The human gut microbiome can influence health through the brain-gut-microbiome axis. Growing evidence suggests that the gut microbiome can influence sleep quality. Previous studies that have examined sleep deprivation and the human gut microbiome have yielded conflicting results. A recent study found that sleep deprivation leads to changes in gut microbiome composition while a different study found that sleep deprivation does not lead to changes in gut microbiome. Accordingly, the relationship between sleep physiology and the gut microbiome remains unclear. To address this uncertainty, we used actigraphy to quantify sleep measures coupled with gut microbiome sampling to determine how the gut microbiome correlates with various measures of sleep physiology. We measured immune system biomarkers and carried out a neurobehavioral assessment as these variables might modify the relationship between sleep and gut microbiome composition. We found that total microbiome diversity was positively correlated with increased sleep efficiency and total sleep time, and was negatively correlated with wake after sleep onset. We found positive correlations between total microbiome diversity and interleukin-6, a cytokine previously noted for its effects on sleep. Analysis of microbiome composition revealed that within phyla richness of Bacteroidetes and Firmicutes were positively correlated with sleep efficiency, interleukin-6 concentrations and abstract thinking. Finally, we found that several taxa (Lachnospiraceae, Corynebacterium, and Blautia) were negatively correlated with sleep measures. Our findings initiate linkages between gut microbiome composition, sleep physiology, the immune system and cognition. They may lead to mechanisms to improve sleep through the manipulation of the gut microbiome.

Chronic sleep deprivation has been demonstrated to diminish cognitive performance, alter mood states, and concomitantly dysregulate inflammation and stress hormones. At present, however, there is little understanding of how an acute sleep deprivation may collectively affect these factors and alter functioning. The present study aimed to determine the extent to which 24-h of sleep deprivation influences inflammatory cytokines, stress hormones, cognitive processing across domains, and emotion states. To that end, 23 participants (mean age = 20.78 years, SD = 2.87) filled out clinical health questionnaires measured by the Pittsburgh Sleep Quality Index, Morningness Eveningness Questionnaire, and Center for Epidemiological Studies Depression Scale. Actigraph was worn for seven days across testing to record sleep duration. At each session participants underwent a series of measures, including saliva and blood samples for quantification of leptin, ghrelin, IL-1β, IL-6, CRP, and cortisol levels, they completed a cognitive battery using an iPad, and an emotion battery. We found that an acute sleep deprivation, limited to a 24 h period, increases negative emotion states such as anxiety, fatigue, confusion, and depression. In conjunction, sleep deprivation results in increased inflammation and decreased cortisol levels in the morning, that are accompanied by deficits in vigilance and impulsivity. Combined, these results suggest that individuals who undergo 24 h sleep deprivation will induce systemic alterations to inflammation and endocrine functioning, while concomitantly increasing negative emotions.