Sleep Debt and Postprandial Metabolic Function in Subclinical Cardiometabolic Pathophysiology.

Abstract

Compared with 4 decades ago, more than twice the adults (37%) are voluntarily restricting sleep from 8.5 hours to less than 7 hours per night [1–3]. Sleep curtailment has consequences that involve not just diminished daytime performance and enhanced sleepiness and fatigue [4], but may also facilitate disease mechanisms, manifesting in a high comorbidity of sleep dysfunction and subclinical cardiometabolic pathophysiology [5,6]. Indeed, epidemiological studies have linked chronic shortened and/or poor sleep with obesity [7,8], and then also with type2diabetes disease and cardiovascular [9–12]. Despite the attention of the health profession, the media, the public and mass educational campaigns about the benefits of healthier diets and increased physical activity, the prevalence of obesity in the United States has more than doubled over the past four decades [13,14]. This increasing prevalence constitutes a major public health challenge. In persons with obesity, cardiometabolic pathogenesis occurs prematurely, and is accelerated by factors that are likely to be a combination of the established risk factors, as well as underlying insulin and glucose metabolic dysfunction associated with prediabetes and metabolic syndrome (MetS) [15]. The impact of sleep curtailment on cardiometabolic processes has not been examined as a function of obesity, prediabetes, or MetS status. Sleep loss could contribute to the development of prediabetes and MetS by deleteriously affecting glycemic regulation and/or by influencing hunger, appetite, and feeding behavior and ultimately result in weight gain and obesity [5]. Evidence suggests that central obesity and insulin resistance may be central mediating pathways by which numerous biobehavioral factors, including sleep debt, drive subclinical cardiometabolic pathophysiology [16].