Sleep and sadness: exploring the relation among sleep, cognitive control, and depressive symptoms in young adults
Open accessAbstract
Background Sleep disturbance is a common feature of depression. However, recent work has found that individuals who are vulnerable to depression report poorer sleep quality compared to their low-risk counterparts, suggesting that sleep disturbance may precede depression. In addition, both sleep disturbance and depression are related to deficits in cognitive control processes. Thus we examined if poor sleep quality predicts subsequent increases in depressive symptoms and if levels of cognitive control mediated this relation.Methods Thirty-five undergraduate students participated in two experimental sessions separated by 3 weeks. Participants wore an actigraph watch between sessions, which provided an objective measure of sleep patterns. We assessed self-reported sleep quality and depressive symptoms at both sessions. Last, individuals completed an exogenous cuing task, which measured ability to disengage attention from neutral and negative stimuli during the second session.Results Using path analyses, we found that both greater self-reported sleep difficulty and more objective sleep stability measures significantly predicted greater difficulty disengaging attention (i.e., less cognitive control) from negative stimuli. Less cognitive control over negative stimuli in turn predicted increased depression symptoms at the second session. Exploratory associations among the circadian locomotor output cycles kaput gene, CLOCK, single nucleotide polymorphism (SNP), rs11932595, as well as sleep assessments and depressive symptoms also are presented.Conclusions These preliminary results suggest that sleep disruptions may contribute to increases in depressive symptoms via their impact on cognitive control. Further, variation in the CLOCK gene may be associated with sleep quality.
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Melatonin, as well as agomelatine, may hinder circadian misalignment and sleep disruption, which has been posited to contribute to increases in depressive symptoms through their effect on cognitive control.
“Melatonin, as well as agomelatine, a melatonergic analogue drug acting as an MT1/MT2 agonist and 5-HT2C antagonist, may hinder circadian misalignment and sleep disruption, which has been posited to contribute to increases in depressive symptoms through their effect on cognitive control [145].”
From Cognitive remission: a novel objective for the treatment of major depression? (2016) · cites this paper as [145]
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- Authors
- Michael Vanderlind, W., Beevers, C. G., Sherman, S. M., Trujillo, L. T., McGeary, J. E., Matthews, M. D., Todd Maddox, W., & Schnyer, D. M.
- Affiliations
- The University of Texas at Austin (US)
- Brown University (US)
- United States Military Academy (US)
- Venue
- Sleep Medicine
- Publisher
- Elsevier BV
- Published
- 2014-01
- Volume
- 15
- Issue
- 1
- Pages
- 144-149
- ISSN
- 1389-9457 (ISSN-L)
- PMC
- PMC4217155
- OpenAlex
- W2036337926
- Cited by
- 117
- References
- 52
- Citations by year
- 2026: 5 · 2025: 13 · 2024: 11 · 2023: 4 · 2022: 9 · 2021: 28 · 2020: 6 · 2019: 10 · 2018: 9 · 2017: 4 · 2016: 3 · 2015: 11 · 2014: 3
- FWCI
- 7.66
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Sleep Medicine (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- Funders
- West Point Network Science Center
- The University of Texas at Austin
- Topics
- Social Sciences › Psychology › Experimental and Cognitive Psychology › Sleep and related disorders
- Life Sciences › Neuroscience › Cognitive Neuroscience › Sleep and Wakefulness Research
- Life Sciences › Neuroscience › Endocrine and Autonomic Systems › Circadian rhythm and melatonin
- Keywords
- sleep quality, depressive symptoms, cognitive control, attentional disengagement, sleep disorders, depression vulnerability, actigraphy, clock genes, young adults, negative stimuli
- MeSH terms
- Adolescent, Circadian Rhythm, Cognition, Depression, Emotions, Female, Genotype, Humans, Male, Sleep, Sleep Wake Disorders, Polymorphism, Single Nucleotide, Young Adult, Actigraphy, CLOCK Proteins
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