Orfeu M. Buxton

Short and long sleep are positively associated with obesity, diabetes, hypertension, and cardiovascular disease among adults in the United States

Research associates short (and to a lesser extent long) sleep duration with obesity, diabetes, and cardiovascular disease; and although 7-8 h of sleep seems to confer the least health risk, these findings are often based on non-representative data. We hypothesize that short sleep (<7 h) and long sleep (>8 h) are positively associated with the risk of obesity, diabetes, hypertension, and cardiovascular disease; and analyze 2004-2005 US National Health Interview Survey data (n=56,507 observations, adults 18-85) to test this. We employ multilevel logistic regression, simultaneously controlling for individual characteristics (e.g., ethnoracial group, gender, age, education), other health behaviors (e.g., exercise, smoking), family environment (e.g., income, size, education) and geographic context (e.g., census region). Our model correctly classified at least 76% of adults on each of the outcomes studied, and sleep duration was frequently more strongly associated with these health risks than other covariates. These findings suggest a 7-8 h sleep duration directly and indirectly reduces chronic disease risk.

Adverse Metabolic Consequences in Humans of Prolonged Sleep Restriction Combined with Circadian Disruption

Sleep deficiency and out-of-synch circadian rhythms impair pancreatic insulin secretion, a possible precursor to metabolic syndrome and diabetes. A Reason to Go to Bed on Time Our own experience tells us that getting too little sleep or traveling across multiple time zones can impair our ability to function. And people who work on the night shift or who habitually sleep too little are more likely to be obese or have diabetes. But what is it about these stresses that translate into faulty physiology? By simulating the life-style of a shift worker or world traveler in controlled laboratory conditions, Buxton et al. now find that prolonged, simultaneous disruption of our normal sleep and circadian rhythms affects the workings of our insulin-secreting pancreatic cells, creating a prediabetic state. And even worse, under these conditions, people show a drop in their resting metabolic rate that could translate into a yearly weight gain of more than 10 pounds. Getting a firm handle on the effects of life-style changes such as sleep, activity schedule, and diet on pancreatic function is much easier in small animals than humans. But Buxton et al. successfully investigated these questions by hosting 21 human participants in a completely controlled environment for almost 6 weeks and simulating disturbances in sleep and circadian rhythms, while keeping diet constant and scheduling all activities. Because sleep and circadian rhythms are intimately related, they designed a special protocol to independently manipulate these variables. After a stabilization segment in which the participants had adequate sleep at the appropriate time within their circadian rhythms, the participants spent 3 weeks in which they got only 5.6 hours of sleep per 24-hour period, while simultaneously experiencing 28-hour circadian days—a state similar to 4 hours of jet lag accumulating each day. During this time, the participants were often trying to sleep at unusual times within their circadian cycle. A segment of 9 recovery days followed. During the 3-week disruption, the participants’ glucose control went haywire, and they were unable to mount a sufficiently high insulin response after a meal, resulting in too much glucose in their blood, in some cases at a level considered prediabetic. This magnitude of disruption, coupled with a lower resting metabolic rate that also emerged during the 3 treatment weeks, could easily set the stage for development of diabetes and obesity, although the exact process by which this happens awaits further study. These results carry a cautionary message for employers to guard against causing adverse metabolic effects in workers by their shift scheduling practices—and a reinforcement of your mother’s message to go to bed on time and get enough sleep. Epidemiological studies link short sleep duration and circadian disruption with higher risk of metabolic syndrome and diabetes. We tested the hypotheses that prolonged sleep restriction with concurrent circadian disruption, as can occur in people performing shift work, impairs glucose regulation and metabolism. Healthy adults spent >5 weeks under controlled laboratory conditions in which they experienced an initial baseline segment of optimal sleep, 3 weeks of sleep restriction (5.6 hours of sleep per 24 hours) combined with circadian disruption (recurring 28-hour “days”), followed by 9 days of recovery sleep with circadian re-entrainment. Exposure to prolonged sleep restriction with concurrent circadian disruption, with measurements taken at the same circadian phase, decreased the participants’ resting metabolic rate and increased plasma glucose concentrations after a meal, an effect resulting from inadequate pancreatic insulin secretion. These parameters normalized during the 9 days of recovery sleep and stable circadian re-entrainment. Thus, in humans, prolonged sleep restriction with concurrent circadian disruption alters metabolism and could increase the risk of obesity and diabetes.

Sleep Restriction for 1 Week Reduces Insulin Sensitivity in Healthy Men

OBJECTIVE Short sleep duration is associated with impaired glucose tolerance and an increased risk of diabetes. The effects of sleep restriction on insulin sensitivity have not been established. This study tests the hypothesis that decreasing nighttime sleep duration reduces insulin sensitivity and assesses the effects of a drug, modafinil, that increases alertness during wakefulness. RESEARCH DESIGN AND METHODS This 12-day inpatient General Clinical Research Center study included 20 healthy men (age 20–35 years and BMI 20–30 kg/m2). Subjects spent 10 h/night in bed for ≥8 nights including three inpatient nights (sleep-replete condition), followed by 5 h/night in bed for 7 nights (sleep-restricted condition). Subjects received 300 mg/day modafinil or placebo during sleep restriction. Diet and activity were controlled. On the last 2 days of each condition, we assessed glucose metabolism by intravenous glucose tolerance test (IVGTT) and euglycemic-hyperinsulinemic clamp. Salivary cortisol, 24-h urinary catecholamines, and neurobehavioral performance were measured. RESULTS IVGTT-derived insulin sensitivity was reduced by (means ± SD) 20 ± 24% after sleep restriction (P = 0.001), without significant alterations in the insulin secretory response. Similarly, insulin sensitivity assessed by clamp was reduced by 11 ± 5.5% (P < 0.04) after sleep restriction. Glucose tolerance and the disposition index were reduced by sleep restriction. These outcomes were not affected by modafinil treatment. Changes in insulin sensitivity did not correlate with changes in salivary cortisol (increase of 51 ± 8% with sleep restriction, P < 0.02), urinary catecholamines, or slow wave sleep. CONCLUSIONS Sleep restriction (5 h/night) for 1 week significantly reduces insulin sensitivity, raising concerns about effects of chronic insufficient sleep on disease processes associated with insulin resistance.

Measuring sleep: Accuracy, sensitivity, and specificity of wrist actigraphy compared to polysomnography

OBJECTIVES We validated actigraphy for detecting sleep and wakefulness versus polysomnography (PSG). DESIGN Actigraphy and polysomnography were simultaneously collected during sleep laboratory admissions. All studies involved 8.5 h time in bed, except for sleep restriction studies. Epochs (30-sec; n = 232,849) were characterized for sensitivity (actigraphy = sleep when PSG = sleep), specificity (actigraphy = wake when PSG = wake), and accuracy (total proportion correct); the amount of wakefulness after sleep onset (WASO) was also assessed. A generalized estimating equation (GEE) model included age, gender, insomnia diagnosis, and daytime/nighttime sleep timing factors. SETTING Controlled sleep laboratory conditions. PARTICIPANTS Young and older adults, healthy or chronic primary insomniac (PI) patients, and daytime sleep of 23 night-workers (n = 77, age 35.0 ± 12.5, 30F, mean nights = 3.2). INTERVENTIONS N/A. MEASUREMENTS AND RESULTS Overall, sensitivity (0.965) and accuracy (0.863) were high, whereas specificity (0.329) was low; each was only slightly modified by gender, insomnia, day/night sleep timing (magnitude of change < 0.04). Increasing age slightly reduced specificity. Mean WASO/night was 49.1 min by PSG compared to 36.8 min/night by actigraphy (β = 0.81; CI = 0.42, 1.21), unbiased when WASO < 30 min/night, and overestimated when WASO > 30 min/night. CONCLUSIONS This validation quantifies strengths and weaknesses of actigraphy as a tool measuring sleep in clinical and population studies. Overall, the participant-specific accuracy is relatively high, and for most participants, above 80%. We validate this finding across multiple nights and a variety of adults across much of the young to midlife years, in both men and women, in those with and without insomnia, and in 77 participants. We conclude that actigraphy is overall a useful and valid means for estimating total sleep time and wakefulness after sleep onset in field and workplace studies, with some limitations in specificity.

Recommended Amount of Sleep for a Healthy Adult: A Joint Consensus Statement of the American Academy of Sleep Medicine and Sleep Research Society.

ABSTRACT Sleep is essential for optimal health. The American Academy of Sleep Medicine (AASM) and Sleep Research Society (SRS) developed a consensus recommendation for the amount of sleep needed to promote optimal health in adults, using a modified RAND Appropriateness Method process. The recommendation is summarized here. A manuscript detailing the conference proceedings and evidence supporting the final recommendation statement will be published in SLEEP and the Journal of Clinical Sleep Medicine.

Spontaneous brain rhythms predict sleep stability in the face of noise

Quality sleep is an essential part of health and well-being. Yet fractured sleep is disturbingly prevalent in our society, partly due to insults from a variety of noises [1]. Common experience suggests that this fragility of sleep is highly variable between people, but it is unclear what mechanisms drive these differences. Here we show that it is possible to predict an individuals ability to maintain sleep in the face of sound using spontaneous brain rhythms from electroencephalography (EEG). The sleep spindle is a thalamocortical rhythm manifested on the EEG as a brief 11-15 Hz oscillation and is thought to be capable of modulating the influence of external stimuli [2]. Its rate of occurrence, while variable across people, is stable across nights [3]. We found that individuals who generated more sleep spindles during a quiet night of sleep went on to exhibit higher tolerance for noise during a subsequent, noisy night of sleep. This result shows that the sleeping brains spontaneous activity heralds individual resilience to disruptive stimuli. Our finding sets the stage for future studies that attempt to augment spindle production to enhance sleep continuity when confronted with noise.

Endogenous circadian system and circadian misalignment impact glucose tolerance via separate mechanisms in humans

Significance It is established that glucose tolerance decreases from the morning to the evening, and that shift work is a risk factor for diabetes. However, the relative importance of the endogenous circadian system, the behavioral cycle (including the sleep/wake and fasting/feeding cycles), and circadian misalignment on glucose tolerance is unclear. We show that the magnitude of the effect of the endogenous circadian system on glucose tolerance and on pancreatic β-cell function was much larger than that of the behavioral cycle in causing the decrease in glucose tolerance from morning to evening. Also, independent from circadian phase and the behavioral cycle, circadian misalignment resulting from simulated night work lowered glucose tolerance—without diminishing effects upon repeated exposure—with direct relevance for shift workers. Glucose tolerance is lower in the evening and at night than in the morning. However, the relative contribution of the circadian system vs. the behavioral cycle (including the sleep/wake and fasting/feeding cycles) is unclear. Furthermore, although shift work is a diabetes risk factor, the separate impact on glucose tolerance of the behavioral cycle, circadian phase, and circadian disruption (i.e., misalignment between the central circadian pacemaker and the behavioral cycle) has not been systematically studied. Here we show—by using two 8-d laboratory protocols—in healthy adults that the circadian system and circadian misalignment have distinct influences on glucose tolerance, both separate from the behavioral cycle. First, postprandial glucose was 17% higher (i.e., lower glucose tolerance) in the biological evening (8:00 PM) than morning (8:00 AM; i.e., a circadian phase effect), independent of the behavioral cycle effect. Second, circadian misalignment itself (12-h behavioral cycle inversion) increased postprandial glucose by 6%. Third, these variations in glucose tolerance appeared to be explained, at least in part, by different mechanisms: during the biological evening by decreased pancreatic β-cell function (27% lower early-phase insulin) and during circadian misalignment presumably by decreased insulin sensitivity (elevated postprandial glucose despite 14% higher late-phase insulin) without change in early-phase insulin. We explored possible contributing factors, including changes in polysomnographic sleep and 24-h hormonal profiles. We demonstrate that the circadian system importantly contributes to the reduced glucose tolerance observed in the evening compared with the morning. Separately, circadian misalignment reduces glucose tolerance, providing a mechanism to help explain the increased diabetes risk in shift workers.

Joint Consensus Statement of the American Academy of Sleep Medicine and Sleep Research Society on the Recommended Amount of Sleep for a Healthy Adult: Methodology and Discussion

The American Academy of Sleep Medicine and Sleep Research Society recently released a Consensus Statement regarding the recommended amount of sleep to promote optimal health in adults. This paper describes the methodology, background literature, voting process, and voting results for the consensus statement. In addition, we address important assumptions and challenges encountered during the consensus process. Finally, we outline future directions that will advance our understanding of sleep need and place sleep duration in the broader context of sleep health.

Acute and Delayed Effects of Exercise on Human Melatonin Secretion

Accumulating evidence suggests that exercise may have both rapid and delayed effects on human melatonin secretion. Indeed, exercise may acutely (i.e., within minutes) alter melatonin levels and result in a shift of the onset of nocturnal melatonin 12 to 24 h later. The presence and nature of both acute and delayed effects appear to be dependent on the timing of exercise. The presence of a detectable acute effect also depends on the duration, intensity, and type of exercise. Late evening exercise during the rising phase of melatonin secretion may blunt melatonin levels. High-intensity exercise during the nighttime period, when melatonin levels already are elevated, consistently results in a further (nearly 50%) elevation of melatonin levels. No effect of low-intensity exercise performed at the same circadian phase could be detected. Irrespective of intensity, exercise near the offset of melatonin secretion or during the daytime has no consistent acute effect on melatonin secretion. Nighttime exercise, whether of moderate or high intensity, results in phase delays of the melatonin onset on the next evening. In support of the concept that a shift of the melatonin onset on the day after nighttime exercise represents a shift of intrinsic circadian timing is the observation that similar phase shifts (in both direction and magnitude) may be observed simultaneously for the onset of the circadian elevation of thyrotropin secretion. The observation of exercise-induced phase shifts of the onset of melatonin secretion is, therefore, interpreted as evidence that, in humans as in rodents, increased physical activity during the habitual rest period is capable of altering circadian clock function.

Sleep Disruption due to Hospital Noises: A Prospective Evaluation

Background Sleep plays a critical role in maintaining health and well-being; however, patients who are hospitalized are frequently exposed to noise that can disrupt sleep. Efforts to attenuate hospital noise have been limited by incomplete information on the interaction between sounds and sleep physiology. Objective To determine profiles of acoustic disruption of sleep by examining the cortical (encephalographic) arousal responses during sleep to typical hospital noises by sound level and type and sleep stage. Design 3-day polysomnographic study. Setting Sound-attenuated sleep laboratory. Participants Volunteer sample of 12 healthy participants. Intervention Baseline (sham) night followed by 2 intervention nights with controlled presentation of 14 sounds that are common in hospitals (for example, voice, intravenous alarm, phone, ice machine, outside traffic, and helicopter). The sounds were administered at calibrated, increasing decibel levels (40 to 70 dBA [decibels, adjusted for the range of normal hearing]) during specific sleep stages. Measurements Encephalographic arousals, by using established criteria, during rapid eye movement (REM) sleep and non-REM (NREM) sleep stages 2 and 3. Results Sound presentations yielded arousal response curves that varied because of sound level and type and sleep stage. Electronic sounds were more arousing than other sounds, including human voices, and there were large differences in responses by sound type. As expected, sounds in NREM stage 3 were less likely to cause arousals than sounds in NREM stage 2; unexpectedly, the probability of arousal to sounds presented in REM sleep varied less by sound type than when presented in NREM sleep and caused a greater and more sustained elevation of instantaneous heart rate. Limitations The study included only 12 participants. Results for these healthy persons may underestimate the effects of noise on sleep in patients who are hospitalized. Conclusion Sounds during sleep influence both cortical brain activity and cardiovascular function. This study systematically quantifies the disruptive capacity of a range of hospital sounds on sleep, providing evidence that is essential to improving the acoustic environments of new and existing health care facilities to enable the highest quality of care. Primary funding source Academy of Architecture for Health, Facilities Guidelines Institute, and The Center for Health Design.