Extending weeknight sleep duration in late-sleeping adolescents using morning bright light on weekends: a 3-week maintenance study.

Study Objectives: Our sleep extension intervention in adolescents showed that gradually shifting weekday bedtime earlier plus one weekend of morning bright light advanced circadian phase and increased weeknight sleep duration. Here, we examine at-home maintenance of these changes. Methods: Fourteen adolescents (15.3-17.9 years; 7 female) completed a 7-week study. After usual sleep at home (2-week baseline), intervention participants (n = 8) gradually advanced weekday bedtime (1 hour earlier than baseline during week 3; 2 hours earlier in week 4) and received bright light (~6000 lux; 2.5 hours) on both mornings of the intervening weekend. During three maintenance weeks, intervention participants were instructed to maintain their school-day wake-up time on all days, keep their early week four bedtimes, except on weekends when they could go to bed up to 1 hour later, and get a 2.5-hour light box exposure within 5 minutes of waking on one morning (Saturday or Sunday) of both weekends at home. Control participants (n = 6) slept as usual at home and did not receive weekend bright light. Dim light melatonin onset (DLMO) was measured after the 2-week baseline, 2-week intervention, and 3-week maintenance in all participants. Actigraphic sleep-wake was collected throughout. Results: After the 2-week intervention, DLMOs advanced more compared to control (37.0 ±â€…40.0 minutes vs. -14.7 ±â€…16.6 minutes), weekday sleep duration increased by 69.7 ±â€…27.8 minutes and sleep onset was 103.7 ±â€…14.2 minutes earlier compared to baseline. After three maintenance weeks, intervention participants showed negligible DLMO delays (-4.9 ±â€…22.9 minutes); weekday fall-asleep times and sleep durations also remained stable. Conclusions: Early circadian phase and extended sleep can be maintained with at-home weekend bright light.

Improving Memory through Better Sleep in Community-dwelling Older Adults: A Tai Chi Intervention Study.

OBJECTIVES: The relationship between sleep and memory has been well documented. However, it remains unclear whether a mind-body exercise, i.e., Tai Chi exercise, can improve memory performance in older adults by improving their subjective and objective sleep. METHOD: A randomized controlled trial was conducted with participants (M = 67.36, 56-79 years) randomly assigned to Tai Chi and control groups. The primary outcomes were sleep, both subjectively reported and objectively assessed by actigraphy, and memory performance, as well as the mediating role of sleep in memory improvement with Tai Chi practice. RESULTS: Tai Chi exercise led to improvements in subjective sleep, as indicated by ISI (p < 0.001, Cohen's d = 0.62) and daytime dysfunction of the PSQI (p = 0.02, Cohen's d = 0.80), and in actigraphy-assessed sleep onset latency (p < 0.01, Cohen's d = 0.61), as well as improved memory performance on digit span forward (p < 0.001, Cohen's d = 1.20) and visual spatial memory tasks (p < 0.01, Cohen's d = 0.83) compared to the control group. Importantly, Tai Chi practice improved digit span forward memory performance through parallel mediation of both subjective sleep (i.e., daytime dysfunction of the PSQI) and objective sleep (i.e., sleep onset latency; b = 0.29, p < 0.01). DISCUSSION: Our findings uncovered the potential benefits of Tai Chi exercise in relation to both subjective and objective sleep in older adults, in turn, how sleep changes played a role in the link between Tai Chi exercise and memory changes in older adults.

REM sleep in narcolepsy.

Narcolepsy is mainly associated with excessive daytime sleepiness, but the characteristic feature is abnormal rapid eye movement (REM) sleep phenomena. REM sleep disturbances can manifest as cataplexy (in narcolepsy type 1), sleep paralysis, sleep-related hallucinations, REM sleep behavior disorder, abnormal dreams, polysomnographic evidence of REM sleep disruption with sleep-onset REM periods, and fragmented REM sleep. Characterization of REM sleep and related symptoms facilitates the differentiation of narcolepsy from other central hypersomnolence disorders and aids in distinguishing between narcolepsy types 1 and 2. A circuit comprising regions within the brainstem, forebrain, and hypothalamus is involved in generating and regulating REM sleep, which is influenced by changes in monoamines, acetylcholine, and neuropeptides. REM sleep is associated with brainstem functions, including autonomic control, and REM sleep disturbances may be associated with increased cardiovascular risk. Medications used to treat narcolepsy (and REM-related symptoms of narcolepsy) include stimulants/wake-promoting agents, pitolisant, oxybates, and antidepressants; hypocretin agonists are a potential new class of therapeutics. The role of REM sleep disturbances in narcolepsy remains an area of active research in pathophysiology, symptom management, and treatment. This review summarizes the current understanding of the role of REM sleep and its dysfunction in narcolepsy.

Heart rate variability during sleep onset in patients with insomnia with or without comorbid sleep apnea.

OBJECTIVES: Pre-sleep stress or hyperarousal is a known key etiological component in insomnia disorder. Despite this, physiological alterations during the sleep onset are not well-understood. In particular, insomnia and obstructive sleep apnea (OSA) are highly prevalent co-morbid conditions, where autonomic regulation may be altered. We aimed to characterize heart rate variability (HRV) during sleep onset as a potential measure of pre-sleep hyperarousal. METHODS: We described the profile of pre-sleep HRV measures and explore autonomic differences in participants with self-reported insomnia disorder (with no OSA, n = 69; with mild OSA, n = 70; with moderate or severe OSA, n = 66), compared to normal sleep controls (n = 123). Heart rate data during the sleep onset process were extracted for HRV analyses. RESULTS: During the sleep onset process, compared to normal sleep controls, participants with insomnia had altered HRV, indicated by higher heart rate (p = 0.004), lower SDNN (p = 0.003), reduced pNN20 (p < 0.001) and pNN50 (p = 0.010) and lower powers (p < 0.001). Participants with insomnia and moderate/severe OSA may have further deteriorated HRV outcomes compared to no/mild OSA patients with insomnia but differences were not significant. Insomnia itself was associated with significantly higher heart rate, lower pNN20, and lower high frequency power even after adjustment for age, gender, BMI and OSA severity. CONCLUSIONS: Participants with insomnia had lower vagal activity during the sleep onset period, which may be compounded by OSA, reflected in higher heart rates and lower HRV. These altered heart rate dynamics may serve as a physiological biomarker for insomnia during bedtime wakefulness, or as a potential tool to evaluate the efficacy of behavioral interventions which target bedtime stress.

Decreased Delta/Beta ratio index as the sleep state-independent electrophysiological signature of sleep state misperception in Insomnia disorder: A focus on the sleep onset and the whole night.

PURPOSE: Sleep State Misperception (SSM) is described as the tendency of Insomnia Disorder (ID) patients to overestimate Sleep Latency (SL) and underestimate Total Sleep Time (TST). Literature exploring topographical components in ID with SSM is scarce and does not allow us to fully understand the potential mechanisms underlying this phenomenon. This study aims to evaluate the existence of sleep EEG topography alterations in ID patients associated with SSM compared to Healthy Controls (HC), focusing on two distinct periods: the Sleep Onset (SO) and the whole night. METHODS: Twenty ID patients (mean age: 43.5 ± 12.7; 7 M/13F) and 18 HCs (mean age: 41.6 ± 11.9; 8 M/10F) underwent a night of Polysomnography (PSG) and completed sleep diaries the following morning upon awakening. Two SSM indices, referring to the misperception of SL (SLm) and TST (TSTm), were calculated by comparing objective and subjective sleep indices extracted by PSG and sleep diary. According to these indices, the entire sample was split into 4 sub-groups: ID +SLm vs HC -SLm; ID +TSTm vs HC -TSTm. RESULTS: Considering the SO, the two-way mixed-design ANOVA showed a significant main effect of Groups pointing to a decreased delta/beta ratio in the whole scalp topography. Moreover, we found a significant interaction effect for the sigma and beta bands. Post Hoc tests showed higher sigma and beta power in anterior and temporo-parietal sites during the SO period in IDs +SLm compared to HC -SLm. Considering the whole night, the unpaired t-test revealed in IDs +TSTm significantly lower delta power during NREM, and lower delta/beta ratio index during NREM and REM sleep compared to HCs -TSTm. Finally, we found diffuse significant negative correlations between SSM indices and the delta/beta ratio during SO, NREM, and REM sleep. CONCLUSION: The main finding of the present study suggests that higher SL overestimation and TST underestimation are both phenomena related to diffuse cortical hyperarousal interpreted as a sleep state-independent electrophysiological correlate of the SSM, both during the SO and the whole night.

Altered sleep onset transition in depression: Evidence from EEG activity and EEG functional connectivity analyses.

OBJECTIVE: Sleep disorders constitute a principal diagnostic criterion for depression, potentially reflecting the abnormal persistence of brain activity during the sleep onset (SO) transition. Here, we sought to explore the differences in the dynamic changes in the EEG activity and the EEG functional connectivity (FC) during the SO transition in depressed patients. METHODS: Overnight polysomnography recordings were obtained from thirty-two depressed patients and thirty-three healthy controls. The multiscale permutation entropy (MSPE) and EEG relative power were extracted to characterize EEG activity, and weighted phase lag index (WPLI) was calculated to characterize EEG FC. RESULTS: The intergroup differences in EEG activity of relative power and MSPE were reversed near SO, which attributed to slower rates of change among depressed patients. Regarding the characteristics of the EEG FC network, depressed patients exhibited significantly higher inter-hemispheric and interregional WPLI values in both delta and alpha bands throughout the SO transition, concomitant with different dynamic properties in the delta band FC. During the process after SO, patients exhibited increased inter-hemispheric long-range links, whereas controls showed more intra-hemispheric ones. Finally, we found significant correlations in the dynamic changes between different EEG measures. CONCLUSIONS: Our research revealed that the abnormal changes during the SO transition in depressed patients were manifested in both homeostatic and dynamic aspects, which were reflected in EEG FC and EEG activity, respectively. SIGNIFICANCE: These findings may elucidate the mechanism underlying sleep disorders in depression from the perspective of neural activity.

Time-Dependent Effects of Altered Prebedtime Light Exposure in Enclosed Spaces on Sleep Performance Associated with Human States.

Purpose: Exposure to artificial light influences human performance, which is essential for maintaining healthy work and sleep. However, existing research has not explored the intrinsic links between sleep performance and human states over time under prebedtime light exposure interventions (LEIs). Methods: To investigate the time-dependent effects of altered prebedtime light exposure, four LEI groupings (#L1 - #L4) and a Time factor (D8, D9, and D10) were chosen for sleep experiments in enclosed spaces. Forty-eight young adults recruited were available for data analysis. Subjective alertness (SA), negative affect (NA), subjective sleep, and objective sleep were measured via the Karolinska Sleepiness Scale, Positive and Negative Affect Schedule, Next-day Self-assessment Sleep Quality, and joint assessment of wrist actigraphy and sleep diaries, respectively. Statistical analysis was used for the effects of light exposure on the human states (corresponding to the SA and NA) and sleep performance, while the process model helped construct the associations between the two. Results: The statistical effects revealed that the Time had a significant main effect on subjective sleep and changes in prebedtime alertness; the LEI had a significant main effect only on sleep onset latency (SOL). After undergoing altered prebedtime light exposure, the mean SA increased at prebedtime of D9 (p = 0.022) and D10 (p = 0.044); No significant effect on the NA was observed; Mean subjective sleep had a significant increase from D8 to D10. Moreover, five actigraphy-estimated sleep parameters were interrelated. In light of this, a chained pathway relationship was identified. The SOL played a mediating predictor between prebedtime state and objective sleep, which was linked to the awakening state through subjective sleep. Conclusion: Our study suggests that time-dependent effects of altered prebedtime light exposure on sleep performance are associated with human states at prebedtime and awakening, with implications for its prediction of sleep health.

Narcolepsy and rapid eye movement sleep.

Since the first description of narcolepsy at the end of the 19th Century, great progress has been made. The disease is nowadays distinguished as narcolepsy type 1 and type 2. In the 1960s, the discovery of rapid eye movement sleep at sleep onset led to improved understanding of core sleep-related disease symptoms of the disease (excessive daytime sleepiness with early occurrence of rapid eye movement sleep, sleep-related hallucinations, sleep paralysis, rapid eye movement parasomnia), as possible dysregulation of rapid eye movement sleep, and cataplexy resembling an intrusion of rapid eye movement atonia during wake. The relevance of non-sleep-related symptoms, such as obesity, precocious puberty, psychiatric and cardiovascular morbidities, has subsequently been recognized. The diagnostic tools have been improved, but sleep-onset rapid eye movement periods on polysomnography and Multiple Sleep Latency Test remain key criteria. The pathogenic mechanisms of narcolepsy type 1 have been partly elucidated after the discovery of strong HLA class II association and orexin/hypocretin deficiency, a neurotransmitter that is involved in altered rapid eye movement sleep regulation. Conversely, the causes of narcolepsy type 2, where cataplexy and orexin deficiency are absent, remain unknown. Symptomatic medications to treat patients with narcolepsy have been developed, and management has been codified with guidelines, until the recent promising orexin-receptor agonists. The present review retraces the steps of the research on narcolepsy that linked the features of the disease with rapid eye movement sleep abnormality, and those that do not appear associated with rapid eye movement sleep.

Novel biomarkers derived from the Maintenance of Wakefulness Test as predictors of sleepiness and response to treatment.

The Maintenance of Wakefulness Test (MWT) is a widely accepted objective test used to evaluate daytime somnolence and is commonly used in clinical studies evaluating novel therapeutics for excessive daytime sleepiness. In the latter, sleep onset latency (SOL) is typically the sole MWT endpoint. Here, we explored microsleeps, sleep probability measures derived from automated sleep scoring, and quantitative electroencephalography (qEEG) features as additional MWT biomarkers of daytime sleepiness, using data from a phase 1B trial of the selective orexin receptor 2 agonist danavorexton (TAK-925) in people with narcolepsy type 1 (NT1) or type 2 (NT2). Danavorexton treatment reduced the rate and duration of microsleeps during the MWT in NT1 (days 1 and 7; p ≤ 0.005) and microsleep rate in NT2 (days 1 and 7; p < 0.0001). Use of an EEG-sleep-staging-derived measure to determine the probability of wakefulness for each minute revealed a novel metric to track changes in daytime sleepiness, which were consistent with the θ/α ratio, a known biomarker of drowsiness. The slopes of line-fits to both the log-transformed sleepiness score or log-transformed θ/α ratio correlated well to (inverse) MWT SOL for NT1 (R = 0.93 and R = 0.83, respectively) and NT2 (R = 0.97 and R = 0.84, respectively), suggesting that individuals with narcolepsy have increased sleepiness immediately after lights-off. These analyses demonstrate that novel EEG-based biomarkers can augment SOL as predictors of sleepiness and its response to treatment and provide a novel framework for the analysis of wake EEG in hypersomnia disorders.

Menstrual-Cycle Symptoms and Sleep Characteristics in Elite Soccer Players.

PURPOSE: To determine whether menstrual-cycle symptoms are associated with sleep in elite female athletes. METHODS: Sleep was assessed for a minimum of 25 nights (range = 25-31) using activity monitoring and sleep diaries. Menstrual-cycle symptoms were collected over the same duration in 12 elite female professional soccer players. Generalized estimating equations were used to examine the relationship between the day of the menstrual cycle (from day 1) and total menstrual-cycle symptoms on sleep characteristics. RESULTS: There was a significant relationship between sleep duration and the day of the menstrual cycle (P = .042) and total symptoms reported that day (P < .001), with sleep duration increasing by 21 minutes for every symptom reported. There was a negative day × symptom interaction on sleep duration (P = .004), indicating that with increased symptoms, the day of the menstrual cycle had a smaller relationship with sleep duration. Sleep efficiency (P = .950), wake after sleep onset (P = .217), and subjective sleep quality (P = .080) were not related to the day of the menstrual cycle. The total symptoms reported had no relationship with sleep efficiency (P = .220), subjective sleep quality (P = .502), or sleep latency (P = .740) but did significantly relate to wake after sleep onset (P < .001), with a significant day × symptom interaction (P < .001). CONCLUSIONS: Sleep duration increased from day 1 of the menstrual cycle and was associated with the number of menstrual-cycle symptoms reported. All other sleep metrics remained unchanged; however, total symptoms reported were related to wake after sleep onset. Monitoring and managing menstrual-cycle symptoms should be encouraged due to a potential relationship with sleep characteristics.

Joint Association of Sleep Onset Time and Sleep Duration With Cardiometabolic Health Outcome.

BACKGROUND: The association of sleep onset time and duration with cardiometabolic health is not well characterized. METHODS AND RESULTS: This study included 6696 adults aged 20 to 80 years from the NHANES (National Health and Nutrition Examination Study) 2015 to 2018. Participants were categorized into 9 groups according to the cross-tabulation of sleep onset time (<22:00 [early], 22:00-23:59 [optimal], and ≥24:00 [late]) and duration (<7 hours [insufficient], 7-8 hours [sufficient], and ≥9 hours [excessive]), with optimal sleep onset time and sufficient duration as the reference. The primary outcomes included hypertension, hypertriglyceridemia, low high-density lipoprotein cholesterol, hyperglycemia, central obesity, and metabolic syndrome. Inappropriate sleep onset time and sleep duration were associated with increased odds of hypertension, hypertriglyceridemia, and metabolic syndrome, especially among participants aged 40 to 59 years. Compared with men reporting optimal onset and sufficient duration, men reporting optimal onset with excessive duration (odds ratio [OR]: 2.01 [95% CI, 1.12-3.58]) and late onset with insufficient duration (OR, 1.74 [95% CI, 1.13-2.68]) had higher odds of metabolic syndrome. Compared with women reporting optimal onset and sufficient duration, women reporting optimal onset and insufficient duration (OR, 1.61 [95% CI, 1.11-2.32]) and early onset and excessive duration (OR, 2.16 [95% CI, 1.30-3.57]) had higher odds of hypertension, and women reporting late onset and excessive duration (OR, 5.64 [95% CI, 1.28-6.77]) were at the highest odds of hypertriglyceridemia. CONCLUSIONS: Late sleep onset as well as insufficient or excessive sleep duration are associated with adverse cardiometabolic outcomes, particularly in participants aged 40 to 59 years.

Out-of-body experiences in relation to lucid dreaming and sleep paralysis: A theoretical review and conceptual model.

Out-of-body experiences (OBEs) are characterized by the subjective experience of being located outside the physical body. Little is known about the neurophysiology of spontaneous OBEs, which are often reported by healthy individuals as occurring during states of reduced vigilance, particularly in proximity to or during sleep (sleep-related OBEs). In this paper, we review the current state of research on sleep-related OBEs and hypothesize that maintaining consciousness during transitions from wakefulness to REM sleep (sleep-onset REM periods) may facilitate sleep-related OBEs. Based on this hypothesis, we propose a new conceptual model that potentially describes the relationship between OBEs and sleep states. The model sheds light on the phenomenological differences between sleep-related OBEs and similar states of consciousness, such as lucid dreaming (the realization of being in a dream state) and sleep paralysis (feeling paralyzed while falling asleep or waking up), and explores the potential polysomnographic features underlying sleep-related OBEs. Additionally, we apply the predictive coding framework and suggest a connecting link between sleep-related OBEs and OBEs reported during wakefulness.

Spatiotemporal EEG dynamics of the sleep onset process in preadolescence.

BACKGROUND: During preadolescence the sleep electroencephalography undergoes massive qualitative and quantitative modifications. Despite these relevant age-related peculiarities, the specific EEG pattern of the wake-sleep transition in preadolescence has not been exhaustively described. METHODS: The aim of the present study is to characterize regional and temporal electrophysiological features of the sleep onset (SO) process in a group of 23 preadolescents (9-14 years) and to compare the topographical pattern of slow wave activity and delta/beta ratio of preadolescents with the EEG pattern of young adults. RESULTS: Results showed in preadolescence the same dynamics known for adults, but with peculiarities in the delta and beta activity, likely associated with developmental cerebral modifications: the delta power showed a widespread increase during the SO with central maxima, and the lower bins of the beta activity showed a power increase after SO. Compared to adults, preadolescents during the SO exhibited higher delta power only in the slowest bins of the band: before SO slow delta activity was higher in prefrontal, frontal and occipital areas in preadolescents, and, after SO the younger group had higher slow delta activity in occipital areas. In preadolescents delta/beta ratio was higher in more posterior areas both before and after the wake-sleep transition and, after SO, preadolescents showed also a lower delta/beta ratio in frontal areas, compared to adults. CONCLUSION: Results point to a general higher homeostatic drive for the developing areas, consistently with plastic-related maturational modifications, that physiologically occur during preadolescence.

A bidirectional model of sleep and technology use: A theoretical review of How much, for whom, and which mechanisms.

The link between technology and sleep is more complex than originally thought. In this updated theoretical review, we propose a new model informed by the growing body of evidence in the area over the past 10 years. The main theoretical change is the addition of bi-directional links between the use of technology and sleep problems. We begin by reviewing the evidence to date for the originally proposed mechanisms of bright light, arousal, nighttime sleep disruptions, and sleep displacement. Then, in support of the new direction of effect (sleep problems preceding technology use), we propose two new mechanisms: technology before sleep might be used as a time filler and/or as an emotional regulation strategy to facilitate the sleep-onset process. Finally, we present potential moderators of the association between technology and sleep, in recognition of protective and vulnerability factors that may mitigate or exacerbate the effects of technology on sleep and vice versa. The goal of this theoretical review is to update the field, guide future public health messages, and to prompt new research into how much technology and sleep affect each other, for whom it may be problematic, and which mechanisms may explain their association.

Exploring sleep characteristics in Chinese patients with narcolepsy: insights from the nocturnal sleep onset rapid eye movement period (nSOREMP).

STUDY OBJECTIVES: This study aimed to investigate the unique characteristics and clinical significance of the nocturnal sleep onset rapid eye movement period (nSOREMP) in the Chinese population with narcolepsy, enhancing our understanding and management of the disorder globally. METHODS: This retrospective analysis investigated narcolepsy in Chinese patients from six hospitals, using the International Classification of Sleep Disorders. A parallel retrospective analysis of the Chinese Clinical Sleep Database focused on polysomnography records was conducted to evaluate nSOREMP prevalence in other sleep disorders. RESULTS: The study found a 2.51% nSOREMP prevalence in other sleep disorders in the Chinese Clinical Sleep Database. Significant differences in age, N2 and rapid eye movement percentages, rapid eye movement latency, and various indexes were noted among patients with narcolepsy with or without nSOREMP and other sleep disorders with nSOREMP in the Chinese Clinical Sleep Database. nSOREMP prevalence in narcolepsy type 1 was 33.33% and in narcolepsy type 2 was 28.30%. Noteworthy disparities in narcolepsy type 1 included N2 percentages, rapid eye movement latency, and SOREMPs on Multiple Sleep Latency Test. In narcolepsy type 2, differences were significant for age, sleep latency, N2 and rapid eye movement latencies, arousal index, mean sleep latency on the Multiple Sleep Latency Test, and Multiple Sleep Latency Test SOREMPs. CONCLUSIONS: This study highlights the distinct characteristics of nSOREMP in the Chinese population. Patients exhibiting symptoms suggestive of the onset of narcolepsy are advised to undergo a Multiple Sleep Latency Test, irrespective of the occurrence of SOREMP during nocturnal polysomnography. CITATION: Zeng S, Feng F, Li W, et al. Exploring sleep characteristics in Chinese patients with narcolepsy: insights from the nocturnal sleep onset rapid eye movement period (nSOREMP). J Clin Sleep Med. 2024;20(8):1349-1355.

Eating habits and sleep quality in individuals with type 1 diabetes on continuous glucose monitoring and insulin pump.

BACKGROUND AND AIMS: Sleep disorders are bidirectionally linked with eating behaviors and glucose metabolism, which could be clinically relevant in type 1 diabetes (T1D). We investigated the relationship between dietary habits and sleep quality in individuals with T1D on insulin pumps and continuous glucose monitoring (CGM). METHODS AND RESULTS: In a cross-sectional study, dietary habits (7-day food diary, EPIC questionnaire) and sleep quality (Pittsburgh Sleep Quality Index questionnaire) were assessed in 59 men and 58 women with T1D, aged 19-79 years, using CGM and insulin pump. Differences in dietary habits and blood glucose after dinner (6 h) between participants differing in sleep quality, sleep duration, and sleep onset latency were evaluated. Bad Sleepers (n = 81) were twice as prevalent as Good Sleepers (n = 36) and had a significantly higher intake of fat than Good Sleepers (dinner: 30.7 ± 10.7 vs. 24.0 ± 10.5 g, p = 0.004). Short sleepers had a significantly higher usual intake (g/1000 kcal) of coffee and tea (90.4 ± 71.7 vs. 62.0 ± 35.6), alcoholic (47.8 ± 51.1 vs. 28.9 ± 31.5) and carbonated beverages (21.8 ± 38.1 vs. 9.3 ± 17.2) (p < 0.05 for all) than Long Sleepers. Long Sleep Onset Latency was associated with a significantly higher fat intake at dinner (41.8 ± 7.4 vs. 38.1 ± 9.1 % total energy, p = 0.029) than Short Sleep Onset Latency. No significant differences in post-dinner blood glucose levels were detected between participants with good or bad sleep quality. CONCLUSION: Sleep disruption is common in T1D and is associated with unhealthy dietary choices, especially at dinner, independently of post-dinner blood glucose control.

Embracing sleep-onset complexity.

Sleep is crucial for many vital functions and has been extensively studied. By contrast, the sleep-onset period (SOP), often portrayed as a mere prelude to sleep, has been largely overlooked and remains poorly characterized. Recent findings, however, have reignited interest in this transitional period and have shed light on its neural mechanisms, cognitive dynamics, and clinical implications. This review synthesizes the existing knowledge about the SOP in humans. We first examine the current definition of the SOP and its limits, and consider the dynamic and complex electrophysiological changes that accompany the descent to sleep. We then describe the interplay between internal and external processing during the wake-to-sleep transition. Finally, we discuss the putative cognitive benefits of the SOP and identify novel directions to better diagnose sleep-onset disorders.

The effect of the interaction of sleep onset latency and age on ischemic stroke severity via inflammatory chemokines.

Objective: Prolonged sleep onset latency (PSOL) and age have been linked to ischemic stroke (IS) severity and the production of chemokines and inflammation, both of which contribute to IS development. This study aimed to explore the relationship between chemokines, inflammation, and the interplay between sleep onset latency (SOL) and age in influencing stroke severity. Methods: A cohort of 281 participants with mild to moderate IS was enrolled. Stroke severity was assessed using the National Institutes of Health Stroke Scale (NIHSS), and SOL was recorded. Serum levels of macrophage inflammatory protein-1alpha (MIP-1α), macrophage inflammatory protein-1beta (MIP-1ß), monocyte chemoattractant protein-1 (MCP-1), interleukin-6 (IL-6), and tumor necrosis factor-alpha (TNF-α) were measured. Results: NIHSS scores of middle-aged participants with PSOL were significantly higher than those with normal sleep onset latency (NSOL) (p = 0.046). This difference was also observed when compared to both the elderly with NSOL (p = 0.022), and PSOL (p < 0.001). Among middle-aged adults with PSOL, MIP-1ß exhibited a protective effect on NIHSS scores (ß = -0.01, t = -2.11, p = 0.039, R2 = 0.13). MIP-1α demonstrated a protective effect on NIHSS scores in the elderly with NSOL (ß = -0.03, t = -2.27, p = 0.027, R2 = 0.12). Conclusion: This study reveals a hitherto undocumented association between PSOL and IS severity, along with the potential protective effects of MIP-1ß in mitigating stroke severity, especially among middle-aged patients.

Sleepiness and the transition from wakefulness to sleep.

The transition from wakefulness to sleep is a progressive process that is reflected in the gradual loss of responsiveness, an alteration of cognitive functions, and a drastic shift in brain dynamics. These changes do not occur all at once. The sleep onset period (SOP) refers here to this period of transition between wakefulness and sleep. For example, although transitions of brain activity at sleep onset can occur within seconds in a given brain region, these changes occur at different time points across the brain, resulting in a SOP that can last several minutes. Likewise, the transition to sleep impacts cognitive and behavioral levels in a graded and staged fashion. It is often accompanied and preceded by a sensation of drowsiness and the subjective feeling of a need for sleep, also associated with specific physiological and behavioral signatures. To better characterize fluctuations in vigilance and the SOP, a multidimensional approach is thus warranted. Such a multidimensional approach could mitigate important limitations in the current classification of sleep, leading ultimately to better diagnoses and treatments of individuals with sleep and/or vigilance disorders. These insights could also be translated in real-life settings to either facilitate sleep onset in individuals with sleep difficulties or, on the contrary, prevent or control inappropriate sleep onsets.

The association between timing of dietary macronutrient and sodium consumption and sleep duration and quality.

Study Objective: The objective of this study was to examine the association between the timing of dietary macronutrients and sodium intake and sleep quantity and quality. Methods: This was a cross-sectional study that included 34 adults between 21 and 50 years of age. The main outcome measures were objective sleep measures assessed from three nights of wrist actigraphy including sleep duration, fragmentation, and wake after sleep onset (WASO), and one night of polysomnography (PSG), including rapid eye movement (REM) sleep, non-REM stage 2 (N2), stage 3 (N3), and WASO. Multiple linear regression models and linear mixed models were used to estimate the associations between sleep measures and dietary measures (carbohydrates, fats, saturated fats, proteins, and sodium). Dietary timing was examined in two ways: (1) the average amount of each nutrient consumed within 3 hours of sleep start, and (2) the interval between the final intake of each nutrient and sleep. Results: Average fat intake within 3 hours of sleep was associated with greater WASO from PSG (ß = 4.48, p = 0.01). No other associations were found between the macronutrients or sodium intake (p > 0.05) within 3 hours of sleep and the sleep parameters from PSG or actigraphy. Similarly, no associations were found between any of the PSG or actigraphy sleep measures and the interval between final nutrient intakes and sleep with sleep duration. Conclusions: The study suggests that greater fat but not carbohydrate, protein, saturated fat, or sodium intake close to sleep may be associated with greater sleep disruption; however, no other associations were observed.