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Current Trends in Endocrinology   Volumes    Volume 10 
Investigating the sleep-cortisol interaction in chronic fatigue syndrome
Cara Tomas, Zoe Gotts, Andrew Close, Steven Rushton, Jason Ellis, Julia L. Newton, Stuart Watson
Pages: 1 - 20
Number of pages: 20
Current Trends in Endocrinology
Volume 10 

Copyright © 2019 Research Trends. All rights reserved

Disturbed sleep is one of the most common symptoms reported by people diagnosed with chronic fatigue syndrome (CFS). The biopsychosocial causes and consequences are poorly understood. The hypothalamic-pituitary-adrenal (HPA) axis is a diurnal hormone cascade responsible for regulating the response to stress; it influences energy metabolism and immune functioning and has been shown to be differently regulated in CFS. We hypothesise that measures of objective sleep and HPA axis function have a bidirectional relationship and have aetiopathogenic significance in CFS. In this preliminary study, polysomnography (PSG) – an all-night recording of sleep physiology – was conducted and analysed for 11 CFS patients. PSG was recorded over three consecutive nights in the homes of the participants. The 3-night protocol improves reliability and allows habituation to the cumbersome equipment. HPA axis function was estimated by collecting saliva samples at 15 minute intervals for 1 hour from wakening, at 4 pm and 11 pm for the 3 days following the sleep recordings. We used a linear mixed-effects modelling approach to examine variation in PSG parameters in patients with CFS as a function of cortisol, Chalder fatigue scale constructs and demographic variables (age, gender, body mass index (BMI), weight and duration of disease). Evidence of the first-night effect in CFS patients was confirmed with more stage-1 and less stage-3 sleep on the first night. We found statistically significant associations between cortisol levels and the duration of wake-periods, and the latency to rapid eye movement (REM) sleep. Determining cause and effect was not possible in this study but the results may be caused by a bidirectional relationship between the PSG parameters and cortisol, with each perpetuating the other.
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