Sleep and Cardio-Metabolic Disease

Francesco P Cappuccio, Michelle A Miller, Francesco P Cappuccio, Michelle A Miller

Abstract

Purpose of review: This review summarises and discusses the epidemiological evidence suggesting a causal relationship between sleep duration and cardio-metabolic risk and outcomes in population.

Recent findings: Sleep duration is affected by a variety of cultural, social, psychological, behavioural, pathophysiological and environmental influences. Changes in modern society-like longer working hours, more shift-work, 24/7 availability of commodities and 24-h global connectivity-have been associated with a gradual reduction in sleep duration and sleeping patterns across westernised populations. We review the evidence of an association between sleep disturbances and the development of cardio-metabolic risk and disease and discuss the implications for causality of these associations. Prolonged curtailment of sleep duration is a risk factor for the development of obesity, diabetes, hypertension, heart disease and stroke and may contribute, in the long-term, to premature death.

Keywords: Cardiovascular disease; Diabetes; Hypertension; Naps; Obesity; Sleep deprivation.

Conflict of interest statement

Conflict of Interest

Francesco P. Cappuccio and Michelle A. Miller declare that they have no conflict of interest.

Human and Animal Rights and Informed Consent

This article does not contain any studies with human or animal subjects performed by any of the authors.

Figures

Fig. 1
Fig. 1
Forest plots of the prospective associations between short duration of sleep and the incidence of hypertension in population studies in adults*. *Results are reported as risk ratio and 95% confidence intervals. (Adapted by permission from Macmillan Publishers Ltd.: Meng L et al. Hypertens Res 2013; 36: 985–95) [28]
Fig. 2
Fig. 2
Possible mechanistic pathways linking short duration of sleep and adverse cardiovascular health. BP blood pressure, HbA1c haemoglobin A1c, HDL high-density lipoprotein cholesterol, HR heart rate, LDL low-density lipoprotein cholesterol, PAI-1 plasminogen activator inhibitor-1, SNS sympathetic nervous system, SWS slow-wave sleep, Trigs triglycerides. (Adapted with permission from Miller MA, Cappuccio FP. J Hum Hypert 2013; 27: 583–588) [42]

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