Journal of Sleep Research最新文献

Multimorbidity and cognitive decline are highly prevalent among older adults. Although sleep disturbances are known to be associated with both conditions, the underlying mechanisms connecting multimorbidity to cognitive impairment remain poorly understood. To address this gap, a multi-center, population-based cross-sectional study was conducted to investigate the potential mediating role of sleep quality in the relationship between multimorbidity and cognitive decline. From June 2023 to March 2024, a total of 3574 community-dwelling adults aged 65 years or older were recruited from eight communities in Shanghai. After excluding participants with missing data (n = 672), the final analytical sample comprised 2902 individuals. Data were analysed using R Statistical Software. Among the 2902 participants (mean age 73.8 ± 7.9 years), fully adjusted models revealed two key findings: first, a significant association was observed between multimorbidity and cognitive decline (odds ratio = 1.152 per unit increase in the Chinese Multimorbidity Weighted Index); and second, sleep quality mediated 12.1% of this relationship (p = 0.004), a result that was confirmed through bootstrap validation for robustness. In conclusion, sleep quality partially mediates the positive association between multimorbidity burden and cognitive decline, accounting for approximately one-eighth of the total effect.

The international Swiss Primary Hypersomnolence and Narcolepsy Cohort Study (iSPHYNCS) is a multicentre study aimed at identifying novel biomarkers for central disorders of hypersomnolence (CDH). We analysed questionnaires and metadata to uncover distinct clusters of participants and explore phenotypic variability within CDH. Data were collected from 227 patients with CDH and 33 healthy controls. Participants completed validated clinical questionnaires and study-specific questions addressing CDH-related symptoms such as excessive daytime sleepiness, fatigue, cataplexy, disrupted sleep, and sleep paralysis. Demographic metadata (age, gender, BMI) were included. After excluding participants with missing over 30% of data (n = 40), missing values were imputed using a multiple random forest algorithm. A robust clustering pipeline was employed: (1) random sampling of 60% of the dataset, (2) dimensionality reduction via UMAP, (3) K-means clustering, and (4) consensus clustering across 500 iterations. Post hoc analysis was performed to identify biomarkers in data not used for clustering. We identified four distinct clusters. One predominantly comprised healthy controls, while another primarily contained individuals with narcolepsy type 1 (NT1). Two clusters represented predominantly the narcolepsy borderland group (NBL), with one distinctly characterised by higher symptom severity and psychiatric comorbidities. The clustering pipeline produced reproducible results, with the NT1 and healthy control clusters serving as internal validation. The differentiation between the two NBL clusters aligns with prior studies, suggesting a possible NBL subtype marked by increased fatigue and psychiatric comorbidities. These findings emphasise the phenotypic heterogeneity of CDH and the potential for cluster-based approaches in management. Trial Registration: ClinicalTrials.gov identifier: NCT04330963.

Sleep is fundamental for infant development and health, playing a critical role in cognitive, socio-emotional, and physical growth. However, environmental factors can impact the quality and duration of sleep in infants. This review synthesises current evidence on the associations between environmental chemical exposures and infant sleep outcomes, with a focus on the first 1000 days of life. Infants may be exposed to environmental pollutants before birth, through the placenta, or after birth, via breastfeeding, diet, and external sources such as inhalation, dust contact, or hand-to-mouth exposure. Given their ongoing development, foetuses and infants are particularly vulnerable to these pollutants. This period of rapid growth and maturation represents a highly sensitive window for environmental exposures. This review covers various categories of environmental pollutants, including persistent organic pollutants (PCBs, dioxins), non-persistent pollutants (phthalates, BPA), air pollutants (particulate matter, second-hand smoke), and water contaminants (nitrates, microplastics). Environmental chemicals exposure could be assessed using parental questionnaires or biological monitoring, while sleep is evaluated using actigraphy, polysomnography, or parental reporting. Some evidence suggests that both prenatal and postnatal exposure to environmental contaminants may be associated with sleep disturbances in children, particularly in girls. Despite the numerous studies on adults and the mechanisms associated with these pollutants (neurotoxicity, endocrine disruption), which suggest an effect on sleep, there is a lack of studies in children, resulting in limited associations in the literature. Therefore, it is imperative to conduct studies on environmental pollutants present in breast milk, diet, and/or ambient air to understand their impact on infant sleep.

Sleep is increasingly understood as a socially embedded phenomenon. This study examined how structural and functional aspects of social support, as well as loneliness, relate to sleep health in a German sample of middle-aged adults (N = 5388). Drawing on the socio-ecological model of sleep health, we assessed the contributions of social support dimensions while accounting for age, sex, and socioeconomic status, as well as psychological covariates. The results of the binary logistic regression showed that functional support (ESSI), friend network size (LSNS6), and loneliness (CES-D item 14) significantly (p < 0.001) predicted sleep health (PSQI), while family network size did not. The portion of explained variance was small (4%-5%). Results remained robust after adjusting for age, sex, and socioeconomic status, but no longer when including psychological covariates (GAD-7, SWLS, CES-D), in which case only the friend network size remained significant (p = 0.019). Women were significantly more affected by poor sleep health than men, and with higher socioeconomic status, fewer people reported suffering from poor sleep (all: p < 0.001). Additional subgroup analysis revealed higher age as a risk factor for worse sleep health in women only, while the friend network was only relevant in men. Our findings highlight the importance of distinguishing between structural and functional dimensions of social support in sleep health research and interventions, and suggest a potential sex-by-age interaction. Future research should promote equity by including diverse populations and longitudinally examine how social support, especially friend networks, affects sleep across genders, ages, and contexts.

Distinguishing non-epileptic events from epileptic seizures remains a clinical challenge, particularly when occurring exclusively during sleep. Sleep-related rhythmical movement disorder (SRRMD) is a benign condition typically seen in early childhood, characterised by stereotyped, rhythmical repetitive movements involving large muscle groups, predominantly during Stage II of non-REM sleep. These movements can closely mimic features of sleep parasomnias, hypermotor seizures or psychogenic non-epileptic seizures (PNES), complicating the diagnostic approach. We present a case of an adolescent female with comorbid SRRMD and PNES and a clinical approach to distinguish between them.

Insomnia is the most prevalent sleep disorder, affecting up to one third of the adult population and is increasingly recognised as a potential contributor to cardiovascular disease (CVD), a leading cause of global morbidity and mortality. This narrative review examines the complex relationship between insomnia and CVD, integrating epidemiological, genetic and mechanistic evidence to assess whether insomnia represents a causal cardiovascular risk factor. Large prospective cohort studies and meta-analyses consistently show that insomnia symptoms and clinically diagnosed insomnia are associated with increased risks of hypertension, myocardial infarction, stroke, heart failure and cardiovascular mortality, with stronger associations observed in individuals with short sleep duration or persistent insomnia. Mendelian randomization studies involving millions of participants further support a likely causal link, suggesting that genetic liability to insomnia increases the risk of multiple cardiometabolic outcomes. Biological plausibility is supported by evidence of autonomic imbalance, hypothalamic-pituitary-adrenal axis activation, inflammation and adverse blood pressure profiles in individuals with insomnia. However, insomnia is a heterogeneous condition, frequently coexisting with other sleep disorders and influenced by psychosocial and circadian factors, which complicates causal inference. Importantly, evidence that treatment of insomnia reduces cardiovascular risk remains limited. While cognitive behavioural therapy for insomnia improves sleep outcomes and some cardiometabolic biomarkers, randomised trials have not demonstrated clear benefits on blood pressure or other cardiovascular endpoints and some pharmacological treatments may even be associated with harm. Overall, current evidence suggests that insomnia is a plausible and potentially causal risk factor for CVD, but definitive proof of reversibility through treatment is lacking. Well-powered, rigorously designed trials targeting patients with clinically defined insomnia are needed to determine whether effective insomnia treatment can meaningfully reduce cardiovascular risk and inform future prevention strategies.

Preterm birth is a significant risk factor for atypical neurodevelopment, yet early electrophysiological markers of brain maturation are still lacking. Non-invasive electroencephalographic (EEG) monitoring of cortical maturation in these patients holds promise as a tool for neurodevelopmental prediction. However, its clinical application is limited by technical challenges in maintaining stable, long-term electrode placement on very small neonate scalps and by the highly specialised, multi-level expertise required to care for these fragile patients. Using video-polysomnographic EEG recordings in very low birth weight (VLBW, < 1500 g) preterm infants, we characterised large-scale neuronal dynamics during distinct vigilance states and tested whether they could serve as indicators of early cortical maturation. We analysed EEG recordings obtained at 33.9 ± 1.4 weeks postmenstrual age (PMA), during active sleep (AS), sleep onset active sleep (SOAS), quiet sleep (QS), and quiet wakefulness (QW). For each vigilance state, we assessed large-scale neuronal dynamics in terms of phase synchronisation, neuronal bistability, and local phase-amplitude coupling (PAC), both globally and separately for anterior and posterior regions, and correlated them with PMA. We found that phase synchronisation peaked in the δ band during QS and in the θ band during more active states (QW, SOAS, AS). δ-band bistability was lower in posterior regions across all states, while δ-PAC was lower posteriorly during sleep but reversed during wakefulness. Also, bistability and PAC decreased with advancing PMA. These findings suggest that vigilance-state-dependent neuronal dynamics capture aspects of early cortical maturation-even with low-density EEG cap-offering novel candidate biomarkers to monitor neurodevelopment in infants born preterm.

Declarative memories are reactivated-and thereby consolidated-during sleep. Real-life memories are typically nested hierarchically (e.g., memory for making coffee nested within memory for one's morning routine). We tested the specificity of memory reactivation during sleep in humans: is it limited to low-tier items or does it extend to wider contexts? To test this, we adapted a well-replicated design using targeted memory reactivation, which uses non-invasive sensory cues to preferentially reactivate memories during sleep. Thirty-two participants (18 women and 14 men) learned two sets of object locations, each paired with a unique odour. By cueing one odour during non-REM sleep, we tested whether reactivation would benefit the entire learning context or selectively enhance the cued set. Our results show no overall benefit for the cued set over the non-cued one. A more nuanced, encoding-strength-dependent reactivation effect was observed for the cued category relative to the non-cued one. Whereas previous studies showed that odour presentation increased spectral activity in the sigma range, putatively reflecting sleep spindles, we found a sustained (~15 s) inhibition following presentation. The results indicate that cueing did not uniformly benefit the targeted memories. One explanation for these results is that cueing benefits may have generalised across the learning context as a whole rather than impacting a single set of memories. Moreover, our results provide more evidence that initial encoding strength dictates the extent of reactivation effectiveness.

Adolescents frequently use smartphones, smartwatches, personal computers, tablets, and other electronic devices during the day and at night. Whilst these devices are kept close to the eyes, they emit artificial light at night (ALAN) and generate noise. ALAN and noise are also emitted from other indoor and outdoor sources, such as home appliances, road traffic, street lighting, and advertising boards. However, the effect of these exposures has been studied mainly in the adult population, and little is known about their combined effect on adolescents. The present study aims to bridge this knowledge gap by examining the combined effect of ALAN and noise on the quality of sleep of junior high and high school students. Study participants included 81 adolescents (age 13-18 years) living in Tamra, a town in northern Israel. A 41-day experiment was carried out during which participants wore smartwatches, connected to Android smartphones, to monitor their exposures to ALAN and noise and their sleep patterns. The collected data were then analysed using statistical tools and showed that an increase in ALAN in a plausible range of 40-150 lx before sleep is estimated to reduce sleep efficiency (SE), all other factors being constant, by ~18% (t < -16, p < 0.01), whilst an increase in noise from 30 to 60 dB was estimated to reduce SE by ~22% (t < -14, p < 0.01). These estimates are higher than those found for the adult population in previous studies, according to which the effects of these environmental risk factors on sleep duration and quality were estimated to be ~8%-9%.

This study aimed to assess caregivers' awareness, use and acceptability of common infant behavioural sleep strategies/interventions and explore differences in awareness and acceptability based on country of residence. A cross-sectional online survey was conducted with caregivers (n = 914) of infants aged between 6 and 18 months residing in Australia, Canada, Turkey, the United Kingdom and the United States. Caregivers were provided descriptions of common infant behavioural sleep interventions and reported their awareness of, use, and level of acceptability (using a validated measure: the acceptability of intervention measure [AIM]) for each intervention. Awareness of interventions ranged from 50% to 70% of caregivers, with significant variability by country. Overall, 70% of caregivers had used at least one intervention, with usage rates varying from 25% to 80% depending on the intervention and 30% to 55% of caregivers ceasing use prematurely. Unmodified extinction (AIM = 2.12; 5 = high acceptability), parental presence (AIM = 2.75) and modified extinction (AIM = 2.85) had lower levels of acceptability compared to responsive settling with gradual reduction (AIM = 3.48) and response-based with settling in arms (AIM = 3.51) and bed (AIM = 3.23). Significant differences in acceptability (AIM) scores by country were evident for most of the interventions. As none of the interventions were universally acceptable, a model of care that provides caregivers with information about a range of interventions and the opportunity to choose based on their preferences, parenting styles and cultural beliefs may increase the likelihood of successful intervention adoption.