The Impact of Sleep: From Ancient Rituals to Modern Challenges.

Although sleep is crucial for mental and physical health, insufficient sleep is a growing problem in our modern society. In general, adults need approximately eight hours of sleep per night, but this is often unfeasible nowadays. This sleep restriction has been observed, and it has worsened, throughout the past two centuries; therefore, it is more attributed to socioeconomic changes than to biological adaptations. The most important factors to contribute to this sleep restriction were the popularization of artificial light and industrialization. The present manuscript briefly overviews, from a socioanthropological perspective, the reasons why sleep has been impacted, disclosing its effects on individuals and on society.

Sleep deprivation and recovery: Endurance racing as a novel model.

The aim of this study was to investigate sleep-wake behavior and gain insights into perceived impairment (sleep, fatigue, and cognitive function) of athletes competing in two international multi-day adventure races. Twenty-four athletes took part across two independent adventure races: Queensland, Australia and Alaska, USA. Individual sleep periods were determined via actigraphy, and racers self-reported their perceived sleep disturbances, sleep impairment, fatigue and cognitive function. Each of these indices was calculated for pre-, during- and post-race periods. Sleep was severely restricted during the race period compared to pre-race (Queensland, 7:46 [0:29] vs. 2:50 [1:01]; Alaska, 7:39 [0:58] vs. 2:45 [2:05]; mean [SD], hh:mm). As a result, there was a large cumulative sleep debt at race completion, which was not 'reversed' in the post-race period (up to 1 week). The deterioration in all four self-reported scales of perceived impairment during the race period was largely restored in the post-race period. This is the first study to document objective sleep-wake behaviors and subjective impairment of adventure racers, in the context of two geographically diverse, multi-day, international adventure races. Measures of sleep deprivation indicate that sleep debt was extreme and did not recover to pre-race levels within 1 week following each race. Despite this objective debt continuing, perceived impairment returned to pre-race levels quickly post-race. Therefore, further examination of actual and perceived sleep recovery is warranted. Adventure racing presents a unique scenario to examine sleep, performance and recovery.

The effect of a dynamic lighting schedule on neurobehavioral performance during a 45-day simulated space mission.

Study Objectives: We previously reported that during a 45-day simulated space mission, a dynamic lighting schedule (DLS) improved circadian phase alignment and performance assessed once on selected days. This study aimed to evaluate how DLS affected performance on a 5-minute psychomotor vigilance task (PVT) administered multiple times per day on selected days. Methods: Sixteen crewmembers (37.4 ±â€…6.7 years; 5F) underwent six cycles of 2 × 8-hour/night followed by 5 × 5-hour/night sleep opportunities. During the DLS (n = 8), daytime white light exposure was blue-enriched (~6000 K; Level 1: 1079, Level 2: 76 melanopic equivalent daytime illuminance (melEDI) lux) and blue-depleted (~3000-4000 K; L1: 21, L2: 2 melEDI lux) 3 hours before bed. In the standard lighting schedule (SLS; n = 8), lighting remained constant (~4500K; L1: 284, L2 62 melEDI lux). Effects of lighting condition (DLS/SLS), sleep condition (5/8 hours), time into mission, and their interactions, and time awake on PVT performance were analyzed using generalized linear mixed models. Results: The DLS was associated with fewer attentional lapses (reaction time [RT] > 500 milliseconds) compared to SLS. Lapses, mean RT, and 10% fastest/slowest RTs were worse following 5 compared to 8 hours of sleep but not between lighting conditions. There was an effect of time into mission on RTs, likely due to sleep loss. Overall performance differed by time of day, with longer RTs at the beginning and end of the day. There were more lapses and slower RTs in the afternoon in the SLS compared to the DLS condition. Conclusions: Future missions should incorporate DLS to enhance circadian alignment and performance. This paper is part of the Sleep and Circadian Rhythms: Management of Fatigue in Occupational Settings Collection.

Acute partial sleep restriction does not impact arterial function in young and healthy humans.

Habitual short sleep durations are associated with several cardiovascular diseases. Experimental research generally supports these findings as metrics of arterial function are impaired after complete deprivation of sleep and after longer periods of partial sleep restriction. The acute influence of a single instance of partial sleep restriction (PSR), however, has not been defined. We evaluated arterial structure and function among 32 university-aged participants on two occasions: once after normal habitual sleep (NS), and again the morning after an acute partial sleep restriction (PSR) intervention involving only 3 h of sleep for a single night. Endothelial function was measured using ultrasonography at the brachial artery via flow-mediated dilatation (FMD), and a ramp peak oxygen uptake test was used to evaluate cardiorespiratory fitness. Blood samples were collected from a subset of participants to investigate the influence of circulatory factors on cellular mechanisms implicated in endothelial function. Sleep duration was lower after a night of PSR compared to NS (P < 0.001); however, there were no appreciable differences in any haemodynamic outcome between conditions. FMD was not different between NS and PSR (NS: 6.5 ± 2.9%; PSR: 6.3 ± 2.9%; P = 0.668), and cardiorespiratory fitness did not moderate the haemodynamic response to PSR (all P > 0.05). Ex vivo cell culture results aligned with in vivo data, showing that acute PSR does not alter intracellular processes involved in endothelial function. No differences in arterial structure or function were observed between NS and acute PSR in healthy and young participants, and cardiorespiratory fitness does not modulate the arterial response to acute sleep restriction.

A pilot time-in-bed restriction intervention behaviorally enhances slow-wave activity in older adults.

Introduction: Identifying intervention methods that target sleep characteristics involved in memory processing is a priority for the field of cognitive aging. Older adults with greater sleep efficiency and non-rapid eye movement slow-wave activity (SWA) (0.5-4 Hz electroencephalographic activity) tend to exhibit better memory and cognitive abilities. Paradoxically, long total sleep times are consistently associated with poorer cognition in older adults. Thus, maximizing sleep efficiency and SWA may be a priority relative to increasing mere total sleep time. As clinical behavioral sleep treatments do not consistently enhance SWA, and propensity for SWA increases with time spent awake, we examined with a proof-of concept pilot intervention whether a greater dose of time-in-bed (TiB) restriction (75% of habitual TiB) would increase both sleep efficiency and SWA in older adults with difficulties staying asleep without impairing memory performance. Methods: Participants were adults ages 55-80 with diary-reported sleep efficiency <90% and wake after sleep onset (WASO) >20 min. Sleep diary, actigraphy, polysomnography (PSG), and paired associate memory acquisition and retention were assessed before and after a week-long TiB restriction intervention (n = 30). TiB was restricted to 75% of diary-reported habitual TiB. A comparison group of n = 5 participants repeated assessments while following their usual sleep schedule to obtain preliminary estimates of effect sizes associated with repeated testing. Results: Subjective and objective sleep measures robustly improved in the TiB restriction group for sleep quality, sleep depth, sleep efficiency and WASO, at the expense of TiB and time spent in N1 and N2 sleep. As hypothesized, SWA increased robustly with TiB restriction across the 0.5-4 Hz range, as well as subjective sleep depth, subjective and objective WASO. Despite increases in sleepiness ratings, no impairments were found in memory acquisition or retention. Conclusion: A TiB restriction dose equivalent to 75% of habitual TiB robustly increased sleep continuity and SWA in older adults with sleep maintenance difficulties, without impairing memory performance. These findings may inform long-term behavioral SWA enhancement interventions aimed at improving memory performance and risk for cognitive impairments.

Role of Thymoquinone on sleep restriction and its mitigating effect on leptin-mediated signaling pathway in rat brain.

BACKGROUND: Sleep and stress interact bidirectionally by acting on brain circuits that affect metabolism. Sleep and its alterations have impact on blood leptin levels, metabolic hormone that regulates appetite. Brain expresses the receptors for the peptide hormone leptin produced from adipocytes. The hypothalamic orexin neurons are low during sleep and active when awake, influenced by a complex interaction with leptin. Thymoquinone was found to be the major bioactive component of Nigella sativa. The aim of this study was to study the role of thymoquinone on sleep restriction and its mitigating effect on leptin-mediated signaling pathway in rat brain. METHODS AND RESULTS: 30 adult male Wistar rats were divided into 5 groups with 6 animals in each group: Control; Thymoquinone (TQ); Corn oil; Chronic Sleep restriction (CSR); and CSR + TQ. After 30 days, behavioral analysis, antioxidant, lipid profile, glucose level, liver and kidney function test, neurotransmitters, neuropeptides, and mRNA expression in in vivo studies were also assessed and pharmacokinetic and docking were done for thymoquinone. Thymoquinone has also shown good binding affinity to the target proteins. CSR has induced oxidative stress in the discrete brain regions and plasma. Current study has shown many evidences that sleep restriction has altered the neurobehavioral, antioxidant status, lipid profile, neurotransmitters, neuropeptide levels, and feeding behavior which damage the Orexin-leptin system which regulates the sleep and feeding that leads to metabolic dysfunction. CONCLUSION: The potentiality of Thymoquinone was revealed in in silico studies, and its action in in vivo studies has proved its effectiveness. The study concludes that Thymoquinone has exhibited its effect by diminishing the metabolic dysfunction by its neuroprotective, antioxidant, and hypolipidemic properties.

Sleep restriction promotes brain oxidative stress and inflammation, and aggravates cognitive impairment in insulin-resistant mice.

Sleep deprivation and insulin resistance (IR) are two risk factors for Alzheimer's disease. As the population of people with IR increases and sleep restriction (SR) due to staying up late becomes the "new normal", it is necessary to investigate the effects and molecular pathogenesis of chronic SR on cognitive function in insulin resistance. In this study, 4-week-old mice were fed a high-fat diet (HFD) for 8 weeks to establish IR model, and then the mice were subjected to SR for 21 days, and related indicators were assessed, including cognitive capacity, apoptosis, oxidative stress, glial cell activation, inflammation, blood-brain barrier (BBB) permeability and adiponectin levels, for exploring the potential regulatory mechanisms. Compared with control group, IR mice showed impaired cognitive capacity, meanwhile, SR not only promoted Bax/Bcl2-induced hippocampal neuronal cell apoptosis and Nrf2/HO1- induced oxidative stress, but also increased microglia activation and inflammatory factor levels and BBB permeability, thus aggravating the cognitive impairment in IR mice. Consequently, changing bad living habits and ensuring sufficient sleep are important intervention strategies to moderate the aggravation of IR-induced cognitive impairment.

Glucose competition between endothelial cells in the blood-spinal cord barrier and infiltrating regulatory T cells is linked to sleep restriction-induced hyperalgesia.

BACKGROUND: Sleep loss is a common public health problem that causes hyperalgesia, especially that after surgery, which reduces the quality of life seriously. METHODS: The 48-h sleep restriction (SR) mouse model was created using restriction chambers. In vivo imaging, transmission electron microscopy (TEM), immunofluorescence staining and Western blot were performed to detect the status of the blood-spinal cord barrier (BSCB). Paw withdrawal mechanical threshold (PWMT) was measured to track mouse pain behavior. The role of infiltrating regulatory T cells (Tregs) and endothelial cells (ECs) in mouse glycolysis and BSCB damage were analyzed using flow cytometry, Western blot, CCK-8 assay, colorimetric method and lactate administration. RESULTS: The 48-h SR made mice in sleep disruption status and caused an acute damage to the BSCB, resulting in hyperalgesia and neuroinflammation in the spinal cord. In SR mice, the levels of glycolysis and glycolysis enzymes of ECs in the BSCB were found significantly decreased [CON group vs. SR group: CD31+Glut1+ cells: p < 0.001], which could cause dysfunction of ECs and this was confirmed in vitro. Increased numbers of infiltrating T cells [p < 0.0001] and Treg population [p < 0.05] were detected in the mouse spinal cord after 48-h SR. In the co-cultured system of ECs and Tregs in vitro, the competition of Tregs for glucose resulted in the glycolysis disorder of ECs [Glut1: p < 0.01, ENO1: p < 0.05, LDHα: p < 0.05; complete tubular structures formed: p < 0.0001; CCK8 assay: p < 0.001 on 24h, p < 0.0001 on 48h; glycolysis level: p < 0.0001]. An administration of sodium lactate partially rescued the function of ECs and relieved SR-induced hyperalgesia. Furthermore, the mTOR signaling pathway was excessively activated in ECs after SR in vivo and those under the inhibition of glycolysis or co-cultured with Tregs in vitro. CONCLUSIONS: Affected by glycolysis disorders of ECs due to glucose competition with infiltrating Tregs through regulating the mTOR signaling pathway, hyperalgesia induced by 48-h SR is attributed to neuroinflammation and damages to the barriers, which can be relieved by lactate supplementation.

Impact of one night of sleep restriction on sleepiness and cognitive function: A systematic review and meta-analysis.

Detrimental consequences of chronic sleep restriction on cognitive function are well established in the literature. However, effects of a single night of sleep restriction remain equivocal. Therefore, we synthesized data from 44 studies to investigate effects of sleep restriction to 2-6 h sleep opportunity on sleepiness and cognition in this meta-analysis. We investigated subjective sleepiness, sustained attention, choice reaction time, cognitive throughput, working memory, and inhibitory control. Results revealed a significant increase in subjective sleepiness following one night of sleep restriction (Standardized Mean Difference (SMD) = 0.986, p < 0.001), while subjective sleepiness was not associated with sleep duration during sleep restriction (ß = -0.214, p = 0.039, significance level 0.01). Sustained attention, assessed via common 10-min tasks, was impaired, as demonstrated through increased reaction times (SMD = 0.512, p < 0.001) and attentional lapses (SMD = 0.489, p < 0.001). However, the degree of impaired attention was not associated with sleep duration (ps > 0.090). We did not find significant effects on choice reaction time, cognitive throughput, working memory, or inhibitory control. Overall, results suggest that a single night of restricted sleep can increase subjective sleepiness and impair sustained attention, a cognitive function crucial for everyday tasks such as driving.

Increasing Restorative Sleep Among Adults With Depressive Symptoms: A Quality Improvement Project.

The Centers for Disease Control and Prevention estimates that 34.8% of adults in the United States experience non-restorative sleep. The restorative theory of sleep is based on sleep as a means for the restoration of cellular function that is needed for activities when awake. Non-restorative sleep leads to awakening feeling unrefreshed and not ready for the activities of the day three or more times weekly. Aims: The aim of this quality improvement project was to increase restorative sleep by increasing the average amount of sleep over units of 24 h, decreasing perceived insufficient sleep, and decreasing episodes of unintended daytime sleep among patients with depressive symptoms ages 18 to 80 years in an outpatient mental health clinic. Methods: Ten patients with depressive symptoms and reporting non-restorative sleep volunteered to participate in the project. Participants kept a sleep diary and followed principles of healthy sleep such as limiting time in bed and going to bed at the same time nightly. The change in and the average amount of sleep over 24 h and daytime sleepiness were evaluated using the Behavioral Risk Factor Surveillance System. Results: All participants achieved at least one more day of restorative sleep, with nine increasing restorative sleep by at least 30 min per day, and nine having no episodes of unintentionally falling asleep.

The dynamic responses of mood and sleep physiology to chronic sleep restriction and subsequent recovery sleep.

Healthy sleep of sufficient duration preserves mood and disturbed sleep is a risk factor for a range of psychiatric disorders. As adults commonly experience chronic sleep restriction (SR), an enhanced understanding of the dynamic relationship between sleep and mood is needed, including whether susceptibility to SR-induced mood disturbance differs between sexes. To address these gaps, data from N=221 healthy adults who completed one of two multi-day laboratory studies with identical 9-day SR protocols were analyzed. Participants randomized to the SR (n=205) condition underwent 5 nights of SR to 4 h time-in-bed and were then randomized to one of seven sleep doses that ranged from 0 h to 12 h in 2 h increments; participants randomized to the control (n=16) condition received 10 h time-in-bed on all study nights. The Profile of Mood States (POMS) was used to assess mood every 2 h during wakefulness and markers of sleep homeostasis (EEG slow-wave activity) were derived via polysomnography. Mood progressively deteriorated across SR with marked disturbances in somatic mood components. Altered sleep physiology contributed to mood disturbance whereby increased EEG slow-wave activity was associated with increased POMS Total Mood Disturbance scores, a finding specific to males. Mood was restored in a dose-response fashion where improvements were greater with longer sleep doses. These findings suggest that when lifestyle and environmental factors are inhibited in the laboratory, the affective consequences of chronic sleep loss are primarily somatic mood disturbances. Altered sleep homeostasis may contribute to mood disturbance, yet sleep-dependent mechanisms may be sex-specific.

Association Between EEG Microarousal During Nocturnal Sleep and Next-Day Selective Attention in Mild Sleep-Restricted Healthy Undergraduates.

Purpose: To explore whether sleep electroencephalogram (EEG) microarousals of different standard durations predict daytime mood and attention performance in healthy individuals after mild sleep restriction. Participants and Methods: Sixteen (nine female) healthy college students were recruited to examine the correlations between nocturnal EEG microarousals of different standard durations (≥3 s, ≥5 s, ≥7 s, ≥9 s) under mild sleep restriction (1.5 h) and the following morning's subjective alertness, mood, sustained attention, and selective attention task performance. Results: Results revealed that mild sleep restriction significantly reduced subjective alertness and positive mood, while having no significant effect on negative mood, sustained attention and selective attention performance. The number of microarousals (≥5 s) was negatively associated with positive mood at 6:30. The number of microarousals was significantly and positively correlated with the response time difference value of disengagement component of the selective attention task at around 7:30 (≥5 s and ≥7 s) and 9:00 (≥5 s). The number of microarousals (≥7 s) was significantly and positively correlated with the inaccuracy difference value of orientation component of the selective attention task at around 9:00. Conclusion: The number of EEG microarousals during sleep in healthy adults with mild sleep restriction was significantly and negatively related to their daytime positive affect while positively associated with the deterioration of disengagement and orientation of selective attention performance, but this link is dependent on the standard duration of microarousals, test time and the type of task.

Sleep and subjective age: protect your sleep if you want to feel young.

The current studies examined the impact of insufficient sleep and sleepiness on the subjective experience of age. Study 1, a cross-sectional study of 429 participants (282 females (66%), 144 males, 3 other gender; age range 18-70), showed that for each additional day of insufficient sleep in the last 30 days, subjective age increased by 0.23 years. Study 2, an experimental crossover sleep restriction study (n = 186; 102 females (55%), 84 males; age range 18-46), showed that two nights of sleep restriction (4 h in bed per night) made people feel 4.44 years older compared to sleep saturation (9 h in bed per night). Additionally, moving from feeling extremely alert (Karolinska Sleepiness Scale (KSS) score of 1) to feeling extremely sleepy (KSS score of 9) was associated with feeling 10 years older in both studies. These findings provide compelling support for insufficient sleep and sleepiness to exert a substantial influence on how old we feel, and that safeguarding sleep is probably a key factor in feeling young.

Effects of Chronic Sleep Restriction on Transcriptional Sirtuin 1 Signaling Regulation in Male Mice White Adipose Tissue.

Chronic sleep restriction (CSR) is a prevalent issue in modern society that is associated with several pathological states, ranging from neuropsychiatric to metabolic diseases. Despite its known impact on metabolism, the specific effects of CSR on the molecular mechanisms involved in maintaining metabolic homeostasis at the level of white adipose tissue (WAT) remain poorly understood. Therefore, this study aimed to investigate the influence of CSR on sirtuin 1 (SIRT1) and the peroxisome proliferator-activated receptor γ (PPARγ) signaling pathway in the WAT of young male mice. Both genes interact with specific targets involved in multiple metabolic processes, including adipocyte differentiation, browning, and lipid metabolism. The quantitative PCR (qPCR) results demonstrated a significant upregulation of SIRT-1 and some of its target genes associated with the transcriptional regulation of lipid homeostasis (i.e., PPARα, PPARγ, PGC-1α, and SREBF) and adipose tissue development (i.e., leptin, adiponectin) in CSR mice. On the contrary, DNA-binding transcription factors (i.e., CEBP-ß and C-myc), which play a pivotal function during the adipogenesis process, were found to be down-regulated. Our results also suggest that the induction of SIRT1-dependent molecular pathways prevents weight gain. Overall, these findings offer new, valuable insights into the molecular adaptations of WAT to CSR, in order to support increased energy demand due to sleep loss.

The temporal expression pattern of classical MHC class I in sleep-restricted mice: Generalizations and broader implications.

The intricate relationship between sleep and leukocyte trafficking has garnered intense attention, particularly their homing dynamics to secondary lymphoid organs under normal and restricted sleep (SR). Considering the scarcity of information regarding circadian rhythms in major histocompatibility class I (MHC-I) expression in SR, we designed a study that assessed the temporal expression of MHC-I in murine lymph nodes and spleen and the subsequent effects of sleep recovery. Male C57BL/6, housed in 12:12 light/dark cycle, were grouped into control (C) and SR. SR was carried for one week before lymphoid tissues were sampled at selected time points and assessed for leukocyte number and MHC-I expression. SR resulted in 21% decrease in granulocyte and 24% increase in agranulocyte numbers. In C, MHC-I expression pattern in lymph nodes was bimodal and relatively higher than splenocytes during the animal's active phase (110.2 ± 1.8 vs 81.9 ± 3.8, respectively; p = 0.002). Splenocytes; however, showed a bimodal pattern upon SR, with higher protein levels during the rest than the activity period (154.6 + 36.2 vs 99.5 + 15.9, respectively; p = 0.002), suggesting preparedness for a potential infection. Furthermore, SR caused a significant drop in MHC-I expression at the onset of rest with 57% and 30% reduction in lymph nodes and splenocytes, respectively. However, the overall protein expression collectively taken from both lymphoid tissues remained stable, emphasizing its indispensable role in immunological homeostasis. This stability coincided with the restoration of protein levels to baseline after a short sleep recovery period, resembling a reset for MHC-I antigen presentation following a week of SR. Understanding the interplay between MHC-I expression and contextual factors could enhance treatment protocols, refining the efficacy and time precision of glucocorticoid-based therapies in immune modulation.

The effects of sustained mild sleep restriction on stress and distress among healthy adults: Findings from two randomized crossover studies.

OBJECTIVE/BACKGROUND: Experimental studies suggest that sleep loss affects psychological outcomes. However, most studies focus on acute severe in-laboratory sleep restriction, with limited ecological validity. This study examines the impact of sustained mild sleep restriction (SR) on stress and distress among healthy adults in a naturalistic home environment. PATIENTS/METHODS: We analyzed data from two randomized crossover studies. Individuals who regularly slept 7-9 h/night completed two 6-wk intervention phases separated by a 6-wk washout: habitual sleep (HS: maintenance of habitual bed and wake times) and SR (delayed bedtime by 1.5 h/night and maintenance of habitual wake time). Adherence to sleep duration requirements was verified with wrist actigraphy and daily sleep diaries during each intervention phase. Measures of perceived stress, subjective anxiety, subjective depression, rumination, and cortisol were collected at baseline and endpoint of each intervention phase. RESULTS: Sixty-two participants (age 36.4 ± 14.0 y, 85.5 % women, 63.3 % racial/ethnic minority) were included in our analyses. Mean total sleep time was 7.4 ± 0.4 h/night during HS and 6.2 ± 0.4 h/night during SR (p < 0.001). Higher perceived stress (3.6 ± 1.0, p = 0.0007) and subjective anxiety (1.1 ± 0.5, p = 0.039) were observed after SR compared to HS. No effect of sleep condition was observed on subjective depression, rumination, and cortisol. CONCLUSIONS: Our findings suggest that prolonged mildly insufficient sleep, similar to what commonly experienced in the real world, can lead to increased perceived stress and subjective anxiety in healthy adults. Addressing sleep loss, even if mild, should be a key component of interventions aimed at promoting mental health in the general population.

The effect of single-component sleep restriction therapy on depressive symptoms: A systematic review and meta-analysis.

Sleep restriction therapy is a behavioural component within cognitive behavioural therapy for insomnia and is an effective standalone treatment for insomnia, but its effect on depressive symptoms remains unclear. This review aimed to synthesise and evaluate the impact of single-component sleep restriction therapy on depressive symptoms relative to a control intervention. We searched electronic databases and sleep-related journals for randomised controlled trials and uncontrolled clinical trials, published from 1 January 1986 until 19 August 2023, that delivered sleep restriction therapy to adults with insomnia. Random-effects meta-analysis of standardised mean differences and Cochrane risk of bias assessment were performed on randomised controlled trials, while uncontrolled clinical trials were discussed narratively. The meta-analysis was pre-registered on PROSPERO (ID: CRD42020191803). We identified seven randomised controlled trials (N = 1102) and two uncontrolled clinical trials (N = 22). Findings suggest that sleep restriction therapy is associated with a medium effect for improvement in depressive symptoms at post-treatment (Nc = 6, g = -0.45 [95% confidence interval = -0.70 to -0.21], p < 0.001) and a small effect at follow-up (Nc = 4, g = -0.31 [95% confidence interval = -0.45 to -0.16], p < 0.001). Five of the seven included randomised controlled trials were judged to have a high risk of bias. Standalone sleep restriction therapy appears to be efficacious for improving depressive symptoms at post-treatment and follow-up. However, conclusions are tentative due to the small number of trials and because none of the trials was performed in a population with clinically defined depression. Large-scale trials are needed to test the effect of sleep restriction therapy in patients experiencing depression and insomnia. Findings also highlight the need to improve the standardisation and reporting of sleep restriction therapy procedures, and to design studies with more rigorous control arms to reduce potential bias.

Sleep restriction alters the integration of multiple information sources in probabilistic decision-making.

The detrimental effects of sleep loss on overall decision-making have been well described. Due to the complex nature of decisions, there remains a need for studies to identify specific mechanisms of decision-making vulnerable to sleep loss. Bayesian perspectives of decision-making posit judgement formation during decision-making occurs via a process of integrating knowledge gleaned from past experiences (priors) with new information from current observations (likelihoods). We investigated the effects of sleep loss on the ability to integrate multiple sources of information during decision-making by reporting results from two experiments: the first implementing both sleep restriction (SR) and total sleep deprivation (TSD) protocols, and the second implementing an SR protocol. In both experiments, participants were administered the Bayes Decisions Task on which optimal performance requires the integration of Bayesian prior and likelihood information. Participants in Experiment 1 showed reduced reliance on both information sources after SR, while no significant change was observed after TSD. Participants in Experiment 2 showed reduced reliance on likelihood after SR, especially during morning testing sessions. No accuracy-related impairments resulting from SR and TSD were observed in both experiments. Our findings show SR affects decision-making through altering the way individuals integrate available sources of information. Additionally, the ability to integrate information during SR may be influenced by time of day. Broadly, our findings carry implications for working professionals who are required to make high-stakes decisions on the job, yet consistently receive insufficient sleep due to work schedule demands.

Selective REM sleep restriction in mice using a device designed for tunable somatosensory stimulation.

BACKGROUND: Sleep perturbation is widely used to investigate the physiological mechanisms that mediate sleep-wake dynamics, and to isolate the specific roles of sleep in health and disease. However, state-of-the-art methods to accomplish sleep perturbation in preclinical models are limited in their throughput, flexibility, and specificity. NEW METHOD: A system was developed to deliver vibro-tactile somatosensory stimulation aimed at controlled, selective sleep perturbation. The frequency and intensity of stimulation can be tuned to target a variety of experimental applications, from sudden arousal to sub-threshold transitions between light and deep stages of NREM sleep. This device was activated in closed-loop to selectively interrupt REM sleep in mice. RESULTS: Vibro-tactile stimulation effectively and selectively interrupted REM sleep - significantly reducing the average REM bout duration relative to matched, unstimulated baseline recordings. As REM sleep was repeatedly interrupted, homeostatic mechanisms prompted a progressively quicker return to REM sleep. These effects were dependent on the parameters of stimulation applied. COMPARISON WITH EXISTING METHODS: Existing sleep perturbation systems often require moving parts within the cage and/or restrictive housing. The system presented is unique in that it interrupts sleep without invading the animal's space. The ability to vary stimulation parameters is a great advantage over existing methods, as it allows for adaptation in response to habituation and/or circadian/homeostatic changes in arousal threshold. CONCLUSIONS: The proposed method of stimulation demonstrates feasibility in affecting mouse sleep within a standard home cage environment, thus limiting environmental stress. Furthermore, the ability to tune frequency and intensity of stimulation allows for graded control over the extent of sleep perturbation, which potentially expands the utility of this technology beyond applications related to sleep.

Awareness of errors is reduced by sleep loss.

The ability to detect and subsequently correct errors is important in preventing the detrimental consequences of sleep loss. The Error Related Negativity (ERN), and the error positivity (Pe) are established neural correlates of error processing. Previous work has shown sleep loss reduces ERN and Pe, indicating sleep loss impairs error-monitoring processes. However, no previous work has examined behavioral error awareness, in conjunction with EEG measures, under sleep loss conditions, and studies of sleep restriction are lacking. Using combined behavioral and EEG measures, we report two studies investigating the impact of total sleep deprivation (TSD) and sleep restriction (SR) on error awareness. Fourteen healthy participants completed the Error Awareness Task under conditions of TSD and 27 completed the same task under conditions of SR. It was found that TSD did not influence behavioral error awareness or ERN or Pe amplitude, however, SR reduced behavioral error awareness, increased the time taken to detect errors, and reduced Pe amplitude. Findings indicate individuals who are chronically sleep restricted are at risk for reduced recognition of errors. Reduced error awareness may be one factor contributing to the increased accidents and injuries seen in contexts where sleep loss is prevalent.