(PS9-A6) Stress Reactivity Mediates the Relationships Between Generalized Anxiety Disorder and Major Depressive Disorder over 18 Years

Introduction: Generalized anxiety disorder (GAD) and major depressive disorder (MDD) are common mental health disorders that often precede each other (Jacobson & Newman, 2017). According to stress reactivity theories, patterns of heightened emotional reactions to stressors may increase vulnerability to developing anxiety and depression symptoms (Gross & Jazaieri, 2014; Schlotz et al., 2011). However, prior cross-sectional research on the topic has hindered directional inferences that approximate causality. Given the heightened prevalence and severity of mental health problems such as GAD and MDD during the COVID-19 pandemic, understanding mechanisms that underlie the longitudinal GAD-MDD relations is important to inform treatment and prevention efforts to reduce the burden arising from the GAD-MDD comorbidity (Li et al., 2020). Thus, the present study tested stress reactivity as a potential mediator in the prospective relations between GAD and MDD symptoms across 18 years. 

Methods: Data were drawn from the Midlife Development in the U.S. (MIDUS) study. The present sample included 3,294 adults (M age = 45.6; SD age = 11.4; % Female = 54.6; % White = 89) who took part in three waves of data collection (T1, T2, and T3), spaced approximately nine years apart. The Composite International Diagnostic Interview–Short Form was used to measure GAD and MDD severity. Stress reactivity was assessed at T2 using the Multidimensional Personality Questionnaire–Stress Reactivity subscale. Data were analyzed using structural equation mediation modeling.

Results: Structural equation modeling showed that T2 stress reactivity significantly mediated the relationship between elevated T1 GAD symptom severity and higher T3 MDD symptoms (β = 0.02, 95% CI [0.01, 0.03], p = .002, d = 0.50). T2 stress reactivity explained 20.22% of the variance of T1 GAD severity positively predicting T3 MDD severity. Moreover, this mediational effect remained significant after adjusting for age, gender, education level, income, and baseline MDD symptoms (d = 0.45–0.49). T2 stress reactivity had an indirect effect in the pathway from elevated T1 MDD symptoms predicting more severe T3 GAD symptoms, but this mediational effect was not significant after controlling for T1 GAD symptom severity. Direct effect analyses indicated that T1 GAD positively predicted T3 MDD (d = 1.29) and vice versa (d = 1.65). 

Conclusions: The results herein suggest that elevated stress reactivity may be a mediator in the 18-year longitudinal relation between GAD severity and future MDD symptoms. These findings support stress reactivity theories of psychopathology and expand on previous cross-sectional studies on the topic. Further, our results suggest that evidence-based cognitive-behavioral treatments for GAD may be enhanced by an increased focus on effectively targeting stress reactivity (e.g., through exposure to negative emotional contrasts), which could potentially reduce the risk of developing subsequent MDD symptoms.