Abstract: Importance Circadian rhythm disturbances occur in symptomatic Alzheimer disease (AD) and have been hypothesized to contribute to disease pathogenesis. However, it is unknown whether circadian changes occur during the presymptomatic phase of the disease. Objective To examine the associations between circadian function, aging, and preclinical AD pathology in cognitively normal adults. Design, Setting, and Participants This cross-sectional study was conducted using community volunteers from the Knight Alzheimer’s Disease Research Center at Washington University in St Louis. Cognitively normal participants (n = 205) underwent 7 to 14 days of actigraphy in their home environment between 2010 and 2012, in addition to clinical assessment, amyloid imaging with Pittsburgh Compound B (PiB), and cerebrospinal fluid biomarker collection. Data collected from 3 years before to 6 months after actigraphy were included. Sixteen participants were excluded owing to incomplete data collection. Main Outcomes and Measures Circadian rhythm analysis was performed on actigraphy data using 3 methods: cosinor, nonparametric, and empirical mode decomposition. Preclinical AD was assessed by longitudinal clinical assessment, amyloid imaging with PiB, and cerebrospinal fluid biomarker collection. Results Data from 189 participants were included in the analyses. The mean (SD) age was 66.6 (8.3) years, and 121 participants (64%) were women. Older age (β = .247; P = .003) and male sex (β = .170; P = .04), in the absence of amyloid pathology, were associated with a significant increase in intradaily variability, a nonparametric measure of rest-activity rhythm fragmentation, as well as decreased amplitude by several measures. After correction for age and sex, the presence of preclinical amyloid plaque pathology, assessed by positive PiB imaging (mean [SD], 0.804 [0.187] for PiB negative vs 0.875 [0.178] for PiB positive; P = .05) or increasing cerebrospinal fluid phosphorylated-tau to amyloid β 42 ratio (β = .231; P = .008), was associated with increased intradaily variability, indicating rest-activity rhythm fragmentation. Conclusions and Relevance Preclinical AD is associated with rest-activity rhythm fragmentation, independent of age or sex. Aging was also associated with circadian dysfunction independently of preclinical AD pathology, particularly in men. The presence of circadian rhythm abnormalities in the preclinical phase of AD suggests that circadian dysfunction could contribute to early disease pathogenesis or serve as a biomarker of preclinical disease.

Abstract: Introduction:The purpose of this guideline is to establish clinical practice recommendations for the use of actigraphy in adult and pediatric patients with suspected or diagnosed sleep disorders or

Abstract: Purpose A literature review is presented that aims to summarize and compare current methods to evaluate sleep. Methods Current sleep assessment methods have been classified according to different criteria; e.g., objective (polysomnography, actigraphy…) vs. subjective (sleep questionnaires, diaries…), contact vs. contactless devices, and need for medical assistance vs. self-assessment. A comparison of validation studies is carried out for each method, identifying their sensitivity and specificity reported in the literature. Finally, the state of the market has also been reviewed with respect to customers' opinions about current sleep apps. Results A taxonomy that classifies the sleep detection methods. A description of each method that includes the tendencies of their underlying technologies analyzed in accordance with the literature. A comparison in terms of precision of existing validation studies and reports. Discussion In order of accuracy, sleep detection methods may be arranged as follows: Questionnaire < Sleep diary < Contactless devices < Contact devices < PolysomnographyA literature review suggests that current subjective methods present a sensitivity between 73% and 97.7%, while their specificity ranges in the interval 50%-96%. Objective methods such as actigraphy present a sensibility higher than 90%. However, their specificity is low compared to their sensitivity, being one of the limitations of such technology. Moreover, there are other factors, such as the patient's perception of her or his sleep, that can be provided only by subjective methods. Therefore, sleep detection methods should be combined to produce a synergy between objective and subjective methods. The review of the market indicates the most valued sleep apps, but it also identifies problems and gaps, e.g., many hardware devices have not been validated and (especially software apps) should be studied before their clinical use.

Abstract: Objectives Actigraphy is widely used to estimate sleep-wake time, despite limited information regarding the comparability of different devices and algorithms. We compared estimates of sleep-wake times determined by two wrist actigraphs (GT3X+ versus Actiwatch Spectrum [AWS]) to in-home polysomnography (PSG), using two algorithms (Sadeh and Cole-Kripke) for the GT3X+ recordings. Subjects and methods Participants included a sample of 35 healthy volunteers (13 school children and 22 adults, 46% male) from Boston, MA, USA. Twenty-two adults wore the GT3X+ and AWS simultaneously for at least five consecutive days and nights. In addition, actigraphy and PSG were concurrently measured in 12 of these adults and another 13 children over a single night. We used intraclass correlation coefficients (ICCs), epoch-by-epoch comparisons, paired t-tests, and Bland-Altman plots to determine the level of agreement between actigraphy and PSG, and differences between devices and algorithms. Results Each actigraph showed comparable accuracy (0.81-0.86) for sleep-wake estimation compared to PSG. When analyzing data from the GT3X+, the Cole-Kripke algorithm was more sensitive (0.88-0.96) to detect sleep, but less specific (0.35-0.64) to detect wake than the Sadeh algorithm (sensitivity: 0.82-0.91, specificity: 0.47-0.68). Total sleep time measured using the GT3X+ with both algorithms was similar to that obtained by PSG (ICC=0.64-0.88). In contrast, agreement between the GT3X+ and PSG wake after sleep onset was poor (ICC=0.00-0.10). In adults, the GT3X+ using the Cole-Kripke algorithm provided data comparable to the AWS (mean bias=3.7±19.7 minutes for total sleep time and 8.0±14.2 minutes for wake after sleep onset). Conclusion The two actigraphs provided comparable and accurate data compared to PSG, although both poorly identified wake episodes (i.e., had low specificity). Use of actigraphy scoring algorithm influenced the mean bias and level of agreement in sleep-wake times estimates. The GT3X+, when analyzed by the Cole-Kripke, but not the Sadeh algorithm, provided comparable data to the AWS.

Abstract: Wrist worn raw-data accelerometers are used increasingly in large scale population research. We examined whether sleep parameters can be estimated from these data in the absence of sleep diaries, which are common in sleep actigraphy. Our heuristic algorithm uses the variance in estimated z-axis angle and makes basic assumptions about sleep interruptions. Detected sleep period time window (SPT-window), was compared against sleep diary in 3741 participants (range=60-83years) and polysomnography in sleep clinic patients (N=28) and in healthy good sleepers (N=22). The SPT-window derived from the algorithm was 10.9 and 2.9 minutes longer compared with sleep diary in men and women, respectively. Average c-statistic to detect the SPT-window compared to polysomnography was 0.86 and 0.83 in clinic and healthy sleepers, respectively. We demonstrated the accuracy of our algorithm to detect the SPT-window. The value of this algorithm lies in studies such as UK Biobank where a sleep diary was not used.

Abstract: Despite the widespread use of actigraphy in pediatric sleep studies, there are currently no age-related normative data. To systematically review the literature, calculate pooled mean estimates of actigraphy-derived pediatric nighttime sleep variables and to examine the magnitude of change with age. A systematic search was performed across eight databases of studies that included at least one actigraphy sleep variable from healthy children aged 0-18 years. Data suitable for meta-analysis were confined to ages 3-18 years with seven actigraphy variables analyzed using random effects meta-analysis and meta-regression performed using age as a covariate. In total, 1334 articles did not meet inclusion criteria; 87 had data suitable for review and 79 were suitable for meta-analysis. Pooled mean estimates for overnight sleep duration declined from 9.68 hours (3-5 years age band) to 8.98, 8.85, 8.05, and 7.4 for age bands 6-8, 9-11, 12-14, and 15-18 years, respectively. For continuous data, the best-fit (R2 = 0.74) equation for hours over the 0-18 years age range was 9.02 - 1.04 × [(age/10)^2 - 0.83]. There was a significant curvilinear association between both sleep onset and offset with age (p These normative values have potential application to assist the interpretation of actigraphy measures from nighttime recordings across the pediatric age range, and aid future research.

Abstract: The present review examines the relations between sleep disturbance and anxiety in children and adolescents. The review begins with a detailed discussion of normative developmental trends in sleep, and the relation between sleep quality and emotion dysregulation in children. The extant literature on sleep disturbance in clinically anxious children with a focus on subjective versus objective measures of sleep is then summarized in detail. Finally, a review of the reciprocal relationship between sleep and emotion regulation is provided. The available research suggests that sleep disturbance is quite prevalent in children with anxiety disorders, although the directionality of the association between sleep disturbance and anxiety in children remains unclear. Despite this limitation, a reciprocal relationship between sleep quality and anxiety appears to be well established. Research using objective measures of sleep quality (e.g. polysomnography, sleep actigraphy, sleep bruxism) is warranted to better understand this relation. Further, complicating factors such as the environment in which sleep quality is measured, the developmental stage of participants, varying severity of anxiety and the timeframe during which assessment takes place should all be considered when examining sleep disturbance in this population.

Abstract: Whether you are a morning lark or a night owl has proven to be a key contributor in the timing of peak athletic performance. Recent evidence suggests that accounting for these differences, known as one’s chronotype, results in significantly different diurnal performance profiles. However, there is limited research investigating multiple measures of performance simultaneously over the course of a socially constrained day. This study aimed to investigate the impact of chronotype on indices of cognitive and physical performance at different times of day in healthy volunteers. We recruited 56 healthy individuals categorised as early (ECT, n = 25) or late (LCT, n = 31) chronotypes using the Munich ChronoType Questionnaire, circadian phase markers and objective actigraphy. Measures of cognitive and physical performance, along with self-reported daytime sleepiness, were taken at multiple times of day (14:00 h, 20:00 h and 08:00 h the following morning). Here, we find significantly different diurnal variation profiles between ECTs and LCTs, for daytime sleepiness, psychomotor vigilance, executive function and isometric grip strength. LCTs were significantly impaired in all measures in the morning compared to ECTs. Our results provide evidence to support the notion that ‘night owls’ are compromised earlier in the day. We offer new insight into how differences in habitual sleep patterns and circadian rhythms impact cognitive and physical measures of performance. These findings may have implications for the sports world, e.g. athletes, coaches and teams, who are constantly looking for ways to minimise performance deficits and maximise performance gains.

Abstract: Sleep disturbances, as well as sleep-wake rhythm disturbances, are typical symptoms of Alzheimer's disease (AD) that may precede the other clinical signs of this neurodegenerative disease. Here, we describe clinical features of sleep disorders in AD and the relation between sleep disorders and both cognitive impairment and poor prognosis of the disease. There are difficulties of the diagnosis of sleep disorders based on sleep questionnaires, polysomnography or actigraphy in the AD patients. Typical disturbances of the neurophysiological sleep architecture in the course of the AD include deep sleep and paradoxical sleep deprivation. Among sleep disorders occurring in patients with AD, the most frequent disorders are sleep breathing disorders and restless legs syndrome. Sleep disorders may influence circadian fluctuations of the concentrations of amyloid-β in the interstitial brain fluid and in the cerebrovascular fluid related to the glymphatic brain system and production of the amyloid-β. There is accumulating evidence suggesting that disordered sleep contributes to cognitive decline and the development of AD pathology. In this mini-review, we highlight and discuss the association between sleep disorders and AD.

Abstract: The study aimed to determine the efficacy of melatonin supplementation for sleep disturbances in patients with traumatic brain injury (TBI). This is a randomised double-blind placebo-controlled two-period two-treatment (melatonin and placebo) crossover study. Outpatients were recruited from Epworth and Austin Hospitals Melbourne, Australia. They had mild to severe TBI (n = 33) reporting sleep disturbances post-injury (mean age 37 years, standard deviation 11 years; 67% men). They were given prolonged-release melatonin formulation (2 mg; Circadin®) and placebo capsules for 4 weeks each in a counterbalanced fashion separated by a 48-hour washout period. Treatment was taken nightly 2 hours before bedtime. Serious adverse events and side-effects were monitored. Melatonin supplementation significantly reduced global Pittsburgh Sleep Quality Index scores relative to placebo, indicating improved sleep quality [melatonin 7.68 vs. placebo 9.47, original score units; difference -1.79; 95% confidence interval (CI), -2.70 to -0.88; p ≤ 0.0001]. Melatonin had no effect on sleep onset latency (melatonin 1.37 vs. placebo 1.42, log units; difference -0.05; 95% CI, -0.14 to 0.03; p = 0.23). With respect to the secondary outcomes, melatonin supplementation increased sleep efficiency on actigraphy, and vitality and mental health on the SF-36 v1 questionnaire (p ≤ 0.05 for each). Melatonin decreased anxiety on the Hospital Anxiety Depression Scale and fatigue on the Fatigue Severity Scale (p ≤ 0.05 for both), but had no significant effect on daytime sleepiness on the Epworth Sleepiness Scale (p = 0.15). No serious adverse events were reported. Melatonin supplementation over a 4-week period is effective and safe in improving subjective sleep quality as well as some aspects of objective sleep quality in patients with TBI. Identifier: 12611000734965; Prospectively registered on 13 July 2011.

Abstract: Background: Delayed Sleep-Wake Phase Disorder (DSWPD) is characterised by sleep initiation insomnia when attempting sleep at conventional times and difficulty waking at the required time for daytime commitments. Although there are published therapeutic guidelines for the administration of melatonin for DSWPD, to our knowledge, randomised controlled trials are lacking. This trial tested the efficacy of 0.5 mg melatonin, combined with behavioural sleep-wake scheduling, for improving sleep initiation in clinically diagnosed DSWPD patients with a delayed endogenous melatonin rhythm relative to patient-desired (or -required) bedtime (DBT). Methods: This randomised, placebo-controlled, double-blind clinical trial was conducted in an Australian outpatient DSWPD population. Following 1-wk baseline, clinically diagnosed DSWPD patients with delayed melatonin rhythm relative to DBT (salivary dim light melatonin onset [DLMO] after or within 30 min before DBT) were randomised to 4-wk treatment with 0.5 mg fast-release melatonin or placebo 1 h before DBT for at least 5 consecutive nights per week. All patients received behavioural sleep-wake scheduling, consisting of bedtime scheduled at DBT. The primary outcome was actigraphic sleep onset time. Secondary outcomes were sleep efficiency in the first third of time in bed (SE T1) on treatment nights, subjective sleep-related daytime impairment (Patient Reported Outcomes Measurement Information System [PROMIS]), PROMIS sleep disturbance, measures of daytime sleepiness, clinician-rated change in illness severity, and DLMO time. Findings: Between September 13, 2012 and September 1, 2014, 307 participants were registered; 116 were randomised to treatment (intention-to-treat n = 116; n = 62 males; mean age, 29.0 y). Relative to baseline and compared to placebo, sleep onset occurred 34 min earlier (95% confidence interval [CI] �60 to �8) in the melatonin group. SE T1 increased; PROMIS sleep-related impairment, PROMIS sleep disturbance, insomnia severity, and functional disability decreased; and a greater proportion of patients showed more than minimal clinician-rated improvement following melatonin treatment (52.8%) compared to placebo (24.0%) (P < 0.05). The groups did not differ in the number of nights treatment was taken per protocol. Post-treatment DLMO assessed in a subset of patients (n = 43) was not significantly different between groups. Adverse events included light-headedness, daytime sleepiness, and decreased libido, although rates were similar between treatment groups. The clinical benefits or safety of melatonin with long-term treatment were not assessed, and it remains unknown whether the same treatment regime would benefit patients experiencing DSWPD sleep symptomology without a delay in the endogenous melatonin rhythm. Conclusions: In this study, melatonin treatment 1 h prior to DBT combined with behavioural sleep-wake scheduling was efficacious for improving objective and subjective measures of sleep disturbances and sleep-related impairments in DSWPD patients with delayed circadian phase relative to DBT. Improvements were achieved largely through the sleep-promoting effects of melatonin, combined with behavioural sleep-wake scheduling. Trial registration: This trial was registered with the Australian New Zealand Clinical Trials Registry, ACTRN12612000425897. © 2018 Sletten et al. http://creativecommons.org/licenses/by/4.0/

Abstract: Summary Sleep is essential for recovery and performance in elite athletes. While actigraphy-based studies revealed suboptimal sleep in athletes, information on their subjective experience of sleep is scarce. Relatively unexplored is also the extent to which athletes’ sleep is adversely affected by environmental conditions and daytime behaviours, that is sleep hygiene. This study aimed to provide insight in sleep quantity, quality and its putative association with sleep hygiene. Participants were 98 elite (youth) athletes competing at the highest (inter-)national level. Sleep quantity, quality and sleep hygiene were assessed once covering a 1-month period by using established (sub)clinical questionnaires, and repeatedly during 7 consecutive days. Sleep quality was generally healthy, although 41% of all athletes could be classified as ‘poor sleeper’, and 12% were identified as having a sleep disorder. Daily self-monitoring revealed sleep durations of 8:11 ± 0:45 h, but elevated wake after sleep onset of 13 ± 19 min. Sleep quality, feeling refreshed, and morning vigor were moderate at best. Regarding sleep hygiene, general measures revealed irregular sleep–wake patterns, psychological strain and activating pre-sleep behaviours. At the daily level, blue-light exposure and late-evening consumption of heavy meals were frequently reported. General sleep hygiene revealed significant associations with sleep quality (0.45 0.50; P < 0.001). Results indicate that there is ample room for optimization, specifically in onset latency and in wake after sleep onset. Subtle improvements in sleep seem possible, and optimizing sleep hygiene, such as regular sleep–wake patterns and reducing psychological strain, may facilitate this sleep upgrading process.

Abstract: Study Objectives To investigate the short- and longer-term impact of a 45-min delay in school start time on sleep and well-being of adolescents. Methods The sample consisted of 375 students in grades 7-10 (mean age ± SD: 14.6 ± 1.15 years) from an all-girls' secondary school in Singapore that delayed its start time from 07:30 to 08:15. Self-reports of sleep timing, sleepiness, and well-being (depressive symptoms and mood) were obtained at baseline prior to the delay, and at approximately 1 and 9 months after the delay. Total sleep time (TST) was evaluated via actigraphy. Results After 1 month, bedtimes on school nights were delayed by 9.0 min, while rise times were delayed by 31.6 min, resulting in an increase in time in bed (TIB) of 23.2 min. After 9 months, the increase in TIB was sustained, and TST increased by 10.0 min relative to baseline. Participants also reported lower levels of subjective sleepiness and improvement in well-being at both follow-ups. Notably, greater increase in sleep duration on school nights was associated with greater improvement in alertness and well-being. Conclusions Delaying school start time can result in sustained benefits on sleep duration, daytime alertness, and mental well-being even within a culture where trading sleep for academic success is widespread.

Abstract: Study Objectives African Americans have been under-represented in obstructive sleep apnea (OSA) research. This study determined the prevalence and correlates of OSA overall and by sex among African Americans in the Jackson Heart Sleep Study. Methods Participants (N = 852) underwent a type 3 in-home sleep apnea study, 7 day wrist actigraphy and completed standardized measurements and questionnaires. OSA was defined as an apnea-hypopnea index (AHI) of ≥15, where hypopneas were defined as ≥ 4% associated desaturation. Physician diagnosis of OSA was self-reported. Logistic regression models were fit to determine the associations of demographics, socioeconomic status, sleep symptoms, actigraphy-based sleep, body mass index (BMI), and comorbidities with OSA. Results Average age was 63.1 (standard deviation = 10.7), 66% were female, and mean BMI was 32.0 (6.9) kg/m2. Approximately 24% had an AHI ≥ 15; of those, 5% had a physician diagnosis of OSA. Prevalence of OSA increased across BMI categories, but not age groups. Men had a 12% higher prevalence of OSA compared with women, p < 0.01. Older age, male sex, higher BMI, larger neck circumference, and report of habitual snoring were independently associated with higher odds of OSA, all p < 0.05. Associations between sleep symptoms and OSA were similar for men and women. Sleepiness and waist circumference were not associated with OSA. Conclusions There was a high prevalence of objectively measured but undiagnosed OSA in this sample of African Americans. Snoring, BMI, and neck circumference were important markers of OSA for men and women. Our results suggest that screening tools that incorporate information on sleepiness and waist circumference may be suboptimal in this population.

Abstract: Irregular and insufficient sleep place youth at risk for adverse psychological and physical health outcomes. Recent research indicates that discrimination constitutes a type of stressor that interferes with adolescent sleep; however, the mechanisms through which discrimination affects sleep are not well understood. This study examined whether ethnic and non-ethnic (i.e., gender, age, and height/weight) discrimination were associated with adolescents’ sleep duration, variability, and quality, and whether loneliness and perceived stress mediated these associations. An ethnically-diverse sample (42% Latino, 29% European American, 23% Asian) of adolescents (N = 316; M age = 16.40 years, 57% girls) reported on their experiences of discrimination, perceived stress, and loneliness. Sleep duration and variability were assessed by actigraphy and sleep quality through self-reports. Ethnic discrimination was related to shorter sleep duration and both ethnic and non-ethnic discrimination were associated with worse sleep quality. Loneliness and perceived stress partially mediated the relation between discrimination and sleep quality. Discriminatory experiences can heighten feelings of loneliness and stress, which, in turn, may contribute to diminished sleep quality during adolescence.

Abstract: Objectives This study compared subjective (questionnaire) and objective (actigraphy) sleep assessments, and examined agreement between these methods, in vulnerable older adults participating in a Veterans Administration Adult Day Health Care (ADHC) program. Methods 59 ADHC participants (95% male, mean age = 78 years) completed sleep questionnaires and 72 continuous hours of wrist actigraphy. Linear regression was used to examine agreement between methods and explore discrepancies in subjective/objective measures. Results Disturbed sleep was common, yet there was no agreement between subjective and objective sleep assessment methods. Compared with objective measures, one-half of participants reported worse sleep efficiency (SE) on questionnaires while one-quarter over-estimated SE. Participants reporting worse pain had a greater discrepancy between subjective and objective SE. Conclusions Vulnerable older adults demonstrated unique patterns of reporting sleep quality when comparing subjective and objective methods. Additional research is needed to better understand how vulnerable older adults evaluate sleep problems. Clinical implications Objective and subjective sleep measures may represent unique and equally important constructs in this population. Clinicians should consider utilizing both objective and subjective sleep measures to identify individuals who may benefit from behavioral sleep treatments, and future research is needed to develop and validate appropriate sleep assessments for vulnerable older adults.

Abstract: Study Objectives Chronic insomnia affects up to 15 per cent of adults. Recent cross-sectional and prospective epidemiological studies report an association between insomnia and hypertension, including incident hypertension, yet mechanisms underlying the association remain unknown. We hypothesized that participants with chronic insomnia would have elevated sympathetic neural outflow, blunted baroreflex sensitivity, and augmented sympathetic neural and cardiovascular reactivity to stress when compared with good-sleeper controls. Methods Twelve participants with chronic insomnia (11 women, 1 man) and 12 controls (8 women, 4 men) underwent one night of laboratory polysomnography, two weeks of at-home wrist actigraphy, and one night of controlled laboratory sleep prior to a comprehensive morning autonomic function test. The autonomic function test consisted of simultaneous recordings of muscle sympathetic nerve activity (MSNA; microneurography), beat-to-beat blood pressure (finger plethysmography), and heart rate (electrocardiogram) during a 10 min supine baseline and a 2 min cold pressor test. Results Baseline blood pressure, heart rate, and MSNA were not different between groups, but sympathetic baroreflex sensitivity was significantly blunted in participants with insomnia (-2.1 ± 1.0 vs. -4.3 ± 1.3 bursts/100 heartbeats/mm Hg; p < 0.001). During the cold pressor test, systolic arterial pressure reactivity (Δ21 ± 11 vs. Δ14 ± 8 mm Hg; time × group = 0.04) and total MSNA reactivity (Δ127%, 54%-208% vs. Δ52%, 30%-81%; time × group = 0.02) were augmented in chronic insomnia. Conclusions Participants with chronic insomnia demonstrated impaired sympathetic baroreflex function and augmented neural cardiovascular responsiveness to stress, when compared with controls. These findings support growing evidence of cardiovascular risk and physiological hyperarousal in chronic insomnia. Clinical Trial Registration NCT02048878. https://clinicaltrials.gov/ct2/show/NCT02048878.

Abstract: Study objectives Sleep is multidimensional, with domains including duration, timing, continuity, regularity, rhythmicity, quality, and sleepiness/alertness. Individual sleep characteristics representing these domains are known to predict health outcomes. However, most studies consider sleep characteristics in isolation, resulting in an incomplete understanding of which sleep characteristics are the strongest predictors of health outcomes. We applied three multivariable approaches to robustly determine which sleep characteristics increase mortality risk in the osteoporotic fractures in men sleep study. Methods In total, 2,887 men (mean 76.3 years) completed relevant assessments and were followed for up to 11 years. One actigraphy or self-reported sleep characteristic was selected to represent each of seven sleep domains. Multivariable Cox models, survival trees, and random survival forests were applied to determine which sleep characteristics increase mortality risk. Results Rhythmicity (actigraphy pseudo-F statistic) and continuity (actigraphy minutes awake after sleep onset) were the most robust sleep predictors across models. In a multivariable Cox model, lower rhythmicity (hazard ratio, HR [95%CI] =1.12 [1.04, 1.22]) and lower continuity (1.16 [1.08, 1.24]) were the strongest sleep predictors. In the random survival forest, rhythmicity and continuity were the most important individual sleep characteristics (ranked as the sixth and eighth most important among 43 possible sleep and non-sleep predictors); moreover, the predictive importance of all sleep information considered simultaneously followed only age, cognition, and cardiovascular disease. Conclusions Research within a multidimensional sleep health framework can jumpstart future research on causal pathways linking sleep and health, new interventions that target specific sleep health profiles, and improved sleep screening for adverse health outcomes.

Abstract: This work examined window/door opening as means of bedroom ventilation and the consequent effect upon occupants' sleep, using data from 17 healthy volunteers. Bedroom CO2 level, temperature, and relative humidity were measured over 5 days, for two cases: open window or door (internal, bedroom door), and closed window and door. Participant filled questionnaires and sleep diary provided subjective measure of sleep quality. Actigraphy objectively monitored the participants during sleep. Additionally, a FlexSensor, placed under pillows of participants, detected movement during sleep. Average CO2 level for the Open conditions was 717 ppm (SD = 197 ppm) and for Closed conditions was 1150 ppm (SD = 463 ppm). Absolute humidity levels were similar for both conditions, while Open conditions were slightly cooler (mean = 19.7°C, SD = 1.8°C) than Closed (mean = 20.1°C, SD = 1.5°C). Results showed significant correlations (P < .001) between actigraphy data and questionnaire responses for: sleep latency (r = .45), sleep length (r = .87), and number of awakenings (r = .28). Of all analyzed sleep parameters, questionnaire-based depth of sleep (P = .002) and actigraphy-based sleep phase (P = .003) were significantly different between Open and Closed conditions.

Abstract: Author(s): Rogers-Soeder, Tara S; Blackwell, Terri; Yaffe, Kristine; Ancoli-Israel, Sonia; Redline, Susan; Cauley, Jane A; Ensrud, Kristine E; Paudel, Misti; Barrett-Connor, Elizabeth; LeBlanc, Erin; Stone, Katie; Lane, Nancy E; Tranah, Greg; Osteoporotic Fractures in Men Study Research Group | Abstract: OBJECTIVE:To examine rest-activity circadian rhythm (RAR) and cognitive decline in older men. DESIGN:Longitudinal. SETTING:Osteoporotic Fractures in Men (MrOS) and ancillary Outcomes of Sleep Disorders in Men (MrOS Sleep) studies. PARTICIPANTS:MrOS and MrOS Sleep participants (N=2,754; mean age 76.0 ± 5.3). MEASUREMENTS:The Modified Mini-Mental State examination (3MS) was used to assess cognition at baseline (2003-05) and follow-up examinations (2005-06 and 2007-09). Wrist actigraphy was used to measure 24-hour activity counts at baseline. RAR variables included amplitude (strength of activity rhythm), mesor (mean activity level), pseudo F-statistic (overall circadian rhythm robustness), and acrophase (time of daily peak activity). RESULTS:After an average of 3.4 ± 0.5 years, men with lower amplitudes, mesors, and pseudo F-statistics had greater decline in 3MS performance (amplitude: -0.7 points Q1 vs -0.5 points Q4, pl.001; mesor: -0.5 points Q1 vs -0.2 points Q4, p=.01; pseudo F-statistic: -0.5 points Q1 vs -0.3 points Q4, pl.001). Lower amplitudes and pseudo-F statistics were associated with greater odds of clinically significant cognitive decline (≥5-point decrease) (amplitude Q1 vs. Q4: odds ratio (OR)=1.4, 95% confidence interval (CI)=1.0-1.9; pseudo-F statistic Q1 vs Q4: OR=1.4, 95% CI=1.0-1.9). Men with phase-advanced acrophase had greater odds of clinically significant cognitive decline (OR=1.8, 95% CI=1.2-2.8). Results were adjusted for multiple confounders. CONCLUSION:Several parameters of disrupted RAR (lower amplitude, pseudo F-statistic, mesor, phase-advanced acrophase) were associated with greater cognitive decline in older community-dwelling men. These findings contribute to a growing body of evidence suggesting that altered RARs are associated with cognitive decline in older adults. J Am Geriatr Soc 66:2136-2143, 2018.

Abstract: Adolescent insomnia can be treated effectively with cognitive behavioural therapy for insomnia (CBTI). However, little is known about effects of CBTI on psychopathology in adolescents. This study aimed to investigate whether (a) CBTI improves psychopathology in Internet- (IT) and face-to-face group treatment (GT) compared to waitlist (WL), (b) improvement in psychopathology can be attributed to reduced insomnia, (c) improvement in psychopathology remains stable for up to 1 year. One hundred and sixteen participants (age = 15.6 years, 25% males) with DSM-5 insomnia, were randomly assigned to IT, GT or WL. http://www.controlledtrials.com (ISRCTN33922163). Assessments of psychopathology, insomnia and objectively and subjectively measured sleep occurred at baseline, post-treatment, and at 2-, 6- and 12-month follow-up. Multilevel and mediation analyses were run to test hypotheses. The CBTI protocol, 'Sleeping Smart' for both IT and GT consisted of six weekly sessions and a booster session after 2 months. Psychopathology symptoms, insomnia and sleep problems as measured by actigraphy and sleep logs decreased substantially in IT and GT compared with WL at 2-month follow-up with medium to large effect sizes (ESs). Psychopathology symptoms remained stable or further improved for up to 12-month follow-up. ESs at 12-month follow-up for IT and GT were respectively: affective (d = -0.87 and -0.97), anxiety (d = -0.81 for IT), somatic (d = -0.38 and d = -0.52), oppositional (d = -0.42 for GT) and attention deficit hyperactivity disorder (ADHD) problems (d = -0.47 and -0.46). Mediation analyses indicated that reduction of insomnia symptoms after CBTI fully mediated the effects of CBTI on affective and anxiety problems, and partially mediated the effect on ADHD problems. This is the first study demonstrating that Internet and face-to-face CBT for insomnia achieves long-term reduction in adolescent psychopathology and does so by improving insomnia. This finding can have profound implications for youth mental health care