Enriched sleep environments lengthen lemur sleep duration
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ABSTRACT:
SUBMITTER: Vining A
PROVIDER: S-EPMC8559942 | biostudies-literature |
REPOSITORIES: biostudies-literature
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Project description:Evening exposure to short-wavelength light has disruptive effects on circadian rhythms and sleep. These effects can be mitigated by blocking short-wavelength (blue) frequencies, which has led to the development of evening blue-depleted light environments (BDLEs). We have previously reported that residing 5 days in an evening BDLE, compared with residing in a normal indoor light environment of similar photopic lux, advances circadian rhythms and increases the duration of rapid eye movement (REM) sleep in a randomized cross-over trial with twelve healthy participants. The current study extends these findings by testing whether residing in the evening BDLE affects the consolidation and microstructure of REM sleep in the same sample. Evening BDLE significantly reduces the fragmentation of REM sleep (p = 0.0003), and REM sleep microarousals in (p = 0.0493) without significantly changing REM density or the latency to first REM sleep episode. Moreover, the increased accumulation of REM sleep is not at the expense of NREM stage 3 sleep. BDLE further has a unique effect on REM sleep fragmentation (p = 0.0479) over and above that of circadian rhythms phase-shift, indicating a non-circadian effect of BDLE. If these effects can be replicated in clinical populations, this may have a therapeutic potential in disorders characterized by fragmented REM sleep.
| S-EPMC9130237 | biostudies-literature
Project description:Short sleep duration is associated with adverse metabolic, cardiovascular, and inflammatory effects. Co-twin study methodologies account for familial (e.g., genetics and shared environmental) confounding, allowing assessment of subtle environmental effects, such as the effect of short habitual sleep duration on gene expression. Therefore, we sought to investigate gene expression in monozygotic twins discordant for actigraphically phenotyped habitual sleep duration. Eleven healthy monozygotic twin pairs (82% female; mean age 42.7 years; SD=18.1), selected based on subjective sleep duration discordance, were objectively phenotyped for habitual sleep duration with two-weeks of wrist actigraphy. Peripheral blood leukocyte (PBL) RNA from fasting blood samples was obtained on the final day of actigraphic measurement and hybridized to Illumina humanHT-12 microarrays. Differential gene expression was determined between paired samples and mapped to functional categories using Gene Ontology. Next, a more comprehensive gene set enrichment analysis was performed based on the entire PBL transcriptome. The mean 24 hour sleep duration of the total sample was 439.2 minutes (SD=46.8 minutes; range 325.4 to 521.6 minutes). Mean within-pair sleep duration difference per 24 hours was 64.4 minutes (SD=21.2; range 45.9 to 114.6 minutes). The twin cohort displayed distinctive pathway enrichment based on sleep duration differences. Short sleep was associated with up-regulation of genes involved in transcription, ribosome, translation and oxidative phosphorylation. Unexpectedly, genes down-regulated in short sleep twins were highly enriched in immuno-inflammatory pathways such interleukin signaling and leukocyte activation, as well as developmental programs, coagulation cascade, and cell adhesion. Objectively assessed habitual sleep duration in monozygotic twin pairs appears to be associated with distinct patterns of differential gene expression and pathway enrichment. By accounting for familial confounding and measuring real life sleep duration, our study shows the transcriptomic effects of short sleep on dysregulated immune response and provides a potential link between sleep deprivation and adverse metabolic, cardiovascular and inflammatory outcomes.
2016-09-09 | GSE80612 | GEO
Project description:Previous studies have found a U-shaped relationship between mortality and (weekday) sleep duration. We here address the association of both weekday and weekend sleep duration with overall mortality. A cohort of 43,880 subjects was followed for 13 years through record-linkages. Cox proportional hazards regression models with attained age as time-scale were fitted to estimate multivariable-adjusted hazard ratios and 95% confidence intervals for mortality; stratified analyses on age (<65 years, ≥65 years) were conducted. Among individuals <65 years old, short sleep (≤5 hr) during weekends at baseline was associated with a 52% higher mortality rate (hazard ratios 1.52; 95% confidence intervals 1.15-2.02) compared with the reference group (7 hr), while no association was observed for long (≥9 hr) weekend sleep. When, instead, different combinations of weekday and weekend sleep durations were analysed, we observed a detrimental association with consistently sleeping ≤5 hr (hazard ratios 1.65; 95% confidence intervals 1.22-2.23) or ≥8 hr (hazard ratios 1.25; 95% confidence intervals 1.05-1.50), compared with consistently sleeping 6-7 hr per day (reference). The mortality rate among participants with short sleep during weekdays, but long sleep during weekends, did not differ from the rate of the reference group. Among individuals ≥65 years old, no association between weekend sleep or weekday/weekend sleep durations and mortality was observed. In conclusion, short, but not long, weekend sleep was associated with an increased mortality in subjects <65 years. In the same age group, short sleep (or long sleep) on both weekdays and weekend showed increased mortality. Possibly, long weekend sleep may compensate for short weekday sleep.
| S-EPMC7003477 | biostudies-literature
Project description:Vascular dysfunction is a hypothesized mechanism linking poor sleep habits to an increased incidence of cardiovascular diseases (CVDs). However, the vascular profile associated with free-living sleep duration and sleep regularity has not been well elucidated, particularly in young adults. Thus, this study aimed to evaluate the associations between mean sleep duration, regularity in sleep duration, and peripheral vascular function in young adult college students. Fifty-one healthy undergraduate students (20 ± 1 years) completed 14 days of 24-hour wrist actigraphy and subsequent vascular assessments. Macrovascular function was measured using brachial artery flow-mediated dilation (FMD) while microvascular function was measured via passive leg movement (PLM). Mean sleep duration was unrelated to FMD and PLM. Conversely, more irregular sleep duration (14-day sleep duration standard deviation [SD]) was unfavorably associated with all three measures of PLM-induced hyperemia (peak leg blood flow [LBF], p = 0.01; change in LBF from baseline to peak, p < 0.01; LBF area under the curve, p < 0.01), and remained significant in regression models which adjusted for sex, body mass index, blood pressure, physical activity, alcohol and caffeine consumption, and sleep duration (all p < 0.05). When using a median split to dichotomize "low" and "high" sleep duration SD groups, those demonstrating high variability in sleep duration exhibited ~45% lower PLM responses compared with those demonstrating low variability. Irregular sleep duration is associated with poorer microvascular function as early as young adulthood. These findings support the growing body of evidence that irregular sleep patterns may be an independent and modifiable risk factor for CVD.
| S-EPMC7879418 | biostudies-literature
Project description:BackgroundObservational studies suggest associations between extremes of sleep duration and myocardial infarction (MI), but the causal contribution of sleep to MI and its potential to mitigate genetic predisposition to coronary disease is unclear.ObjectivesThis study sought to investigate associations between sleep duration and incident MI, accounting for joint effects with other sleep traits and genetic risk of coronary artery disease, and to assess causality using Mendelian randomization (MR).MethodsIn 461,347 UK Biobank (UKB) participants free of relevant cardiovascular disease, the authors estimated multivariable adjusted hazard ratios (HR) for MI (5,128 incident cases) across habitual self-reported short (<6 h) and long (>9 h) sleep duration, and examined joint effects with sleep disturbance traits and a coronary artery disease genetic risk score. The authors conducted 2-sample MR for short (24 single nucleotide polymorphisms) and continuous (71 single nucleotide polymorphisms) sleep duration with MI (n = 43,676 cases/128,199 controls), and replicated results in UKB (n = 12,111/325,421).ResultsCompared with sleeping 6 to 9 h/night, short sleepers had a 20% higher multivariable-adjusted risk of incident MI (HR: 1.20; 95% confidence interval [CI]: 1.07 to 1.33), and long sleepers had a 34% higher risk (HR: 1.34; 95% CI: 1.13 to 1.58); associations were independent of other sleep traits. Healthy sleep duration mitigated MI risk even among individuals with high genetic liability (HR: 0.82; 95% CI: 0.68 to 0.998). MR was consistent with a causal effect of short sleep duration on MI in CARDIoGRAMplusC4D (Coronary ARtery DIsease Genome wide Replication and Meta-analysis plus Coronary Artery Disease Genetics Consortium) (HR: 1.19; 95% CI: 1.09 to 1.29) and UKB (HR: 1.21; 95% CI: 1.08 to 1.37).ConclusionsProspective observational and MR analyses support short sleep duration as a potentially causal risk factor for MI. Investigation of sleep extension to prevent MI may be warranted.
| S-EPMC6785011 | biostudies-literature
Project description:In this study, we hypothesized that dynamics of sleep time obtained over consecutive days of extended sleep in a laboratory reflect an individual's optimal sleep duration (OSD) and that the difference between OSD and habitual sleep duration (HSD) at home represents potential sleep debt (PSD). We found that OSD varies among individuals and PSD showed stronger correlation with subjective/objective sleepiness than actual sleep time, interacting with individual's vulnerability of sleep loss. Furthermore, only 1 h of PSD takes four days to recover to their optimal level. Recovery from PSD was also associated with the improvement in glycometabolism, thyrotropic activity and hypothalamic-pituitary-adrenocortical axis. Additionally, the increase (rebound) in total sleep time from HSD at the first extended sleep would be a simple indicator of PSD. These findings confirmed self-evaluating the degree of sleep debt at home as a useful clinical marker. To establish appropriate sleep habits, it is necessary to evaluate OSD, vulnerability to sleep loss, and sleep homeostasis characteristics on an individual basis.
| S-EPMC5075948 | biostudies-literature
Project description:Aims: Abnormally short or long durations of sleep have been proposed as a risk factors for diabetes and its micro- and macro-vascular complications. However, the relationship between sleep duration and diabetic kidney disease (DKD) has not been well-characterized. Thus, we aimed to examine the association of sleep duration with DKD in two Asian populations. Methods: We included 1,258 persons (Malay, n = 403; Indian, n = 855) aged 40-80 years with diabetes from a population-based cross-sectional sample from Singapore. DKD was defined by low estimated glomerular filtration rate (eGFR <60 mL/min/1.73 m2) and albuminuria (urinary albumin-to-creatinine ratio ?30 mg/g, only measured in Indian participants). Self-reported habitual sleep duration was categorized into 4 categories: very short (<5 h), short (5-6.9 h), normal (7-8 h) and long (>8 h). The associations of sleep duration with low eGFR and albuminuria were analyzed using multivariable logistic regression models adjusted for multiple potential confounders (including classic risk factors such as HbA1c and hypertension). Results: In total, 268 (21.3%) participants had low eGFR, and 271 (34.7% in Indians) had albuminuria. The number (%) of individuals with very short, short, normal, and long durations of sleep were 117 (9.3%), 629 (50.0%), 429 (34.1%), and 83 (6.6%), respectively. Long sleep duration was associated with a higher odds of renal insufficiency compared to normal sleep duration (OR [95% CI]: 2.31 [1.27-4.19]) on multivariable analysis. Similarly, both long and very short durations of sleep were associated with higher odds of albuminuria (OR [95%]: 2.44 [1.36, 4.38] and 2.37 [1.25, 4.50], respectively) in Indian participants (where data on albuminuria were available). Conclusions: Our study suggests that abnormally short or long durations of sleep were associated with DKD, manifesting as either a reduced eGFR or increased albuminuria. However, further longitudinal data would be required for confirmation.
| S-EPMC6340267 | biostudies-literature
Project description:A primary goal of sleep research is to understand the molecular basis of sleep. Although some sleep/wake-promoting circuits and secreted substances have been identified, the detailed molecular mechanisms underlying the regulation of sleep duration have been elusive. Here, to address these mechanisms, we developed a simple computational model of a cortical neuron with five channels and a pump, which recapitulates the cortical electrophysiological characteristics of slow-wave sleep (SWS) and wakefulness. Comprehensive bifurcation and detailed mathematical analyses predicted that leak K+ channels play a role in generating the electrophysiological characteristics of SWS, leading to a hypothesis that leak K+ channels play a role in the regulation of sleep duration. To test this hypothesis experimentally, we comprehensively generated and analyzed 14 KO mice, and found that impairment of the leak K+ channel (Kcnk9) decreased sleep duration. Based on these results, we hypothesize that leak K+ channels regulate sleep duration in mammals.
| S-EPMC6176580 | biostudies-literature
Project description:To investigate the prevalence and possible determinants of sleep quality and quantity, we used data from a cross-sectional study conducted in 2019 on a sample of 3120 subjects, representative of the general Italian adult population. Sleep dissatisfaction was reported by 14.2% and insufficient sleep (duration) by 29.5% of adults. Sleep dissatisfaction and insufficient sleep were directly related with age (p for trend < 0.001), and inversely related with socioeconomic class (p for trend < 0.001) and income (p for trend < 0.001). Sleep dissatisfaction was higher among women (odds ratio, OR 1.30; 95% confidence interval, CI 1.05-1.60). Insufficient sleep was inversely related to education (p for trend < 0.001) and more frequent in current compared to never smokers (OR 1.32; 95% CI 1.08-1.61). Sleep dissatisfaction was higher among divorced/separated compared with married subjects (OR 1.75; 95% CI 1.20-2.58) and lower among subjects living with children aged 0-14 years (OR 0.48, 95% CI 0.33-0.70). Pet owners more frequently had sleep dissatisfaction (OR 1.35, 95% CI 1.08-1.68) and insufficient sleep (OR 1.46, 95% CI 1.23-1.73). In Italy, self-perceived sleep problems appear to be increasing. Sleep problems can contribute to aggravating health disparities in the society. The unfavourable relationship with pets (and the favourable ones with children) should be confirmed by longitudinal studies.
| S-EPMC7578786 | biostudies-literature
Project description:Sleep duration varies widely across individuals and appears to be trait-like. Differences in the stability of underlying sleep processes may underlie this phenomenon. To investigate underlying mechanisms, we examined the relationship between sleep duration and sleep continuity in baseline polysomnography (PSG) recordings from three independently collected datasets: 1) 134 healthy controls (ages 37 ± 13 years) from the São Paulo Epidemiologic Sleep Study, who spent one night in a sleep laboratory, 2) 21 obstructive sleep apnea (OSA) patients who were treated with continuous positive airway pressure for at least 2 months (45 ± 12 years, respiratory disturbance index <15), who spent one night in a sleep laboratory with previous experience of multiple PSG studies, and 3) 62 healthy controls (28 ± 6 years) who, as part of larger experiments, spent 2 consecutive nights in a sleep laboratory. For each dataset, we used total sleep time (TST) to separate subjects into those with shorter sleep (S-TST) and those with longer sleep (L-TST). In all three datasets, survival curves of continuous sleep segments showed greater sleep continuity in L-TST than in S-TST. Correlation analyses with TST as a continuous variable corroborated the results; and the results also held true after controlling for age. There were no significant differences in baseline waking performance and sleepiness between S-TST and L-TST. In conclusion, in both healthy controls and treated OSA patients, sleep continuity was positively correlated with sleep duration. These findings suggest that S-TST may differ from L-TST in processes underlying sleep continuity, shedding new light on mechanisms underlying individual differences in sleep duration.
| S-EPMC5386280 | biostudies-literature