Lower Sleep Efficiency Research Articles

Phenotypes of sleep health among adults with chronic heart failure in a randomized controlled trial of cognitive behavioral therapy for insomnia.

Poor sleep contributes to adverse health in heart failure. However, studies are limited to isolated sleep characteristics. To evaluate changes in sleep health phenotypes after cognitive behavioral therapy for insomnia or attention control and associations between sleep health phenotypes, symptoms, stress, functional performance, and emergency department visits and hospitalizations. Secondary analysis of a randomized controlled trial of cognitive behavioral therapy for insomnia among adults with heart failure. We measured sleep (rest-activity rhythms, sleep duration, quality, and efficiency, insomnia severity, daytime sleepiness), symptoms, cognitive ability, vigilance, and 6-minute walk distance at baseline and 3-, 6-, and 12-month postintervention and collected hospitalizations and emergency department visits. We used K-means cluster analysis and generalized linear mixed models, generalized estimating equations, and Cox proportional hazard models. Among 166 participants (M age=63.2 (SD=12.6) years; 57% male; 23% NewYork Heart Association Class III/IV), there were four sleep health phenotypes ("Unstable Sleep" (15%); "Short Sleep" (39%); "Low Sleep Efficiency" (25%); and "Good Sleep" (21%)) at baseline. The healthiest phenotype was associated with the lowest fatigue. The proportions of participants in the healthiest sleep group increased from pre- to post-treatment. Low sleepiness (p=.0188) and a robust circadian quotient (p=.007) predicted transition to the healthiest phenotype. The poorest sleep phenotype at baseline predicted time to hospitalizations and emergency department visits (hazard ratios 0.35-0.60) after adjusting for covariates. Sleep phenotypes predict heart failure outcomes. Tailored interventions targeting phenotypes may be more effective than approaches that focus on single sleep characteristics.

Move more today, sleep better tonight? Daily associations between physical activity and sedentary behavior with sleep among young adults with and without insomnia symptoms

ObjectiveAt the between-person level, it is well-documented that individuals with more physical activity (PA) and less sedentary behavior (SB) tend to have better sleep outcomes than their peers. However, the associations at the within-person level remain unclear. This study investigated the daily associations between PA and SB with nighttime sleep among young adults with and without insomnia symptoms. MethodsData was collected through activity trackers and online questionnaires for 7 consecutive days among 147 university students, including time spent on moderate to vigorous physical activity (MVPA), light physical activity (LPA), and SB, along with sleep duration, sleep efficiency, and sleep quality. Participants were classified into two subgroups according to the presence of insomnia symptoms, which were determined by a self-reported insomnia scale. Multilevel compositional data analysis was conducted on the total sample, and separately on subsamples characterized by the presence and absence of insomnia symptoms. ResultsIn the total sample and subsample without insomnia symptoms, substitutions among MVPA, LPA, and SB were not associated with changes in sleep outcomes at the daily level. However, in the subsample with insomnia symptoms, days with more MVPA or SB and less LPA were associated with higher sleep efficiency, while days with more LPA at the expense of MVPA or SB were associated with lower sleep efficiency. ConclusionsFor young adults with insomnia symptoms, replacing LPA with MVPA on a given day may improve their sleep efficiency that night.

Factors associated with poor sleep in children with drug-resistant epilepsy.

We aimed to investigate sleep in children with drug-resistant epilepsy (DRE), including developmental and epileptic encephalopathies (DEEs). Next, we examined differences in sleep macrostructure and microstructure and questionnaire outcomes between children with well-controlled epilepsy (WCE) and children with DRE. Furthermore, we wanted to identify factors associated with poor sleep outcome in these children, as some factors might be targets to improve epilepsy and neurodevelopmental outcomes. A cross-sectional study was conducted in children 4 to 18-years-old. Children without epilepsy, with WCE, and with DRE were included. Overnight electroencephalography (EEG), including chin electromyography and electrooculography, to allow sleep staging, was performed. Parents were asked to fill out a sleep questionnaire. Classical five-stage sleep scoring was performed manually, spindles were automatically counted, and slow wave activity (SWA) in the first and last hour of slow wave sleep was calculated. One hundred eighty-two patients were included: 48 without epilepsy, 75 with WCE, and 59 with DRE. We found that children with DRE have significantly lower sleep efficiency (SE%), less time spent in rapid eye movement (REM) sleep, fewer sleep spindles, and a lower SWA decline over the night compared to children with WCE. Subjectively more severe sleep problems were reported by the caregivers and more daytime sleepiness was present in children with DRE. Least absolute shrinkage and selection operator (LASSO) regression showed that multifocal interictal epileptiform discharges (IEDs), benzodiazepine treatment, and longer duration of epilepsy were associated with lower SE% and lower REM sleep time. The presence of multifocal discharges and cerebral palsy was associated with fewer spindles. Benzodiazepine treatment, drug resistance, seizures during sleep, intellectual disability, and older age were associated with lower SWA decline. Both sleep macrostructure and microstructure are severely impacted in children with DRE, including those with DEEs. Epilepsy parameters play a distinct role in the disruption REM sleep, spindle count, and SWA decline.

Childhood Adversity and Adolescent Epigenetic Age Acceleration: The Role of Adolescent Sleep Health.

We investigated how a dimension of early life adversity (ELA) capturing threat in the home relates to later epigenetic age acceleration in adolescence through sleep (duration, efficiency, and timing), to empirically test theoretical models suggesting the importance of sleep as a key mechanism linking ELA with poor health outcomes, and to expand the limited literature on sleep and epigenetic aging among youth. We utilized data from 861 participants from the Future of Families and Child Wellbeing Study (FFCWS) who participated in the actigraphy sub study at age 15. Sleep variables used were average total sleep time (TST), sleep efficiency (SE), and sleep onset timing. Home threat was determined at ages 3, 5, and 9 from parent reports on the Child Conflict Tactics Scale (CTS-PC), and epigenetic aging was measured through DNA methylation analyses of saliva samples collected at age 15. Higher levels of childhood home threat exposure were associated with less adolescent TST, lower SE, and later sleep onset timing. Adolescent SE and timing were associated with a faster pace of aging and epigenetic age acceleration. Sleep efficiency and timing mediated the link between childhood home threat exposure and adolescent epigenetic aging. Epigenetic embedding of childhood threat exposure in the home may occur through adversity-related sleep disturbances in adolescence. Findings warrant greater attention to pediatric sleep health in theoretical models of biological embedding of adversity and point to the examination of improving sleep health as a potential way to prevent adversity-related epigenetic age acceleration.

Biopsychosocial factors intersecting with weekly sleep difficulties in the menopause transition

ObjectivesSleep difficulties are common in the menopause transition and increase risk for a variety of physical and psychological problems. The current study investigated potential interactions between psychosocial variables and within-person changes in ovarian hormones in predicting perimenopausal sleep problems as well as the potential interactions between poor sleep and psychosocial factors in predicting worsened mood, affect, and attention. Study designThe sample included 101 perimenopausal individuals. Participants completed 12 weekly assessments of self-reported sleep outcomes, depressive mood and affect, and attention function, and of estrone glucuronide (E1G) and pregnanediol glucuronide (PdG) levels (urinary metabolites of estradiol and progesterone, respectively); they also had 24-h tracking of vasomotor symptoms. Other psychosocial variables such as trauma history and stressful life events were assessed at baseline. ResultsA history of depression, baseline depressive symptoms, trait anxiety, and more severe and bothersome vasomotor symptoms predicted worsened sleep outcomes. Recent stressful life events, trauma history, and person-centred E1G and PdG changes did not predict sleep outcomes. However, there was an interaction whereby person-centred E1G decreases predicted lower sleep efficiency in those with higher baseline depressive symptoms. Higher baseline depression and trauma history also amplified the effect of vasomotor symptoms on sleep outcomes. In evaluating the effect of poor sleep on psychological and cognitive outcomes, stressful life events emerged as a moderating factor. Finally, trauma history and poor sleep interacted to predict worsened attention function. ConclusionsThe current study suggests that certain individuals may be at greater risk of perimenopausal sleep problems and the resulting negative effects on mood and cognition.

Associations between habitual sleep characteristics and cardiometabolic disease risk in corporate executives

ObjectivesCorporate executive job demands may lead to poor sleep habits, increasing their risk for cardiometabolic disease. This study aimed to describe and explore associations between objectively measured habitual sleep characteristics and cardiometabolic disease risk of corporate executives, while accounting for occupational, psychological, and lifestyle factors. MethodsHabitual sleep was measured using wrist-worn actigraphy and a sleep diary over seven consecutive days in 61 (68.3% men) corporate executives aged 46.4 ± 8.7years. A composite cardiometabolic disease risk score was determined using body mass index, waist circumference, blood pressure and fasting glucose and lipid concentrations. Prediction models were built using a backward stepwise selection approach to explore associations between sleep characteristics and cardiometabolic disease risk factors adjusting for occupational, psychological, and lifestyle covariates. ResultsAverage total sleep time was 6.60 ± 0.75 hours, with 51.7% of participants reporting poor sleep quality and 26.2% extending their weekend sleep. Adjusted models showed that lower sleep efficiency (β = −0.25, 95%CI: −0.43; −0.08, P = .006), shorter weekday total sleep time (β = −1.37, 95% CI: −2.41, −0.32; P = .011) and catch-up sleep (β = 0.84, 95%CI: 0.08, 1.60, P = .002) were associated with higher cardiometabolic disease risk scores. Adjusted models also found that shorter average time-in-bed (ß=−2.00, 95%CI: −3.76; −0.18, P = .031), average total sleep time (ß=1.98, 95%CI: −3.70; −0.25, P = .025) and weekday total sleep time (β = −2.13, 95%CI: −3.56; −0.69, P = .025) as well as catch-up sleep (β = 1.67, 95% CI: 0.52; 2.83; P = .012) were all associated with a higher body mass index. ConclusionCorporate executives who compromise sleep duration during the working week may increase their risk for obesity and future cardiometabolic disease.

Comparing sleep measures in cancer survivors: self-reported sleep diary versus objective wearable sleep tracker.

Cancer survivors are increasingly using wearable fitness trackers, but it is unclear if they match traditional self-reported sleep diaries. We aimed to compare sleep data from Fitbit and the Consensus Sleep Diary (CSD) in this group. We analyzed data from two randomized clinical trials, using both CSD and Fitbit to collect sleep outcomes: total sleep time (TST), wake time after sleep onset (WASO), number of awakenings (NWAK), time in bed (TIB), and sleep efficiency (SE). Insomnia severity was measured by Insomnia Severity Index (ISI). We used the Wilcoxon signed rank test, Spearman's rank correlation coefficients, and the Mann-Whitney test to compare sleep outcomes and assess their ability to distinguish insomnia severity levels between CSD and Fitbit data. Among 62 participants, compared to CSD, Fitbit recorded longer TST by an average of 14.6 (SD = 84.9) minutes, longer WASO by an average of 28.7 (SD = 40.5) minutes, more NWAK by an average of 16.7 (SD = 6.6) times per night, and higher SE by an average of 7.1% (SD = 14.4); but shorter TIB by an average of 24.4 (SD = 71.5) minutes. All the differences were statistically significant (all p < 0.05), except for TST (p = 0.38). Moderate correlations were found for TST (r = 0.41, p = 0.001) and TIB (r = 0.44, p < 0.001). Compared to no/mild insomnia group, participants with clinical insomnia reported more NWAK (p = 0.009) and lower SE (p = 0.029) as measured by CSD, but there were no differences measured byFitbit. TST was the only similar outcome between Fitbit and CSD. Our study highlights the advantages, disadvantages, and clinical utilization of sleep trackers in oncology.

A cross-sectional study on the relationship between infant sleep, temperament and bedtime practices.

To explore the interplay between infant temperament, sleep characteristics, and bedtime practices. We conducted a cross-sectional study involving a large sample of 9-13 month old infants (N = 623). Sleep data were collected through auto-videosomnography, allowing for objective, non-invasive assessment of sleep in an infants' ecological environment. Infant temperament and bedtime practices were assessed with questionnaires completed by parents. Results revealed significant correlations between negative affectivity and disrupted sleep patterns, including shorter sleep duration, more night awakenings, and increased parental interventions. Infants falling asleep while being breast/bottle feeding or while being hold/rocked had shorter nocturnal sleep duration, lower sleep efficiency, later bedtime, earlier wake up time, and more parent interventions. Regression analyses indicated that bedtime practices accounted for a substantial portion of variance in sleep metrics, emphasizing their role in influencing infant sleep. The study highlights the intricate interconnections between infant temperament, sleep, and caregiving practices, emphasizing the need for a nuanced understanding of individual differences to tailor effective parenting strategies for promoting healthy sleep in infants.

Actigraphy-based sleep and muscle sympathetic nerve activity in humans.

Short and insufficient sleep are prevalent and associated with cardiovascular disease, with the sympathetic nervous system as a suspected mediator. The purpose of the present study was to investigate the association between objective, actigraphy-based total sleep time (TST), sleep efficiency (SE), and cardiovascular and sympathetic regulation in healthy adults. We hypothesized that short TST and low SE would be associated with elevated resting blood pressure, heart rate (HR), and muscle sympathetic nerve activity (MSNA). Participants included 94 individuals [46 males, 48 females, age: 30 ± 15 yr, body mass index (BMI): 26 ± 4 kg/m2]. All participants underwent at least 7 days of at-home, wristwatch actigraphy monitoring (avg: 10 ± 3 days). Seated blood pressures were assessed using brachial blood pressure measurements, followed by a 10-minute supine autonomic testing session consisting of continuous HR (electrocardiogram), beat-by-beat blood pressure (finger plethysmograph), and MSNA (microneurography) monitoring. Partial correlations were used to determine the relationship between sleep and cardiovascular parameters while accounting for the influence of age, sex, and BMI. TST was not associated with MAP (R = -0.105, P = 0.321), HR (R = 0.093, P = 0.383), or MSNA burst frequency (BF; R = -0.168, P = 0.112) and burst incidence (BI; R = -0.162, P = 0.124). Similarly, SE was not associated with MAP (R = -0.088, P = 0.408), HR (R = -0.118, P = 0.263), MSNA BF (R = 0.038, P = 0.723), or MSNA BI (R = 0.079, P = 0.459). In contrast to recent preliminary findings, our results do not support a significant association between actigraphy-based sleep duration or efficiency and measures of resting blood pressure, heart rate, and MSNA.NEW & NOTEWORTHY The present study investigated the independent association between actigraphy-based sleep duration, efficiency, and measures of blood pressure, heart rate, and muscle sympathetic nerve activity (MSNA) in adult males and females. Contrary to our hypothesis, the findings do not support an independent association between habitual sleep and cardiovascular or sympathetic neural activity. However, these findings do not preclude a potential association between these parameters in populations with sleep disorders and/or cardiovascular disease.

The relationship between wearable-derived sleep features and relapse in Major Depressive Disorder

BackgroundChanges in sleep and circadian function are leading candidate markers for the detection of relapse in Major Depressive Disorder (MDD). Consumer-grade wearable devices may enable remote and real-time examination of dynamic changes in sleep. Fitbit data from individuals with recurrent MDD were used to describe the longitudinal effects of sleep duration, quality, and regularity on subsequent depression relapse and severity. MethodsData were collected as part of a longitudinal observational mobile Health (mHealth) cohort study in people with recurrent MDD. Participants wore a Fitbit device and completed regular outcome assessments via email for a median follow-up of 541 days. We used multivariable regression models to test the effects of sleep features on depression outcomes. We considered respondents with at least one assessment of relapse (n = 218) or at least one assessment of depression severity (n = 393). ResultsIncreased intra-individual variability in total sleep time, greater sleep fragmentation, lower sleep efficiency, and more variable sleep midpoints were associated with worse depression outcomes. Adjusted Population Attributable Fractions suggested that an intervention to increase sleep consistency in adults with MDD could reduce the population risk for depression relapse by up to 22 %. LimitationsLimitations include a potentially underpowered primary outcome due to the smaller number of relapses identified than expected. ConclusionOur study demonstrates a role for consumer-grade activity trackers in estimating relapse risk and depression severity in people with recurrent MDD. Variability in sleep duration and midpoint may be useful targets for stratified interventions.

Polysomnography parameters in a large cohort of people with multiple sclerosis

BackgroundDisordered and disturbed sleep is quite common among people with multiple sclerosis (PwMS). It is associated with fatigue one of most disabling symptoms in MS. This study aims at comparing polysomnographic (PSG) sleep parameters in a large single cohort of PwMS from a single center to that of the published norms. Hence establishing PSG parameters in PwMS. MethodsThis is a retrospective review of 299 consecutive adult PwMS who were seen and evaluated with an overnight PSG at a Comprehensive MS Care Center between 11/19/2001 to 9/17/2014. Data extracted from the PSG included Total Sleep Time (TST), sleep efficiency (SE), sleep onset latency (SOL), Relative REM latency, total apnea-hypopnea indices (AHI), spontaneous arousal indices (AI), total periodic leg movements indices (PLMI) and, sleep architecture metrics including percentage spent in stages N1/N2, N3, and REM. ResultsPwMS, compared to normative data, had, on average, 85.9 min shorter TST (p < 0.001), 27.3 min longer SOL (p < 0.0001), 62.1 min longer REM latency (p < 0.0001), 10.7 % lower SE (p < 0.0001), 16.4 % more N1/N2 (p < 0.0001) and 11.4 % less N3 (p < 0.0001). REM latency The prevalence of Obstructive Sleep Apnea (OSA) was high at 60.7 % and the mean AHI was higher by 11.1 events per hour (p < 0.0001). ConclusionsThis study establishes PSG parameters in the largest PwMS cohort reported to date. It is important to be vigilant of sleep complaints in PwMS. Future prospective large single cohort studies with standardized methods are needed to further understand sleep disturbances in PwMS as well as their causes and implications.

Brain metabolites are associated with sleep architecture and cognitive functioning in older adults.

Sleep deficits are a possible risk factor for development of cognitive decline and dementia in older age. Research suggests that neuroinflammation may be a link between the two. This observational, cross-sectional study evaluated relationships between sleep architecture, neuroinflammation and cognitive functioning in healthy older adults. Twenty-two adults aged ≥60 years underwent whole-brain magnetic resonance spectroscopic imaging (in vivo method of visualizing increased brain temperatures as a proxy for neuroinflammation), supervised laboratory-based polysomnography, and comprehensive neurocognitive testing. Multiple regressions were used to assess relationships between magnetic resonance spectroscopic imaging-derived brain temperature and metabolites related to inflammation (choline; myo-inositol; N-acetylaspartate), sleep efficiency, time and % N3 sleep and cognitive performance. Choline, myo-inositol and N-acetylaspartate were associated with sleep efficiency and cognitive performance. Higher choline and myo-inositol in the bilateral frontal lobes were associated with slower processing speed and lower sleep efficiency. Higher choline and myo-inositol in bilateral frontoparietal regions were associated with better cognitive performance. Higher N-acetylaspartate around the temporoparietal junction and adjacent white matter was associated with better visuospatial function. Brain temperature was not related to cognitive or sleep outcomes. Our findings are consistent with the limited literature regarding neuroinflammation and its relationships with sleep and cognition in older age, which has implicated ageing microglia and astrocytes in circadian dysregulation, impaired glymphatic clearance and increased blood-brain barrier integrity, with downstream effects of neurodegeneration and cognitive decline. Inflammatory processes remain difficult to measure in the clinical setting, but magnetic resonance spectroscopic imaging may serve as a marker of the relationship between neuroinflammation, sleep and cognitive decline in older adults.

Self-supervised learning of accelerometer data provides new insights for sleep and its association with mortality

Sleep is essential to life. Accurate measurement and classification of sleep/wake and sleep stages is important in clinical studies for sleep disorder diagnoses and in the interpretation of data from consumer devices for monitoring physical and mental well-being. Existing non-polysomnography sleep classification techniques mainly rely on heuristic methods developed in relatively small cohorts. Thus, we aimed to establish the accuracy of wrist-worn accelerometers for sleep stage classification and subsequently describe the association between sleep duration and efficiency (proportion of total time asleep when in bed) with mortality outcomes. We developed a self-supervised deep neural network for sleep stage classification using concurrent laboratory-based polysomnography and accelerometry. After exclusion, 1113 participant nights of data were used for training. The difference between polysomnography and the model classifications on the external validation was 48.2 min (95% limits of agreement (LoA): −50.3 to 146.8 min) for total sleep duration, −17.1 min for REM duration (95% LoA: −56.7 to 91.0 min) and 31.1 min (95% LoA: −67.3 to 129.5 min) for NREM duration. The sleep classifier was deployed in the UK Biobank with ~100,000 participants to study the association of sleep duration and sleep efficiency with all-cause mortality. Among 66,262 UK Biobank participants, 1644 mortality events were observed. Short sleepers (<6 h) had a higher risk of mortality compared to participants with normal sleep duration 6–7.9 h, regardless of whether they had low sleep efficiency (Hazard ratios (HRs): 1.36; 95% confidence intervals (CIs): 1.18 to 1.58) or high sleep efficiency (HRs: 1.29; 95% CIs: 1.04–1.61). Deep-learning-based sleep classification using accelerometers has a fair to moderate agreement with polysomnography. Our findings suggest that having short overnight sleep confers mortality risk irrespective of sleep continuity.

Sleep as a contributor to socioeconomic disparities in hypertension: The Midlife in the United States (MIDUS II) Study.

Hypertension is highly prevalent and is a major risk factor for cardiovascular disease. There is a higher burden of hypertension among individuals of lower socioeconomic status (SES), yet the role of sleep in understanding socioeconomic disparities in hypertension is unclear. We investigated whether sleep quality is a partial mediator of the association between SES and hypertension. We used data from the Midlife in the United States II Study, 2004-2009 (n = 426). Analyses were conducted in 2023. Participants underwent 7-day actigraphy and clinical assessments. Sleep quality measures included actigraphy-defined wakefulness after sleep onset (WASO) and sleep efficiency. Hypertension was measured via three consecutive blood pressure readings, and SES was measured via educational attainment. Models were fit adjusting for age, gender, race, body mass index, and perceived stress. Participants had a mean age of 53.5 years (SD = 12.4) and 41.0% were African American. The prevalences of poor WASO (>30 minutes), low sleep efficiency (<85%), and hypertension were 77.7%, 67.1%, and 61.0%, respectively. Education was not associated with hypertension. However, individuals with low vs. high sleep efficiency had 24% higher prevalence of hypertension (aPR = 1.24, 95% CI: 1.02 to 1.51), higher systolic blood pressure (aβ = 4.61, 95% CI: 0.69 to 8.53), and higher diastolic blood pressure (aβ = 2.50, 95% CI: 0.10 to 4.89). Education was not significantly associated with sleep after adjustment. There was no evidence of sleep mediating the SES-hypertension relation. Effective interventions to lower hypertension prevalence should consider targeting sleep quality. Future research should explore the intersectionality of SES and race in hypertension.

Device-estimated sleep metrics do not mediate the relation between race and blood pressure dipping in young black and white women.

Short, disturbed, and irregular sleep may contribute to blunted nocturnal blood pressure (BP) dipping, a predictor of cardiovascular disease. Black women (BLW) demonstrate less BP dipping and poorer sleep health than White women (WHW). However, it remains unclear whether device-estimated sleep health metrics mediate the relation between race and BP dipping in young women. We hypothesized that the relation between race and BP dipping would be partly mediated by sleep health metrics of sleep duration, sleep efficiency, and sleep regularity. Participants (20 BLW, 17 WHW) were 18-29 years old, normotensive, nonobese, and without evidence of sleep disorders. Systolic and diastolic BP dipping were derived from 24-h ambulatory BP monitoring. Habitual sleep duration and sleep efficiency were estimated via 14 days of wrist actigraphy. Sleep duration regularity was calculated as the standard deviation (SD) of nightly sleep duration (SDSD). Sleep timing regularity metrics were calculated as the SD of sleep onset and sleep midpoint (SMSD). Mediation analysis tested the mediating effect of each sleep metric on the relation between race and BP dipping. BLW experienced less systolic (P=.02) and diastolic (P=.01) BP dipping. Sleep duration (P=.14) was not different between groups. BLW had lower sleep efficiency (P<.01) and higher SDSD (P=.02), sleep onset SD (P<.01) and SMSD (P=.01). No sleep metrics mediated the relation between race and BP dipping (all indirect effects P>.38). In conclusion, mediation pathways of sleep health metrics do not explain racial differences in nocturnal BP dipping between young BLW and WHW.

Worse sleep architecture but not self-reported insomnia and sleepiness is associated with higher cortisol levels in menopausal women

ObjectiveWorsening of sleep quality during menopause is well recognized. However, the underlying hormonal regulation is insufficiently described. In this study, we evaluated associations between sleep and cortisol levels. Study designSeventeen perimenopausal and 18 postmenopausal women were enrolled in a three-night sleep study. Diurnal blood sampling was performed during the third night and the following day. Main outcome measuresSelf-reported insomnia and sleepiness were evaluated with the Basic Nordic Sleep Questionnaire and sleep architecture with all-night polysomnography. Diurnal cortisol samples were collected at 20-min intervals. Correlation analyses and generalized linear models adjusted by age, body mass index, vasomotor symptoms and depressive symptoms were conducted. ResultsIn correlation analyses, self-reported insomnia and sleepiness were not associated with cortisol levels. Lower sleep efficiency, slow-wave sleep and stage 1 percentages, number of slow-wave sleep and of rapid-eye-movement (REM) periods, longer slow-wave sleep latency and higher wake after sleep onset percentage were associated with higher cortisol levels (all p < 0.05). Further, lower slow-wave sleep percentage and longer slow-wave sleep latency correlated with steeper daytime cortisol slope (i.e. day cortisol decrease, both p < 0.05). In adjusted generalized linear models, lower sleep efficiency and number of rapid-eye-movement periods as well as higher wake after sleep onset percentage correlated with higher cortisol levels; lower slow-wave sleep percentage correlated with higher cortisol awakening response. ConclusionsWorse sleep architecture but not worse self-reported insomnia and sleepiness was associated with higher cortisol levels. This is important for understanding sleep in women, especially during the menopausal period.

An Evaluation of DNA Methylation Levels and Sleep in Relation to Hot Flashes: A Cross-Sectional Study.

Objectives: We aimed to evaluate the DNA methylation levels in perimenopausal and postmenopausal women, measured through Long Interspersed Element-1 (LINE-1) and Alu, and the sleep parameters in relation to the presence of hot flashes (HFs). Methods: This cross-sectional study included 30 peri- or postmenopausal women aged between 45 and 55. The menopausal status was determined according to STRAW + 10 criteria and all participants had a low cardiovascular disease (CVD) risk profile determined by Framingham risk score. The sample was divided into two groups based on the presence or absence of HFs documented in their medical history during their initial visit: Group 1 (n = 15) with HFs present and Group 2 (n = 15) with HFs absent. The patients had polysomnography test and HFs were recorded both by sternal skin conductance and self-report overnight. Genomic DNA was extracted from the women's blood and methylation status was analyzed by fluorescence-based real-time quantitative PCR. The quantified value of DNA methylation of a target gene was normalized by β-actin. The primary outcome was the variation in methylation levels of LINE-1 and Alu and sleep parameters according to the presence of HFs. Results: LINE-1 and Alu methylation levels were higher in Group 1 (HFs present), although statistically non-significant. LINE-1 methylation levels were negatively correlated with age. Sleep efficiency was statistically significantly lower for women in Group 1 (HFs present) (74.66% ± 11.16% vs. 82.63% ± 7.31%; p = 0.03). The ratio of duration of awakening to total sleep time was statistically significantly higher in Group 1 (HFs present) (22.38% ± 9.99% vs. 15.07% ± 6.93, p = 0.03). Objectively recorded hot flashes were significantly higher in Group 1 (4.00 ± 3.21 vs. 1.47 ± 1.46, p = 0.03). None of the cases in Group 2 self-reported HF despite objectively recorded HFs during the polysomnography. The rate of hot flash associated with awakening was 41.4% in the whole sample. Conclusions: Women with a history of hot flashes exhibited lower sleep efficiency and higher awakening rates. Although a history of experiencing hot flashes was associated with higher LINE-1 and Alu methylation levels, no statistical significance was found. Further studies are needed to clarify this association. This study was funded by the Scientific Research Projects Coordination Unit of Istanbul University-Cerrahpasa. Project number: TTU-2021-35629.

A comparison of sleep, insomnia and health-related quality of life between mothers and fathers of preterm versus full-born infants: a longitudinal study from Norway

BackgroundPoor sleep may negatively affect parents’ health-related quality of life (HRQoL). This longitudinal study aimed to describe and compare sleep, insomnia and HRQoL in mothers and fathers of preterm and full-born infants, and to assess possible associations between sleep, insomnia, and HRQoL from birth up to 12 months in the total sample.MethodsA longitudinal study of parents of preterm (n = 25 couples) and full-born (n = 76 couples) infants was conducted. To assess sleep, parents wore wrist actigraphs and filled out sleep diaries for 2 consecutive weeks before responding to a digital questionnaire regarding insomnia symptoms and HRQoL. Actigraphy and sleep diary data were collected at the infant age of 2 months, while questionnaire data on insomnia and HRQoL were collected at the infant ages of 2, 6, and 12 months. Statistical analyses included linear regression and linear mixed models for repeated measures.ResultsThere were no statistically significant differences in total sleep time (actigraphy and sleep diary) between the parent groups (preterm and full-born) at 2 months postpartum. Sleep efficiency was significantly higher for the full-born group. All mothers reported significantly shorter total sleep time and lower sleep efficiency compared to fathers (all p < 0.01). In the whole sample, insomnia incidence at 2 months postpartum was high (> 43.5%), and for mothers, it remained high at 6 and 12 months (> 50%). No significant HRQoL differences were identified between the parent groups over time. Fathers in both groups reported significantly higher physical HRQoL levels compared to mothers (p = 0.04). There were no significant associations between total sleep time or sleep efficiency and HRQoL at 2 months postpartum. Insomnia symptoms were associated with reduced mental and physical HRQoL at all measurement points.ConclusionsSleep efficiency (actigraphy and sleep diary) was significantly higher for the full-born group compared to the preterm group. Mothers (both groups) experienced significantly shorter total sleep time and lower sleep efficiency compared to fathers. The incidences of insomnia symptoms were high at 2 months postpartum for the whole sample and remained high at follow-up for mothers. Fathers (both groups) reported higher physical HRQoL compared to mothers. Insomnia symptoms had a significantly negative impact on parents’ long-term HRQoL.

The sleep problems in individuals with Rett syndrome and their caregivers

Sleep problems are prevalent among individuals with Rett syndrome. We aimed to investigate sleep problems in individuals with Rett syndrome and their caregivers. A total of 29 participants diagnosed with Rett syndrome and their respective 29 caregivers were included. The Children Sleep Habits Questionnaire (CSHQ), the Pittsburgh Sleep Quality Index (PSQI), the Center for Epidemiologic Studies Depression Scale (CES-D), and the actigraphy data collected from Actiwatch 2 were used to investigate the change of sleep pattern. Based on the CSHQ questionnaire, 75.9% (22/29) of the patients reported sleep disturbances. The younger patients exhibited higher CSHQ scores. Actigraphy data revealed that both young and older patients had short total sleep duration, low sleep efficiency, long sleep-onset latency, long awaking duration, and fragmented sleep. The caregivers reported significantly higher PSQI scores, mildly declined sleep efficiency, and shorter total sleep duration in the actigraphy study. Associations were identified between smaller head circumference and shorter total sleep duration, more severe motor dysfunction and longer wake after sleep onset, worsen scoliosis and more awakenings per night. Sleep efficiency was inversely associated with epilepsy and positively associated with somatic growth. Sleep disturbances are common and should be investigated in individuals with Rett syndrome and their caregivers. Lay abstract Sleep problems are common and impactful among individuals with Rett syndrome (RTT) and their caregivers. We examined the sleep patterns of 29 RTT patients and their primary caregivers using various assessment tools. The study found that a majority of the patients experienced sleep disturbances, with younger patients showing more sleep difficulties. Caregivers also reported poor sleep quality. The findings emphasize the need to address sleep problems in RTT management, as improving sleep quality can positively impact the well-being of individuals with RTT and their caregivers.

Sleep disturbance in children with attention-deficit hyperactivity disorder: relationship with melatonin and behavior

ABSTRACT Aim To evaluate the prevalence and types of sleep problems and their correlations with melatonin content and behavior in Attention-Deficit Hyperactivity Disorder (ADHD) children. Method Sleep in ADHD children and typically developing children (TD) aged 6–14 was assessed by the Sleep Disorders Scale for Children (SDSC) and actigraphy, salivary melatonin quantified by ELISA, and behavior was analyzed using the Strengths and Difficulties Questionnaire. Results ADHD children showed a higher frequency of sleep disturbances, higher sleep latency, and lower sleep efficiency than in the TD group. The ADHD group presented lower melatonin nocturnal content compared to the TD group. Disorders of Initiating and Maintaining Sleep (DIMS) was moderately associated with nocturnal melatonin. The total behavior difficulties were correlated with Disorders of Initiating and Maintaining Sleep (DIMS), Sleep/Wake Transition Disorders (SWTD), Disorders of Excessive Somnolence (DES), Sleep Hyperhidrosis (SHY) and Total SDSC Score. The behavior was the only determinant of the total SDSC score (R2 = 0.499; p < 0.002). Conclusion This study provides, for the first time, evidence that among the frequent sleep disturbances in ADHD, the disorders in initiating and maintaining sleep are associated with the low levels of melatonin found in this population. Additionally, these, along with other sleep disturbances, are linked to behavioral problems in ADHD.