Respiratory frequency is a critical biomarker in sleep medicine and circadian biology. We investigated whether the high-frequency (HF) component of heart-rate variability (HRV)—which reflects respiratory sinus arrhythmia (RSA)—can serve as a non-invasive proxy for breathing rate estimation from ECG or PPG. We employed a two-stage validation design: (1) a physiologically calibrated simulation study (N = 30 per condition, five conditions, 180 s recordings) for controlled error characterization using the PhysioNet ECG-ID Database (Electrocardiogram Identification Database, DOI: 10.13026/C2XW26) as the processing pipeline reference; and (2) pilot real-data validation in N = 10 older adult participants (mean age 71.3 years) with simultaneous ECG and thermistor respiratory reference measured using the East Medic Biotope Mini (1000 Hz). Results: Under controlled resting conditions, simulation yielded MAE = 0.46 bpm (SNR = 4.8). An empirical error formula MAE = 2.017 × SNR^(−1.187) (R2 = 0.71) was derived. In the real-data validation, 4/10 participants achieved MAE ≤ 2.0 bpm; the remaining 6/10 showed errors of 6–17 bpm attributable to non-respiratory HF oscillations, harmonic confusion, and breathing rate variability. The HF-peak method is reliable when SNR is high and breathing is regular but requires additional quality criteria beyond SNR alone in older adult populations where non-respiratory HF oscillations may confound spectral peak detection.
Professional drivers are exposed to work conditions that may affect sleep quality. Although poor sleep quality has been associated with lower mental health (MH) and vitality (VT), its relationship with these outcomes in professional drivers remains unclear. This cross-sectional study examined the association between sleep quality and selected health-related quality-of-life (HRQoL) domains among 399 professional drivers. Sleep quality was assessed using the Pittsburgh Sleep Quality Index (PSQI). At the same time, HRQoL was evaluated using the Mental Health, Vitality, and Bodily Pain domains of the 36-Item Short Form Health Survey. Correlation and regression analyses were performed. The mean PSQI score was 8.59, indicating overall poor sleep quality. Higher PSQI scores were negatively associated with MH (ρ = −0.384, p < 0.001) and VT (ρ = −0.495, p < 0.001). Sleep quality remained an independent predictor of MH (B = −2.47, p < 0.001; R2 = 0.155) and VT (B = −4.10, p < 0.001; R2 = 0.268), whereas age showed a modest association only with VT (B = −0.235, p = 0.035). Poor sleep quality was associated with lower MH and VT scores among professional drivers. The stronger association observed for VT suggests that sleep quality may be particularly relevant to energy levels and daily functioning in this study population.
Obstructive sleep apnea (OSA) is associated with renin-angiotensin-aldosterone system (RAAS) dysregulation. This study examined the relationship between salivary aldosterone and OSA severity, identified predictors of salivary aldosterone, evaluated the moderating role of mean arterial pressure (MAP), and compared the diagnostic performance of salivary aldosterone with the STOP-BANG questionnaire. This cross-sectional study included 67 adults grouped as healthy or mild OSA (apnea-hypopnea index [AHI] < 15; n = 34) versus moderate-to-severe OSA (AHI ≥ 15; n = 33). Morning salivary aldosterone was measured using enzyme-linked immunosorbent assay. Generalized linear models assessed independent predictors, MAP moderation was tested using PROCESS Model 1, and diagnostic performance was evaluated using receiver operating characteristic analysis. Salivary aldosterone did not differ between OSA severity groups and showed poor diagnostic performance. Age was negatively associated with aldosterone levels, while MAP moderated the relationship between AHI and salivary aldosterone. In contrast, the STOP-BANG questionnaire demonstrated acceptable discriminative ability and significantly higher specificity. Salivary aldosterone is not a reliable standalone OSA screening biomarker. However, MAP moderated the OSA-aldosterone relationship, suggesting potential utility in OSA patients with elevated MAP. Age independently predicted lower aldosterone, likely reflecting age-related RAAS decline. These findings support selective utility of salivary aldosterone in OSA patients with elevated blood pressure.
BACKGROUND:Sleep quality plays an essential role in cognitive performance, memory consolidation, learning efficiency, and overall wellbeing. University students are particularly vulnerable to sleep disturbances because of academic stress, irregular sleep schedules, and lifestyle-related factors. Poor sleep quality has been associated with impaired academic performance and reduced cognitive functioning. OBJECTIVE:This study aimed to evaluate the relationship between sleep patterns, sleep quality, and academic performance among female university students. METHODS:A cross-sectional study was conducted among 201 female university students at Qassim University, Saudi Arabia. Data were collected using an electronic self-administered questionnaire that included demographic characteristics, sleep-related behaviors, and the Pittsburgh Sleep Quality Index (PSQI). Academic performance was assessed using self-reported Grade Point Average (GPA). Statistical analysis included descriptive statistics, Spearman correlation analysis, one-way ANOVA with Tukey post hoc analysis, Chi-square tests, and multiple linear regression analysis. RESULTS:The mean GPA of the participants was 4.13 ± 0.60 (on a 5-point scale), while the mean PSQI score was 8.81 ± 3.26, indicating generally poor sleep quality. A significant negative correlation was observed between PSQI score and GPA (rho = -0.200, p = 0.0047). Students with good sleep quality demonstrated significantly higher GPA scores compared with students with poor sleep quality (F(2,194) = 6.31, p = 0.0022). Significant associations were also identified between sleep quality and both bedtime (p = 0.0009) and sleep duration category (p = 0.0002). However, after adjustment for other variables, the independent effect of PSQI on GPA was attenuated and did not reach statistical significance (p = 0.138). This discrepancy between the significant bivariate correlation (rho = -0.200, p = 0.005) and the non-significant multivariate result represents the most important finding of this study, suggesting that sleep quality alone does not independently predict GPA when other academic and behavioral factors are considered. CONCLUSION:Poor sleep quality was highly prevalent among female university students and showed a significant bivariate association with lower academic performance, though this relationship was attenuated in the multivariate model. Promoting healthy sleep behaviors may support student wellbeing and academic functioning, cognitive wellbeing, quality of life, and the advancement of Sustainable Development Goal 3 (Good Health and Well-Being).
Rising global temperatures and more frequent heat waves pose a growing threat to public health, particularly among older adults. Age-related declines in thermoregulatory capacity such as reduced sweating, impaired vasodilation, and diminished hypothalamic responsiveness make it more difficult to cope with elevated nighttime temperatures. These thermal challenges disrupt sleep by prolonging sleep onset, fragmenting slow-wave and REM sleep, and suppressing melatonin secretion. Importantly, sex-related differences in thermoregulatory aging-particularly menopause-associated vasomotor instability in women and testosterone-related autonomic changes in men-further modulate individual vulnerability to heat-induced sleep disruption. Beyond sleep, heat-induced stress affects metabolic, cardiovascular, and immune systems, promoting insulin resistance, endothelial dysfunction, sympathetic overactivation, and chronic inflammation. Socioeconomic disparities, urban heat island exposure, and differential access to cooling infrastructure function as critical environmental modifiers that amplify biological vulnerability, particularly in disadvantaged older populations. This narrative review aims to synthesize current knowledge on the specific thermoregulatory mechanisms of sleep disruption induced by heat stress in older adults. Understanding these interactions is crucial for developing effective interventions, including environmental cooling, circadian-aligned behaviors, and targeted public health strategies, to mitigate the compounded risks of heat exposure and preserve healthy sleep in aging populations. However, many proposed mechanistic pathways are primarily derived from animal models, and controlled human studies specifically targeting heat-exposed older adults remain scarce.
Heatwaves and tropical nights are emerging as significant public health challenges under accelerating climate change, with middle-aged and older adults demonstrating heightened vulnerability. This scoping review maps the existing evidence on how nocturnal heat affects sleep in middle-aged and older adults aged 45 and above, synthesizing findings from experimental and observational studies published in English over the past decade. A comprehensive search of PubMed and Scopus, supplemented by reference screening, identified 31 relevant studies. Data on study design, population characteristics, heat exposure metrics, sleep outcomes, and interventions were charted and synthesized narratively due to methodological heterogeneity. Across studies, elevated nighttime temperatures consistently reduced total sleep time and sleep efficiency, increased wake after sleep onset, and disrupted sleep architecture, particularly REM and N3 stages. Environmental, behavioral, and physiological interventions such as improved ventilation, targeted cooling strategies, and pre-sleep thermal management partially mitigated heat-related sleep disruption. Overall, the findings highlight gaps in standardized exposure metrics and harmonized sleep assessment, providing guidance for future research and public health strategies aimed at protecting sleep health in middle-aged and aging populations amid increasingly frequent extreme heat events.
Circadian rhythms, sleep homeostasis, and chronotype interact to modulate cognitive processes such as attention and executive functions, leading to fluctuations in performance throughout the day and significant impairments under conditions of misalignment or sleep deprivation. The study was conducted in two phases and included the assessment of subjective measures of sleepiness, vigor, affect, sleep quality, and individual chronotype. In the first phase, 32 healthy participants (19 females; mean age = 24.9 ± 3.14) were tested at four different times of the day to examine diurnal variations in attentional performance. In the second phase, a subsample of 8 participants (4 females; mean age = 24.4 ± 2.20) underwent a total sleep-deprivation protocol and completed the AD-Task over two consecutive days to evaluate the impact of prolonged wakefulness on attentional and executive functioning. In the first phase, results revealed a progressive decline in selective attention across the day (F(3.93) = 3.188; p = 0.027; η2p = 0.093) and significantly slower reaction times in divided attention during the morning (F(3.93) = 7.3134; p < 0.001; η2p = 0.191), indicating a time-of-day modulation of attentional resources. In the second phase, total sleep deprivation led to a marked impairment in performance, reflected by slower reaction times (F(11.77) = 1.948; p = 0.046; η2p = 0.218) and reduced discriminative ability (d'; F(11.77) = 13.438; p < 0.001; η2p = 0.657), particularly in task-switching conditions. These findings suggest increased vulnerability of executive functions under sleep deprivation, likely associated with reduced efficiency of prefrontal cortical processes. The results confirm that time of the day and pressure of sleep significantly affect attention and cognitive flexibility and further affirm the validity of the AD-Task as a reliable instrument for detecting these variations under ecologically relevant conditions.
Internalized weight bias-the self-directed endorsement of weight-related stereotypes-has emerged as a psychologically potent correlate of health outcomes in individuals with overweight and obesity, yet its relationship with sleep remains largely unexplored. In a cross-sectional manner, 495 Greek adults with a history of overweight/obesity were assessed regarding sleep quality and duration, internalized weight bias (Modified Weight Bias Internalization Scale; WBIS-M), and expressed anti-fat attitudes (Anti-Fat Attitudes Questionnaire, AFA: Dislike, Fear of Fat, Willpower). Insomnia prevalence, assessed with the Athens Insomnia Scale (AIS), was high at 57.6%-nearly doubling across ascending WBIS-M tertiles (39.9% to 73.1%). In hierarchical linear regression models, AIS score remained independently associated with WBIS-M after adjustment for depression, anxiety, BMI, and a comprehensive range of sociodemographic and clinical covariates (B = 0.058; 95% CI: 0.036-0.079; p < 0.001), with the fully adjusted model explaining 58.5% of total variance in WBIS-M. AFA subscales did not remain significant in the model post-full adjustment, and sleep duration failed to show independent association with either bias dimensions. The sleep-weight bias association was therefore specific to the internalized dimension and to sleep quality, rather than quantity. These findings highlight a clinically relevant and dimension-specific link between insomnia symptoms and internalized weight stigma, and suggest that routine sleep assessment may be warranted in individuals with a history of overweight or obesity presenting with elevated internalized weight bias-and vice versa.
Melatonin occupies a paradoxical position in contemporary sleep medicine: despite its physiological role as a regulator of circadian timing, it is frequently used and perceived as a nonspecific "natural" hypnotic. Although melatonin demonstrates modest benefits for sleep initiation and clearer efficacy in circadian rhythm sleep-wake disorders, its clinical use is often undermined by diagnostic imprecision, inappropriate dosing, mistimed administration, inconsistent formulations, and inadequate patient counseling. Circadian disorders can be misclassified as primary insomnia, leading to symptomatic treatment approaches that fail to address the underlying phase misalignment. At the same time, supraphysiological doses and reflexive bedtime administration have become normalized despite evidence that melatonin acts primarily as a chronobiotic whose effects depend more on timing than dose. Regulatory inconsistencies and substantial variability in over-the-counter preparations further complicate safe and reproducible use. These factors contribute to avoidable treatment failure, inaccurate labeling of nonresponse, and persistent misconceptions regarding melatonin's mechanism of action. Therefore, melatonin should be approached as a pharmacological intervention requiring the same diagnostic rigor, individualized dosing, and longitudinal assessment expected of other sleep therapeutics, particularly when integrated with behavioral and circadian interventions.
Sleep characteristics have been associated with body mass index (BMI) among adolescents, but population-representative evidence on sleep timing and variation across demographic subgroups remains limited. We conducted a cross-sectional analysis of 2017-2018 California Health Interview Survey data from 880 adolescents aged 12-17 years. Weeknight sleep duration was obtained from the CHIS-derived sleep-duration variable, based on reported school-night bedtimes and school-day wake times. Sleep-timing measures included bedtime, wake time, and the derived sleep midpoint. Pooled survey-weighted linear and logistic regression models used 160 jackknife replicate weights and adjusted for age, sex, race/ethnicity, household poverty category, and survey year; sensitivity models additionally adjusted for dietary and behavioral factors. Sleep duration was not associated with BMI overall (p = 0.161) or with the odds of having overweight or obesity (p = 0.36). The association between sleep duration and BMI varied by age group (p for interaction = 0.042). Each additional hour of sleep was associated with a lower BMI among adolescents aged 14-17 years (β = -0.895 kg/m2; 95% CI: -1.464 to -0.326; p = 0.002), but not among those aged 12-13 years. However, there was no evidence of an interaction when age was modeled continuously (p for interaction = 0.36). Bedtime, wake time, and sleep midpoint were not independently associated with BMI. Exploratory evidence that the association between sleep duration and overweight or obesity varied by race/ethnicity was attenuated after adjustment for dietary and behavioral factors (p for interaction changed from 0.04 to 0.05). In this cross-sectional study, neither sleep duration nor sleep timing was associated with BMI in the overall sample, and sleep duration was not associated with BMI-defined weight status. Subgroup findings were not consistent across model specifications and should be examined in longitudinal studies using objective and repeated measures of sleep.
Athletes often experience situations in which they do not obtain adequate sleep at night. One strategy to overcome this issue is to supplement nighttime sleep with a daytime nap. However, little is known about how well athletes sleep during daytime naps. The aims of this study were to (i) determine the ability of athletes to fall asleep during an afternoon nap and (ii) examine the composition of the sleep obtained. In a counterbalanced, repeated-measures cross-over design, 12 young male semi-professional soccer players were given a 1 h (15:00-16:00) or 2 h (14:00-16:00) nap opportunity following a normal night's sleep (7-8 h time in bed) in a laboratory. Sleep was monitored using polysomnography and variables were compared between naps using generalized estimating equation models. In the 1 h nap, participants took 6.5 min to fall asleep and spent 52/60 min asleep (87% efficiency); in the 2 h nap, participants took 7.5 min to fall asleep and spent 105/120 min asleep (87% efficiency). There was no difference in wake after sleep onset (p = 0.168) or time spent in stage N3 sleep (p = 0.110) between the 1 h and 2 h nap, but participants fell asleep faster (p < 0.001), obtained more sleep (p < 0.001), and spent more time in stage N1 sleep (p = 0.003), stage N2 sleep (p < 0.001), and Stage REM sleep (p = 0.004) in the 2 h nap. Athletes sleep well during 1 h and 2 h afternoon naps and could use this as a strategy to help meet sleep duration recommendations (i.e., 7-9 h).
Human African trypanosomiasis (HAT) or sleeping sickness is a neglected tropical disease with a progressive central nervous system (CNS) involvement and marked sleep and circadian rhythm abnormalities. Even though this is a prominent feature of HAT, the connection between parasite neuroinvasion, neuroinflammation, circadian dysfunction, and neurological impairment is not fully understood. This narrative review aims to summarize the most up-to-date knowledge about sleep and circadian disturbance in HAT and proposes an integrated approach for the Trypanosome-Associated Sleep Disorder (TASD). The relevant literature was identified by searching major biomedical databases for HAT, sleep disorders, circadian rhythms, neuroinflammation, and CNS invasion. The review covers the steps by which the CNS becomes invaded, how the barriers are disrupted, how the CNS becomes activated by inflammatory responses, and how the hypothalamic and circadian regulatory networks are disrupted. The evidence suggests that excessive daytime sleepiness, fragmented nocturnal sleep, circadian misalignment, and neuropsychiatric manifestations are related to the activation of inflammatory cytokines, altered neurotransmitter signaling, activation of the kynurenine pathway, dysregulation of clock genes, and disruption of the suprachiasmatic nucleus. We also discuss TASD as a syndrome-like phenotype of CNS involvement and propose a three-stage model of sleep-wake dysfunction in HAT. The review unites these integral mechanisms in a single mechanistic framework to offer a unified understanding of the sleep pathology associated with HAT. There are still important gaps in our knowledge of biomarkers, disease staging, and irreversible neuronal damage, which indicate priorities for future research and better clinical management.
The belief that the moon disturbs sleep is widespread, but the factors associated with it remain poorly understood. I therefore examined how frequently poor sleep is attributed to moon phases, whether this varied across the lunar cycle, and which personal and environmental factors were associated with “moon blaming”. Data were derived from an ongoing online survey. At the time of analysis, 1815 participants had completed a 16-item questionnaire assessing sleep quality, sleep duration, sleep timing on workdays and free days, alarm clock use, environmental and personal sleep-disturbing factors, residential setting, age, gender, attention to lunar phases, and whether the moon was perceived as a cause of poor sleep. The primary outcome was endorsement of the moon as a sleep-disturbing factor. Logistic regression with stepwise Akaike information criterion selection was used to identify the strongest predictors of attributing the moon for poor sleep. Questionnaire timing was also examined across the lunar cycle. Among environmental factors, the moon was the most frequently endorsed cause of poor sleep (36%), followed by outdoor temperature (31%), indoor noise (26%), and bad weather (22%). Rumination was the most commonly reported personal factor (73%), but it did not predict moon attribution. Instead, the strongest correlates were weather-related sleep complaints, tracking lunar phases, age, and gender, with endorsement increasing with age and being more common among women. Moon-related complaints also peaked during the week after the full moon. These findings suggest that perceived lunar effects on sleep are shaped, at least in part, by attributional and expectation-related processes.
The rest-activity rhythm (RAR) is a key marker of circadian regulation and is commonly assessed using actigraphy. Emerging evidence suggests that characteristics of RAR, such as amplitude, stability, and regularity, may be associated with pain-related outcomes. However, no systematic review has yet synthesized this evidence across populations and pain conditions. This systematic review aimed to provide an overview of current approaches to measuring and defining RAR and to examine its associations with pain outcomes in both healthy individuals and clinical populations experiencing acute or chronic pain. A systematic search of PubMed, Web of Science, Scopus, and Embase was conducted, with the final search completed on 20 May 2025. Observational studies reporting associations between at least one RAR characteristic and a pain outcome were eligible. Article selection and risk-of-bias assessment using the ROBINS-E tool were performed independently by two reviewers, and findings were synthesized narratively. Seven cross-sectional studies were included, employing diverse analytic methods such as cosinor and non-parametric analyses. Overall, the findings were heterogeneous, suggesting that associations between RAR and pain vary according to the RAR metric used, the analytical approach, and the population studied. Nevertheless, the evidence generally indicates that more robust and well-consolidated circadian rhythms are associated with lower pain, whereas regularity and timing appear to play more context-dependent roles, highlighting the potential relevance of RAR metrics as modifiable targets and the need for standardized measurement approaches.
Population-based evidence on sleep quality in Kazakhstan remains limited. This study describes sleep quality as a multidimensional construct among adults in Kazakhstan using data collected during the first national survey wave after the adoption of a single national time zone. The survey was designed as a national post-transition baseline assessment and not as an evaluation of the causal impact of the time-zone reform. Associations with socio-demographic, behavioural, clinical, and regional factors were examined. We conducted a nationally representative cross-sectional survey of adults aged 18-69 years in Kazakhstan from May to October 2025 using a multistage stratified cluster design. Sleep quality was assessed with the Pittsburgh Sleep Quality Index (PSQI). Poor sleep quality was defined as a global PSQI score > 5. Complete PSQI data were available for 5872 participants. Descriptive analyses examined the global PSQI score and the seven component scores. Survey-weighted multivariable logistic regression was used to identify factors independently associated with poor sleep quality. The weighted prevalence of poor sleep quality was 28.1%, and the weighted mean global PSQI score was 4.43. The greatest component burden was attributable to sleep latency (mean 0.87), subjective sleep quality (0.82), and sleep disturbances (0.80), whereas use of sleep medication contributed minimally (0.11). Poor sleep quality was more common among women, older adults, urban residents, and participants with diabetes, current smoking, heavy episodic drinking, and depressive symptoms. In the adjusted model, female sex (aOR 1.37, 95% CI 1.19-1.57), age 55 years or older versus 18-24 years (1.98, 1.53-2.55), diabetes (1.47, 1.22-1.78), current smoking (1.28, 1.10-1.50), heavy episodic drinking (1.43, 1.16-1.76), and depressive symptoms (4.26, 3.52-5.15) were independently associated with higher odds of poor sleep quality. Rural residence was inversely associated with the outcome (0.71, 0.61-0.84). Compared with the North, higher odds were observed in the Central region (2.00, 1.46-2.74), East (1.94, 1.48-2.53), West (1.48, 1.17-1.88), and Almaty city (2.18, 1.72-2.76). Poor sleep quality is common among adults in Kazakhstan and is characterized primarily by difficulties with sleep initiation, perceived sleep quality, and nocturnal disturbances. The findings provide national post-transition baseline evidence and suggest that sleep health surveillance in Kazakhstan should prioritize demographic, mental health, behavioural, and regional inequalities while avoiding causal interpretation of the time-zone reform itself.
The current use of artificial light during the natural dark phase has acquired contaminant dimensions, known as "light pollution". It is well known that exposure to dim light at night (dLAN) during the postnatal period severely impairs the immune system and related organs, but few reports have demonstrated the effects of dLAN during the fetal period. This study, therefore, examines whether exposure to dim light at night during two critical developmental windows (i.e., prenatal and postnatal periods) leads to long-lasting dysregulation of circadian, behavioral, and immune organization, as well as spleen immune responses, in early adulthood. To address this question, these outcomes were assessed using two defined sampling time points. To answer this question, we exposed two groups of C57BL/6J male mice to dim night light during the gestational and postnatal periods and compared them with control groups that were exposed to light-dark conditions (12 h each, LD). Parametric and non-parametric activity/rest values were analyzed with circular statistics. Compared to their controls, we found differences in alpha, onset, offset, M10, and L5 start time in dLAN groups. We also assessed the transcript levels of clock genes and inflammatory mediators in spleen tissue and found a dampening of daily variation in mRNA expression in both experimental groups. Finally, we used an ovalbumin (OVA) allergy challenge to test the B-cell response in the spleen and found a significantly higher cell recruitment to the spleen and more anti-OVA IgE. Together, these results clearly show that dLAN, at two ZT sampling points, affects peripheral molecular clocks and responses in the spleen, and that these effects are independent of the life stage at which exposure to dim light at night occurs.
Sleep disturbances and poor sleep quality are growing public health concerns, adversely affecting both physical and mental health. While exogenous melatonin supplements are used to manage the condition, there is limited evidence available on the efficacy of sustained-release (SR) melatonin formulations. This multicenter, randomized, double-blind, placebo-controlled clinical trial evaluated the efficacy and safety of melatonin-SR capsules (2 mg) in healthy adults with poor sleep quality. Participants aged 30-60 years with poor sleep quality received melatonin-SR (2 mg) or a placebo capsule at night for 28 days. Changes from baseline to day 28 in polysomnography (PSG)-derived sleep parameters, Pittsburgh Sleep Quality Index (PSQI), WHO-5 Well-Being Index, sleep diary parameters, and safety profile were evaluated. Of 62 enrolled participants, 59 (melatonin-SR, n = 28; placebo, n = 31) completed the study. Compared with placebo, melatonin-SR supplementation resulted in significant improvements at day 28 in PSG-derived sleep efficiency (change from baseline: 3.49 for melatonin-SR vs. -6.30% for placebo; p = 0.001) and total sleep time (change from baseline: 23.83 for melatonin-SR vs. -39.25 min for placebo; p = 0.001), along with significant reductions in sleep onset latency (change from baseline: -10.28 for melatonin-SR vs. 16.70 min for placebo; p = 0.031) and wake after sleep onset (change from baseline: -14.92 for melatonin-SR vs. 24.71 min for placebo; p = 0.001). Melatonin-SR supplementation demonstrated a large treatment effect for the improvement in sleep efficiency compared with placebo (Cohen's d = 0.9). A significant reduction in PSQI global scores was observed in the melatonin-SR group from day 07 onwards (change from baseline on day 07: -2.21 vs. -0.23; day 14: -4.86 vs. -0.65; and day 28: -5.61 vs. -0.65 for melatonin-SR and placebo, respectively; p = 0.001). Improvement in subjective psychological well-being was significant from day 14 onwards (change from baseline on day 14: 9.86 vs. 0.77; and day 28: 13.29 vs. 0.77 for melatonin-SR and placebo, respectively; p = 0.001). A significant improvement in subjective sleep parameters at day 28 (p < 0.05) was observed. Reported adverse events in both groups were mild and transient in nature. Supplementation with melatonin-SR 2 mg capsule at night for 28 days was found to be effective and safe in improving objective and subjective sleep quality outcomes and overall well-being in the trial population.
This study investigated the diurnal dynamics of the gut microbiota and core clock gene expression in the red swamp crayfish, Procambarus clarkii. Samples were collected at four time points (06:00, 12:00, 18:00, and 24:00) over a 24 h period. Gut microbiota characteristics were analyzed using 16S rRNA gene sequencing, while quantitative real-time polymerase chain reaction (qPCR) was used to examine the expression patterns of core clock genes, including Cycle (Cyc), Clock (Clk), and cryptochrome type 1 (Cry1), in the hepatopancreas and eyestalk. The results showed that Kruskal-Wallis tests for α-diversity indices (Shannon, Simpson, ACE, Chao1) and PERMANOVA for β-diversity (Bray-Curtis) of the gut microbiota revealed no significant diurnal variation across the four time points (all p > 0.05). Firmicutes, Proteobacteria, and Bacteroidota were the dominant phyla, with norank_o_RsaHf231, ZOR0006, and Bacteroides as the predominant genera. Although the overall microbial structure remained stable, several taxa, including unclassified_c_Bacilli, unclassified_f_Caulobacteraceae, Gemmobacter, unclassified_f_Rhodobacteraceae, Allorhizobium-Neorhizobium-Pararhizobium-Rhizobium, Lactobacillus, and unclassified_f_Vibrionaceae exhibited time-dependent fluctuations. In addition, the relative mRNA expression levels of Cyc, Clk, and Cry1 in the hepatopancreas and eyestalk showed significant diurnal variation. This study reveals the diurnal dynamic characteristics of the gut microbiota and core clock gene expression in P. clarkii, providing a foundation for further investigation of diurnal regulatory mechanisms and physiological adaptations.
Sleep disturbance is a central feature of depression and a proposed pathway through which Bright-Light Therapy (BLT) exerts antidepressant effects. However, little is known about how sleep reorganises day by day during BLT or whether these dynamics relate to symptom improvement. We analysed daily sleep diaries from 66 patients with depression undergoing three weeks of BLT in routine outpatient care. Generalised Additive Mixed Models characterised daily trajectories in sleep timing, continuity, duration, and Subjective Sleep Quality, and weekly changes in sleep regularity were assessed using Root Mean Square of the Successive Differences. Structural Equation Modelling examined whether within-person deviations in sleep parameters mediated changes in depressive symptoms. Sleep timing showed gradual adjustment across treatment, with a progressive 48 min advance in weekday sleep onset. Sleep regularity improved from Week 1 to Week 2 before partially reversing, and the probability of nocturnal awakenings followed a non-linear trajectory. Other sleep parameters showed weaker directional trends. Improvements in Subjective Sleep Quality accounted for a modest portion of the association between treatment progression and reductions in depressive symptoms, whereas changes in sleep timing and regularity were not associated with symptom change. These findings indicate that sleep reorganises gradually during outpatient BLT, with different sleep dimensions evolving on distinct timescales and Subjective Sleep Quality emerging as one observable component linked to symptom improvement. More broadly, the results highlight the value of day-to-day modelling for understanding sleep-mood dynamics during real-world chronotherapy.
While the health benefits of pet ownership are well-documented, research on co-sleeping with pets has yielded conflicting results, often contrasting objective sleep disturbances with subjective satisfaction. This study examined the association between dog or cat co-sleeping and well-being across two age groups: adults and youths. Data were collected through two cross-sectional online surveys involving adults (n = 2675) and youths (n = 1050). Participants reported their pet ownership, co-sleeping status, and well-being using the five-item World Health Organization Well-being Index (WHO-5). Analysis of covariance (ANCOVA) was used to compare WHO-5 scores among three groups: non-owners, owners who do not co-sleep, and co-sleepers. In adults, dog co-sleepers exhibited significantly higher well-being scores compared to non-owners (p = 0.025). However, no significant associations were observed in the youth sample. These findings suggest that while pet co-sleeping is often perceived as disruptive, it may be positively associated with subjective well-being in adult populations. Further longitudinal research is needed to clarify the causal relationship and the specific mechanisms underlying this “pet effect” in the context of shared sleep environments.
