bluuebunny/crossref_metadata_2025_split huggingface dataset:
O019 The Association between Later Circadian Timing and Higher Depressive Symptoms in Early Adolescence is Ameliorated by Longer Sleep Duration
Authors: Chachos E , Lu S , Hand A , Carskadon M , Klerman E , Lockley S , Wiley J , Phillips A , Rajaratnam S , Bei B , Stone J 
Published: November 2022

Abstract

Background
Circadian phase and sleep-wake timing delays are hallmark adolescent development features. These delays contribute to shorter sleep duration in combination with early school schedules. Both delayed circadian phase and insufficient sleep are associated with increased prevalence/severity of mood problems. This study examined associations between circadian phase, sleep duration, and mood in early adolescence.

Methods
157 Year 7 Australian students (M±SD=12.81±0.40 years, 56.7% female) wore actiwatches and completed sleep diaries for two weeks in school term. Circadian phase was measured via salivary dim light melatonin onset (DLMO) on the final Friday of sleep monitoring. PROMIS Paediatric Depression and Anxiety measured depression/anxiety symptom severity. Sleep duration/efficiency were calculated using actigraphy and self-reports. Multiple linear regression quantified the relationships between sleep duration and efficiency and circadian phase and mood (depression/anxiety) associations, adjusting for sex.

Results
DLMO occurred at the expected time for early adolescents [continuous decimal time; M±SD=20.52±1.20; range:17.52-24.03]. Sleep duration (p=.03), but not sleep efficiency (p=.89), moderated associations between DLMO and depression (but not anxiety; p-values&gt;.08). Simple slope analyses showed that in individuals with shorter average sleep duration, a one-hour circadian phase delay was associated with 1.84 t-score increase in depressive symptom severity (p=.03). These associations were non-significant in individuals with longer average sleep duration (p=.44).

Conclusion
Although delayed circadian phase is a developmental norm, its association with increased depressive symptom severity was ameliorated in young adolescents who obtained longer sleep duration. Addressing sleep duration, a modifiable protective factor (e.g., by delaying school start times), may yield mood-related benefits for adolescents.
O020 Sleep regularity is a stronger predictor of all-cause mortality than sleep duration or sleep efficiency in ~60 000 UK Biobank participants
Authors: Windred D , Burns A , Lane J , Phillips A , Cain S 
Published: November 2022

Abstract
Sleep duration and sleep efficiency are observed risk factors for all-cause mortality, but the role of sleep regularity is unknown. Irregular sleep patterns are associated with ageing, cancer, depressed mood, and cardio-metabolic diseases, and may therefore increase risk of mortality. We extracted Sleep Regularity Index (SRI) scores, sleep duration, and sleep efficiency from one week of actigraphy in 60,997 UK Biobank participants (62.8±7.8 years, 55.6% female). Using Cox Proportional Hazards models, we assessed whether SRI, sleep duration, and sleep efficiency predicted all-cause mortality up to 7.6 years post-actigraphy. A one standard deviation increase in SRI score (+10.7), indicating more regular sleep patterns, predicted a 20.4±2.0% reduced hazard of all-cause mortality (p &lt; .0001). This relationship remained robust after controlling for age, sex, ethnicity, education, income, and employment status (+1SD in SRI predicted an 18.7±2.4% hazard reduction, p &lt; .0001). SRI was a relatively stronger predictor of mortality hazard than sleep duration (explaining 19.0±2.1% vs. 12.4±2.6% of hazard reduction) or sleep efficiency (19.0±2.1% vs. 13.1±2.6%) in two additional Cox models. Sleep regularity may play a causal role in mortality, via contribution to poor health outcomes, or it may be a marker of poor health leading to mortality. These findings suggest that sleep regularity should be monitored and/or adjusted alongside traditional sleep metrics for optimal health and longevity.
O021 Investigation of a novel LED lighting strategy designed to accelerate circadian entrainment to night shift-work in an encapsulated environment
Authors: Guyett A , Scott H , Lechat B , Manners J , Stuart N , Lack L , Kemps E , Eckert D , Micic G , Banks S , Dorrian J , Adams R , Catcheside P , Lovato N 
Published: November 2022

Abstract

Introduction
Shift-work results in misalignment between circadian timing and the sleep/wake schedule, negatively impacting sleep and performance. In encapsulated environments (e.g., submarines), the lack of strong daily lighting cues impairs circadian entrainment. This study tested whether circadian-informed LED lighting promotes greater circadian phase delays to adjust to night shift-work compared to standard lighting.

Method
To date, 11 healthy sleepers (7 males, mean±SD age27.6±8.5 y, N=24 anticipated) have completed two separate 8-day experimental conditions (circadian-informed lighting versus standard lighting). After a baseline sleep from 22:00 – 07:00 (day 1) and salivary dim light melatonin onset ([DLMO], day 2), participants undertook simulated night shift-work (00:00 - 08:00) and slept during the daytime (10:00 - 19:00) for days 3-7 followed by a post-DLMO assessment on day 8. Ingestible capsules collected core body temperature (CBT) continuously throughout days 2-8. The standard lighting condition mimicked current lighting on submarines (largely dim, blue-depleted light), while the circadian-informed lighting administered bright, blue-enriched and dim, blue-depleted lighting at times estimated to facilitate rapid circadian delay. Cosine curve fitting was applied to the CBT data to estimate temperature minima (CBTmin) and determine phase delay magnitude for comparison across conditions.

Results
There was a significant day-by-condition interaction on CBTmin (F4, 88=2.82, p=0.030). By day 6, the CBTmin delay was (mean±SD) 3.2±.97 hours greater in the circadian-informed lighting versus standard lighting, p=0.001.

Conclusions
These preliminary analyses support that circadian-informed lighting accelerates circadian re-adjustment to night shift-work. Such interventions could improve sleep, performance, and safety in shift-workers who work in encapsulated environments.
O024 Modifying light environments according to individual circadian light sensitivity
Authors: Stone J , Cain S , Phillips A 
Published: November 2022

Abstract

Introduction
Large inter-individual differences exist in how sensitive the circadian system is to light. Circadian light sensitivity can be affected by medications, such as antidepressants, and varies as a function of age and some mood disorders. Using a computational model, we investigated how differences in an individual’s light sensitivity can be offset by changes in their light environment to maintain stable circadian timing.

Methods
A previously validated computational model was used to simulate sleep and circadian timing under realistic assumptions about light and sleep schedules in day workers across two weeks. The model predicted circadian phase (dim light melatonin onset) and sleep onset/offset times for each day. Simulations were repeated varying two parameters: (i) light sensitivity, representing changes in the dose-response curve to light, and (ii) evening illuminance, representing home lighting levels after sunset.

Results
Higher light sensitivity and higher evening illuminance levels resulted in systematically later predicted sleep and circadian timing. The effects of increasing light sensitivity could be offset by reducing the level of evening illuminance, with this relationship holding over a wide range of light sensitivity values. Low light sensitivity combined with high evening illuminance produced a non-entrained (non-24) phenotype; decreasing evening illuminance from this state resulted in stable entrainment.

Discussion
We are only beginning to understand the influence of medications and health conditions on circadian light sensitivity. Our results show how modifications to evening light levels can be used to offset impacts of variable light sensitivity on sleep and circadian timing.
O029 Sleep architecture differs for individuals manifesting excessive daytime sleepiness with and without obstructive sleep apnea
Authors: Chen X , Korkalainen H , Kainulainen S , Leppänen T , Oksenberg A , Töyräs J , Terrill P 
Published: November 2022

Abstract

Introduction
The mechanism underlying the development of excessive daytime sleepiness (EDS) in obstructive sleep apnea (OSA) remains unclear. Thus, we characterised the association between sleep architecture and EDS in individuals with and without OSA.

Methods
1876 suspected OSA patients reporting daytime sleepiness underwent in-lab polysomnography and next-day multiple sleep latency test (MSLT). We investigated sleep architecture characteristics in OSA (apnea-hypopnea index [AHI]≥5, n=1508) and non-OSA (AHI&lt;5, n=368) patients with and without EDS (MSLT≤10-minutes and MSLT&gt;10-minutes). Sleep architecture was quantified by N1, N2, N3, REM, total sleep time (TST), and wake after sleep onset (WASO).

Results
OSA patients with EDS had less N1 (median: 10.0 vs 12.0-minutes, p&lt;0.05) and N3 (60.2 vs 71.5-minutes, p&lt;0.05) sleep, less WASO (43.0 vs 51.0-minutes, p&lt;0.05), more N2 (210.5 vs 189.0-minutes, p&lt;0.05) sleep, and higher TST (365.0 vs 351.5-minutes, p&lt;0.05) than non-EDS patients. No difference was observed in the amount of REM (70.0 vs 67.5-minutes, p=0.46) sleep.
Non-OSA patients with EDS had less WASO (31.5 vs 40.0-minutes, p&lt;0.05), more N2 (188.5 vs 177.5-minutes, p&lt;0.05) sleep, and higher TST (374.5 vs 359.0-minutes, p&lt;0.05) and the amount of REM sleep (76.5 vs 68.5-minutes, p&lt;0.05) than non-EDS patients.

Discussion
While EDS was associated with less WASO and greater TST and N2 in both OSA and non-OSA groups, there was also characteristic differences. Non-OSA patients with EDS have greater REM sleep duration, while OSA patients with EDS have less N3 sleep. There is likely a complex bi-directional relationship between sleep architecture and EDS reflecting acute/chronic sleep disruption and compensatory mechanisms.
O034 Autonomic control of heart rate stabilises with improvement of sleep disordered breathing in children with Down syndrome
Authors: Walter L , Varkey J , Gu C , Bassam A , Davey M , Nixon G , Horne R 
Published: November 2022

Abstract

Background
Sleep disordered breathing (SDB) alters autonomic function, assessed using heart rate variability (HRV) in typically developing (TD) and children with Down syndrome (DS). SDB resolution in TD children normalises HRV, but the effects in children with DS are unknown. We compared HRV in children with DS with improved SDB (decrease in obstructive apnoea hypopnoea index (OAHI) to ≤ 50% of baseline OAHI) to those with unimproved SDB 2 y following baseline study.

Methods
24 children (3-19 y at baseline) were included. Power spectral analysis of the ECG determined low frequency (LF, parasympathetic and sympathetic activity), high frequency (HF, parasympathetic activity) power and LF/HF (sympathovagal balance). Children were grouped into Improved (n=12; 7 treated between studies) and Unimproved (n=12; 2 treated between studies).

Results
OAHI decreased between studies in the Improved group (baseline, 29.5 (1.6,154.0) [mean (min,max)] events/h; follow-up, 8.4 (0,77.0); p&lt;0.05), and worsened in the Unimproved group (baseline 6.1 (0,22.9); follow-up 14.4 (0.3, 54.6); p&lt;0.05). LF power was lower at follow-up in the Unimproved group compared to baseline during Total Sleep (p&lt;0.05), N3 (p&lt;0.05) and REM (p&lt;0.01). HF power was also lower at follow-up in the Unimproved group during REM (p&lt;0.05). HRV remained unchanged between baseline and follow-up for the Improved group.

Conclusion
Autonomic control worsened as indicated by lower sympathetic and parasympathetic activity in children whose SDB was not improved. In contrast, in those children with improved SDB autonomic control remained the same, suggesting improvement in SDB severity prevents further worsening of autonomic control in children with DS.
O051 Insomnia predicts persistent symptoms of anxiety and depression during the COVID-19 pandemic: A 12-month longitudinal cohort study
Authors: Saunders W , Meaklim H , Byrne M , Junge M , Varma P , Finck W , Jackson M 
Published: November 2022

Abstract

Introduction
Insomnia increases risk of affective disorders. This study assessed whether individuals with insomnia symptoms at the beginning of the pandemic, either new-onset or pre-existing, were at increased vulnerability to anxiety and depressive symptoms longitudinally compared to those who continued sleeping normally. Sleep-related factors (e.g., pre-sleep arousal) were also examined for their influence on risk of clinically significant anxiety and depression.

Method
Between April 2020 and May 2021, 2069 participants (M=46.16 years, SD=13.42; 75.3% female) with new-onset, pre-existing, or no insomnia symptoms responded to a global online survey with 3-, 6-, and 12-month follow-ups. Data were analysed using mixed-effects and logistic regression models.

Results
New-onset and pre-existing insomnia were stronger predictors of anxiety and depressive symptoms over time (p’s &lt;.001) than other established risk factors such as, age, sex, and past psychiatric diagnoses. Although depressive symptoms in both insomnia groups declined from acutely elevated baseline levels, they remained clinically significant at the majority of timepoints whereas normal sleepers remained below threshold. Pre-sleep arousal was identified as a risk factor for clinically significant symptoms of anxiety (OR=1.05) and depression (OR=1.09) at 12-months. Sleep effort predicted anxiety (OR=1.06), whereas dysfunctional sleep-related attitudes and beliefs contributed to clinically significant depression (OR=1.22).

Discussion
Insomnia and associated sleep-related factors are key modifiable risks for persistent symptoms of anxiety and depression. This study highlights sleep as an opportunity for intervention into the enduring mental health ramifications of the COVID-19 pandemic and underlines the need to integrate insomnia treatment into routine mental health care.
O053 Obstructive sleep apnea is a distinct physiological phenotype in individuals with comorbid insomnia and sleep apnea (COMISA)
Authors: Brooker E , Thomson L , Landry S , Drummond S , Edwards B 
Published: November 2022

Abstract

Introduction
Obstructive sleep apnea (OSA) pathophysiology varies among individuals, though the influence of comorbid insomnia on this pathophysiology is unknown. We examined whether upper airway collapsibility, muscle compensation, loop gain, and the arousal threshold differ between OSA patients with and without comorbid insomnia disorder.

Methods
We noninvasively determined the four traits using the ventilatory flow pattern captured from standard polysomnography in 34 comorbid insomnia and obstructive sleep apnea (COMISA) and 34 OSA patients without insomnia (OSA-only). Participants had mild-to-severe OSA (

AHI
25.8±2.0 events/h) and were matched according to age (50.2±1.5 years) sex (42M:26F), and body mass index (29.3±0.6 kg/m²).

Results
COMISA patients had significantly lower respiratory arousal thresholds (128.9 [118.1–137.1] vs. 147.7 [132.3–165.0] %Veupnea, U=261, p&lt;.001), less collapsible upper airways (i.e., higher

Vpassive
88.2 [85.5–94.6] vs. 72.9 [64.7–79.2] %Veupnea, U=1081, p&lt;.001) and more stable ventilatory control (i.e., lower loop gain: 0.51 [0.44–0.56] vs. 0.58 [0.49–0.70], U=402, p=.03) relative to OSA-only controls. Muscle compensation did not significantly differ between groups.

Discussion
OSA patients with comorbid insomnia appear to have OSA driven more by heightened nocturnal arousability than by the contribution of anatomical factors, compared to OSA patients without insomnia. Heightened nocturnal arousability as the driver of apneic events in COMISA suggests the conditioned arousal perpetuating insomnia may also increase risk or severity of OSA. Further research should investigate whether targeting increased arousal propensity (e.g., through CBT-I) provides therapeutic benefit to individuals with COMISA.
O057 Effects of oral appliance therapy on upper airway collapsibility pre- versus post-treatment
Authors: Osman A , Eckert D 
Published: November 2022

Abstract

Introduction
A key predictive mechanism of improvement in obstructive sleep apnoea (OSA) severity with oral appliance therapy (OAT) is a less collapsible upper airway. In this study, we investigate the effects of acute versus longer-term use of OAT on upper airway collapsibility.

Methods
To investigate potential changes in upper airway collapsibility we studied 10 treatment naïve people (2 female) with OSA (AHI=40±31events/h, age=51±11years, BMI=29±4kg/m-2) at baseline and following 4-6 weeks oral appliance therapy acclimatization. The upper airway collapsibility index was measured during wakefulness with/without the oral appliance in place at two time points (pre/post treatment). All participants were instrumented with standard polysomnography equipment, two pressure catheters (one at the level of the choanae, and the other at the epiglottis), a pneumotachograph, sealed nasal mask and a short tubing connected to a breathing circuit to allow rapid delivery of negative pressure ~-11cmH₂O to the mask.

Results
The upper airway collapsibility index measured during early inspiration was reduced by 11% (33±19 vs. 22±16%, n=10, p=0.02) with OAT in place in treatment naïve participants. Similarly, following acclimatization, the upper airway collapsibility index also reduced by 7% with OAT in place (25±15 vs. 18±15%, n=9, p=0.03).

Conclusions
While further work is required to determine if long-term OAT independently improves upper airway collapsibility, these data show sustained improvements in upper airway collapsibility with OAT over time and highlight the potential for this approach to help predict OAT treatment outcomes.
O062 Sleep behaviour modification in shift workers: Applying models of arousal dynamics tailored to individual shift schedules and personal commitments
Authors: Varma P , Postnova S , Rajaratnam S , Phillips A , Howard M , Sletten T 
Published: November 2022

Abstract

Introduction
Circadian-based biomathematical models of sleep-wake and alertness regulation can improve sleep health in shift workers by providing physiologically optimal times for sleep. It is unclear whether they can be successfully implemented in real-world contexts. This study, for the first time examined associations between model-based sleep-wake recommendations and modification of sleep behaviours in shift workers.

Methods
Nurses (n=28; 37.2±9.6yrs) with matching-rotating shift schedules received personalised sleep recommendations from either the Phillips-Robinson Model or Model of Arousal Dynamics. Nurses used sleep diaries to record sleep-wake behaviours: (i) pre-exposure to recommendations (baseline, 1-week), (ii) upon exposure (1-week) and completed PROMIS-sleep disturbance, sleep-related impairments pre and post.

Results
During baseline, participants usual bedtimes and waketimes were at least 180mins away from recommended times from both models. Upon exposure to recommendations, sleep behaviours were aligned within: (i) 62±11mins for bedtime, 71±9mins for waketime (Model of Arousal Dynamics), (ii) 104±16mins for bedtime, 89±12mins for waketime (Phillips-Robinson model) with large effect sizes (p&lt;.00001 for both models). Participants sleep windows had better compliance with recommended sleep windows for the CRC Alertness model (79% overlap) compared to the Phillips-Robinson model (69% overlap). Sleep disturbance and sleep-related impairments improved significantly upon study conclusion (small-effect sizes both groups). Participants reported that automated recommendation delivery, and use of diurnal preference and real-time sleep behaviours to further personalise recommendations will facilitate greater uptake.

Conclusion
The study provides positive proof-of-concept for the implementation of biomathematical models of sleep-wake dynamics in shift work contexts. Accounting for individual differences may improve applicability of recommendations.
O063 Impact of sleep deprivation on distributed team performance and cohesion
Authors: Greer E , Matthews R , Owen M , Grosser L , Roma P , Banks S 
Published: November 2022

Abstract
Distributed teams often have limited contact resulting in less effective collaboration and decreased cohesion. Those in 24/7 industries are further impacted by fatigue and sleep loss which threatens workers’ safety, productivity, and performance. To date little is known about distributed team cohesion with extended periods of time awake. Hence, this study examined the impact of sleep deprivation on distributed team performance and cohesion.
22 healthy individuals (M=22.81,SD=4.4 years,11f) aged 18-45 years participated in a five-day sleep study. Participants were randomly allocated into teams consisting of four members and underwent 62h of total sleep deprivation (TSD). Distributed teams completed the COHESION task at 10h intervals throughout the wake period. COHESION required distributed teams to attempt resource movements, while avoiding visible and invisible barriers. Team members could dedicate time to reveal barriers to all, making successful resource movements easier. Distributed team performance was assessed using team successful resource movements. Distributed team cohesion was assessed through team members’ barrier reveal responses in relation to their total responses.
Data were analysed using linear mixed models. Results showed that distributed team cohesion decreased with TSD (F(5,495.19)=3.18,p=.008), and there were significant differences between teams (F(5,21.99)=8.74,p&lt;.001). Team performance also decreased with TSD (F(5,144)=3.01,p=.013), with significant differences between teams (F(5,21.01)=7.03,p&lt;.001).
This study found distributed team cohesion was reduced with TSD, as was overall team performance. We found each distributed team used a different strategy to manage the team task during sleep deprivation and these differences impacted their overall team performance.
O065 The impact of breaking up sitting on vigilant attention during the workday when sleep restricted
Authors: Gupta C , Ferguson S , Vandelanotte C , Duncan M , Tucker P , Lastella M , Tuckwell G , Vincent G 
Published: November 2022

Abstract

Introduction
Sleep restriction is associated with impairments to cognitive performance. A current strategy to improve cognitive performance at work is breaking up prolonged sitting with light-intensity walking. However, it is unknown whether this strategy can counteract the impact of sleep restriction. This study investigated the effect of breaking up sitting on cognitive performance under conditions of sleep restriction.

Method
84 healthy adults (age M±

SD
23.1±4.5 years; 41 females) participated in a 7-day laboratory study, with 5 simulated workdays (0900-1700). Participants were randomly allocated to a condition: Breaking up sitting and 9-h sleep (Break9; n=20), Breaking up sitting and 5h sleep (Break5; n=20), Sedentary and 9-h sleep (Sit9; n=22), Sedentary and 5-h sleep (Sit5; n=22). Sleep opportunity prior to each workday was 9-h (2200-0700) or 5-h (0200-0700) depending on condition. Every 30-min during the workday participants in the breaking up sitting conditions completed 3-min bouts of light-intensity walking, while participants in the sedentary conditions remained sitting. At 0900, 1100, 1300, 1500, and 1700, participants completed a 10-min Psychomotor Vigilance Task and the Karolinska Sleepiness Scale.

Results
Mixed model ANOVAs revealed no significant 2-way or 3-way interactions between condition (Break9, Break5, Sit9 and Sit5), time of day, and workday for vigilant attention (reciprocal mean response time and mean lapses) or subjective sleepiness.

Discussion
Breaking up prolonged sitting with light-intensity walking did improve cognitive performance. Higher doses of physical activity may be needed to counteract the effects of sleep restriction on cognitive performance. Findings highlight the acute cognitive deficits associated with inadequate sleep.