Cognitive predictors of stress-induced mood malleability in depression

ABSTRACT

Background & objectives

Basic attentional control, negative biases in attention and interpretation, and rumination are all cognitive processes associated with depression; however, less is known about their predictive role in depressive mood reactivity and -recovery in response to stress, and their relation to severity of depression.

Design & methods

We experimentally induced stress based on an autobiographical imagery script in a sample of 92 participants with Major Depressive Disorder with or without comorbid anxiety disorders. We used simple regression analysis for investigating the roles of state- and trait rumination, attentional networks, and attentional and interpretation biases for predicting stress-induced depressive mood reactivity and -recovery, respectively, and whether they in parallel mediated the association between cognitive processes and depression severity.

Results

Stress-induced depressive mood reactivity was predicted by better orienting ability and more state rumination. Better recovery was predicted by better orienting efficiency and lower negative interpretation bias. Furthermore, the relation between state rumination and depression severity was partially mediated by depressive mood reactivity, however limited by the lack of temporal precedence in the analysis.

Conclusions

We characterized the relation between cognitive processes and mood malleability in response to stress. Findings could refine theoretical models of depression if causality is established.

Trial registration

ClinicalTrials.gov identifier: NCT04137367.

KEYWORDS:

• Depression
• stress
• reactivity
• recovery
• cognition
• mood

Acknowledgements

Author contributions: All authors contributed to the study’s conception, methods, and design. NIL acquired the funding. RB and BK collected and analyzed the data. RB wrote the first draft. All authors collaborated in the writing and editing of the final manuscript and approved the final version of the manuscript for submission.

Disclosure statement

NIL has received consultancy fees and travel expenses from Lundbeck outside this work. CJH has received consultancy fees from P1vital, Lundbeck, Sage Therapeutics, Compass Pathways, Zogenix outside of this work. The remaining author(s) declared that there were no conflicts of interest with respect to the authorship or the publication of this article.

Data availability statement

Data are not publicly available.

Additional information

Funding

This work was supported by the Foundation Dam [grant number 2019/FO249225], the South-Eastern Norway Regional Health Authority [grant number 2020021], University of Oslo, and NIHR Oxford Health Biomedical Research Centre. The funding agencies had no role in design and conduct of the study; collection, management, analysis, and interpretation of the data; and preparation, review, or approval of the manuscript.