Sleep Rhythms Research Articles

Sex differences in baseline sleep and dark phase rebound sleep after chronic sleep fragmentation in the APPXPS1 and 5XFAD mouse models

AbstractBackgroundFragmentation of the daily sleep‐wake rhythm is a risk factor for Alzheimer’s disease (AD) (Li et al, Lancet Healthy Longev 1:e96‐e105 [2020]). While women have a higher AD incidence than men, whether women are more sensitive to sleep fragmentation (SF) is not known. Studies in female 3xTg‐AD mice (8‐11 months old) show that chronic SF for four weeks alters the daily sleep‐wake rhythm and stimulates AD‐like neuropathology (Duncan et al, Neuroscience 481:111‐122 [2022]).MethodTo investigate possible sex differences in the effects of sleep fragmentation, we studied two AD mouse models and matching wild‐type controls, APPxPS1‐knock‐in mice (6.2‐11 months old; N = 127) and 5XFAD mice (2.3‐3.3 months old; N = 52). All mice were exposed to 3‐4 weeks of SF or undisturbed sleep while individually housed in cages interfaced for piezo electric sleep recording for monitoring of daily sleep‐wake rhythms. SF consisted of four daily sessions (1 hour each) of enforced wakefulness (induced with toys and paintbrush stimulation) that were evenly distributed during the light phase, for 5 days/week. Immediately after the last SF session, mice in both groups were euthanized and cortical and hippocampal tissue was dissected and frozen. Amyloid‐beta levels were determined in soluble fractions using ELISA.ResultsSF redistributed sleep from the light phase (loss) to the dark phase (gain) in APPxPS1‐ki (p<0.0001) and 5XFAD (p<0.05) mice and WT controls. Overall, females slept less than males (p<0.001) and were more affected by SF. Dark phase “rebound” sleep after SF was greater in APPxPS1‐ki females (∼70% of undisturbed controls) than in APPxPS1 males or WT mice of either sex (∼20% of undisturbed controls) (p<0.001). Cortical amyloid‐beta levels were higher in female than male AD mice, but surprisingly, neither cortical nor hippocampal amyloid‐beta levels were affected by SF in either strain.ConclusionThese findings suggest an interaction between sex, AD mutations, and neuropathology on dark phase rebound sleep after chronic SF. To elucidate this interaction, on‐going studies are investigating the role of amyloid‐beta in sex‐differences in SF‐induced rebound sleep and potential sex differences in SF effects on gene expression in brain regions regulating sleep or circadian rhythms.

Curcumin mitigates the sleep-deprivation impacts on rat hypothalamic paraventricular nucleus

IntroductionThe paraventricular nucleus of the hypothalamus (PVH) is an important efferent system that relays the circadian rhythm of sleep and stress information to the periphery. Chronic REM sleep deprivation (CSD) is thought to damage this system. We evaluated the effects of CSD after 21 days on the spatial arrangement of PVH in male rats and the anti-apoptotic effects of curcumin on cell loss in sleep-deprived rats. MethodsThe rats received 1 mL of 100 mg/kg/day of curcumin in 3 groups: the CSD (through a modified multiple platform apparatus, 18 h/day), grid-floor control, and cage-control along with the same set of matched groups which received 1 mL PBS. In the grid-floor control group, as a control for CSD, animals were placed on stainless-steel-mesh grids positioned upon the CSD apparatus and then allowed to sustain the chance to sleep. After 21 days, their brains were removed for stereological estimations, Voronoi tessellation, and TUNEL assay. In an unbiased stereological approach, Cavalieri’s principle and an optical disector were used for estimating the volume and total cell number of the PVH, respectively. The Voronoi tessellation was measured using Image J software. ResultsSignificant reductions (P < 0.05) in the PVH volume and cell number, along with an increase in dead neurons, were found in CSD animals. The spatial pattern of two types of PVH neurons (parvocellular and magnocellular) showed random distributions after CSD, whereas curcumin not only increased the volume and neuronal number but also retrieved the spatial distribution to a regular one. ConclusionsCSD decreased the volume and altered the spatial arrangement of the neurons in PVH by increasing apoptosis and decreasing the cell number. However, oral use of curcumin could protect PVH from these changes.

The Impact of Immunotherapy on Sleep and Circadian Rhythms in Patients with Cancer.

Immunotherapy has revolutionized treatments for both early and advanced cancers, and as their role evolves, their impact on sleep and circadian rhythms continues to unfold. The recognition, evaluation, and treatment of sleep and circadian rhythm disturbance leads to improved symptom management, quality of life and treatment outcomes. An intricate complex relationship exists in the microenvironment with immunity, sleep and the tumor, and these may further vary based on the cancer, addition of standard chemotherapy, and pre-existing patient factors. Sleep and circadian rhythms may offer tools to better utilize immunotherapy in the care of cancer patients, leading to better treatment outcome, reduced symptom burden, and increased quality of life.

Sleep and circadian rhythm disturbance in kidney stone disease: a narrative review.

The circadian rhythm generated by circadian clock genes functions as an internal timing system. Since the circadian rhythm controls abundant physiological processes, the circadian rhythm evolved in organisms is salient for adaptation to environmental change. A disturbed circadian rhythm is a trigger for numerous pathological events. Recently, accumulated data have indicated that kidney stone disease (KSD) is related to circadian rhythm disturbance. However, the mechanism between them has not been fully elucidated. In this narrative review, we summarized existing evidence to illustrate the possible association between circadian rhythm disturbance and KSD based on the epidemiological studies and risk factors that are linked to circadian rhythm disturbance and discuss some chronotherapies for KSD. In summary, KSD is associated with systemic disorders. Metabolic syndrome, inflammatory bowel disease, and microbiome dysbiosis are the major risk factors supported by sufficient data to cause KSD in patients with circadian rhythm disturbance, while others including hypertension, vitamin D deficiency, parathyroid gland dysfunction, and renal tubular damage/dysfunction need further investigation. Then, some chronotherapies for KSD were confirmed to be effective, but the molecular mechanism is still unclear.

Delaying circadian sleep phase under ultradian light cycle causes time-of-day-dependent alteration of cognition and mood

Light exerts powerful and pervasive effects on physiology and behaviour. These effects can be indirect, through clock synchronization and phase adjustment of circadian rhythms, or direct, independent of the circadian process. Exposure to light at inappropriate times, as commonly experienced in today’s society, leads to increased prevalence of circadian, sleep and mood disorders as well as cognitive impairments. In mice, exposure to an ultradian 3.5 h light/3.5 h dark cycle (T7) for several days has been shown to impair behaviour through direct, non-circadian, photic effects, a claim we challenge here. We first confirmed that T7 cycle induces a lengthening of the circadian period resulting in a day by day phase-delay of both activity and sleep rhythms. Spatial novelty preference test performed at different circadian time points in mice housed under T7 cycle demonstrated that cognitive deficit was restrained to the subjective night. Mice under the same condition also showed a modification of stress-induced despair-like behaviour in the forced swim test. Therefore, our data demonstrate that ultradian light cycles cause time-of-day-dependent alteration of cognition and mood through clock period lengthening delaying circadian sleep phase, and not through a direct photic influence. These results are of critical importance for the clinical applications of light therapy in the medical field and for today’s society to establish lighting recommendations for shift work, schools, hospitals and homes.

Effects of thermal environment on body temperature rhythm and thermal sensation before and after getting into bed: A laboratory study in Shanghai, China

Body temperature rhythm serves as a crucial bridge connecting thermal environment and sleep rhythm. While previous studies have extensively confirmed the significant effects of thermal environment on sleep process, a quantitative exploration elucidating the relationships between sleeping thermal environment and body temperature rhythm has persistently been absent. This research aimed to investigate the persistent effects of three stable thermal environments (16 °C, 20 °C and 24 °C) on body temperature rhythm and thermal sensation during complete sleep process. In a laboratory with strictly controlled environment, 14 participants underwent a continuous four-day sleep experiment over a two-month period. Throughout three distinct phases (pre-bed sitting, awake lying in bed, and sleep after lights-off), core body temperature at gastro-intestinal tract, as well as skin temperature at nine specific locations, were continuously monitored. Concurrently, regular questionnaires were employed to periodically collect data on participants’ thermal sensation. The data confirmed that (1) three hours after lights-off, core-to-skin temperature gradient consistently fluctuated around 2 °C across three conditions, and this observation may aid in elucidating the physiological significance of sleeping thermal environment; (2) thermal environment before getting into bed exerted a significant influence on body temperature rhythm and can further regulate the duration of sleep onset latency; (3) bedding system significantly diminished the impact of thermal environment on body temperature rhythm, and future bedding microenvironment deserves more attention; and (4) existing methods for sleeping thermal sensation evaluation varying degrees of limitation, and a novel prediction method was proposed. In general, this study provided valuable insights for the design and regulation of bedroom thermal environment from a thermophysiological perspective.

Major depressive episode with insomnia and excessive daytime sleepiness: A more homogeneous and severe subtype of depression

Previous studies have noted the crucial role of excessive daytime sleepiness (EDS) in the course of depressive illness, and more recently, a few studies documented its strong associations with an increased risk of suicide. While insomnia is associated with heightened emotional reactivity, suicidal behaviors, and increased relapses and recurrence. Our main hypothesis is that major depressive episodes (MDE) with insomnia and EDS are associated with more severe manifestations of depression. However, to date, no study has directly compared MDE with insomnia without EDS (Ins), and MDE with insomnia with EDS (InsEDS) using both subjective biomarkers (administration of self-assessment questionnaires for psychiatric evaluation and sleep complaints) and objective biomarkers (of sleep and circadian rhythms (using actigraphy). The InsEDS group, compared to the Ins group, exhibited significantly increased suicidal ideation, larger seasonal impacts on mood, alterations in sleep duration, weight, appetite, energy levels, and social activities throughout the year. Furthermore, they had significant delayed onset of daily activity measured with actigraphy. These findings provided new insights into the link between suicide, sleep, alertness, and biological clock. They also hold significant implications for identifying individuals with more severe depressive manifestations and for developing tailored and personalized therapeutic strategies.

Role of age, menopausal status, and symptoms in midlife women: Examination of sleep patterns and rest-activity circadian rhythms

BackgroundMidlife women experience menopausal transition at different ages with a variety of symptoms. This study aimed to identify the effects of age, menopausal status, and symptoms in women on their actigraphy-based sleep patterns and circadian rhythms. MethodsA total of 87 women aged 45–60 from the community and a gynecology clinic in Taiwan who had their sleep and circadian rhythms recorded with a 7-day actigraphy were analyzed. Multiple linear regression was used to estimate the association of age, menopausal status, and symptoms with sleep parameters and circadian rhythms. ResultsA sleep efficiency below 85 % was observed in 46.0 % of women, and those with severe somatic-vegetative or psychological symptoms tended to have problems with sleep latency (β = 0.22 and β = 0.42, respectively) and efficiency (β = −0.26 and β = −0.36, respectively). Women with more severe urogenital symptoms only experienced significantly longer sleep latency (β = 0.33). There was a weak correlation between circadian rhythms and symptoms. Additionally, perimenopausal (β = 0.30 and β = 0.35, respectively) and late postmenopausal (β = 0.67 and β = 0.59, respectively) women had higher relative amplitude and stability in circadian rhythms than premenopausal women. Age had no significant effect on sleep parameters or circadian rhythms. ConclusionsPremenopausal women had the most unstable day-to-day rhythms compared to their peri- and postmenopausal counterparts. Women with higher somatic-vegetative, psychological, and urogenital symptoms showed greater sleep problems. Psychological symptoms (e.g., depression, irritability, anxiety, exhaustion) were the strongest predictors for all sleep parameters. The mechanisms underlying these associations warrant investigation.

Disruption in Sleep and Circadian Rhythm: A Potential Accelerator in Alzheimer’s Disease Progression

Disruption in Sleep and Circadian Rhythm: A Potential Accelerator in Alzheimer’s Disease Progression

What role do sleep and circadian rhythms play in psychological functioning including motivation, emotion, cognition, and performance?

The influence of sleep and circadian rhythms on daytime functioning has long been noted. Psychologists and psychology-oriented researchers were among the first to investigate the role of sleep and circadian rhythms in motivation, emotion, cognition, and performance. At the dawn of modern sleep science, psychological fellow, F. B. Dresslar found that telegram tapping speed varied according to time of day providing the first clues to the role of circadian rhythms on performance (Dresslar 1892). Marie de Manacéïne was the first to experimentally demonstrate that sleep was critical to life and that the brain and behaviour were adversely impacted by sleep loss (de Manacéïne 1894) Patrick and Gilbert elaborated on the role of sleep on psychological functioning and were the first to experimentally study the impact of sleep loss in humans (Patrick and Gilbert 1896). The past century has seen an explosion of interest in understanding which aspects of sleep and circadian rhythms relate to which aspects of daytime psychological functioning.

The low ratio of ghrelin in plasma and cerebrospinal fluid might be beneficial to sleep

ObjectiveGhrelin is physiologically important for maintaining sleep rhythm. Cigarette smoking has been demonstrated to significantly increase the risk of insufficient sleep by regulating ghrelin at the central and peripheral levels. No research has been published to study the relationship between active smoking and sleep via ghrelin level in cerebrospinal fluid (CSF). MethodsA total of 139 Chinese males were recruited and divided into active smokers (n = 77) and non-smokers (n = 62). The levels of CSF and plasma ghrelin were measured. The Pittsburgh Sleep Quality Index (PSQI) was used to evaluate sleep. ResultsNon-smokers had lower PSQI scores (1.71 ± 1.93) than active smokers (3.70 ± 1.78). Non-smokers have significantly lower plasma ghrelin levels and lower plasma/CSF ghrelin ratio but higher CSF ghrelin than active smokers. Among non-smokers, plasma ghrelin levels were not correlated with PSQI scores (all p > 0.05), CSF ghrelin levels were positively correlated with PSQI scores (r = 0.309, p = 0.019), and the plasma/CSF ghrelin ratio was negatively correlated with PSQI scores (r = −0.346, p = 0.008). ConclusionsThis study is the first to reveal the relationship between cigarette smoking, high CSF ghrelin levels and insufficient sleep, suggesting that maintaining a normal plasma/CSF ghrelin ratio may be the physiological mechanism of healthy sleep, and the insufficient sleep population must quit smoking.

The impact of dietary and sleep rhythms on blood pressure in children and adolescents: a cross-sectional study.

Evidence about the relationship between meal and sleep time and CVD in children is scarce. The aims of this study were to describe the association between life rhythm patterns and blood pressure in children. This research was conducted among 5,608 children aged 6 to 15 years old in Chongqing and Sichuan provinces in 2021 and 2022. Dietary and sleep rhythms information was collected. The time of the first meal and last meal, and sleep time, were obtained. The mean age was 10.48 ± 2.24 years old, with 2958 (52.75%) male participants. The mean feeding window on weekdays was 11.69 h, 12.42 h, and 13.23 h for participants aged 6-7 years old, 8-12 years old and 13-15 years old, respectively. Weekday feeding window and last mealtime were positively correlated with blood pressure levels. And the changes in the feeding window between weekdays and weekends were significantly correlated with BP. Sleep duration and change in wake time were significantly correlated with SBP. Based on these results, this study identified the optimal combination of dietary and sleep rhythm interventions for children younger than 12 years of age and aged 12 and older, respectively. Disorder dietary and sleep rhythms disorders may correlate with elevated blood pressure levels, suggesting developing optimal dietary and sleep rhythm patterns could prevent the incidence of CVDs in children. The optimal dietary rhythm was defined by the indexes of breakfast time, dinner time and daily feeding window. As good meal patterns are defined as satisfied the following three items: for children younger than 12 years should have breakfast after 7:30 am; aged 12 years and over should have breakfast after 7 am; having dinner before 6 pm; daily feeding window less than 12.5 h. And less optimal dietary rhythm should satisfy any condition or eat dinner between 6 pm and 8 pm; and poor dietary rhythm should not satisfy any of the three criteria and eat dinner after 8 pm. Children with optimal dietary rhythm (in group A) had lower SBP (P < 0.001), DBP (P = 0.002) and MAP (P < 0.001) than those in group C.

Dopamine pathways mediating affective state transitions after sleep loss

The pathophysiology of affective disorders-particularly circuit-level mechanisms underlying bidirectional, periodic affective state transitions-remains poorly understood. In patients, disruptions of sleep and circadian rhythm can trigger transitions to manic episodes, whereas depressive states are reversed. Here, we introduce a hybrid automated sleep deprivation platform to induce transitions of affective states in mice. Acute sleep loss causes mixed behavioral states, featuring hyperactivity, elevated social and sexual behaviors, and diminished depressive-like behaviors, where transitions depend on dopamine (DA). Using DA sensor photometry and projection-targeted chemogenetics, we reveal that elevated DA release in specific brain regions mediates distinct behavioral changes in affective state transitions. Acute sleep loss induces DA-dependent enhancement in dendritic spine density and uncaging-evoked dendritic spinogenesis in the medial prefrontal cortex, whereas optically mediated disassembly of enhanced plasticity reverses the antidepressant effects of sleep deprivation on learned helplessness. These findings demonstrate that brain-wide dopaminergic pathways control sleep-loss-induced polymodal affective state transitions.

54 Sleep and Circadian Rhythms in Premanifest Huntington’s disease: Relationship with Cognition

Objective:Huntington’s disease (HD) is a neurodegenerative disease characterised by motor, psychiatric and cognitive decline. Currently, no treatments have been identified in HD for slowing down cognitive decline or improving cognitive function. We are interested in identifying potentially modifiable factors in HD that can be targeted to improve or maintain cognitive function. Sleep and circadian disruption stand out as possible modifiable targets because sleep and circadian symptoms are common in HD, and such disruptions are known to impact cognition in the general population. Despite some emerging evidence that sleep quality correlates with cognition in manifest HD, whether these same relationships exist in the premanifest period is unknown. Further, whether circadian rhythms relate to cognition in premanifest HD remains open. Therefore, we aimed to determine whether sleep and circadian parameters relate to cognitive performance in premanifest HD.Participants and Methods:To date, we have recruited 27 premanifest HD participants to a two-week remote sleep study. During the study, participants wore an Actiwatch-2 and completed a sleep diary for 14 consecutive days to assess their sleep and rest-activity patterns. Participants also completed online sleep and mood questionnaires and a cognitive assessment using videoconference. We calculated Pearson correlations to examine whether cognitive performance relates to subjective sleep quality, objective sleep parameters and circadian rest-activity rhythms. Thus far, we have analysed data from 15 female participants with premanifest HD (Mage = 43.20, SD = 11.58).Results:Preliminary results indicate that measures of subjective sleep quality, insomnia severity, daytime sleepiness, and fatigue severity in premanifest HD do not correlate with cognitive performance. Increases in objectively measured sleep efficiency, however, strongly correlated with better performance on the Hopkins-Verbal Learning Test-Revised (HVLT-R) immediate (r = 0.562, p &lt; 0.05) and delayed recall trials (r = 0.597, p &lt; 0.05) and the Trail Making Test Part B (TMT-B; r = 0.550, p &lt; 0.05). More time spent awake (i.e., wake after sleep onset) was strongly linked to reduced performance on the TMT-B (r = -0.542, p &lt; 0.05) and Symbol Digit Modalities Test (r = -0.556, p &lt; 0.05). Further, increases in total sleep time were associated with better performance on the HVLT-R immediate (r = 0.682, p &lt; 0.05) and delayed recall trial (r = 0.616, p &lt; 0.05). For our circadian parameters, less fragmented day-today rest-activity rhythms (i.e., higher intra-daily variability) strongly correlated with higher scores on the HVLT-R immediate (r = 0.768, p &lt; 0.001) delayed recall trials (r = 0.7276, p &lt; 0.05) and TMT-B (r = 0.516, p &lt; 0.05), whereas consistent and stable day-to-day rest-activity rhythms (i.e., higher inter-daily stability) was associated with poorer performance on ERT (r = -0.587, p &lt; 0.05).Conclusions:Preliminary results suggest that fragmented sleep, sleep inefficiency, reduced total sleep time, rest-activity rhythm stability and fragmentation relate to poorer cognitive performance in people with premanifest HD. Should analysis of our whole sample confirm these preliminary findings, targeting sleep in HD (e.g., through sleep hygiene and/or psychoeducation) may be a useful strategy to improve or maintain cognition.

Effect of Acute and Chronic Sleep Deficit on Working and Long-Term Memory in Rats

It is known that insufficient sleep or diurnal rhythm disturbances of sleep and wakefulness exert a detrimental effect on cognitive functions. It was thought for a long period that memory consolidation is the most vulnerable link, i.e., information transfer from short-term/working memory to long-term memory. However, there is a progressive number of studies indicating that the most negative consequences of sleep loss are observed in working memory. In our study, we undertook an effort to assess possible disturbances in working memory and long-term memory following sleep loss impact with different protocols in acute and chronic experiment in rats. Sleep in Wistar rats was deprived/restricted by swinging platform technique according to the following protocols: 1 – total sleep deprivation for 18 h; 2 – partial sleep restriction for 24 h (3 h of sleep deprivation alternated with 1 h of sleep opportunity – totally 18 h of sleep deprivation); 3 – chronic partial sleep restriction (conditions 2 for five consistent days). Total sleep deprivation in Y-maze test was shown to result in a significant decrease in spontaneous alternations of maze arms that indicates working memory impairment. This impact in Barnes test did not exert an effect on long-term memory – time spent for seeking a shelter did not change in this task. Acute and chronic sleep restriction induced no changes in working memory and long-term memory. The results obtained allow us to come to conclusion that working memory (in contrast to long-term memory) is a vulnerable component of cognitive function under total sleep deprivation conditions. This negative effect was abolished if periods of sleep deprivation alternated with short periods of sleep opportunities that indicate protective significance of short sleep periods for cognitive functions during sleep deficit. Hence, short-term sleep is helpful for cognitive health and protects working memory, whereas continuous long-term wakefulness impairs it.

Thalamic Stroke: An Opportunity to Study the Brain Mechanisms of Sleep–Wake and Cognition

The thalamus, and its projections to the cerebral cortex, are crucial for regulating sleep rhythms, such as sleep spindles, and for maintaining arousal and sleep homeostasis. Moreover, they play a significant role in memory, executive functioning, and attention. Altered thalamocortical circuitry caused by vascular lesions affects sleep–wake architecture and may contribute to cognitive deficits observed in thalamic stroke patients. This review summarizes the biology of the thalamus and current knowledge regarding the impact of thalamic circuitry on sleep regulation and cognition, drawing from clinical and pre-clinical studies. Furthermore, deep brain stimulation and transcranial magnetic stimulation are discussed as possible therapeutic approaches targeting thalamic circuits. Understanding the role of the thalamus in sleep and cognition opens new avenues for developing novel therapeutic strategies to improve sleep and cognitive functions in affected individuals.

A two-process model of Drosophila sleep reveals an inter-dependence between circadian clock speed and the rate of sleep pressure decay.

Sleep is controlled by two processes-a circadian clock that regulates its timing and a homeostat that regulates the drive to sleep. Drosophila has been an insightful model for understanding both processes. For four decades, Borbély and Daan's two-process model has provided a powerful framework for understanding sleep regulation. However, the field of fly sleep has not employed such a model as a framework for the investigation of sleep. To this end, we have adapted the two-process model to the fly and established its utility by showing that it can provide empirically testable predictions regarding the circadian and homeostatic control of fly sleep. We show that the ultradian rhythms previously reported for loss-of-function clock mutants in the fly are robustly detectable and a predictable consequence of a functional sleep homeostat in the absence of a functioning circadian system. We find that a model in which the circadian clock speed and homeostatic rates act without influencing each other provides imprecise predictions regarding how clock speed influences the strength of sleep rhythms and the amount of daily sleep. We also find that quantitatively good fits between empirical values and model predictions were achieved only when clock speeds were positively correlated with rates of decay of sleep pressure. Our results indicate that longer sleep bouts better reflect the homeostatic process than the current definition of sleep as any inactivity lasting 5 minutes or more. This two-process model represents a powerful framework for work on the molecular and physiological regulation of fly sleep.

Sleep and circadian rhythms during pregnancy, social disadvantage, and alterations in brain development in neonates.

Pregnant women in poverty may be especially likely to experience sleep and circadian rhythm disturbances, which may have downstream effects on fetal neurodevelopment. However, the associations between sleep and circadian rhythm disturbances, social disadvantage during pregnancy, and neonatal brain structure remains poorly understood. The current study explored the association between maternal sleep and circadian rhythm disturbances during pregnancy and neonatal brain outcomes, examining sleep and circadian rhythm disturbances as a mediator of the effect of social disadvantage during pregnancy on infant structural brain outcomes. The study included 148 mother-infant dyads, recruited during early pregnancy, who had both actigraphy and neuroimaging data. Mothers' sleep was assessed throughout their pregnancy using actigraphy, and neonates underwent brain magnetic resonance imaging in the first weeks of life. Neonatal structural brain outcomes included cortical gray matter, subcortical gray matter, and white matter volumes along with a measure of the total surface area of the cortex. Neonates of mothers who experienced greater inter-daily deviations in sleep duration had smaller total cortical gray and white matter volumes and reduced cortical surface areas. Neonates of mothers who had higher levels of circadian misalignment and later sleep timing during pregnancy showed smaller subcortical gray matter volumes. Inter-daily deviations in sleep duration during pregnancy mediated the association between maternal social disadvantage and neonatal structural brain outcomes. Findings highlight the importance of regularity and rhythmicity in sleep schedules during pregnancy and bring to light the role of chronodisruption as a potential mechanism underlying the deleterious neurodevelopmental effects of prenatal adversity. RESEARCH HIGHLIGHTS: Social disadvantage was associated with sleep and circadian rhythm disturbances during pregnancy, including later sleep schedules, increased variability in sleep duration, circadian misalignment, and a higher proportion of the sleep period spent awake. Maternal sleep and circadian rhythm disturbances during pregnancy were associated with decreased brain volume and reduced cortical surface area in neonates. Maternal inter-daily deviations in sleep duration during pregnancy mediated the association between social disadvantage and neonatal brain volume and cortical surface area.

How are psychological factors involved in the evaluation and treatment of sleep and circadian rhythm disorders?

Clinical sleep psychology is a branch of psychological science that aims to understand and harness psychological factors (i.e., affective, behavioral, cognitive, social, and environmental) that are involved in sleep and circadian disorders. Behavioral Sleep Medicine, a branch of sleep medicine, has a similar focus (https://www.behavioralsleep.org/). Collectively, these clinical branches of sleep psychology aim to effectively evaluate and treat sleep and circadian rhythm disorders to promote sleep health. Clinical sleep psychology has a long history, including early work in the areas of insomnia, behavioral treatment for pediatric sleep disorders, dream psychology, and hypnotic sleep (Jacobson 1934; McReynolds 1997; Mower and Mower 1938; Münsterberg 1915; Watson 1928). The past 100 years have seen considerable progress in identifying psychological factors involved in sleep and circadian rhythm disorders and their treatment, particularly in insomnia and pediatric sleep disorders. Barriers to advancement persist.

P019 Sleep and Circadian Interventions for Mental Health and Mood in Athletes

Abstract Introduction There are only a small number of evidence-based interventions that address sleep and circadian rhythms in athletes despite it being well-recognized that sleep has a bidirectional relationship with mental health conditions, wellbeing, mood disorders and may be protective against concussions and injury risk. Athletes, both during and after their career, face unique stressors that, if not well managed and mitigated, could become a source of mental health issues. The aim of this review was to discuss the current evidence on sleep and circadian interventions to improve mental health and mood in athletes. Methods The following databases—PubMed, Scopus, EMBASE, SPORTDiscus, and Google Scholar—were searched for initial studies of interest from inception to July 2023. Results Very few sleep and circadian strategies have been implemented in sporting environments to improve the mental health and mood of athletes. The interventions that have been investigated are constrained by limited sample sizes, lack of female representation, low quality study design and inconsistent measurement of mental health and mood, making it difficult to draw definitive conclusions of the efficacy of these strategies. Overall, the evidence base for the effectiveness of the interventions was limited. Discussion There remains a need for larger, adequately powered interventions that are individually tailored, with considerations for the specific challenges of athletes at different levels of professionalism, season time and in particular sporting contexts.