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Sleep duration and cardiometabolic risk: A review of the epidemiologic evidence

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Laboratory studies have found that short-term sleep restriction is associated with impairments in glucose metabolism, appetite regulation and blood pressure regulation. This chapter reviews the epidemiologic evidence for an association between habitual sleep duration and quality and risk of cardiometabolic diseases including obesity, diabetes and hypertension. Multiple studies observed a cross-sectional association between short sleep duration (generally <6 h per night) and increased body mass index or obesity, prevalent diabetes and prevalent hypertension. Many studies also reported an association between self-reported long sleep duration (generally >8 h per night) and cardiometabolic disease. There have been a few prospective studies and several, but not all, have found an association between short sleep and incident diabetes, hypertension and markers of cardiovascular disease. Future prospective epidemiologic studies need to include objective measures of sleep, and intervention studies are needed in order to establish a causal link between impaired or insufficient sleep and cardiometabolic disease risk.

Introduction

Cardiometabolic risk has been defined as a cluster of metabolic and cardiovascular abnormalities, including abdominal obesity, insulin resistance, hypertension, dyslipidemia and atherosclerosis, that predispose individuals to cardiovascular disease (CVD) and type 2 diabetes.1, 2 CVD, type 2 diabetes and overweight/obesity are closely linked conditions. For example, approximately 70% of total mortality in type 2 diabetes is due to CVD, and individuals with the metabolic syndrome, which is a clustering of risk factors including obesity, dyslipidemia, high blood pressure and insulin resistance, are at increased risk of developing type 2 diabetes and CVD.3 The prevalence and impact of these cardiometabolic diseases is enormous. The World Health Organization estimates that worldwide in 2004–2005 approximately 1.6 billion adults were overweight, 400 million were obese, over 190 million people had diabetes and 17.1 million people died of cardiovascular disease.4 In addition to increased mortality risk, CVD, diabetes, and obesity are associated with reduced quality of life and an increased economic burden on both the individual and on society.5, 6, 7, 8 Thus, an important goal of global public health is to reduce cardiometabolic risk.

Efforts to reduce the burden of these diseases require a better understanding of the mechanisms underlying increased cardiometabolic risk. Poor diet and limited physical activity certainly play an important role, but an additional possible explanation for the epidemic of cardiometabolic diseases is reduced sleep duration and quality. There is some evidence in the US that the number of adults obtaining insufficient sleep has increased over the same time period that the prevalence of obesity and diabetes has increased.9, 10, 11, 12, 13 For example, a report from the National Health Interview Survey indicated the percentage of adults report sleeping 6 h or less increased by approximately 5–6% between 1985 and 2004.14 Sleep loss may be the result of either a voluntary restriction of time spent in bed or as a result of a sleep disorder, such as insomnia and obstructive sleep apnea (OSA). Unfortunately, most epidemiologic studies cannot distinguish between voluntary sleep curtailment and sleep loss due to a pathological condition. Section 4 will discuss the impact of sleep disorders such as OSA on metabolism. Laboratory studies involving experimental restriction of time in bed provided the initial evidence that sleep loss can increase cardiometabolic risk and other papers in this issue will discuss these laboratory studies (see Section 1). One limitation of laboratory studies, however, is that they are short-term, lasting a few weeks at most. This raises the question of whether the associations observed in the laboratory persist in the real world when sleep loss is chronic. Epidemiologic studies provide some insight into the associations between sleep and health outside of the laboratory. This paper will review the epidemiologic evidence linking sleep duration and/or quality to cardiometabolic risk, including the relationship between sleep and body mass index (BMI) or obesity, appetite regulation, type 2 diabetes, hypertension and cardiovascular disease.

Section snippets

Sleep and BMI, obesity and appetite regulation

Several observational studies have examined the association between sleep and obesity or BMI. Over 65 published articles have presented cross-sectional analyses and most found a significant association between short sleep duration (generally <6 h per night) and increased prevalence of obesity or higher BMI in both adults and children from various countries (see*15, *16, 17 for reviews). Some of these studies also observed higher mean BMI associated with longer sleep durations (generally >8 h

Sleep and diabetes

Several large observational studies have reported cross-sectional associations between short sleep duration or impaired sleep and greater prevalence of diabetes or impaired glucose tolerance (see17 for a review). Most of these studies found an increased odds of diabetes associated with short sleep durations (≤5 h or ≤6 h per night) and some also found an increased odds of diabetes among long sleepers (≥8 or ≥9 h). One study found stronger associations in older people 43 and another observed a

Sleep and cardiovascular disease

Sleep duration and quality have also been associated with blood pressure in epidemiologic studies.49, 50, 51, 52, 53, 54 Cross-sectional studies have generally found that self-reported short sleep durations or subjectively poor sleep quality are associated with higher blood pressure or higher prevalence of hypertension.43, 49, 51, 52, 53, 55, 56 Some of these studies also observed higher blood pressure among long sleepers.43, 49 Two of these studies observed a significant association in women

Limitations

The majority of the observational studies described above had consistent findings, but we must still consider the methodological limitations of these studies. First, the vast majority of these studies relied on a self-reported measure of sleep duration, which may not be very accurate. Recent analysis comparing sleep durations estimated from wrist actigraphy to self-reported sleep in a sample of over 600 middle-aged adults indicated only moderate agreement between these measures (r = 0.47).67 In

Potential mechanisms

The mechanisms underlying the association between cardiometabolic disease risk and sleep duration or quality are not fully understood. However, laboratory studies have provided some clues about potential pathways leading from insufficient or disturbed sleep to diabetes and obesity. The figure below presents potential pathways linking disturbed or insufficient sleep to the development of obesity, type 2 diabetes and cardiovascular disease (CVD) or hypertension (HTN). It is unlikely that any

Summary

The accumulated evidence from numerous observational studies suggests that insufficient or disturbed sleep may play a role in the development of cardiometabolic disease risk. Potential pathways through which sleep could lead to the development of obesity, diabetes, cardiovascular disease and hypertension have been discussed. In particular, these pathways involve impairments in glucose metabolism, appetite regulation, and sympatho-vagal balance. However, more research is required to better

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