W Michael Vanderlind1, Christopher G Beevers2, Stephanie M Sherman3, Logan T Trujillo3, John E McGeary4, Michael D Matthews5, W Todd Maddox6, David M Schnyer6. 1. Department of Psychology, Northwestern University, United States. Electronic address: wmvanderlind@u.northwestern.edu. 2. Department of Psychology, The University of Texas at Austin, United States; Institute for Mental Health Research, The University of Texas at Austin, United States. 3. Department of Psychology, The University of Texas at Austin, United States. 4. Providence Veterans Affairs Medical Center and Division of Behavioral Genetics, Rhode Island Hospital, Brown University, United States. 5. Department of Behavioral Sciences & Leadership, United States Military Academy at West Point, United States. 6. Department of Psychology, The University of Texas at Austin, United States; Institute for Neuroscience, The University of Texas at Austin, United States; Institute for Mental Health Research, The University of Texas at Austin, United States.
Abstract
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.
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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