The COVID-19 pandemic has had medical, economic and behavioral implications on a global scale and was argued to have negatively impacted the population’s mental health as well. The current study utilizes longitudinal data to assess such an assertion. An international group of 218 participants completed measures of depression, anxiety, rumination and distress intoler-ance at two baselines six months apart as well as at the height of the COVID-19 pandemic ex-actly 12 months later. Contrary to expectations, depression, rumination, and distress intolerance were at equivalent levels during the pandemic as they were at baseline. Anxiety was reduced by a trivial degree (d = .10). Furthermore, a comparison of quantitative explanatory models indi-cated that symptom severity and pandemic-related environmental stressors predicted pandem-ic-related distress, but pandemic-related distress did not predict symptom severity. These find-ings underscore the necessity of longitudinal designs and diathesis-stress models in the study of mental health during the COVID-19 pandemic.

Bipolar spectrum disorders are characterized by alternating intervals of extreme positive and negative affect. We performed a meta-analysis to test the hypothesis that such disorders would be related to dysregulated reinforcement sensitivity. First, we reviewed 23 studies that reported the correlation between self-report measures of (hypo)manic personality and measures of reinforcement sensitivity. A large relationship was found between (hypo)manic personality and BAS sensitivity (g = .74), but not with BIS sensitivity (g = -.08). This stands in contrast to self-reported depression which has a small, negative relationship with BAS sensitivity and a large positive one with BIS sensitivity (Katz et al., 2020). Next, we reviewed 33 studies that compared reinforcement sensitivity between euthymic, bipolar participants and healthy controls. There, bipolar disorder had a small, positive relationship with BAS sensitivity (g = .20) and a medium, positive relationship with BIS sensitivity (g = .64). These findings support a dual-system theory of bipolar disorders, wherein BAS sensitivity is more closely related to mania and BIS sensitivity more closely to bipolar depression. Bipolar disorders show diatheses for both states with euthymic participants being BAS- and BIS- hypersensitive. Implications for further theory and research practice are expounded upon in the discussion.

Reinforcement Sensitivity Theory (RST) posits that individual differences in reward and punishment processing predict differences in cognition, behavior, and psychopathology. We performed a quantitative review of the relationships between reinforcement sensitivity, depression and anxiety, in two separate sets of analyses. First, we reviewed 204 studies that reported either correlations between reinforcement sensitivity and self-reported symptom severity or differences in reinforcement sensitivity between diagnosed and healthy participants, yielding 483 effect sizes. Both depression (Hedges’ g = .99) and anxiety (g = 1.21) were found to be high on punishment sensitivity. Reward sensitivity negatively predicted only depressive disorders (g = -.21). More severe clinical states (e.g., acute vs remission) predicted larger effect sizes for depression but not anxiety. Next, we reviewed an additional 39 studies that reported correlations between reinforcement sensitivity and both depression and anxiety, yielding 156 effect sizes. We then performed meta-analytic structural equation modeling to simultaneously estimate all covariances and control for comorbidity. Again we found punishment sensitivity to predict depression (β = .37) and anxiety (β = .35), with reward sensitivity only predicting depression (β = -.07). The transdiagnostic role of punishment sensitivity and the discriminatory role of reward sensitivity support a hierarchical approach to RST and psychopathology. Highlights: Sensitivity to punishment positively predicts both depression and anxiety. Sensitivity to reward discriminates between them, negatively predicting depression. This pattern was ob-served even when directly controlling for comorbidity. Depression’s effect sizes are uniquely sensitive to clinical state. Depression’s effect sizes are also moderated by method of clinical assessment.Data, analysis code, supplementary material: https://osf.io/n6gv4/

Bipolar spectrum disorders are characterized by alternating intervals of extreme positive and negative affect. We performed a meta-analysis to test the hypothesis that such disorders would be related to dysregulated reinforcement sensitivity. First, we reviewed 22 studies that reported the correlation be-tween self-report measures of (hypo)mania and measures of reinforcement sensitivity. A large relation-ship was found between (hypo)mania and reward sensitivity (g = .75), but not with punishment sensi-tivity (g = -.05). This stands in contrast to self-reported depression which was found to have a small, negative relationship with reward sensitivity and a large positive one with punishment sensitivity (Katz et al., 2020). Next, we reviewed 32 studies that compared reinforcement sensitivity between euthymic, bipolar participants and healthy controls. There, bipolar disorder had a small, positive relationship with reward sensitivity (g = .19) and a medium, positive relationship with punishment sensitivity (g = .64). These findings support a dual-system theory of bipolar disorders, wherein reward sensitivity is more closely related to mania and punishment sensitivity more closely to bipolar depression. Bipolar disorders show diatheses for both states with euthymic participants being hypersensitive to both rewards and punishments. Implications for further theory and research practice are expounded upon in the discussion.

Accompanying materials for: Ariela Friedman, Benjamin A. Katz, Inbal Halavy Cohen & Iftah Yovel (2020) Expanding the Scope of Implicit Personality Assessment: An Examination of the Questionnaire-Based Implicit Association Test (qIAT), Journal of Personality Assessment, DOI: 10.1080/00223891.2020.1754230