ABSTRACT
Sleep disturbances are emerging as novel risk factors for cardiometabolic disease development, including risks of obesity, prediabetes, type 2 diabetes (T2D), and atherosclerotic disease. The effects of sleep loss on glucose metabolism are likely multifactorial, involving several interacting pathways that include hormonal dysregulation, high levels of inflammatory cytokines, sympathetic nervous system overactivity, and orexin system hyperactivity. Night shift workers are at higher risk for T2D due to the adverse effects of circadian misalignment. It is likely that an internal desynchronization between tissue clocks in the liver, muscle, and pancreas further contributes to the observed effects of circadian misalignment on glucose metabolism. A temporal pattern of light exposure and excessive screen time also influences body weight, insulin resistance, risk of T2D, and development of the metabolic syndrome independent of sleep timing and duration. It is important to acknowledge the unique health effects of screen time that are independent from those of non-screen sedentary behavior. Obstructive sleep apnea (OSA) plays an important role in this population. OSA leads to high levels of sympathetic nervous system activity, intermittent hypoxia, and sleep fragmentation, all leading to dysregulation of the hypothalamic-pituitary axis, endothelial dysfunction, and alterations in cytokines and adipokines. Accumulating evidence suggests that metabolic abnormalities can be partially corrected by continuous positive airway pressure treatment.
