Overeem, S. | bioRxiv Science

bioRxiv2020

Home-EEG assessment of possible compensatory mechanisms for sleep disruption in highly irregular shift workers - The ANCHOR study

Study objectivesWhile poor sleep quality has been related to increased risk of Alzheimers disease, long-time shift workers (maritime pilots) did not manifest evidence of early Alzheimers disease in a recent study. We explored two hypotheses of possible compensatory mechanisms for sleep disruption: Increased efficiency in generating deep sleep during workweeks (model 1) and rebound sleep during rest weeks (model 2). MethodsWe used data from ten male maritime pilots (mean age: 51.6{+/-}2.4 years) with a history of approximately 18 years of irregular shift work. Subjective sleep quality was assessed with the Pittsburgh Sleep Quality Index (PSQI). A single lead EEG-device was used to investigate sleep in the home/work environment, quantifying total sleep time (TST), deep sleep time (DST), and deep sleep time percentage (DST%). Using multilevel models, we studied the sleep architecture of maritime pilots over time, at the transition of a workweek to a rest week. ResultsMaritime pilots reported worse sleep quality in workweeks compared to rest weeks (PSQI=8.2{+/-}2.2 vs. 3.9{+/-}2.0; p<0.001). Model 1 showed a trend towards an increase in DST% of 0.6% per day during the workweek (p=0.08). Model 2 did not display an increase in DST% in the rest week (p=0.87). ConclusionsOur findings indicated that increased efficiency in generating deep sleep during workweeks is a more likely compensatory mechanism for sleep disruption in the maritime pilot cohort than rebound sleep during rest weeks. Compensatory mechanisms for poor sleep quality might mitigate sleep disruption-related risk of developing Alzheimers disease. These results should be used as a starting point for future studies including larger, more diverse populations of shift workers.

neuroscience↗

bioRxiv2017

Enhanced food-related responses in the ventral medial prefrontal cortex in orexin-deficient narcolepsy patients

BackgroundNarcolepsy Type 1 is a chronic sleep disorder caused by a deficiency of orexin (hypocretin). In addition to sleep regulation, orexin is important for motivated control processes. Weight gain and obesity are common in narcolepsy. However, the neurocognitive processes associated with food-related control and overeating in orexin-deficient patients are unknown. We explored the neural correlates of general and food-related attentional control in narcolepsy patients (n=23) and healthy BMI-matched controls (n=20). In secondary analyses, we included patients with idiopathic hypersomnia (n=15) to assess sleepiness-related influences.\n\nMethodsWe measured attentional bias to food words with a Food Stroop task and general executive control with a Classic Stroop task during fMRI. Moreover, with correlational analyses, we assessed the relative contribution of the neural findings on the Food Stroop and Classic Stroop tasks to spontaneous snack intake.\n\nResultsRelative to healthy controls, narcolepsy patients showed enhanced ventral medial prefrontal cortex responses and connectivity with motor cortex during the Food Stroop task, but attenuated dorsal medial prefrontal cortex responses during the Classic Stroop task. The ventral medial prefrontal cortex responses on the Food Stroop task, not the dorsal medial prefrontal cortex responses on the Classic Stroop task, were a significant predictor of snack intake. Comparing the narcolepsy patients with idiopathic hypersomnia patients revealed similar results.\n\nConclusionsThese findings demonstrate that orexin deficiency is associated with decreased dorsal medial prefrontal cortex responses during general executive control and enhanced ventral medial prefrontal cortex responses during food-driven attention, with the latter predicting increases in food intake.\n\nStatement of SignificancePatients with orexin (hypocretin) deficient narcolepsy type-1 often suffer from obesity as well as increased food craving, in addition to the sleep symptoms. However, whether and how orexin deficiency relates to neural differences in food-directed attention is unclear. We employed a Food Stroop task during fMRI and provide experimental evidence that the ventral medial prefrontal cortex responds more strongly to food words in narcolepsy patients than in controls. The hypothesis that this mechanism contributes to weight problems in narcolepsy is strengthened by the observation that ventral medial prefrontal cortex responses during the Food Stroop task were predictive of snack intake. These mechanistic data might thus advance the development of treatment targets for obesity in narcolepsy.

neuroscience↗