Sleep duration, cardiovascular disease, and proinflammatory biomarkers

Michael A Grandner,1,2 Megan R Sands-Lincoln,3 Victoria M Pak,2,4 Sheila N Garland1,5 1Behavioral Sleep Medicine Program, Department of Psychiatry, Perelman School of Medicine, University of Pennsylvania, PA, USA; 2Center for Sleep and Circadian Neurobiology, University of Pennsylvania, PA, USA; 3Center for Evidence Based Medicine, Elsevier Inc, Philadelphia, PA, USA; 4Division of Sleep Medicine, Perelman School of Medicine, University of Pennsylvania, PA, USA; 5Department of Family Medicine and Community Health, Perelman School of Medicine, University of Pennsylvania, PA, USA Abstract: Habitual sleep duration has been associated with cardiometabolic disease, via several mechanistic pathways, but few have been thoroughly explored. One hypothesis is that short and/or long sleep duration is associated with a proinflammatory state, which could increase risk for cardiovascular and metabolic diseases. This hypothesis has been largely explored in the context of experimental sleep deprivation studies which have attempted to demonstrate changes in proinflammatory markers following acute sleep loss in the laboratory. Despite the controlled environment available in these studies, samples tend to lack generalization to the population at large and acute sleep deprivation may not be a perfect analog for short sleep. To address these limitations, population based studies have explored associations between proinflammatory markers and habitual sleep duration. This review summarizes what is known from experimental and cross-sectional studies about the association between sleep duration, cardiovascular disease, and proinflammatory biomarkers. First, the association between sleep duration with both morbidity and mortality, with a focus on cardiovascular disease, is reviewed. Then, a brief review of the potential role of proinflammatory markers in cardiovascular disease is presented. The majority of this review details specific findings related to specific molecules, including tumor necrosis factor-α, interleukins-1, -6, and -17, C-reactive protein, coagulation molecules, cellular adhesion molecules, and visfatin. Finally, a discussion of the limitations of current studies and future directions is provided. Keywords: sleep duration, inflammation, cardiovascular disease, cytokine