For some time sleep disturbance has been implicated as important in bipolar disorder (e.g., Ehlers et al., 1988
) and evidence now supports these claims (e.g., Harvey, 2009
). Few studies have prospectively examined the relationships of sleep with symptoms and functioning, especially in a larger sized bipolar cohort. Our results revealed significant concurrent and prospective associations between SV and TST with both mood symptoms and functioning in bipolar disorder.
We note that the results of the present study need to be interpreted within the confines of several limitations. First, the existing sleep variables in the STEP-BD database were limited in several ways. Specifically, measures of sleep functioning from the CMF were measured using single score estimates of the maximum and minimum sleep averaged across the previous week, unlikely to fully reflect the central tendency of sleep patterns and variability in over this time period. For example, estimates of both SV and TST might be susceptible to retrospective memory biases as compared to daily sleep diaries, actigraphy, and polysomnography. Furthermore, it was not possible to make formal diagnoses of insomnia or hypersomnia based on the CMF and so future work is needed to replicate these findings when formal insomnia and hypersomnia diagnoses are made. Second, our measure of global functioning may not have been sensitive enough to capture sleep-related impairment. Third, the medication regimens of patients were variable and changed over the 12-month follow-up period. Research indicates that frequently prescribed medications for bipolar disorder may influence sleep architecture (e.g., Eidelman et al., 2010
). Future studies should systematically assess medication influences on sleep duration and variability.
Considering these limitations, the present study represents a step forward in examining sleep functioning in bipolar disorder. More specifically, our first aim examined concurrent associations between sleep at study entry (i.e., baseline) with mood symptoms and functioning. Interestingly, lower TST was associated with more severe mania symptoms, whereas greater SV was associated with more severe mania and depression symptoms. Taking TST first, this finding is consistent with research documenting cross-sectional associations between short sleep durations and increased mania or hypomania (Bauer et al., 2006
; Colombo et al., 1999
; Gruber et al., 2009
; Kasper and Wehr, 1992
; Wehr et al., 1987
). For SV, the results suggest that greater variability in sleep may be associated with more severe mood symptoms. These findings are broadly consistent with the finding that disruptions in social rhythms, including sleep, are associated with greater depressive symptomatology in adolescents (Goldstein et al., 2008
). Moreover, disrupted social rhythms have been associated with increased risk for manic and depressive symptom severity and poorer treatment outcome (Frank et al., 2005
Our second aim examined prospective associations between sleep functioning with mood symptoms and functioning across a 12-month period using mixed-effects modeling. Consistent with concurrent associations at baseline, TST was associated with increased mania severity though TST was not associated with depression severity over time. This is inconsistent with the notion that extended sleep duration, or hypersomnia, is associated with greater symptoms of depression (Kaplan and Harvey, 2009
). However, the relationship is likely more complicated, given that depression can be characterized by either insomnia or hypersomnia (American Psychiatric Association, 2000
Increased sleep variability was associated with greater manic and depressive symptom severity across the 12-month period. These results are consistent concurrent associations between SV and mood symptoms in prior work (e.g., Perlman et al., 2006
). A tendency towards an inconsistent sleep pattern in bipolar disorder may precipitate the onset of mood episodes. Alternatively, prodromal mood symptoms may aggravate sleep regularity leading to the exacerbation of mood symptoms. A third possibility is that a bi-directional escalating vicious cycle is operating whereby sleep and mood progressively feed into the other worsening (Wehr et al., 1987
). Either way, there is likely to be value in exploring specific sleep variables in future research.
In sum, the present study suggests that longer total sleep duration was associated with more severe concurrent and prospective mania, but not depression, symptom severity in bipolar disorder. Furthermore, greater variability in sleep was associated with worsened concurrent and prospective mania and depression symptom profiles. No associations between sleep duration or variability emerged with global functioning. The present findings represent an important initial step towards identifying aspects of sleep functioning that may contribute to clinical impairment in bipolar disorder. Furthermore, this research underscores the importance of incorporating interventions that target sleep functioning aimed at promoting illness stabilization.