SUMMARY Existing research has demonstrated associations between sleep duration and obesity, diabetes, cardiovascular disease and mortality. Sleep disorders research has shown that sleep apnoea, insomnia and other sleep disorders confer risk for cardiometabolic disease, particularly in the presence of reduced sleep duration. The aim of the present study was to examine the associations between general sleep disturbance, operationalized as ‘difficulty falling asleep, staying asleep, or sleeping too much’ as measured in a large, nationally representative sample, and self-reported history of myocardial infarction, stroke, coronary artery disease, diabetes and obesity. Data from the Behavioral Risk Factor Surveillance System were analysed. Complete data were available for 138 201 individuals. A hierarchical logistic regression analysis examined associations before and after adjustment for demographic, socioeconomic, medical and psychological factors. After adjusting for demographic, socioeconomic and health risk factors, sleep duration was associated with obesity [odds ratio (OR) = 1.18, P < 0.0005), diabetes (OR = 1.18, P < 0.005), myocardial infarction (OR = 1.36, P < 0.0005), stroke (OR = 1.22, P < 0.05) and coronary artery disease (OR = 1.59, P < 0.0005). In fully adjusted models that included physical health, significant relationships remained for obesity (OR = 1.14, P < 0.0005), myocardial infarction (OR = 1.23, P < 0.005) and coronary artery disease (OR = 1.43, P < 0.0005). Sleep disturbance is a significant risk factor for obesity, diabetes, myocardial infarction, stroke and coronary artery disease, and effects for obesity, myocardial infarction and coronary artery disease are the most robust after adjustment. This study demonstrates that sleep disturbance is a novel risk factor that is potentially modifiable. Future research should determine whether sleep intervention could reduce the cardiometabolic consequences of sleep disturbance.

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.

SUMMARY Over 20 years of evidence indicates a strong association between obstructive sleep apnea (OSA) and cardiovascular disease. Although inflammatory processes have been heavily implicated as an important link between the two, the mechanism for this has not been conclusively established. Atherosclerosis may be one of the mechanisms linking OSA to cardiovascular morbidity. This review addresses the role of circulating adhesion molecules in patients with OSA, and how these may be part of the link between cardiovascular disease and OSA. There is evidence for the role of adhesion molecules in cardiovascular disease risk. Some studies, albeit with small sample sizes, also show higher levels of adhesion molecules in patients with OSA compared to controls. There are also studies that show that levels of adhesion molecules diminish with continuous positive airway pressure therapy. Limitations of these studies include small sample sizes, cross-sectional sampling, and inconsistent control for confounding variables known to influence adhesion molecule levels. There are potential novel therapies to reduce circulating adhesion molecules in patients with OSA to diminish cardiovascular disease. Understanding the role of cell adhesion molecules generated in OSA will help elucidate one mechanistic link to cardiovascular disease in patients with OSA.

The ODSI is a brief, valid, easy-to-administer three-item assessment that can screen for excessive daytime sleepiness among elderly patients with OSA.