Circadian rhythms and psychiatric profiles in young adults with unipolar depressive disorders

Kristy-Lee Feilds,Sharon L Naismith,Daniel F Hermens,Sarah Fares,Elizabeth M Scott,Ashlee B Grierson,Joanne S Carpenter,Ian B Hickie,Rébecca Robillard,Nick Glozier,Sharon J Mullin,Naomi L Rogers

doi:10.1038/s41398-018-0255-y

Abstract

Abnormalities in circadian rhythms have been reported in people with mood disorders, but these abnormalities are marked by considerable inter-individual variability. This study aimed to identify pathophysiological subgroups on the basis of circadian markers and evaluate how these subgroups relate to psychiatric profiles. Thirty-five young adults (18–31 years old) receiving clinical care for unipolar depressive disorders and 15 healthy controls took part to this study. The Hamilton Rating Scale for Depression and the Young Mania rating scale were used to evaluate the severity of mood symptoms in participants with depressive disorders. All participant underwent ambulatory sleep monitoring with actigraphy for about 12 days before attending a laboratory-based chronobiological assessment which included repeated salivary samples to determine dim light melatonin onset (DLMO) and continuous core body temperature (CBT) monitoring using an ingestible temperature sensor. Cluster analyses were conducted across all participants to identify subgroups with consistent circadian timing profiles based on DLMO and the nocturnal minima of CBT. Two clusters were identified: ‘delayed’ and ‘conventional timing’ circadian phase. Descriptive analyses showed that the delayed cluster was characterised by abnormal time relationships between circadian phase markers and the sleep–wake cycle. Importantly, individuals from the delayed cluster had worse depression severity (t(28) = −2.7, p = 0.011) and hypomanic symptoms (Z = −2.2, p = 0.041) than their peers with conventional circadian timing. These findings suggest that delayed and disorganised circadian rhythms may be linked to worse psychiatric profiles in young people with depressive disorders.

Highlights

The biological clock in the suprachiasmatic nuclei regulates the temporal coordination of physiological rhythms to optimise brain and body functions across the different phases of the 24-h cycle
Based on the variables included in the cluster analysis, one of the clusters was characterised by later dim light melatonin onset (DLMO) and CBTmin (i.e. ‘delayed’ cluster) compared to the other cluster (i.e. ‘conventional timing’ cluster)
DLMO and CBTmin, respectively, occurred 3.7 and 3.0 h later in the ‘delayed’ cluster compared to the ‘conventional timing’ cluster

Summary

Introduction

The biological clock in the suprachiasmatic nuclei regulates the temporal coordination of physiological rhythms to optimise brain and body functions across the different phases of the 24-h cycle. The temporal organisation of these rhythms is important for several aspects of physical and mental health (for a review, see ref.[1]). Experimentally induced alterations in the temporal relationship between the light–dark cycle and circadian rhythms can induce mood impairments[2,3]. It has been hypothesised that circadian rhythms disruption may play a role in the pathophysiology of mood disorders The temporal alignment of endogenous rhythms with the 24-h patterns of sleep, wakefulness, feeding and physical activity supports variations in physiological functions at times that best match behavioural schedules

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