Abstract
Depression and its related mood disorders are a major global health issue that disproportionately affects young adults. A number of factors that influence depressive symptoms are particularly relevant to the young adult developmental stage, including sleep loss, poor sleep quality, and the tendency toward eveningness in circadian preferences. However, relatively few studies have examined the relationship between sleep and circadian phenotypes, and their respective influences on mood, or considered potential molecular mechanisms driving these associations. Here, we use a multi-year, cross-sectional study of 806 primarily undergraduates to examine the relationships between sleep-wake chronotype, sleep disturbance, depression and genotypes associated with the PER3 variable number of tandom repeats (VNTR) polymorphism—circadian gene variants associated with both chronotype and sleep homeostatic drive. In addition, we use objective, Fitbit-generated sleep structure data on a subset of these participants (n = 67) to examine the relationships between chronotype, depression scores, actual measures of sleep duration, social jetlag, and the percent of deep and rapid eye movement (REM) sleep per night. In this population, chronotype is weakly associated with depressive symptoms and moderately correlated with self-reported sleep disturbance. Sleep disturbance is significantly associated with depression scores, but objective sleep parameters are not directly correlated with Beck Depression Inventory (BDI-II) scores, with the exceptions of a moderate correlation between social jetlag and depression scores in females and a marginal correlation between sleep duration and depression scores. Multiple regression and path analyses reveal that chronotype effects on depressive symptoms in this population are mediated largely by sleep disturbance. The PER3 VNTR genotype significantly predicts depressive symptoms in a model with objective sleep parameters, but it does not significantly predict depressive symptoms in a model with chronotype or subjective sleep disturbance. Interestingly, PER35,5 genotypes, in males only, are independently related to chronotype and depression scores. Our results support hypotheses linking subjective sleep quality and chronotype and provide a first step in understanding how objective sleep structure may be linked to chronotype and depressive symptoms. Our results also suggest that circadian gene variants may show sex-specific effects linking sleep duration and sleep structure to depression.
Highlights
Depression and related disorders, such as anxiety, affect nearly one-fifth of the global population and disproportionately affect young adults (Steel et al, 2014); studies of sleep patterns in depressed individuals highlight a robust relationship between sleep duration and depression, with extreme long and short sleep duration associated with increased depression (Watson et al, 2014; Zhai et al, 2015; Kalmbach et al, 2017)
mid-sleep point on a free day (MSF) chronotype scores are weakly correlated with BDI-II depression scores (Figure 1A; R2 = 0.07, F = 3.39, df = 223, p = 0.002) with evening-types reporting greater symptoms of depression
Our study reveals complex and, potentially, sex-specific relationships between depressive symptoms and chronotype, sleep disturbance, and sleep structure
Summary
Depression and related disorders, such as anxiety, affect nearly one-fifth of the global population and disproportionately affect young adults (Steel et al, 2014); studies of sleep patterns in depressed individuals highlight a robust relationship between sleep duration and depression, with extreme long and short sleep duration associated with increased depression (Watson et al, 2014; Zhai et al, 2015; Kalmbach et al, 2017). Mutations in core regulatory clock genes are associated with both sleep and mood disorders, suggesting that molecular mechanisms affecting sleep and mood are influenced, in part, by the circadian clock (Randler, 2008; Mendlewicz, 2009; Soria et al, 2010; Lee et al, 2011; Courtet and Olié, 2012; McCarthy and Welsh, 2012; McClung, 2013; Robillard et al, 2013; Sivertsen et al, 2015; Antypa et al, 2016) and may utilize similar downstream pathways. The molecular basis for extreme chronotypes involves geneticallyprogrammed advanced or delayed circadian phase (the timing of peak arousal driven by oscillations in clock genes) – extreme morning-types have advanced phases and extreme eveningtypes have delayed phases in oscillations relative to intermediate types, corresponding to their sleep-wake cycles (McClung, 2013; Robillard et al, 2013)
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