Original ArticleShift work disorder, depression, and anxiety in the transition to rotating shifts: the role of sleep reactivity
Introduction
Labor statistics estimate that at least 2.5% of the US workforce is scheduled on rotating shifts [1], which include both rapid shifting (eg, multiple changes in work hours during a week) and slow rotations (eg, three weeks per shift schedule). Owing to the constant flux of rotating shifts, work-related sleep–wake schedules often conflict with internal circadian rhythms. Sleep–wake disturbances in response to a circadian challenge are highly variable between individuals [2], [3], but a substantial subset of shift workers are unable to recalibrate the timing of their circadian clocks to their work-related sleep–wake schedules [4], [5]. Indeed, up to 26% of rotating shift workers develop shift work disorder (SWD) [4], which is characterized by persistent and severe sleep disturbance during the sleep period and/or excessive sleepiness during the wake period [6]. In addition to sleep–wake complaints, shift workers report poorer mental health and lower quality of life [7], [8], [9]. To improve preventative efforts against SWD and comorbid psychiatric complaints, it is important to identify trait characteristics corresponding to adverse response to shift-work-related challenges to the circadian system. Previous research has shown that normal sleepers with high sleep reactivity – that is, a sensitive sleep system – are prone to transient sleep disturbance and increased wake-time sleepiness in response to a single night of circadian misalignment [10]. However, no studies to date have compared normal sleepers with high versus low sleep reactivity in their risk for developing a circadian rhythm sleep disorder and associated psychiatric complaints.
Disruptions in sleep and wake patterns can reflect normative adjustment to shift-work exposure and circadian misalignment [11], [12]. In comparison to normal sleep–wake characteristics of shift workers, due to inability to sufficiently adjust to shift work, SWD is marked by chronic and severe sleep–wake disturbances [11], [12]. The cardinal features of SWD are sleep disturbance during the sleep period and/or excessive sleepiness during the wake period as a direct result of a mismatch between the endogenous timing of the circadian rhythm and the exogenous work-related sleep–wake schedule [6]. One previously identified trait characteristic predictive of shift-work tolerance is diurnal preference, or morningness versus eveningness [13], which has been linked to a polymorphism of the clock gene, PERIOD3 [14], [15]. Individuals with morningness preference, associated with the homozygotic PERIOD35/5 polymorphism [14], [15], are less tolerant to shift-work-related circadian disruption [13] and sleep loss [15]. Much of the research on sequelae related to diurnal preference and the PERIOD3 gene following a circadian challenge largely focuses on the degree to which sleep loss impairs wake functioning [12], [15], [16]. However, previous research has also demonstrated a certain vulnerability to insomnia to be sensitive to circadian misalignment [10], which may further elucidate trait characteristics that predispose vulnerable individuals to sleep disturbance following a circadian challenge.
Sleep reactivity is a heritable predisposition to sleep disturbance and insomnia that manifests in a sleep system that is sensitive or “reactive” to stress [17], [18], [19], [20], [21]. Although previous research has shown highly reactive sleepers to be more sensitive to major life events [19] and stimulant use [17] among other situational stressors, only one previous study has investigated the effects of circadian disruption on good sleepers with robust versus sensitive sleep systems. In a laboratory setting, Bonnet and Arand [10] found that good sleepers with high sleep reactivity – as evidenced by sensitivity to first night laboratory effects and caffeine intake – experienced significantly greater sleep disturbance and subsequent daytime sleepiness in response to a 6-h phase advance in comparison to good sleepers with more robust sleep systems. Despite demonstrating the sensitivity of reactive sleepers in response to a phase advance, it is at present unclear whether these findings would translate outside of the laboratory. In addition, it is not known whether highly reactive sleepers eventually adapt to circadian misalignment or if they continue to suffer.
The impact of sleep reactivity may not be limited to work-related sleep–wake disturbances, but also to co-occurring changes in mood. Previous research has shown sleep problems to facilitate the relationship between sleep reactivity and depression, such that highly reactive sleepers are predisposed to sleep disturbance and insomnia, which, in turn, elevate risk for depression [18], [19]. As such, it is possible that high sleep reactivity constitutes a trait vulnerability to shift-work-related changes in mood, and that SWD may facilitate this relationship. Despite data showing circadian desynchrony to elicit sleep–wake symptoms in highly reactive normal sleepers [10], and that sleep reactivity increases risk for sleep problems and resultant mood difficulties [18], the role of sleep reactivity in the development of SWD and shift-work-related affective symptoms has not been explored. To address these gaps in the literature, we explored the role of trait sleep reactivity in the development of SWD and work-related changes in depression and anxiety following transition to rotating shifts.
Using the transition to rotating shift work as a naturalistic model of circadian misalignment, we investigated premorbid sleep reactivity as a trait risk factor for developing SWD and related elevations in depression and anxiety. Workers belonging to the rotational shift are unique in that their shifts are in constant flux, thus presenting a persistent challenge to the circadian system. As such, rotating shifts may confer a particularly robust challenge for individuals whose sleep systems are sensitive to such disruptions. We hypothesized that highly reactive sleepers would be more vulnerable to developing SWD in comparison to nonreactive individuals. In addition, we predicted that individuals with high sleep reactivity would experience greater increases in symptoms of depression and anxiety after transitioning to rotating shifts, and that SWD would mediate these relationships.
Section snippets
Participants
Data were collected from a large community sample in Southeastern Michigan using two similar protocols as part of the Evolutions of Pathways to Insomnia Cohort (EPIC) study, a 3-year National Institute of Mental Health (NIMH)-funded investigation (see Table 1 for sample characteristics). The EPIC study is a prospective investigation of a large community-based sample with no previous/current history of insomnia at baseline. For both protocols, recruitment procedures and broader demographic
Sample characteristics
Approximately half of the sample was classified as having high sleep reactivity at baseline (N = 52/96). We observed 18 new cases of SWD after transitioning to rotating shifts, representing an incidence rate of 18.8% in the overall sample. We then compared normal sleepers and individuals with SWD on a number of sleep parameters and daytime impairment indices (see Table 2). Expectedly, individuals with SWD reported shorter TST on weekdays and weekends than good sleepers. When examining changes
Discussion
Using the transition to rotating shift work as a naturalistic challenge to the circadian system, this investigation sought to use a trait measure of sleep reactivity to identify normal sleepers at elevated risk for SWD and shift-work-related changes in depression and anxiety. Rotating workers with high sleep reactivity were at substantially elevated risk for SWD. Importantly, results also indicated that highly reactive sleepers experienced escalations in depression and anxiety symptoms, but
Conclusions
This study demonstrated high sleep reactivity to be an important premorbid vulnerability to incident SWD and elevations in depression and anxiety in response to desynchrony between endogenous circadian timing and exogenous sleep patterns among rotating shift workers. By demonstrating the capability of premorbid sleep reactivity in identifying these at-risk individuals before work-related circadian disruption, preventative care and early identification may be appropriately directed. In addition,
Conflict of interest
This study was supported by an National Institute of Health (NIH) Grant R01 MH082785 to Dr. Christopher L. Drake. Dr. Drake has severed as consultant for Teva; has received research support from Merck and Teva; and has served on speakers' bureau for Jazz, Purdue, and Teva. The other authors have indicated no financial conflict of interest.
The ICMJE Uniform Disclosure Form for Potential Conflicts of Interest associated with this article can be viewed by clicking on the following link: //dx.doi.org/10.1016/j.sleep.2015.09.007
Acknowledgment
This study was supported by an NIMH Grant (R01 MH082785; PI: Drake) and an investigator-initiated research award from Merck & Co., Inc. (50562) (PI: Drake).
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Institution: Sleep Disorders and Research Center, Henry Ford Hospital, Detroit, MI, USA.