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We created Sleep for Inpatients: Empowering Staff to Act (SIESTA), which combines electronic "nudges" to forgo nocturnal vitals and medications with interprofessional education on improving patient sleep. In one "SIESTAenhanced unit," nurses received coaching and integrated SIESTA into daily huddles; a standard unit did not. Six months pre- and post-SIESTA, sleep-friendly orders rose in both units (foregoing vital signs: SIESTA unit, 4% to 34%; standard, 3% to 22%, P < .001 both; sleeppromoting VTE prophylaxis: SIESTA, 15% to 42%; standard, 12% to 28%, P < .001 both). In the SIESTAenhanced unit, nighttime room entries dropped by 44% (-6.3 disruptions/room, P < .001), and patients were more likely to report no disruptions for nighttime vital signs (70% vs 41%, P = .05) or medications (84% vs 57%, P = .031) than those in the standard unit. The standard unit was not changed. Although sleep-friendly orders were adopted in both units, a unit-based nursing empowerment approach was associated with fewer nighttime room entries and improved patient experience., (© 2019 Society of Hospital Medicine.)

Study Objectives: Sleep duration has been associated with risk of dementia and stroke, but few studies have investigated the relationship between sleep duration and brain MRI measures, particularly in middle age., Methods: In a prospective cohort of 613 black and white adults (mean age = 45.4 years) enrolled in the Coronary Artery Risk Development in Young Adults (CARDIA) study, participants reported typical sleep duration, dichotomized into moderate sleep duration (> 6 to ≤ 8 h) and short sleep duration (≤ 6 h) at baseline (2005-2006). Five years later, we obtained brain MRI markers of white matter including fractional anisotropy, mean diffusivity, and white matter hyperintensities., Results: Compared to moderate sleepers, short sleepers had an elevated ratio of white matter hyperintensities to normal tissue in the parietal region (OR = 2.31, 95% CI: 1.47, 3.61) adjusted for age, race/sex, education, hypertension, stroke/TIA, depression, smoking status, and physical activity. White matter diffusivity was also higher, approximately a 0.2 standard deviation difference, in frontal, parietal, and temporal white matter regions, among those reporting shorter sleep duration in (P < 0.05 for all)., Conclusions: Short sleep duration was associated with worse markers of white matter integrity in midlife. These mid-life differences in white matter may underlie the link between poor sleep and risk of dementia and stroke., (© 2016 Associated Professional Sleep Societies, LLC.)

Objective: To determine the association between objectively measured sleep and 10-year changes in estimated glomerular filtration rate (eGFR)., Methods: From 2003 to 2005, an ancillary sleep study was conducted at the Chicago site of the Coronary Artery Risk Development in Young Adults (CARDIA) study. Community-based black and white adults (aged 32-51 years) wore a wrist actigraph for up to six nights to record sleep duration and fragmentation. Sleep quality was measured with the Pittsburgh Sleep Quality Index (PSQI). Participants without history of cardiovascular or chronic kidney diseases, proteinuria, or hypertension at the 2000-2001 CARDIA examination were followed over 10 years (n = 463). eGFR was estimated from serum creatinine (eGFRCr) at the 2000-2001, 2005-2006, and 2010-2011 CARDIA examinations, whereas cystatin-C-estimated eGFR (eGFRCys) was measured at the 2000-2001 and 2005-2006 examinations. Generalized estimating equation regression and linear models estimated the associations of each sleep parameter with changes in eGFRCr and eGFRCys, controlling for cardiovascular and renal risk., Results: Sleep parameters were not related to 5-year change in eGFRCys. However, each 1 h decrease in sleep duration was significantly associated with a 1.5 mL/min/1.73 m2 higher eGFRCr [95% confidence interval (CI), 0.2-2.7], and each one-point increase in PSQI was significantly associated with a 0.5 mL/min/1.73 m2 higher eGFRCr (95% CI, 0.04-0.9) over 10 years., Conclusion: In this community-based sample, shorter sleep and poorer sleep quality were related to higher kidney filtration rates over 10 years., (Copyright © 2014 Elsevier B.V. All rights reserved.)

Sleep is a biological imperative associated with cardiometabolic disease risk. As such, a thorough discussion of the sociocultural and demographic determinants of sleep is warranted, if not overdue. This paper begins with a brief review of the laboratory and epidemiologic evidence linking sleep deficiency, which includes insufficient sleep and poor sleep quality, with increased risk of chronic cardiometabolic diseases such as obesity, diabetes and hypertension. Identification of the determinants of sleep deficiency is the critical next step to understanding the role sleep plays in human variation in health and disease. Therefore, the majority of this paper describes the different biopsychosocial determinants of sleep, including age, gender, psychosocial factors (depression, stress and loneliness), socioeconomic position and race/ethnicity. In addition, because sleep duration is partly determined by behavior, it will be shaped by cultural values, beliefs and practices. Therefore, possible cultural differences that may impact sleep are discussed. If certain cultural, ethnic or social groups are more likely to experience sleep deficiency, then these differences in sleep could increase their risk of cardiometabolic diseases. Furthermore, if the mechanisms underlying the increased risk of sleep deficiency in certain populations can be identified, interventions could be developed to target these mechanisms, reduce sleep differences and potentially reduce cardiometabolic disease risk., (Copyright © 2012 Elsevier Ltd. All rights reserved.)

Study Objective: Loneliness has been shown to predict poor health. One hypothesized mechanism is that lonely individuals do not sleep as well as individuals who feel more connected to others. Our goal was to test whether loneliness is associated with sleep fragmentation or sleep duration., Design: Cross-sectional study., Setting: Members of a traditional, communal, agrarian society living in South Dakota., Participants: Ninety-five participants (mean age 39.8 years, 55% female) who were ≥ 19 years of age at the study's inception., Interventions: Not applicable., Measurements and Results: We conducted interviews querying loneliness, depression, anxiety, and stress, as well as subjective sleep quality and daytime sleepiness. Study participants wore a wrist actigraph for one week to measure objective sleep properties; the two studied here were sleep fragmentation and sleep duration. Higher loneliness scores were associated with significantly higher levels of sleep fragmentation (β = 0.073, t = 2.55, P = 0.01), controlling for age, sex, body mass index, risk of sleep apnea, and negative affect (a factor comprising symptoms of depression and anxiety, and perceived stress). Loneliness was not associated with sleep duration or with either subjective sleep measure., Conclusions: Loneliness was a significant predictor of sleep fragmentation. Humans' social nature may partly be manifest through our dependence on feeling secure in our social environment to sleep well.

Background: The clinical significance of rapid eye-movement (REM)-related obstructive sleep apnea (OSA) is unknown. Moreover, it is unclear what the determinants of sleepiness and quality of life (QoL) are among these patients. Our aim was to identify whether the apnea-hypopnea index during REM sleep (AHI(REM)), AHI during NREM sleep (AHI(NREM)), depressive symptoms, or obesity are independent predictors of excessive daytime sleepiness and reduced QoL in patients with REM-related OSA. We also assessed if these characteristics were predictors of sleepiness and QoL in all patients with OSA (AHI ≥ 5) as well as in non-stage specific OSA., Methods: This was a cross-sectional analysis of a clinic-based population with OSA. In order to minimize the contribution of AHI(NREM), we defined REM-related OSA using the following criteria: an overall AHI ≥ 5, AHI(REM)/AHI(NREM) ≥ 2, AHI(NREM) the lowest quartile of the entire cohort. We examined the predictors of subjective sleepiness using the Epworth Sleepiness Scale (ESS) and QoL using the short-form quality of life questionnaire-12 (SF-12)., Results: Of 1019 consecutive adults that were referred for their first in-laboratory polysomnogram for suspicion of OSA over a 10 month period, 931 had OSA. REM-related OSA was present in 126 patients. In adjusted linear regression models, AHI(NREM) was a significant predictor of sleepiness in the entire cohort of patients with OSA as well as non-stage specific OSA, but not in the REM-related OSA group. AHI(REM) was not a significant predictor of ESS or QoL in any of the three groups. However, greater depressive symptoms and body mass index were significant independent predictors of ESS and reduced QoL in the REM-related OSA group., Conclusion: Higher depression scores and obesity, rather than the severity of OSA (as measured by AHI(NREM) and AHI(REM)), were predictive of sleepiness and QoL scores in patients with REM-related OSA., (Copyright © 2011 Elsevier B.V. All rights reserved.)

Study Objectives: To determine (1) whether short sleep has increased over 31 years; (2) whether trends in short sleep differed by employment status; (3) which sociodemographic factors predict short sleep; and (4) how short sleepers spend their time., Design: Time diaries from eight national studies conducted between 1975 and 2006., Patients or Participants: U.S. adults > or = 18 years., Measurements and Results: Short sleepers were defined as those reporting < 6 hours of sleep in their time diary. Unadjusted percentages of short sleepers ranged from 7.6% in 1975 to 9.3% in 2006. The 1998-99 study had the highest odds of short sleep. The odds ratio for the 31-year period predicting short sleep was 1.14 (95% CI: 0.92, 1.50, P = 0.22), adjusting for age, sex, education, employment, race, marital status, income, and day of week. When stratified by employment, there was a significant increase for full-time workers (P = 0.05), who represented over 50% of participants in all studies, and a significant decrease for students (P = 0.01), who represented < 5% of participants. The odds of short sleep were lower for women, those > or = 65 years, Asians, Hispanics, and married people. The odds were higher for full-time workers, those with some college education, and African Americans. Short sleepers in all employment categories spent more time on personal activities. Short sleepers who were full- and part-time workers spent much more time working., Conclusions: Based on time diaries, the increase in the odds of short sleep over the past 31 years was significant among full-time workers only. Work hours are much longer for full-time workers sleeping < 6 hours.

Sleep is an important modulator of neuroendocrine function and glucose metabolism in children as well as in adults. In recent years, sleep curtailment has become a hallmark of modern society with both children and adults having shorter bedtimes than a few decades ago. This trend for shorter sleep duration has developed over the same time period as the dramatic increase in the prevalence of obesity. There is rapidly accumulating evidence from both laboratory and epidemiological studies to indicate that chronic partial sleep loss may increase the risk of obesity and weight gain. The present article reviews laboratory evidence indicating that sleep curtailment in young adults results in a constellation of metabolic and endocrine alterations, including decreased glucose tolerance, decreased insulin sensitivity, elevated sympathovagal balance, increased evening concentrations of cortisol, increased levels of ghrelin, decreased levels of leptin, and increased hunger and appetite. We also review cross-sectional epidemiological studies associating short sleep with increased body mass index and prospective epidemiological studies that have shown an increased risk of weight gain and obesity in children and young adults who are short sleepers. Altogether, the evidence points to a possible role of decreased sleep duration in the current epidemic of obesity.

During the past few decades, sleep curtailment has become a very common in industrialized countries. This trend for shorter sleep duration has developed over the same time period as the dramatic increase in the prevalence of obesity and diabetes. Evidence is rapidly accumulating to indicate that chronic partial sleep loss may increase the risk of obesity and diabetes. Laboratory studies in healthy volunteers have shown that experimental sleep restriction is associated with an adverse impact on glucose homeostasis. Insulin sensitivity decreases rapidly and markedly without adequate compensation in beta cell function, resulting in an elevated risk of diabetes. Prospective epidemiologic studies in both children and adults are consistent with a causative role of short sleep in the increased risk of diabetes. Sleep curtailment is also associated with a dysregulation of the neuroendocrine control of appetite, with a reduction of the satiety factor, leptin, and an increase in the hunger-promoting hormone, ghrelin. Thus, sleep loss may alter the ability of leptin and ghrelin to accurately signal caloric need, acting in concert to produce an internal misperception of insufficient energy availability. The adverse impact of sleep deprivation on appetite regulation is likely to be driven by increased activity in neuronal populations expressing the excitatory peptides orexins that promote both waking and feeding. Consistent with the laboratory evidence, multiple epidemiologic studies have shown an association between short sleep and higher body mass index after controlling for a variety of possible confounders.

The prevalence of diabetes and obesity is increasing at an alarming rate worldwide, and the causes of this pandemic are not fully understood. Chronic sleep curtailment is a behavior that has developed over the past 2-3 decades. Laboratory and epidemiological studies suggest that sleep loss may play a role in the increased prevalence of diabetes and/or obesity. Current data suggest the relationship between sleep restriction, weight gain and diabetes risk may involve at least three pathways: (1) alterations in glucose metabolism; (2) upregulation of appetite; and (3) decreased energy expenditure. The present article reviews the current evidence in support of these three mechanisms that might link short sleep and increased obesity and diabetes risk.

The popularity of energy drinks has increased rapidly in the past decade. One of the main reasons people use energy drinks is to counteract effects of insufficient sleep or sleepiness. Risks associated with energy drink use, including those related to sleep loss, may be disproportionately borne by racial minorities and those of lower socioeconomic status. In this review, a brief introduction to the issue of health disparities is provided, population-level disparities and inequalities in sleep are described, and the social-ecological model of sleep and health is presented. Social and demographic patterns of energy drink use are then presented, followed by discussion of the potential ways in which energy drink use may contribute to health disparities, including the following: 1) effects of excessive caffeine in energy drinks, 2) effects of energy drinks as sugar-sweetened beverages, 3) association between energy drinks and risk-taking behaviors when mixed with alcohol, 4) association between energy drink use and short sleep duration, and 5) role of energy drinks in cardiometabolic disease. The review concludes with a research agenda of critical unanswered questions. [ABSTRACT FROM AUTHOR]

The prevalence of obesity is increasing rapidly worldwide, which is cause for concern because obesity increases the risk of cardiovascular disease and diabetes, reduces life expectancy, and impairs quality of life. A better understanding of the risk factors for obesity is therefore a critical global health concern, and human biologists can play an important role in identifying these risk factors in various populations. The objective of this review is to present the evidence that inadequate sleep may be a novel risk factor associated with increased vulnerability to obesity and associated cardiometabolic disease. Experimental studies have found that short-term sleep restriction is associated with impaired glucose metabolism, dysregulation of appetite, and increased blood pressure. Observational studies have observed cross-sectional associations between short sleep duration (generally <6 h per night) and increased body mass index or obesity, prevalent diabetes, and prevalent hypertension. Some studies also reported an association between self-reported long sleep duration (generally >8 h per night) and cardiometabolic disease. A few prospective studies have found a significant increased risk of weight gain, incident diabetes, and incident hypertension associated with inadequate sleep. Given the potential link between inadequate sleep and obesity, a critical next step is to identify the social, cultural, and environmental determinants of sleep, which would help to identify vulnerable populations. Future human biology research should consider variation in sleep characteristics among different populations and determine whether the associations between sleep and obesity observed in Western populations persist elsewhere. © 2012 Wiley Periodicals, Inc. [ABSTRACT FROM AUTHOR]

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. [ABSTRACT FROM AUTHOR]

The author discusses a study by J. C.Yoder et al which showed that patients' sleep suffers significantly from hospital noise and the detrimental effect of hospital noise on sleep adversely affects recovery from a disease. It cites a study which linked impairment of early phase of adaptive immune response of patients exposed to an influenza antigen after they have been subjected to recurrent partial sleep deprivation.

The authors respond to the commentary "How Much Do We Really Sleep?," by Stuart Quan. They express enjoyment in reading Quan's perspective on the importance of sleep. They note that Quan addressed two possible sources of bias: that actigraphy might underestimate sleep compared with other measurement modes and that actigraphy is sleep deprived. The authors agree that persons in metropolitan areas in the U.S. might sleep less than other persons. They express excitement about the growing epidemiologic interest in sleep.