Abstract
The current dissertation investigated a conceptual model whereby stress impairs reward processing and subsequently reduces daily behavioral activation to confer risk for anhedonic depression symptoms in emerging adulthood. This model was tested piecewise in three studies.
In study 1, a between-subject experiment was conducted to examine whether individuals exposed to a controllable stressor, compared to those exposed to an uncontrollable one, would show better reward learning and higher appraisals of rewards. No effects on reward learning were found. However, the uncontrollable stressor group reported lower stressor controllability than the controllable stressor group; in turn, individuals reporting lower stressor controllability also reported feeling less rewarded during a reward learning task, even after controlling for appraisals of stressor intensity, revealing a unique effect of perceived stress controllability on reward sensitivity.
In study 2, blunted reward sensitivity predicted lower behavioral activation averaged over the following 21 days, which predicted higher anhedonic depression symptoms up to 10 months later. On the same timescale, lower behavioral activation also mediated the association between poor reward learning and higher anhedonic depression symptoms. These findings suggested that deficits in behavioral activation were predicted by multiple sources of reward dysfunction to confer risk for long-term anhedonic depression symptoms. In addition, multilevel analyses revealed within-person effects whereby decreases in behavioral activation predicted elevations in anhedonic depression symptoms on the next day and vice versa, pointing to bidirectional processes that evolved within person over time.
Building on studies 1 and 2, study 3 drew direct links between stressor frequency with behavioral activation and anhedonic depression. Higher stressor frequency (aggregated across 21 days) was associated with lower behavioral activation (aggregated across the same 21 days), which predicted higher anhedonic depression symptoms up to 10 months later. While replication in a fully longitudinal model is needed, these models identified behavioral activation as a potential mechanism driving the depressogenic effects of stress. Further, multilevel analyses revealed between-person and within-person concurrent within-day, but not lagged next-day, relations between stressor frequency and anhedonic depression symptoms, highlighting the short timescale of these within-person processes.
Collectively, the three studies supported key aspects of the conceptual model, delineating how dimensions of stress influence those of reward function to dampen behavioral activation and confer vulnerability for anhedonic depression in emerging adulthood.