Mechanisms Linking Insomnia and Cardiometabolic Disease Risk

About 10% to 15% of the adult population reports frequent, chronic insomnia symptoms of difficulty initiating or maintaining sleep associated with daytime impairment (ie, insomnia disorder). An additional 30% to 40% report insomnia symptoms at any given time. Not only is insomnia disproportionally more prevalent in individuals with cardiometabolic diseases, but evidence also demonstrates that insomnia, particularly when coupled with objective short sleep duration, increases the risk of developing cardiometabolic diseases. Insomnia is a disorder of 24-hour hyperarousal, a multidimensional construct ranging from cognitive to physiological dysregulation. Physiological hyperarousal in insomnia occurs in the form of hyperactivation of wake-promoting and emotion-regulating areas (eg, glucose metabolism in the ascending reticular activating system), hypothalamic-pituitary-adrenal axis (eg, cortisol levels), sympatho-adrenomedullary axis (eg, norepinephrine levels), cardiac sympathetic-parasympathetic system (eg, heart rate variability), and low-grade inflammation (eg, cytokine levels). Physiological hyperarousal in insomnia inhibits sleep ability, leading to objective short sleep, and increases cardiometabolic disease risk. This brief review summarizes the evidence on the pathophysiologic mechanisms associating insomnia with cardiometabolic disease risk, including current knowledge on the phenotypic heterogeneity of insomnia based on objective sleep duration. Future studies need to test the molecular, cellular, and behavioral mechanisms at play in increasing cardiometabolic disease risk across robustly identified insomnia phenotypes.