Acute total sleep deprivation decreases brain activation in the fronto-parietal attention network (prefrontal cortex and intraparietal sulcus) and in the salience network (insula and medial frontal cortex). Increased thalamic activation after sleep deprivation may reflect a complex interaction between the de-arousing effects of sleep loss and the arousing effects of task performance on thalamic activity.
Shorter sleep duration may impair insulin sensitivity and beta-cell function in nondiabetic white men, possibly contributing to later type 2 diabetes and cardiovascular disease.
The current findings demonstrate that total sleep deprivation and chronic circadian misalignment modulate cortisol levels and that chronic circadian misalignment increases plasma concentrations of pro- and anti-inflammatory proteins.
Sleep deprivation has been associated with altered feeding patterns. This study reports the relationship between sleep deprivation, caloric consumption, and connectivity in affected regions of the brain. Human subjects were sleep deprived for one night, compared to the control group (normal sleep), sleep deprived individuals consumed more food during the extra wake period, and in the recovery period consumed similar total calories but with significantly more fat and less carbohydrate composition than controls. Functional MRI scanning revealed connectivity differences between the dorsal anterior cingulate cortex (dACC) and multiple regions of the brain, with the pathways between the dACC and putamen and dACC and insula being most highly correlated with increased fat and decreased carbohydrate consumption. Based on what is known of these pathways the authors suggest a connectivity mechanism by which attentiveness and reward centers (insula and putamen) interact with homeostatic-stress centers (dACC) to explain the increased consumption of fat after sleep deprivation.