Article

Association of Sleep Time With Diabetes Mellitus and Impaired Glucose Tolerance

The Pulmonary Center, Boston University School of Medicine, VA Boston Healthcare System, 715 Albany St, Mail Stop R-304, Boston, MA 02118, USA.
Archives of Internal Medicine (Impact Factor: 17.33). 05/2005; 165(8):863-7. DOI: 10.1001/archinte.165.8.863
Source: PubMed

ABSTRACT

Experimental sleep restriction causes impaired glucose tolerance (IGT); however, little is known about the metabolic effects of habitual sleep restriction. We assessed the cross-sectional relation of usual sleep time to diabetes mellitus (DM) and IGT among participants in the Sleep Heart Health Study, a community-based prospective study of the cardiovascular consequences of sleep-disordered breathing.
Participants were 722 men and 764 women, aged 53 to 93 years. Usual sleep time was obtained by standardized questionnaire. Diabetes mellitus was defined as a serum glucose level of 126 mg/dL or more (> or =7.0 mmol/L) fasting or 200 mg/dL or more (> or =11.1 mmol/L) 2 hours following standard oral glucose challenge or medication use for DM. Impaired glucose tolerance was defined as a 2-hour postchallenge glucose level of 140 mg/dL or more (> or =7.8 mmol/L) and less than 200 mg/dL. The relation of sleep time to DM and IGT was examined using categorical logistic regression with adjustment for age, sex, race, body habitus, and apnea-hypopnea index.
The median sleep time was 7 hours per night, with 27.1% of subjects sleeping 6 hours or less per night. Compared with those sleeping 7 to 8 hours per night, subjects sleeping 5 hours or less and 6 hours per night had adjusted odds ratios for DM of 2.51 (95% confidence interval, 1.57-4.02) and 1.66 (95% confidence interval, 1.15-2.39), respectively. Adjusted odds ratios for IGT were 1.33 (95% confidence interval, 0.83-2.15) and 1.58 (95% confidence interval, 1.15-2.18), respectively. Subjects sleeping 9 hours or more per night also had increased odds ratios for DM and IGT. These associations persisted when subjects with insomnia symptoms were excluded.
A sleep duration of 6 hours or less or 9 hours or more is associated with increased prevalence of DM and IGT. Because this effect was present in subjects without insomnia, voluntary sleep restriction may contribute to the large public health burden of DM.

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    • "Moreover, disruption of the sleep–wake cycle alters some parameters related to nutritional balance and metabolism, such as glycaemic control (Spiegel et al. 1999;Gottlieb et al. 2005;van Leeuwen et al. 2010), and increases cholesterol and triglycerides levels (Karlsson et al. 2003;Gangwisch et al. 2010). Given that sleep deprivation or restriction causes all these changes in metabolic regulation, they have been associated with higher prevalence of metabolic syndrome (Karlsson et al. 2003;Sabanayagam & Shankar, 2012;Choi et al. 2011;Katano et al. 2011;Kobayashi et al. 2011;Ju & Choi, 2013;Yoo & Franke, 2013;Parkes, 2002), dyslipidaemia (Romon et al. 1992;Lennernäs et al. 1994;Gangwisch et al. 2010) and diabetes mellitus (Ayas et al. 2003;Gottlieb et al. 2005;Cappuccio et al. 2008Cappuccio et al. , 2010Nilsson et al. 2004;Knutson & Van Cauter, 2008;van Leeuwen et al. 2010). Animal studies reveal some common metabolic outcomes of distinct methods of sleep deprivation (unremitting exposure of animals to sleep suppression), including hyperphagia (Everson & Wehr, 1993;Suchecki et al. 2003;Martins et al. 2010;Moraes et al. 2014), weight loss (Kushida et al. 1989;Brock et al. 1994;Suchecki & Tufik, 2000;HipólideHip´Hipólide et al. 2006;Rodrigues et al. 2015) and augmented energy expenditure (Bergmann et al. 1989;Koban & Swinson, 2005;HipólideHip´Hipólide et al. 2006;Caron & Stephenson, 2010). "
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    ABSTRACT: Sleep curtailment is associated with obesity and metabolic changes in adults and children. The aim of the present study was to evaluate the immediate and long-term metabolic alterations produced by sleep restriction in pubertal male rats. Twenty-eight-day old male Wistar rats were distributed in two groups: control (CTL) and sleep restricted (SR), which was accomplished by the single platform technique for 18 h/day for 21 days, These groups were further distributed in four periods of assessment: sleep restriction, 1 month, 2 months and 4 months of recovery. Body weight and food intake were monitored during all experimental periods. At the end of each period, blood was collected for metabolic profiling, and the carcasses were processed for measurement of body composition and energy balance. During the sleep restriction period, SR animals consumed less food in the home-cages. This group also displayed lower body weight, body fat, triglycerides and glucose levels than CTL rats. At the 1(st) month of recovery, despite eating as much as CTL rats, SR animals showed greater energy and body weight gain, increased gross food efficiency and decreased energy expenditure. At the 2(nd) and 4(th) months of recovery, the groups were no longer different, except for energy gain and gross food efficiency, which remained higher in SR animals. In conclusion, sleep restriction affected weight gain of young animals, due to reduction of fat stores. Two months were sufficient to recover this deficit, and to reveal that SR rats tended to save more energy and to store more fat. This article is protected by copyright. All rights reserved.
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    • "This increased risk is linked to cognitive deficits associated with impaired glycemic control in T2DM (Cukierman- Yaffe et al., 2009). Over the last decade, compelling evidence has identified disrupted sleep as an independent T2DM risk factor (Gottlieb et al., 2005; Knutson et al., 2006, 2007; Laposky et al., 2008; Gale et al., 2011; Touma and Pannain, 2011; Wan Mahmood et al., 2013), contributing to diabetes progression (Gale et al., 2011) and severity (Knutson et al., 2007). Poor sleep quality (as measured by the Pittsburgh Sleep Quality Index; PSQI) is predictive of higher levels of hemoglobin-A1c (HbA1c; Knutson et al., 2007; Wan Mahmood et al., 2013), which is the gold standard for indexing glycemic control and diabetes selfmanagement (Canadian Diabetes Association Clinical Practice Guidelines Expert Committee, 2013). "
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    ABSTRACT: As of 2010, the worldwide economic impact of dementia was estimated at $604 billion USD; and without discovery of a cure or effective interventions to delay disease progression, dementia’s annual global economic impact is expected to surpass $1 trillion USD as early as 2030. Alzheimer’s disease (AD) is the leading cause of dementia accounting for over 75% of all cases. Toxic accumulation of amyloid beta (Aβ), either by overproduction or some clearance failure, is thought to be an underlying mechanism of the neuronal cell death characteristic of AD—though this amyloid hypothesis has been increasingly challenged in recent years. A compelling alternative hypothesis points to chronic neuroinflammation as a common root in late-life degenerative diseases including AD. Apolipoprotein-E (APOE) genotype is the strongest genetic risk factor for AD: APOE-ε4 is proinflammatory and individuals with this genotype accumulate more Aβ, are at high risk of developing AD, and almost half of all AD patients have at least one ε4 allele. Recent studies suggest a bidirectional relationship exists between sleep and AD pathology. Sleep may play an important role in Aβ clearance, and getting good quality sleep vs. poor quality sleep might reduce the AD risk associated with neuroinflammation and the ε4 allele. Taken together, these findings are particularly important given the sleep disruptions commonly associated with AD and the increased burden disrupted sleep poses for AD caregivers. The current review aims to: (1) identify individuals at high risk for dementia who may benefit most from sleep interventions; (2) explore the role poor sleep quality plays in exacerbating AD type dementia; (3) examine the science of sleep interventions to date; and (4) provide a road map in pursuit of comprehensive sleep interventions, specifically targeted to promote cognitive function and delay progression of dementia.
    Full-text · Article · Dec 2014 · Frontiers in Aging Neuroscience
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    • "Recent research has identified sleep quality and sleep duration as important factors in cardiovascular disease risk [Buxton and Marcelli, 2010; Laugsand et al., 2013]. Indeed, insufficient sleep duration and poor sleep quality appear to contribute to increased cardiovascular disease risk [Buxton and Marcelli, 2010; Cappuccio et al., 2010], and have been linked to elevated body mass index [Hasler et al., 2004; Kohatsu et al., 2006], weight gain [Patel et al., 2004, 2008], obesity [Taheri et al., 2004; Cizza et al., 2005; Gangwisch et al., 2005; Buxton et al., 2013], and diabetes mellitus [Ayas et al., 2003a; Gottlieb et al., 2005; Buxton et al., 2013]. "
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