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The timing, duration, and consolidation of sleep result from the interaction of the circadian timing system with a sleep-wake homeostatic process. When aligned and functioning optimally, this allows for wakefulness throughout the day and a long consolidated sleep episode at night. Changes to either the sleep regulatory process or how they interact can result in an inability to fall asleep at the desired time, difficulty remaining asleep, waking too early, and/or difficulty remaining awake throughout the day. This mismatch between the desired timing of sleep and the ability to fall asleep and remain asleep is a hallmark of a class of sleep disorders called the circadian rhythm sleep-wake disorders. In this updated article, we discuss typical changes in the circadian regulation of sleep with aging; how age influences the prevalence, diagnosis, and treatment of circadian rhythm sleep disorders; and how neurologic diseases in older patient impact circadian rhythms and sleep.

Noise and light levels during hospitalizations can disrupt sleep and circadian health, resulting in worse health outcomes. This study describes patterns of noise and light in an inpatient room of children undergoing stem cell transplants. Objective meters tracked noise and light levels every minute for 6 months. Median overnight sound was 55dB (equivalent to conversational speech), which exceeded recommendations. There were 3.4 loud noises (>80dB) per night on average. Children spent 62% of the 24-hour cycle in non-optimal lighting, with daytime light dimmer than recommended 98% of the time. These data suggest improvements for hospital environment in pediatric cancer patients.

Objectives Rotating shift work is associated with adverse outcomes due to circadian misalignment, sleep curtailment, work-family conflicts, and other factors. We tested a bright light countermeasure to enhance circadian adaptation on a counterclockwise rotation schedule. Methods Twenty-nine adults (aged 20–40 years; 15 women) participated in a 4-week laboratory simulation with weekly counterclockwise transitions from day, to night, to evening, to day shifts. Each week consisted of five 8-hour workdays including psychomotor vigilance tests, two days off, designated 8-hour sleep episodes every day, and an assessment of circadian melatonin secretion. Participants were randomized to a treatment group (N=14), receiving intermittent bright light during work designed to facilitate circadian adaptation, or a control group (N=15) working in indoor light. Adaptation was measured by how much of the melatonin secretion episode overlapped with scheduled sleep timing. Results On the last night shift, there was a greater overlap between melatonin secretion and scheduled sleep time in the treatment group [mean 4.90, standard deviation (SD) 2.8 hours] compared to the control group (2.62, SD 2.8 hours; P=0.002), with night shift adaptation strongly influenced by baseline melatonin timing (r 2 =-0.71, P=0.01). While the control group exhibited cognitive deficits on the last night shift, the treatment group’s cognitive deficits on the last night and evening shifts were minimized. Conclusions In this laboratory setting, intermittent bright light during work hours enhanced adaptation to night work and subsequent readaptation to evening and day work. Light regimens scheduled to shift circadian timing should be tested in actual shift workers on counterclockwise schedules as a workplace intervention.

The 2019 coronavirus disease (COVID-19) has become a global health and economic crisis. Recent evidence from small samples suggest that it has increased mood and sleep disturbances, including insomnia, around the world. This study aimed to estimate the effect of COVID-19 on insomnia levels worldwide and in the United States during the acute phase of the pandemic.We analyzed search query data recorded between January 2004 and May 2020 from Google Trends and Google Keyword Planner for the search term "insomnia".The number of search queries for insomnia has increased over the past decade and is greater than the number of search queries for other major sleep disorders. The COVID-19 pandemic increased search queries for insomnia both worldwide and in the United States, with the number in the United States increasing by 58% during the first 5 months of 2020 compared with the same months from the previous 3 years. There is a robust diurnal pattern in insomnia search queries in the United States, with the number of queries peaking around 3 am and the overall pattern remaining stable during the pandemic.These results highlight the impact the COVID-19 pandemic has had on sleep health and the urgent need for making effective interventions accessible. Future studies will be needed to determine whether the increase in insomnia symptoms will persist and lead to higher rates of chronic insomnia in the population.

Circadian misalignment remains a distinct challenge for night shift workers. Variability in individual sleep-wake/light-dark patterns might contribute to individual differences in circadian alignment in night shift workers. In this simulation study, we compared the predicted phase shift from a mathematical model of the effect of light on the human circadian pacemaker to the observed melatonin phase shift among individuals who completed one of four interventions during simulated night shift work. Two inputs to the model were used to simulate circadian phase: sleep-wake/light-dark patterns measured from a wrist monitor (Simulation 1) and sleep-wake/light-dark patterns measured from a wrist monitor enhanced by known light levels measured at the level of the eye during simulated night shifts (Simulation 2). The estimated phase shift from the model was within 2 hours of the observed phase shift in ~80% of night shift workers for both simulations; none of the model-predicted phase shifts was more than ~3 hours from the observed phase shift. Overall, the root-mean-square error between observed and predicted phase shifts was better for Simulation 1. The light input from the wrist monitor informed by actual light level measured at the eye performed better in the sub-group exposed to bright light during their night shifts. The findings from this simulation study suggest that using a mathematical model combined with sleep-wake and light exposure data from a wrist monitor can facilitate the design of shift work schedules to enhance circadian alignment, which is expected to improve sleep, alertness, and performance.

Aging is associated with changes in sleep, and improving sleep may have important consequences for the health, cognition, and quality of life of older adults. Many prescription sleep aids increase the risk of nighttime falls, have adverse effects on next-day cognition, and are associated with increased mortality. Melatonin, a hormone secreted at night, increases sleep duration in young adults but only when administered during the day when endogenous levels are low. In a month-long cross-over study, we randomized 24 healthy older (age55, mean 64.2 ± 6.3 years) participants to receive 2 weeks of placebo and 2 weeks of either a low (0.3 mg) or high (5.0 mg) dose of melatonin 30 min before lights out. Sleep was polysomnographically recorded and was scheduled during both the biological day and night using a forced desynchrony design. Although 0.3 mg melatonin had a trend towards increasing sleep efficiency (SE) overall, this was due to its effects on sleep during the biological day. In contrast, 5 mg melatonin significantly increased SE during both biological day and night, mainly by increasing the duration of Stage 2 non-rapid eye movement sleep and slightly shortening awakenings. Melatonin should be further explored as a sleep aid for older adults.

Chronic sleep restriction (CSR) has been associated with adverse effects including cognitive impairment and increased risk of diabetes and cardiovascular disease. Yet, sleep restriction therapy is an essential component of most behavioral treatments for insomnia. Moreover, little is known about the impact of CSR on sleep continuity and structure in healthy people whose need for sleep is satiated. We investigated the impact of CSR on sleep continuity and structure in nine healthy participants. They had 4 nights of sleep extension, 2 nights of post-extension sleep, 21 nights of CSR (5/5.6-hour time-in-bed), and 9 nights of recovery sleep. Compared to postextension sleep, during CSR sleep duration was reduced by 95.4 ± 21.2 min per night, Slow-Wave Activity was significantly increased, and sleep was more consolidated. During recovery, sleep duration was increased by 103.3 ± 23.8 min compared to CSR, and the CSR-induced increase in Slow-Wave Activity persisted, particularly after the 5-hour exposure. Yet, we found that sustained vigilant attention was not fully recovered even after nine nights of recovery sleep. Our results suggest that CSR improves traditional metrics of sleep quality and may have a persistent impact on sleep depth, which is consistent with the reported benefits on sleep continuity and structure of sleep restriction therapy. However, these improvements in traditional metrics of sleep quality were associated with deterioration rather than improvement in neurobehavioral performance, demonstrating that sleep duration should be included in assessments of sleep quality. These results have implications for the long-term use of sleep restriction in the behavioral treatment of insomnia. Clinical Trial Registration: Impact of Chronic Circadian Disruption vs. Chronic Sleep Restriction on Metabolism (https://clinicaltrials.gov/ct2/show/; #NCT02171273).

Sudden cardiac death (SCD) is the sudden, unexpected death due to abrupt loss of heart function secondary to cardiovascular disease. In certain populations living with cardiovascular disease, SCD follows a distinct 24-hour pattern in occurrence, suggesting day/night rhythms in behavior, the environment, and endogenous circadian rhythms result in daily spans of increased vulnerability. The National Heart, Lung, and Blood Institute convened a workshop, Understanding Circadian Mechanisms of Sudden Cardiac Death to identify fundamental questions regarding the role of the circadian rhythms in SCD. Part 2 summarizes research gaps and opportunities in the areas of population and clinical research identified in the workshop. Established research supports a complex interaction between circadian rhythms and physiological responses that increase the risk for SCD. Moreover, these physiological responses themselves are influenced by several biological variables, including the type of cardiovascular disease, sex, age, and genetics, as well as environmental factors. The emergence of new noninvasive biotechnological tools that continuously measure key cardiovascular variables, as well as the identification of biomarkers to assess circadian rhythms, hold promise for generating large-scale human data sets that will delineate which subsets of individuals are most vulnerable to SCD. Additionally, these data will improve our understanding of how people who suffer from circadian disruptions develop cardiovascular diseases that increase the risk for SCD. Emerging strategies to identify new biomarkers that can quantify circadian health (eg, environmental, behavioral, and internal misalignment) may lead to new interventions and therapeutic targets to prevent the progression of cardiovascular diseases that cause SCD.

Sudden cardiac death (SCD), the unexpected death due to acquired or genetic cardiovascular disease, follows distinct 24-hour patterns in occurrence. These 24-hour patterns likely reflect daily changes in arrhythmogenic triggers and the myocardial substrate caused by day/night rhythms in behavior, the environment, and endogenous circadian mechanisms. To better address fundamental questions regarding the circadian mechanisms, the National Heart, Lung, and Blood Institute convened a workshop, Understanding Circadian Mechanisms of Sudden Cardiac Death. We present a 2-part report of findings from this workshop. Part 1 summarizes the workshop and serves to identify research gaps and opportunities in the areas of basic and translational research. Among the gaps was the lack of standardization in animal studies for reporting environmental conditions (eg, timing of experiments relative to the light dark cycle or animal housing temperatures) that can impair rigor and reproducibility. Workshop participants also pointed to uncertainty regarding the importance of maintaining normal circadian rhythmic synchrony and the potential pathological impact of desynchrony on SCD risk. One related question raised was whether circadian mechanisms can be targeted to reduce SCD risk. Finally, the experts underscored the need for studies aimed at determining the physiological importance of circadian clocks in the many different cell types important to normal heart function and SCD. Addressing these gaps could lead to new therapeutic approaches/molecular targets that can mitigate the risk of SCD not only at certain times but over the entire 24-hour period.

Circadian clocks drive cyclic variations in many aspects of physiology, but some daily variations are evoked by periodic changes in the environment or sleep-wake state and associated behaviors, such as changes in posture, light levels, fasting or eating, rest or activity and social interactions; thus, it is often important to quantify the relative contributions of these factors. Yet, circadian rhythms and these evoked effects cannot be separated under typical 24-h day conditions, because circadian phase and the length of time awake or asleep co-vary. Nathaniel Kleitman's forced desynchrony (FD) protocol was designed to assess endogenous circadian rhythmicity and to separate circadian from evoked components of daily rhythms in multiple parameters. Under FD protocol conditions, light intensity is kept low to minimize its impact on the circadian pacemaker, and participants have sleep-wake state and associated behaviors scheduled to an imposed non-24-h cycle. The period of this imposed cycle, Τ, is chosen so that the circadian pacemaker cannot entrain to it and therefore continues to oscillate at its intrinsic period (τ, ~24.15 h), ensuring circadian components are separated from evoked components of daily rhythms. Here we provide detailed instructions and troubleshooting techniques on how to design, implement and analyze the data from an FD protocol. We provide two procedures: one with general guidance for designing an FD study and another with more precise instructions for replicating one of our previous FD studies. We discuss estimating circadian parameters and quantifying the separate contributions of circadian rhythmicity and the sleep-wake cycle, including statistical analysis procedures and an R package for conducting the non-orthogonal spectral analysis method that enables an accurate estimation of period, amplitude and phase.

Nearly 14% of Americans experience chronic circadian disruption due to shift work, increasing their risk of obesity, diabetes, and other cardiometabolic disorders. These disorders are also exacerbated by modern eating habits such as frequent snacking and consumption of high-fat foods.We investigated the effects of recurrent circadian disruption (RCD) on glucose metabolism in C57BL/6 mice and in human participants exposed to non-24-h light-dark (LD) schedules vs. those on standard 24-h LD schedules. These LD schedules were designed to induce circadian misalignment between behaviors including rest/activity and fasting/eating with the output of the near-24-h central circadian pacemaker, while minimizing sleep loss, and were maintained for 12 weeks in mice and 3 weeks in humans. We examined interactions of these circadian-disrupted schedules compared to control 24-h schedules with a lower-fat diet (LFD, 13% in mouse and 25-27% in humans) and high-fat diet (HFD, 45% in mouse and 45-50% in humans). We also used young vs. older mice to determine whether they would respond differently to RCD.When combined with a HFD, we found that RCD caused significant weight gain in mice and increased body fat in humans, and significantly impaired glucose tolerance and insulin sensitivity in both mice and humans, but this did not occur when RCD was combined with a LFD. This effect was similar in both young and older mice.These results in both humans and a model organism indicate that circadian disruption has an adverse effect on metabolism among individuals eating a high-fat Western-style diet, even in the absence of significant sleep loss, and suggest that reducing dietary fat may protect against the metabolic consequences of a lifestyle (such as shift work) that involves chronic circadian disruption.

Background: Musculoskeletal disorders (MSDs) are the leading cause of pain and disability among nurses and are frequently accompanied by depression. However, the association between the comorbidity of MSDs and depression and working conditions has not been studied, which was the aim of this study. Methods: In 2015, all nurses ( n = 1,102) employed at a community hospital in the Northeast United States were invited to participate in this cross-sectional study. A survey was distributed in which participants were asked to report on MSDs, depressive symptoms, as well as subjective working conditions assessed including physical demands, psychological demands, decision authority, social support, and work–family conflict. Findings: 397 nurses responded (36%), and the prevalence of the comorbidity of MSDs and depression was 14.5%. Poisson regression (PR) models suggested that work–family conflict was associated with increased risk of the comorbidity (PR = 2.18; 95% confidence interval [CI] = 1.33–3.58), as was 8-hour night shift (PR = 2.77; 95% CI = [1.22, 6.31]) or 12-hour day shift (PR = 2.20; 95% CI = [1.07, 4.50]). Other working conditions were not directly associated with the comorbidity. Conclusions/Application to Practice: The comorbidity of MSDs and depression is prevalent among hospital nurses, and work–family conflict and working night shift or longer shifts were significantly associated with this. Effective workplace programs are needed to address nurses’ working conditions to reduce their work–family conflict, thereby improving their musculoskeletal and mental health.

There are strong individual differences in performance during sleep deprivation. We assessed whether baseline features of Psychomotor Vigilance Test (PVT) performance can be used for classifying participants’ relative attentional vulnerability to total sleep deprivation. In a laboratory, healthy adults (n = 160, aged 18–30 years) completed a 10-min PVT every 2 h while being kept awake for ≥24 hours. Participants were categorized as vulnerable (n = 40), intermediate (n = 80), or resilient (n = 40) based on their number of PVT lapses during one night of sleep deprivation. For each baseline PVT (taken 4–14 h after wake-up time), a linear discriminant model with wrapper-based feature selection was used to classify participants’ vulnerability to subsequent sleep deprivation. Across models, classification accuracy was about 70% (range 65–76%) using stratified 5-fold cross validation. The models provided about 78% sensitivity and 86% specificity for classifying resilient participants, and about 70% sensitivity and 89% specificity for classifying vulnerable participants. These results suggest features derived from a single 10-min PVT at baseline can provide substantial, but incomplete information about a person’s relative attentional vulnerability to total sleep deprivation. In the long term, modeling approaches that incorporate baseline performance characteristics can potentially improve personalized predictions of attentional performance when sleep deprivation cannot be avoided.

This White Paper presents the results from a workshop cosponsored by the Sleep Research Society (SRS) and the Society for Research on Biological Rhythms (SRBR) whose goals were to bring together sleep clinicians and sleep and circadian rhythm researchers to identify existing gaps in diagnosis and treatment and areas of high-priority research in circadian rhythm sleep–wake disorders (CRSWD). CRSWD are a distinct class of sleep disorders caused by alterations of the circadian time-keeping system, its entrainment mechanisms, or a misalignment of the endogenous circadian rhythm and the external environment. In these disorders, the timing of the primary sleep episode is either earlier or later than desired, irregular from day-to-day, and/or sleep occurs at the wrong circadian time. While there are incomplete and insufficient prevalence data, CRSWD likely affect at least 800,000 and perhaps as many as 3 million individuals in the United States, and if Shift Work Disorder and Jet Lag are included, then many millions more are impacted. The SRS Advocacy Taskforce has identified CRSWD as a class of sleep disorders for which additional high-quality research could have a significant impact to improve patient care. Participants were selected for their expertise and were assigned to one of three working groups: Phase Disorders, Entrainment Disorders, and Other. Each working group presented a summary of the current state of the science for their specific CRSWD area, followed by discussion from all participants. The outcome of those presentations and discussions are presented here.

Daily rhythms in several physiological processes are important for cardiometabolic health. The lipid panel is used clinically to assess cardiovascular disease risk, but previous attempts to demonstrate circadian variation in lipids have failed to uncouple the endogenous circadian rhythm from the effects of meals and wake duration. Changes in basal lipid levels and dampening of circadian rhythms have been reported with aging, but it is unknown whether aging is also associated with changes in the rhythmic variation of lipids. We measured fasting lipid panels (triglycerides, total cholesterol, high‐density lipoprotein, and low‐density lipoprotein) in blood at wake time in 21 healthy adults using a specialized laboratory protocol that uncouples sleep–wake and activity‐related effects from the endogenous circadian rhythm. Young and older adults exhibited endogenous circadian variations in fasting triglycerides, with both groups peaking in the early biological morning. Young adults also exhibited significant circadian rhythmicity in total cholesterol and low‐density lipoprotein, while older adults did not exhibit circadian rhythmicity in any other lipids. These results reveal that triglyceride metabolism may be regulated by the central circadian pacemaker. Moreover, our findings may have clinical implications in assessing cardiovascular risk in shift workers and younger adults, since routine measurement of morning/fasting lipids may not fully and reliably assess triglyceride‐ and other lipid‐related biomarkers of cardiovascular disease risk in these groups., Daily rhythms in several physiological processes are important for cardiometabolic health. Young and older adults exhibited endogenous circadian variations in fasting triglycerides, with both groups peaking in the early biological morning. These results reveal that triglyceride metabolism may be regulated by the central circadian pacemaker, and may have clinical implications in assessing cardiovascular risk in shift workers and younger adults.

Age-related disrupted sleep has been associated with modifications in the timing of endogenous circadian rhythms. There are studies suggesting a decreased sensitivity of the aging circadian pacemaker to light. In this study, we aimed to test whether a moderate illuminance light stimulus would produce significant phase shifts in older adults, and whether those would fall in a range consistent with the illuminance response curve (IRC) we previously reported in older adults. We conducted an 8-day in-patient study with 12 healthy older participants (mean age [SD], 58.3 [4.2] y, 5 females). A 6.5-h polychromatic white light exposure with a target illuminance of 270 lux was administered beginning in the early biological night. Before and after the light exposure, a circadian phase estimation procedure was carried out, with plasma melatonin data used as a circadian phase marker. The mean phase delay produced by the light stimulus was 1.78 ± 0.77 h. Ten of the 12 phase delay shifts at ~270 lux fell within the 95% predictive interval of the model fit to data from our previous IRC in older adults. This finding demonstrates that the circadian system of healthy older adults is sensitive to the phase-delaying effects of a moderate intensity light stimulus. The magnitude of the observed phase shifts is consistent with the previously described IRC in older adults.

Good sleep is necessary for good health. Sleep health is increasingly recognized as important for physical and mental health by both the medical profession and the general public, and there is great interest in how to avoid and treat sleep disorders and problems. Recent research indicates that insufficient sleep, disrupted sleep, and sleep disorders affect many aspects of human health including sexual function. In fact, patients with urological disorders or erectile dysfunction (ED) may have a sleep disorder that contributes to their urological or sexual dysfunction. Obstructive sleep apnea, insomnia, shift work disorder, and restless legs syndrome are all common sleep disorders and are associated with ED and/or other urological disorders. Therefore, careful attention should be paid to the diagnosis and treatment of concomitant sleep disorders in patients with sexual dysfunction. In this review, we provide an overview of what sleep is and how it is assessed in the clinic or laboratory; our current understanding of the functions of sleep and sleep health; a description of common sleep disorders, as well as how they are diagnosed and treated; and how sleep and its disorders are associated with male sexual dysfunction. Sleep is considered to be a ‘third pillar of health’, along with diet and exercise. With an understanding of common sleep disorders and how they can impact male sexual function, the urologist can ensure that sleep disorders are considered as a contributor to sexual dysfunction in their patients in order to provide them with the optimal treatment for overall health.

More than a third of US adults report fewer than 6 hours of sleep a night, making chronic sleep restriction a growing public health concern. Sleep curtailment is associated with an increase in industrial accidents, motor vehicle accidents, medical and other occupational errors. Young adults are more vulnerable to acute sleep deprivation than older adults, but less is known about how young vs. older adults respond to the more commonly experienced chronic sleep restriction. To test the hypothesis that young adults are more vulnerable to chronic sleep loss than older adults, we compared data from young and older adults who underwent three weeks of chronic sleep restriction (equivalent to 5.6 hours/24 hours) combined with recurrent circadian disruption in an experiment that enabled us to separate the influences of the sleep-wake homeostatic process, the circadian timing system, and the chronic sleep deficit. We found that while young and older adults reported similar levels of subjective sleepiness, objective measures of sleepiness revealed that young adults were more vulnerable and had more attentional failures than the older adults. These results have important public health implications, particularly related to prevention of sleep-related motor vehicle crashes in young drivers. Further research is needed to understand the neurobiological basis of these age-related differences.

Introduction Sleep deficiency is a severe problem faced by night shift workers. Approximately one-third of night workers report insomnia during daytime sleep and excessive sleepiness during nighttime work; when severe, these symptoms characterize shift work disorder (SWD). Difficulty sustaining 7 to 9 hours of sleep during the daytime is partly due to a circadian drive for wakefulness. Not much is known, however, about how non-work activities contribute to the inability to obtain recovery sleep. We sought to explore how much time night workers are able to allocate for daytime sleep, and how this relates to insomnia-like symptoms and the likelihood of developing SWD. Methods Night shift workers (n=452, 19–69 years old, 54% men) from various occupations who worked at least four night shifts per month completed an online survey. This included questions related to shift duration, hours per workday of non-optional non-work activities, self-rated sleep need, the Insomnia Severity Index (ISI) and a validated 4-item SWD screening questionnaire. For each participant, we calculated the duration of work plus non-optional activities and compared the remaining available time for sleep to their self-described sleep need. Non-parametric Chi-square analyses and Pearson correlations were conducted. Results On average, shift duration was 8.9±1.6 hours, non-optional activities were 3.6±2.9 hours, and sleep need was 7.6±1.6 hours, leaving 15% of shift workers with insufficient free time to obtain the amount of sleep they needed. The percentage of workers at high risk for SWD was significantly greater among those who did not have enough free time for sleep compared to those whose schedules allowed sufficient sleep time (72% vs. 42%; χ2=20.2, p Conclusion About 15% of night workers have non-optional activities outside work that limit their time to obtain sufficient sleep, and this contributes to greater insomnia-like symptoms and increased risk for SWD. Future research should focus on understanding what these non-optional activities are and whether they differ between night and day workers. These insights will enable personalized countermeasures to maximize the sleep and health of shift workers. Support (if any) Supported by US NIH grant R01-AG044416.

The risk for developing heparin-induced thrombocytopenia in healthy individuals is thought to be low, but monitoring recommendations remain controversial. Therefore, a retrospective cohort study was conducted to identify the incidence of thrombocytopenic events in a healthy research population exposed and re-exposed to continuous intravenous (IV) unfractionated heparin. The Division of Sleep Medicine and the Centre for Clinical Investigations at Brigham and Women's Hospital, Boston, Massachusetts, United States, instituted a standardized platelet monitoring procedure for all research protocols that involved heparin to detect platelet count decreases. Protocol-related frequent blood sampling required use of continuous IV unfractionated heparin infusion (5,000 unit/L in 0.45% saline at 40 mL/h) to maintain line patency over extended periods of IV access. From the years 2009 to 2012, a total of 273 healthy volunteers enrolled in Sleep Medicine research protocols met study criteria as having been exposed and/or re-exposed to continuously infused intravenous heparin for at least 4 hours. The mean continuous heparin exposure time was 88 ± 82 SD hours with a total of 397 heparin exposure and re-exposure events. Platelet count measurements were obtained on 629 occasions, representing a range from 2 to 9 draws per participant. No platelet count decrease of more than 50% was detected. There were no detected adverse bleeding or thrombotic events. In this retrospective study of healthy volunteers involved in a rigorously applied inpatient platelet monitoring protocol, heparin exposure and re-exposure did not lower platelet concentration and, therefore, does not appear to be associated with increased risk of HIT in this population.

Nurses are at a high risk for work-family conflict due to long and irregular work hours and multiple physical and psychosocial stressors in their work environment. Nurses report higher rates of depressive symptoms than the general public, leading to a high rate of burnout, absenteeism, and turnover. Work-family conflict is associated with negative consequences in nurses including physical illnesses and mental disorders.Past research on this topic has not examined the mechanisms for the effect of work family conflict on depression. Studies rarely examine the influence of health behaviors such as sleep in explaining this association. Our study identified significant association of sleep disturbances with both work-family conflict and depressive symptoms in nurses. Our main contribution is reporting the important role of sleep disturbances in translating the effect of work-family conflict on depressive symptoms among nurses.Nurses need to receive training in best practices for maintaining their own sleep and mental health. Organizations should include sleep health education and training in workplace health programs. Evidence-based interventions to promote healthy sleep practices such as cognitive behavioral therapy and complementary and integrative approaches should be evaluated for their effectiveness in addressing the impact of work-family conflict on the mental health of nurses. Healthcare organizations should incorporate mental health services as part of their Employee Assistance Program for nurses and include psychological and sleep disorders screening, counseling, and follow-up.Introduction Depression has been identified as the leading cause of disability worldwide. Nurses report higher rates of depression than the general public. Work-family conflict is challenging for nurses and may lead to depression and poor health. However, the mechanisms for the effect of work-family conflict on depression have not been well understood. Aim The objective is to use a cross-sectional design to examine the role of sleep disturbances in the association between work-family conflict and depressive symptoms in nurses. Methods Questionnaires, measuring working conditions, work-family conflict, sleep disturbances and depressive symptoms were collected from 397 nurses at a not-for-profit community hospital in the north-eastern United States. Results We observed a significant association between work-family conflict and depressive symptoms (β = 2.22, p .001) among nurses. Sleep disturbances partially mediated this association by 40.54%. Discussion Sleep disturbances play an important role in translating work-family conflict into depressive symptoms. Implications Evidence-based interventions to promote healthy sleep practices should be evaluated for their effectiveness in addressing the impact of work-family conflict on mental health. Organizations should include sleep education and training as a component of workplace health promotion and employee assistance programmes to mitigate the effect of work-family conflict and promote overall health in nurses.

Introduction The pathogenesis of multiple sclerosis (MS)-related fatigue is multi-factorial, including neurogenic, inflammatory, endocrine, metabolic, mood, as well as sleep disorder-related mechanisms. The confounding effect of sleep disorders on the association between fatigue and neurodegenerative changes in the brain has not been investigated. Our objectives were to assess the prevalence of sleep apnea and periodic limb movements in the framework of a prospective study which investigates the neurogenic causation of treatment-resistant fatigue in MS. Methods MS patients enrolled in a National MS Society-funded prospective study (grant identifier RG-1501-03141) underwent a one-night at-home sleep test (HST) using a NOX T3 portable monitor. HST recordings were scored by a registered polysomnographic technologist. Respiratory Event (REI) and Periodic Limb Movement (PLMI) Indices were calculated for each patient. Results Out of 36 patients, 7 (20%) had mild (REI=5-14), 1 (3%) had moderate (REI=15-29), and 1 (3%) had severe sleep-disordered breathing (REI≥30). Fourteen (42%) of the patients had mild (PLMI=5-24), 4 (11%) had moderate (PLMI=25-49), and 7 (19%) had severe periodic limb movements (PLMI≥50). Overall, 81% of the patients had at least mild sleep-disordered breathing and/or periodic limb movements. Conclusion Sleep abnormalities (i.e., sleep apnea and periodic limb movements) are highly prevalent in patients with MS. We plan to compare the MRI exams of subgroups of MS patients with fatigue, to test the hypothesis that fronto-striatal circuitry is more affected by lesions in patients without sleep apnea compared to those with sleep apnea. Support This investigation was supported by a grant from the National Multiple Sclerosis Society (grant identifier RG-1501-03141). The home sleep test equipment was provided by a DURIP grant from the Office of Naval Research (grant N00014-15-1-2917).

Introduction The aim of this study was to investigate the efficacy of changing sleep timing to afternoon-evening following nightshifts in hospital nurses with three rapid rotating shift schedules. Methods Hospital nurses with three rotating shift schedules were enrolled for a 1-month pre-intervention and a 1-month intervention study. During the Intervention, sleep timing following nightshifts was directed to afternoon-evening sleep for 8h time-in-bed (TIB) after 1 PM, and ad-lib sleep schedule for other shifts. Baseline and follow-up evaluation included sleep schedule, sleep duration, Epworth sleepiness scale (ESS), insomnia severity index (ISI) for each shift, Beck depression inventory (BDI), and Beck anxiety inventory (BAI). Sleep was assessed by sleep diary and actigraphy. Alertness during the night shift was evaluated using the Karolinska sleepiness scale (KSS) in the beginning and at the end of the shift by texts sent to their cell phones. The participants were asked to give feedback and a willingness to continue this intervention. Results A total of 26 subjects (30.7±8.5years, 25 female) finished the study among 29 nurses who participated in the study. The shift work was 6.5±8.0years. The mean morningness-eveningness scale was 42.1±8.0(31-62). TIB following nightshifts were 379.9±91.2 and 478.4±48.7 min for preintervention and intervention, respectively (p=0.001). Total sleep time (TST) was 328.0±91.0 vs. 361.0±70.4min, respectively following nightshifts (p=0.187, Cohen’s drm = 0.467). BDI, BAI, ESS, and ISI were significantly improved after the intervention. 60.7% and 49% of the participants reported improved alertness, and work efficiency during the nightshift. 17.9% and 42.9% of the participants reported increased sleep duration, and improved sleep quality after nightshift, respectively. Only eight participants were willing to continue the afternoon-evening sleep schedule following night shifts. KSS was not different between pre-intervention and intervention. Conclusion The afternoon-evening sleep schedule modestly increased total sleep time following nightshift. The overall mood, sleepiness and insomnia scale improved after the intervention although the alertness assessed by KSS failed to show the difference. The individual difference should be considered for applying afternoon-evening sleep for rapid rotating shift schedules. Support 2018 Research award grants from the Korean sleep research society and NRF-2019R1A2C1090643 funded by the Korean national research foundation

Introduction Nearly 14% of Americans experience chronic circadian disruption due to shift work, increasing their risk of obesity and cardiometabolic disorders. These disorders are also exacerbated by modern eating habits such as frequent snacking and consumption of high-fat foods. Here we used a forced desynchrony protocol to investigate the effect of 3 weeks of recurrent circadian disruption (RCD) with minimal sleep loss on glucose metabolism in humans on a lower or higher fat diet (LFD and HFD, respectively). Methods Six healthy adults (38-69yrs; 3f) participated in a 37-day inpatient protocol with LFD (25–27% fat) and 15.67-hr fasting duration, or HFD (45–50% fat) and 13-hr fasting duration. The protocol included three weeks of RCD consisting of 28-hr “days” with 11.67-hr sleep opportunities (=10hrs/24hr). Glucose and insulin responses to a standardized breakfast were conducted at baseline, at an aligned circadian phase after 2–3 weeks of exposure to RCD, and after 1 week of recovery. Frequent blood samples were assayed for glucose and insulin; the Area-Under-Curve was calculated from start of breakfast through postprandial minute 180. Results Total Sleep Time was similar in Baseline and RCD in both groups. Participants on the LFD showed no change in glucose AUC during RCD compared to Baseline. Insulin AUC was lower during RCD (p=0.0269) and Recovery (p=0.0443) than Baseline. In contrast, participants on the HFD showed a significant increase in glucose AUC during RCD compared to Baseline (p Conclusion RCD (in the absence of sleep loss) led to impaired glucose tolerance when combined with HFD, but not when combined with LFD. These results suggest that LFD may be part of healthy strategies for people experiencing RCD. Support Study supported by P01AG009975 and conducted in the Brigham and Women’s Hospital Center for Clinical Investigation, part of Harvard Clinical and Translational Science Center supported by UL1TR001102. Authors supported by a fellowship from the Finnish Cultural Foundation (KMZ); T32HL007901 and F32HL143893 (RKY); T32HL007901 and F32AG051325 (NV); K24HL105664 (EBK); R01HL118601 (FAJLS).

No abstract available. Article truncated after 150 words. Sleep is more important now than ever. Getting enough sleep and maintaining a regular schedule for optimal circadian rhythm health is a challenge for most of us even in the best of times, but the schedule changes and added stress from the COVID-19 pandemic has likely impacted your sleep schedule over the past few weeks. Sleep does more than just make us feel better the next day. It allows us to pay close attention, remember new information, and multi-task. Regularity of sleep and wake also maintains the health and optimal function of the circadian timing system (our internal biological clock). Insufficient sleep and irregular sleep-wake schedules can impair our health, weaken our immune system, increase inflammation, and even lead to increased vulnerability to viral illnesses. Given how important regular, sufficient, sleep is for our safety, health, and quality of life, the following tips may help to optimize circadian and sleep …

Sleep has been demonstrated to improve consolidation of many types of new memories. However, few prior studies have examined how sleep impacts learning of face-name associations. The recognition of a new face along with the associated name is an important human cognitive skill. Here we investigated whether post-presentation sleep impacts recognition memory of new face-name associations in healthy adults. Fourteen participants were tested twice. Each time, they were presented 20 photos of faces with a corresponding name. Twelve hours later, they were shown each face twice, once with the correct and once with an incorrect name, and asked if each face-name combination was correct and to rate their confidence. In one condition the 12-h interval between presentation and recall included an 8-h nighttime sleep opportunity (“Sleep”), while in the other condition they remained awake (“Wake”). There were more correct and highly confident correct responses when the interval between presentation and recall included a sleep opportunity, although improvement between the “Wake” and “Sleep” conditions was not related to duration of sleep or any sleep stage. These data suggest that a nighttime sleep opportunity improves the ability to correctly recognize face-name associations. Further studies investigating the mechanism of this improvement are important, as this finding has implications for individuals with sleep disturbances and/or memory impairments.

ObjectivesThis study investigated whether an intervention designed to reduce homeostatic sleep pressure would improve night shift performance and alertness in older adults.MethodsNon-shift workers aged 57.9±4.6 (mean±SD) worked four day (07:00–15:00) and four night shifts (23:00–07:00). Two intervention groups were instructed to remain awake until ~13:00 after each night shift: the sleep timing group (ST; n=9) was instructed to spend 8 hours in bed attempting sleep, and the sleep ad-lib group (n=9) was given no further sleep instructions. A control group (n=9) from our previous study was not given any sleep instructions. Hourly Karolinska Sleepiness Scales and Psychomotor Vigilance Tasks assessed subjective sleepiness and performance.ResultsThe ST group maintained their day shift sleep durations on night shifts, whereas the control group slept less. The ST group were able to maintain stable performance and alertness across the initial part of the night shift, while the control group’s alertness and performance declined across the entire night. Wake duration before a night shift negatively impacted sustained attention and self-reported sleepiness but not reaction time, whereas sleep duration before a night shift affected reaction time and ability to sustain attention but not self-reported sleepiness.ConclusionsA behavioural change under the control of the individual worker, spending 8 hours in bed and waking close to the start of the night shift, allowed participants to acquire more sleep and improved performance on the night shift in older adults. Both sleep duration and timing are important factors for night shift performance and self-reported sleepiness.

The PERIOD2 (PER2) gene is a core molecular component of the circadian clock and plays an important role in the generation and maintenance of daily rhythms. Rs35333999, a missense variant of PER2 common in European populations, has been shown to associate with later chronotype. Chronotype relates to the timing of biological and behavioral activities, including when we sleep, eat, and exercise, and later chronotype is associated with longer intrinsic circadian period (cycle length), a fundamental property of the circadian system. Thus, we tested whether this PER2 variant was associated with circadian period and found significant associations with longer intrinsic circadian period as measured under forced desynchrony protocols, the ‘gold standard’ for intrinsic circadian period assessment. Minor allele (T) carriers exhibited significantly longer circadian periods when determinations were based on either core body temperature or plasma melatonin measurements, as compared to non-carriers (by 12 and 11 min, respectively; accounting for ~7% of inter-individual variance). These findings provide a possible underlying biological mechanism for inter-individual differences in chronotype, and support the central role of PER2 in the human circadian timing system.