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Abstract The main objective of this study was to evaluate the association of the insomnia-anxiety comorbidity with incident type 2 diabetes (T2D) in a large prospective cohort. We selected adults without diabetes at baseline from the French NutriNet-Santé cohort who had completed the trait anxiety subscale of the Spielberger State-Trait Anxiety Inventory (STAI-T, 2013–2016) and a sleep questionnaire (2014); insomnia was defined according to established criteria. Using multivariable Cox models, we compared T2D risk across 4 groups: no insomnia or anxiety (reference), insomnia alone, anxiety alone (STAI-T ≥ 40), and comorbid anxiety and insomnia. Among 35,014 participants (mean baseline age: 52.4 ± 14.0 years; 76% women), 378 (1.1%) developed T2D over a mean follow-up of 5.9 ± 2.1 years. Overall, 28.5% of the sample had anxiety alone, 7.5%—insomnia alone, and 12.5%—both disorders. In the fully-adjusted model, a higher T2D risk was associated with anxiety-insomnia comorbidity (HR = 1.40; 95% CI 1.01, 1.94), but not with each disorder separately, compared to the group without insomnia or anxiety. The findings supported a positive association between anxiety-insomnia comorbidity and incident T2D among general-population adults. Future research using clinical diagnoses of mental disorders could confirm the findings and guide diabetes prevention programs.

A high percentage of people worldwide complain of sleep disturbances; however, the vast majority do not meet the diagnostic criteria for insomnia or other classic sleep disorders. Therefore, the ‘classical’ concept of poor sleep remains undetected, and patients stay ignored and unidentified. Also, poor sleep has been strongly associated with increased daytime function impairment, morbidity and mortality and is considered a risk factor for developing mental disorders. Poor sleep is the individual experience of insufficient restorative sleep and/or sleep satisfaction in adults who do not fulfil the criteria for sleep disorders. This article provides a review on the impact of poor sleep on a healthy life within the multidimensional concept of sleep health, including the COVID-19-affected period. We propose a wide definition of poor sleep and the key characteristics of poor sleepers and tools for (self) detection. We discuss sleep assessment methods that combine the ability to capture the subjective perception of the sleep experience and measure objective sleep parameters. We then report selected strategies to improve sleep health, focusing on healthy sleep habits, cognitive behavioural therapy, diet, exercise, food supplements and other sleep aids. Considering the current megalopolis way of life, young people are following a 24/24 hours 7 days/week rhythm of life, with increased exposure to noise and light pollution, night-shift work, higher commute time, increased global temperature and overuse of smartphones and screens. Therefore, there is an urgent need for increasing awareness of poor sleep and stimulating educational efforts targeted at poor sleepers and primary care specialists.

Abstract Background Quantitative electroencephalography (EEG) analysis offers the opportunity to study high-level cognitive processes across psychiatric disorders. In particular, EEG microstates translate the temporal dynamics of neuronal networks throughout the brain. Their alteration may reflect transdiagnostic anomalies in neurophysiological functions that are impaired in mood, psychosis, and autism spectrum disorders, such as sensorimotor integration, speech, sleep, and sense of self. The main questions this study aims to answer are as follows: 1) Are EEG microstate anomalies associated with clinical and functional prognosis, both in resting conditions and during sleep, across psychiatric disorders? 2) Are EEG microstate anomalies associated with differences in sensorimotor integration, speech, sense of self, and sleep? 3) Can the dynamic of EEG microstates be modulated by a non-drug intervention such as light hypnosis? Methods This prospective cohort will include a population of adolescents and young adults, aged 15 to 30 years old, with ultra-high-risk of psychosis (UHR), first-episode psychosis (FEP), schizophrenia (SCZ), autism spectrum disorder (ASD), and major depressive disorder (MDD), as well as healthy controls (CTRL) (N = 21 × 6), who will be assessed at baseline and after one year of follow-up. Participants will undergo deep phenotyping based on psychopathology, neuropsychological assessments, 64-channel EEG recordings, and biological sampling at the two timepoints. At baseline, the EEG recording will also be coupled to a sensorimotor task and a recording of the characteristics of their speech (prosody and turn-taking), a one-night polysomnography, a self-reference effect task in virtual reality (only in UHR, FEP, and CTRL). An interventional ancillary study will involve only healthy controls, in order to assess whether light hypnosis can modify the EEG microstate architecture in a direction opposite to what is seen in disease. Discussion This transdiagnostic longitudinal case–control study will provide a multimodal neurophysiological assessment of clinical dimensions (sensorimotor integration, speech, sleep, and sense of self) that are disrupted across mood, psychosis, and autism spectrum disorders. It will further test the relevance of EEG microstates as dimensional functional biomarkers. Trial registration ClinicalTrials.gov Identifier NCT06045897.

Abstract Background Ageing is accompanied by changes in sleep, while poor sleep is suggested as a risk factor for several health outcomes. Non-pharmacological approaches have been proposed to improve sleep in elderly; their impact remains to be investigated. The aim of this study was to examine the independent day-to-day associations of physical behaviours and daylight exposure with sleep characteristics among older adults. Methods Data were drawn from 3942 participants (age range: 60–83 years; 27% women) from the Whitehall II accelerometer sub-study. Day-to-day associations of objectively-assessed daytime physical behaviours (sedentary behaviour, light-intensity physical activity (LIPA), moderate-to-vigorous physical activity (MVPA), mean acceleration, physical activity chronotype) and daylight exposure (proportion of waking window with light exposure > 1000 lx and light chronotype) with sleep characteristics were examined using mixed models. Results A 10%-increase in proportion of the waking period spent sedentary was associated with 5.12-minute (4.31, 5.92) later sleep onset and 1.76-minute shorter sleep duration (95%confidence interval: 0.86, 2.66). Similar increases in LIPA and MVPA were associated with 6.69 (5.67, 7.71) and 4.15 (2.49, 5.81) earlier sleep onset respectively and around 2-minute longer sleep duration (2.02 (0.87, 3.17) and 2.23 (0.36, 4.11), respectively), although the association was attenuated for MVPA after adjustment for daylight exposure (1.11 (− 0.84, 3.06)). A 3-hour later physical activity chronotype was associated with a 4.79-minute later sleep onset (4.15, 5.43) and 2.73-minute shorter sleep duration (1.99, 3.47). A 10%-increase in proportion of waking period exposed to light> 1000 lx was associated with 1.36-minute longer sleep (0.69, 2.03), independently from mean acceleration. Associations found for sleep duration were also evident for duration of the sleep windows with slightly larger effect size (for example, 3.60 (2.37, 4.82) minutes for 10%-increase in LIPA), resulting in associations with sleep efficiency in the opposite direction (for example, − 0.29% (− 0.42, − 0.16) for 10%-increase in LIPA). Overall, associations were stronger for women than for men. Conclusions In this study, higher levels of physical activity and daylight exposure were associated with slightly longer sleep in older adults. Given the small effect sizes of the associations, increased physical activity and daylight exposure might not be enough to improve sleep.

IntroductionInsomnia is highly prevalent in the general population, and is commonly associated with somatic and psychiatric comorbidities. However, its origins remain poorly-understood. Recently, adverse childhood events (ACE), including traumatic experiences, have been found to be significantly associated with both insomnia and Post-Traumatic Stress Disorders (PTSD). Many patients with PTSD suffer from sleep disorders. However, we know much less about traumatic childhood experiences in patients with insomnia and PTSD.MethodsOur exploratory study investigated a cohort of 43 patients (14 males, 29 females) clinically diagnosed with chronic insomnia at a sleep center, and systematically evaluated their condition using the trauma history questionnaire (THQ), and the PTSD checklist (PCL-5).ResultsOur results show that 83.72% of insomnia patients reported at least one traumatic event, while the prevalence of PTSD symptoms was 53.49%. For 11.6% of patients, insomnia began in childhood, while for 27.07% it began in adolescence. PCL-5 scores were associated with higher Insomnia Severity Index (ISI) scores, but not trauma. ISI scores were also higher for women, and positive relationships were observed between ISI scores, PCL-5 scores and the number of self-reported traumatic events among women.ConclusionsThese exploratory results highlight that the relationship between PTSD symptoms and insomnia could be sex-specific. They also highlight the importance of PTSD symptoms screening for patients diagnosed with chronic insomnia.

Background Sleep duration has been shown to be associated with individual chronic diseases but its association with multimorbidity, common in older adults, remains poorly understood. We examined whether sleep duration is associated with incidence of a first chronic disease, subsequent multimorbidity and mortality using data spanning 25 years. Methods and findings Data were drawn from the prospective Whitehall II cohort study, established in 1985 on 10,308 persons employed in the London offices of the British civil service. Self-reported sleep duration was measured 6 times between 1985 and 2016, and data on sleep duration was extracted at age 50 (mean age (standard deviation) = 50.6 (2.6)), 60 (60.3 (2.2)), and 70 (69.2 (1.9)). Incidence of multimorbidity was defined as having 2 or more of 13 chronic diseases, follow-up up to March 2019. Cox regression, separate analyses at each age, was used to examine associations of sleep duration at age 50, 60, and 70 with incident multimorbidity. Multistate models were used to examine the association of sleep duration at age 50 with onset of a first chronic disease, progression to incident multimorbidity, and death. Analyses were adjusted for sociodemographic, behavioral, and health-related factors. A total of 7,864 (32.5% women) participants free of multimorbidity had data on sleep duration at age 50; 544 (6.9%) reported sleeping ≤5 hours, 2,562 (32.6%) 6 hours, 3,589 (45.6%) 7 hours, 1,092 (13.9%) 8 hours, and 77 (1.0%) ≥9 hours. Compared to 7-hour sleep, sleep duration ≤5 hours was associated with higher multimorbidity risk (hazard ratio: 1.30, 95% confidence interval = 1.12 to 1.50; p < 0.001). This was also the case for short sleep duration at age 60 (1.32, 1.13 to 1.55; p < 0.001) and 70 (1.40, 1.16 to 1.68; p < 0.001). Sleep duration ≥9 hours at age 60 (1.54, 1.15 to 2.06; p = 0.003) and 70 (1.51, 1.10 to 2.08; p = 0.01) but not 50 (1.39, 0.98 to 1.96; p = 0.07) was associated with incident multimorbidity. Among 7,217 participants free of chronic disease at age 50 (mean follow-up = 25.2 years), 4,446 developed a first chronic disease, 2,297 progressed to multimorbidity, and 787 subsequently died. Compared to 7-hour sleep, sleeping ≤5 hours at age 50 was associated with an increased risk of a first chronic disease (1.20, 1.06 to 1.35; p = 0.003) and, among those who developed a first disease, with subsequent multimorbidity (1.21, 1.03 to 1.42; p = 0.02). Sleep duration ≥9 hours was not associated with these transitions. No association was found between sleep duration and mortality among those with existing chronic diseases. The study limitations include the small number of cases in the long sleep category, not allowing conclusions to be drawn for this category, the self-reported nature of sleep data, the potential for reverse causality that could arise from undiagnosed conditions at sleep measures, and the small proportion of non-white participants, limiting generalization of findings. Conclusions In this study, we observed short sleep duration to be associated with risk of chronic disease and subsequent multimorbidity but not with progression to death. There was no robust evidence of an increased risk of chronic disease among those with long sleep duration at age 50. Our findings suggest an association between short sleep duration and multimorbidity. Using data from the Whitehall II cohort study, Severine Sabia and colleagues investigate whether sleep duration is associated with subsequent risk of developing multimorbidity among adults age 50, 60, and 70 years old in England. Author summary Why was this study done? The prevalence of multimorbidity is on the rise as reflected in over half of older adults having at least 2 chronic diseases in high-income countries, making multimorbidity a major challenge for public health. Both short and long sleep duration has been shown to be associated with individual chronic diseases, but their associations with multimorbidity and subsequent mortality risk remain unclear. What did the researchers do and find? We used data on more than 7,000 men and women from the Whitehall II cohort study to extract sleep duration at age 50, 60, and 70 and examined its association with incident multimorbidity over 25 years of follow-up. Role of sleep duration at age 50 in transitions from a healthy state to a first chronic disease, multimorbidity, and mortality was also examined using a multistate model. We found a robust association of sleep duration ≤5 hours at age 50, 60, and 70 (separate analyses) with higher risk of incident multimorbidity, while the association with sleep duration ≥9 hours was observed only when measured at age 60 and 70. Analysis of transitions in health states showed short sleep duration at age 50 to be associated with 20% increased risk of a first chronic disease, and with a similar increased risk of subsequent multimorbidity, but within this framework there was no clear evidence of associations with mortality. There was no robust association between sleep duration ≥9 hours at age 50 and risk of 1 chronic disease or multimorbidity. However, in those with a chronic condition there was some evidence of higher risk of multimorbidity. What do these findings mean? Our comprehensive analyses of the association of sleep duration with multimorbidity and the natural course of chronic disease show short sleep duration to be associated with the onset of chronic disease and multimorbidity but not with subsequent mortality in those with chronic disease(s). There was no clear evidence for an association between long sleep duration at age 50 and risk of chronic disease. Rather the increased risk of multimorbidity associated with long sleep duration at older ages and in those with existing disease might reflect the need for longer sleep in those with underlying chronic conditions.

ObjectivesWe aimed to examine the effects of circadian and sleep rhythm disruptions on immune biomarkers among hospital healthcare professionals working night shifts and rotating day shifts.MethodsHospital nurses working either as permanent night shifters (n=95) or as day shifters rotating between morning and afternoon shifts (n=96) kept a daily diary on their sleep and work schedules over a full working week. Blood samples were collected at the beginning and end of the last shift during the week, and participants were categorized into three groups based on work shift: morning shift (39 day shifters sampled at 7:00 and 14:00), afternoon shift (57 day shifters sampled at 14:00 and 21:00), and night shift (95 night shifters sampled at 21:00 and 7:00). Circulating blood counts in immune cells, interleukin-6 and C-reactive protein concentrations as well as total sleep time per 24 hours during work days (TST24w) and free days (TST24f), sleep debt (TST24f — TST24w) and social jet-lag (a behavioral proxy of circadian misalignment) were assessed.ResultsCompared with day shifters, night shifters had shorter sleep duration (TST24w=5.4 ± 1.4h), greater sleep debt (3.2 ± 1.4 h) and social jet-lag (6.7 ± 2.4 h). Variations of immune biomarkers concentrations were consistent with the expected diurnal variations among day shifters (i.e., low level in the morning, increase during the day, peak value in the evening). By contrast, in night shifters, blood concentrations of total lymphocytes, T-helper cells, cytotoxic T-cells, memory B-cells and interleukin-6 were lower at 21:00, increased during the night, and reached higher values at 7:00. Multivariate analyses ruled out significant impact of TST24w, sleep debt, and social jet-lag on immune biomarkers concentrations among day shifters. In contrast, among night shifters, multivariate analyses indicated a combined effect of total sleep time (TST24w), sleep debt and social jet-lag for total lymphocytes and T-helper cells but only a social jet-lag effect for interleukin-6 and a single total sleep time effect for neutrophil and B-Cells.ConclusionsAltogether, our results point to intricate response patterns of immune rhythms to circadian misalignment and sleep debt in night shifters. Specifically, these altered pattern expressions of immune cells may increase vulnerability to infections and reduce vaccination efficiency in night workers.

Summary: Background: Telemonitoring of circadian and sleep cycles could identify shift workers at increased risk of poor health, including cancer and cardiovascular diseases, thus supporting personalized prevention. Methods: The Circadiem cross-sectional study aimed at determining early warning signals of risk of health alteration in hospital nightshifters (NS) versus dayshifters (DS, alternating morning and afternoon shifts). Circadian rhythmicity in activity, sleep, and temperature was telemonitored on work and free days for one week. Participants wore a bluetooth low energy thoracic accelerometry and temperature sensor that was wirelessly connected to a GPRS gateway and a health data hub server. Hidden Markov modelling of activity quantified Rhythm Index, rest quality (probability, p1-1, of remaining at rest), and rest duration. Spectral analyses determined periods in body surface temperature and accelerometry. Parameters were compared and predictors of circadian and sleep disruption were identified by multivariate analyses using information criteria-based model selection. Clusters of individual shift work response profiles were recognized. Findings: Of 140 per-protocol participants (133 females), there were 63 NS and 77 DS. Both groups had similar median rest amount, yet NS had significantly worse median rest-activity Rhythm Index (0·38 [IQR, 0·29-0·47] vs. 0·69 [0·60-0·77], p

New information can be learned during sleep but the extent to which we can access this knowledge after awakening is far less understood. Using a novel Associative Transfer Learning paradigm, we show that, after hearing unknown Japanese words with sounds referring to their meaning during sleep, participants could identify the images depicting the meaning of newly acquired Japanese words after awakening (N = 22). Moreover, we demonstrate that this cross-modal generalization is implicit, meaning that participants remain unaware of this knowledge. Using electroencephalography, we further show that frontal slow-wave responses to auditory stimuli during sleep predicted memory performance after awakening. This neural signature of memory formation gradually emerged over the course of the sleep phase, highlighting the dynamics of associative learning during sleep. This study provides novel evidence that the formation of new associative memories can be traced back to the dynamics of slow-wave responses to stimuli during sleep and that their implicit transfer into wakefulness can be generalized across sensory modalities.

Objectives Sleep is important for human health and well-being. No previous study has assessed whether the COVID-19 pandemic impacts sleep and daytime function across the globe.Methods This large-scale international survey used a harmonised questionnaire. Fourteen countries participated during the period of May–August 2020. Sleep and daytime problems (poor sleep quality, sleep onset and maintenance problems, nightmares, hypnotic use, fatigue and excessive sleepiness) occurring ‘before’ and ‘during’ the pandemic were investigated. In total, 25 484 people participated and 22 151 (86.9%) responded to the key parameters and were included. Effects of COVID-19, confinement and financial suffering were considered. In the fully adjusted logistic regression models, results (weighted and stratified by country) were adjusted for gender, age, marital status, educational level, ethnicity, presence of sleep problems before COVID-19 and severity of the COVID-19 pandemic in each country at the time of the survey.Results The responders were mostly women (64%) with a mean age 41.8 (SD 15.9) years (median 39, range 18–95). Altogether, 3.0% reported having had COVID-19; 42.2% reported having been in confinement; and 55.9% had suffered financially. All sleep and daytime problems worsened during the pandemic by about 10% or more. Also, some participants reported improvements in sleep and daytime function. For example, sleep quality worsened in about 20% of subjects and improved in about 5%. COVID-19 was particularly associated with poor sleep quality, early morning awakening and daytime sleepiness. Confinement was associated with poor sleep quality, problems falling asleep and decreased use of hypnotics. Financial suffering was associated with all sleep and daytime problems, including nightmares and fatigue, even in the fully adjusted logistic regression models.Conclusions Sleep problems, fatigue and excessive sleepiness increased significantly worldwide during the first phase of the COVID-19 pandemic. Problems were associated with confinement and especially with financial suffering.

IntroductionObstructive sleep apnea (OSA) is a frequent condition. In the absence of treatment, OSA is associated with a higher risk of traffic accidents and a large variety of diseases. The objectives of this study were to describe the characteristics of patients treated for OSA in France and assess the time trends in treatment.MethodsThe French National Health Data System is an individual database with data on all healthcare reimbursements for the entire French population. Based on this database, we included all patients aged 20 years or over who were treated with continuous positive airway pressure (CPAP) or mandibular advancement splint (MAS) between 2009 and 2018. Negative binomial models, adjusted for age, were used to assess time trends in treatment prevalence and incidence rates.ResultsIn 2017, 2.3% of French adults aged ≥20 years were treated with CPAP (men: 3.3%; women: 1.3%). The highest prevalence was observed in people aged 70-74 years (5.0%). From 2009 to 2018, the annual prevalence of CPAP increased 3-fold and the annual incidence 1.9-fold. During the same period, the rate of patients reimbursed for MAS (first prescription or renewal) was multiplied by 7.6. The proportion of patients treated with CPAP in 2017 who were no longer treated in the subsequent year was 6.9%.DiscussionThe sharp increase in the incidence of OSA treatment probably reflects a better recognition of the disease in France. However, the prevalence of OSA treatment remains lower than expected based on the international literature. Further studies are needed to identify the obstacles to an optimal management of individuals with OSA in France.

Sleep debt is becoming a better acknowledged cause of physiological stress and neurobehavioral deficits with major public-health concerns. We investigated whether exposure to blue light during daytime could be an efficient countermeasure to limit sleep restriction’s impact on relevant behavioral (stress, sleepiness, sustained attention, and memory performance) and physiological (saliva cortisol, testosterone, and alpha-amylase) markers. Our semi-ecological, crossover, randomized design included 17 young men that underwent two sleep-restricted nights (3 h each) followed or not by blue light exposure (30-min-long sessions at 100 lux repeated four times throughout the day). Behavioral and physiological measurements were performed in the lab but outside these periods the participants kept following their usual routine. After sleep restriction, morning cortisol and testosterone, and afternoon alpha-amylase levels decreased. In parallel, subjective ratings of stress and sleepiness increased while performance on the sustained attention and memory tasks deteriorated. In contrast, after periods of blue light exposure, all these parameters were largely restored to baseline levels, despite an identical sleep restriction procedure, although this restorative effect was reduced for the memory task. Our findings suggest that even short exposure to blue light could trigger persistent beneficial effects throughout the day and could be potentially efficient in real-life settings.

Several genetic polymorphisms differentiate between healthy individuals who are more cognitively vulnerable or resistant during total sleep deprivation (TSD). Common metrics of cognitive functioning for classifying vulnerable and resilient individuals include the Psychomotor Vigilance Test (PVT), Go/noGo executive inhibition task, and subjective daytime sleepiness. We evaluated the influence of 14 single-nucleotide polymorphisms (SNPs) on cognitive responses during total sleep deprivation (continuous wakefulness for 38 h) in 47 healthy subjects (age 37.0 ± 1.1 years). SNPs selected after a literature review included SNPs of the adenosine-A2A receptor gene (including the most studied rs5751876), pro-inflammatory cytokines (TNF-α, IL1-β, IL-6), catechol-O-methyl-transferase (COMT), and PER3. Subjects performed a psychomotor vigilance test (PVT) and a Go/noGo-inhibition task, and completed the Karolinska Sleepiness Scale (KSS) every 6 h during TSD. For PVT lapses (reaction time >500 ms), an interaction between SNP and SDT (p < 0.05) was observed for ADORA2A (rs5751862 and rs2236624) and TNF-α (rs1800629). During TSD, carriers of the A allele for ADORA2A (rs5751862) and TNF-α were significantly more impaired for cognitive responses than their respective ancestral G/G genotypes. Carriers of the ancestral G/G genotype of ADORA2A rs5751862 were found to be very similar to the most resilient subjects for PVT lapses and Go/noGo commission errors. Carriers of the ancestral G/G genotype of COMT were close to the most vulnerable subjects. ADORA2A (rs5751862) was significantly associated with COMT (rs4680) (p = 0.001). In conclusion, we show that genetic polymorphisms in ADORA2A (rs5751862), TNF-α (rs1800629), and COMT (rs4680) are involved in creating profiles of high vulnerability or high resilience to sleep deprivation. (NCT03859882).

Though memory and sleep are related, it is still unclear whether new memories can be formed during sleep. Here, authors show that people could learn new sounds during REM or light non-REM sleep, but that learning was suppressed when sounds were played during deep NREM sleep.

Recent research has shown that auditory closed-loop stimulation can enhance sleep slow oscillations (SO) to improve N3 sleep quality and cognition. Previous studies have been conducted in lab environments. The present study aimed to validate and assess the performance of a novel ambulatory wireless dry-EEG device (WDD), for auditory closed-loop stimulation of SO during N3 sleep at home. The performance of the WDD to detect N3 sleep automatically and to send auditory closed-loop stimulation on SO were tested on 20 young healthy subjects who slept with both the WDD and a miniaturized polysomnography (part 1) in both stimulated and sham nights within a double blind, randomized and crossover design. The effects of auditory closed-loop stimulation on delta power increase were assessed after one and 10 nights of stimulation on an observational pilot study in the home environment including 90 middle-aged subjects (part 2).The first part, aimed at assessing the quality of the WDD as compared to a polysomnograph, showed that the sensitivity and specificity to automatically detect N3 sleep in real-time were 0.70 and 0.90, respectively. The stimulation accuracy of the SO ascending-phase targeting was 45 ± 52°. The second part of the study, conducted in the home environment, showed that the stimulation protocol induced an increase of 43.9% of delta power in the 4 s window following the first stimulation (including evoked potentials and SO entrainment effect). The increase of SO response to auditory stimulation remained at the same level after 10 consecutive nights. The WDD shows good performances to automatically detect in real-time N3 sleep and to send auditory closed-loop stimulation on SO accurately. These stimulation increased the SO amplitude during N3 sleep without any adaptation effect after 10 consecutive nights. This tool provides new perspectives to figure out novel sleep EEG biomarkers in longitudinal studies and can be interesting to conduct broad studies on the effects of auditory stimulation during sleep.

Several aspects of human physiology and behavior are dominated by 24-h circadian rhythms with key impacts on health and well-being. These include mainly the sleep–wake cycle, vigilance and performance patterns, and some hormone secretions. The rhythms are generated spontaneously by an internal “pacemaker,” the suprachiasmatic nuclei within the anterior hypothalamus. This master clock has, for most humans, an intrinsic rhythm slightly longer than 24 h. Daily retinal light exposure is necessary for the synchronization of the circadian rhythms with the external 24-h solar environment. This daily synchronization process generally poses no problems for sighted individuals except in the context of jetlag or working night shifts being conditions of circadian desynchrony. However, many blind subjects with no light perception had periodical circadian desynchrony, in the absence of light information to the master clock leading to poor circadian rhythm synchronization. Affected patients experience cyclical or periodic episodes of poor sleep and daytime dysfunction, severely interfering with social, academic, and professional life. The diagnosis of Non-24 Sleep–Wake Rhythm Disorder, also named free-running disorder, non-entrained disorder, or hypernycthemeral syndrome, remains challenging from a clinical point of view due to the cyclical symptoms and should be confirmed by measurements of circadian biomarkers such as urinary melatonin to demonstrate a circadian period outside the normal range. Management includes behavioral modification and melatonin. Tasimelteon, a novel melatonin receptor 1 and 2 agonist, has demonstrated its effectiveness and safety with an evening dose of 20 mg and is currently the only treatment approved by the FDA and the European Medicines Agency.

To investigate pain sensitivity after sleep restriction and the restorative effect of napping.A strictly controlled randomized crossover study with continuous polysomnography monitoring was performed.Laboratory-based study.11 healthy male volunteers.Volunteers attended two three-day sessions: "sleep restriction" alone and "sleep restriction and nap". Each session involved a baseline night of normal sleep, a night of sleep deprivation and a night of free recovery sleep. Participants were allowed to sleep only from 02:00 to 04:00 during the sleep deprivation night. During the "sleep restriction and nap" session, volunteers took two 30-minute naps, one in the morning and one in the afternoon.Quantitative sensory testing was performed with heat, cold and pressure, at 10:00 and 16:00, on three areas: the supraspinatus, lower back and thigh. After sleep restriction, quantitative sensory testing revealed differential changes in pain stimuli thresholds, but not in thermal threshold detection: lower back heat pain threshold decreased, pressure pain threshold increased in the supraspinatus area and no change was observed for the thigh. Napping restored responses to heat pain stimuli in the lower back and to pressure stimuli in the supraspinatus area.Sleep restriction induces different types of hypersensitivity to pain stimuli in different body areas, consistent with multilevel mechanisms, these changes being reversed by napping. The napping restorative effect on pain thresholds result principally from effects on pain mechanisms, since it was independent of vigilance status.

BackgroundA significant U-shaped association between sleep duration and several morbidity (obesity, diabetes or cardiovascular disease) and mortality risks has been regularly reported. However, although the physiological pathways and risks associated with "too short sleep" (PurposeTo explore socio-demographic characteristics and comorbidities of "long sleepers" (over 10 hours/day) from a nationally representative sample of adults.MethodsA cross-sectional nationally representative sample of 24,671 subjects from 15 to 85-year-old. An estimated total sleep time (TST) on non-leisure days was calculated based on a specifically designed sleep log which allows to distinguish "long sleepers" from "short sleepers" (ResultsThe average TST was 7 hours and 13 minutes (+/- 17 minutes). Six hundred and twelve subjects were "long sleepers" (2.7%) and 1969 "short sleepers" (7.5%). Compared to the whole group, "long sleepers" were more often female, younger (15-25 year-old) or older (above 65 year-old), with no academic degree, mostly clerks and blue collar workers. "Long sleepers" were significantly more likely to have psychiatric diseases and a greater body mass index (BMI). However, long sleep was not significantly associated with the presence of any other chronic medical disease assessed. Conversely, short sleep duration was significantly associated with almost all the other chronic diseases assessed.ConclusionsIn the general population, sleeping too much was associated with psychiatric diseases and higher BMI, but not with other chronic medical diseases.