| Summary: | Studies suggest that sleep disturbance may be an important etiological factor in the development of comorbid anxiety and depressive disorders, whereby anxiety leads to sleep difficulties, which in turn increase the vulnerability for depression. The primary aim of this study was to determine whether the sequential comorbidity patterns observed at the disorder level (i.e., where anxiety disorders most often precede insomnia, and insomnia most often precedes depression) were also present in daily fluctuations of symptoms. The secondary aim was to explore possible moderators of any observed temporal associations. Participants were 15 patients with generalized anxiety disorder (GAD; mean age = 28.9 years, SD = 9.8) and 15 good sleeper controls (mean age = 27.1 years, SD = 8.3) who were comparable in female:male ratio (73% female vs. 67% female). For 14 days, participants wore an actigraph to objectively assess sleep quality (sleep onset latency, total sleep time, wake after sleep onset, sleep efficiency) and completed daily symptom ratings multiple times each day using their smartphones to assess symptoms of anxiety, depressed mood, and subjective sleep quality.
Study aims were assessed using multilevel modeling, with daily symptoms nested within individuals. Many of the analyses were lagged such that the time-varying predictor variable preceded the time-varying outcome variable temporally. Consistent with hypotheses, results demonstrated that anxious mood was predictive of later subjective and objective sleep disturbance in individuals with GAD, and this effect was strongest among individuals with higher levels of neuroticism, negative affect, and dysfunctional beliefs about sleep. Anxious mood was not associated with later subsequent sleep disturbance in healthy controls. In the GAD group, subjective and objective sleep disturbance predicted later depressed mood; this effect was moderated by temperament and dysfunctional beliefs about sleep. For the control group, the effect of subjective sleep disturbance on later depressed mood was moderated by neuroticism and the effect of objective sleep disturbance was moderated by dysfunctional beliefs about sleep, suggesting that sleep disturbance may increase vulnerability for depressed mood even in healthy individuals. These results suggest that explicitly targeting sleep disturbance during the treatment of GAD may attenuate the experience of depressive symptoms.
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