these aspects of reactivity may operate synergistically in the development of depression and that the lack of physiological recovery may amplify the negative effects of different cognitive styles. The joint effects of cognitive and biological reactivity can enhance our understanding of reactions to stressful events and lead to more personalized treatment. Approaches that incorporate mindfulness and relaxation strategies may be particularly relevant to the regulation of physiological reactivity to stress that may reduce the prolonged feelings associated with stressful events. Overall, the results from the current study provide a more nuanced understanding of the relationship between stress responses and move beyond prior research on risk factors for depression.