Epidemiological evidence for the links between sleep, circadian rhythms and metabolism

Authors

  • J. E. Gangwisch

    1. Columbia University, College of Physicians and Surgeons, Department of Psychiatry, Division of Cognitive Neuroscience, New York, NY, USA
    Search for more papers by this author

JE Gangwisch, Columbia University, College of Physicians and Surgeons, Department of Psychiatry, Division of Cognitive Neuroscience, 1051 Riverside Drive, Unit 74, New York, NY 10032, USA. E-mail: jeg64@columbia.edu

Summary

Epidemiological data reveal parallel trends of decreasing sleep duration and increases in metabolic disorders such as obesity, diabetes and hypertension. There is growing evidence that these trends are mechanistically related. The seasonal expression of the thrifty genotype provides a conceptual framework to connect circadian and circannual rhythms, sleep and metabolism. Experimental studies have shown sleep deprivation to decrease leptin, increase ghrelin, increase appetite, compromise insulin sensitivity and raise blood pressure. Habitually short sleep durations could lead to insulin resistance by increasing sympathetic nervous system activity, raising evening cortisol levels and decreasing cerebral glucose utilization that over time could compromise β-cell function and lead to diabetes. Prolonged short sleep durations could lead to hypertension through raised 24-h blood pressure and increased salt retention resulting in structural adaptations and the entrainment of the cardiovascular system to operate at an elevated pressure equilibrium. Cross-sectional and longitudinal epidemiological studies have shown associations between short sleep duration and obesity, diabetes and hypertension. If metabolic changes resulting from sleep restriction function to increase body weight, insulin resistance and blood pressure then interventions designed to increase the amount and improve the quality of sleep could serve as treatments and as primary preventative measures for metabolic disorders.

Ancillary