“Omics” Approaches for Sleep and Circadian Rhythm Research: Biomarkers for Identifying Differential Vulnerability to Sleep Loss

Abstract

The two-process model of sleep-wake regulation asserts a neurobiological drive for sleep that varies homeostatically (increasing as a saturating exponential during wakefulness and decreasing in a similar manner during sleep) and a circadian process that neurobiologically modulates the homeostatic drive for sleep and waking performance and alertness. Sleep deprivation increases homeostatic sleep drive and degrades waking neurobehavioral functions as reflected in fatigue, sleepiness, attention, memory, and cognitive speed. Notably, there are robust individual differences in neurobehavioral responses to sleep loss which are trait-like and phenotypic and not explained by baseline functioning or other possible predictors. This review discusses “omics” methodologies (transcriptomics, epigenomics, and metabolomics) in sleep and circadian rhythm research. Since the molecular mechanisms underlying differential vulnerability remain virtually unknown, such methodologies can be used to yield biomarkers for predicting individual differences in neurobehavioral responses to sleep loss in humans. Reliable prediction of who is more or less likely to experience neurobehavioral decrements from sleep loss would provide more targeted use of biological countermeasures and optimization of personnel in a variety of occupational settings.