bluuebunny/crossref_metadata_2025_split huggingface dataset:
0114 Interplay of School and Free Days on the Association of Circadian Misalignment with Heart Rate Variability in Adolescents
Authors: Morales-Ghinaglia Natasha , He Fan , Calhoun Susan , Liao Jason , Vgontzas Alexandros , Bixler Edward , Liao Duanping , Fernandez-Mendoza Julio 
Published: May 2023

Abstract

Introduction
The circadian timing system, which governs the sleep-wake cycle, is involved in cardiometabolic and autonomic regulation. Heart rate variability (HRV), a marker of cardiac autonomic modulation (CAM), is known to predict cardiovascular morbidity. Therefore, circadian misalignment of the sleep-wake cycle, which is highly prevalent in adolescents and may express differently if youth are in school or free-days, is likely to impact CAM. We examined whether deviations in the circadian timing of sleep are associated with blunted HRV in adolescents as a function of being entrained to school or not.

Methods
We studied 337 population-based randomly-selected adolescents from the Penn State Child Cohort (median 16 years; 47% female; 21% racial/ethnic minority) who had at least 3-night at-home actigraphy (ACT), in-lab 9-h polysomnography (PSG) and 24-h Holter-monitoring heart rate variability (HRV) data. ACT-measured sleep midpoint (SM) was calculated as the midpoint of the sleep period for weekdays (5-nights) and weekends (2-nights), whereas ACT-measured sleep regularity (SR) was calculated as the intra-individual standard deviation of the SM across 5- and 7-nights. Frequency and time-domain HRV indices were primary outcomes. Linear regression models were stratified by “in school” and “on break” to test SM and SR as predictors of HRV indices while accounting for sex, race/ethnicity, age, BMI percentile, ACT-sleep duration, ACT-sleep variability, and PSG-apnea/hypopnea index.

Results
Lower SR on schooldays was associated with lower nighttime Log-HF, Log-LF and SDNN, yet higher HR (all p&lt; 0.01); e.g., each standard deviation increase in SR on schooldays (i.e., 45m higher) was associated with -7.15ms (2.57) in nighttime SDNN (p=0.006). A later SM on free weekends was associated with lower nighttime Log-HF, Log-LF, SDNN and RMSSD, yet higher HR and LF-HF ratio (all p&lt; 0.03); e.g., each standard deviation increase in SM on free weekends (i.e., 1.5h later) was associated with -7.33ms (2.85) in nighttime RMSSD (p=0.011).

Conclusion
A delayed and an irregular sleep midpoint during breaks and during schooldays, respectively, were associated with impaired CAM in adolescents. These data suggest that not only circadian misalignment contributes to adverse cardiovascular outcomes but its distinct metrics require measurement under different entrainment conditions in adolescents.

Support (if any)
NIH (R01HL136587,R01MH118308,UL1TR000127), American Heart Association (23PRE1011962).
0118 Association between TNF-α G308A Polymorphism (rs1800629) and Insomnia Vulnerability in Fertile Age Women with Primary Dysmenorrhea
Authors: Hung Ching-Sui , Wei Shyh-Yuh , Lin Chen-Li , Tu Cheng-Hao , Liu Yu-Huei , Ho Ying-Jui , Yang Chien-Ming , Hsieh Jen-Chuen 
Published: May 2023

Abstract

Introduction
Higher tumor necrosis factor-alpha (TNF-α) gene expression has been revealed in the peripheral blood monocytes across the menstrual cycle in patients with primary dysmenorrhea (PDM) than in the unaffected control. Sleep quality is affected by environmental factors, endocrine function abnormalities and genetic factors. The aim of this study was to evaluate the effect of TNF-α G308A polymorphism (rs1800629) on the self-reported sleep, health, menstrual pain severity as well as peri-ovulatory serum TNF-α level in women with and without PDM.

Methods
Sleep, psychological and physiological characteristics and menstrual pain severity were collected with questionnaires and sleep/menstrual diary within a menstrual cycle from a cohort of 43 PDM women and 42 healthy controls (aged 20-30 years, right-handed, non-smoking and non-shift workers without psychiatric, sleep and neurological comorbidity). Chi-square tests were used to check if the genotype proportions of the investigated gene fitted the Hardy-Weinberg equilibrium (HWE) and to evaluate if the genotypic and allelic distribution is associated with PDM. Chi-square tests or analysis of variance were used to examine the effects of genotype, group and/or genotype x group interaction with the sleep, mind and the body health variables.

Results
Neither allele frequencies nor genotypes of TNF-α G-308A gene could serve as an independent risk factor of PDM in the Taiwanese population. Circulating serum TNF-α did not correspond with the -308 TNF-α promoter polymorphism, either, which might be due to a multifactorial control process. The TNF-α 308 A allele carriers (28.6%) which was less common than the G allele carriers (71.4%), showed lower Beck depression score, lower bodily pain and better physical health and higher subjective sleep quality. Furthermore, in G allele carriers, the PDM group showed higher insomnia severity and lower sleep duration than that of the control group.

Conclusion
Present results suggested that TNF-alpha polymorphism conferred no prediction to PDM risk and peri-ovulatory serum TNF-α level. However, our findings were evident that the A allele at the TNFα 308 locus, as compared to the more common G allele, was associated to better health and better sleep, with an indication of a genetic underpinning to their better resistance from the risk of PDM.

Support (if any)
0127 Effects of pre-sleep alcohol consumption on sleep and heart rate (HR)
Authors: Rosenzweig Rebecca , McCullar Katie , McGeary John , Carskadon Mary 
Published: May 2023

Abstract

Introduction
Sympathetic nervous system (SNS) activity is relatively low, parasympathetic NS (PNS) relatively high, and heart rate (HR) is slow in NREM sleep. In tonic REM sleep, PNS activity remains high, but phasic REM sleep is associated with brief alterations of SNS/PNS balance along with irregular and phasic changes in HR. Alcohol elevates SNS activity, producing an overall increased HR during sleep. We propose to examine HR in NREM N2, N3, and REM sleep to determine whether the alcohol-related HR increase is present in these states.

Methods
27 healthy adults [(mean ± SD) 32.8 ± 12.4 y, 13 women] completed the study. Participants kept a consistent 8-9hr sleep schedule at home followed by 2 nonconsecutive in-lab nights with order of alcohol vs. mixer counterbalanced. Alcohol condition included vodka + mixer (dose adjusted by sex/height/weight/age) to target peak breath alcohol concentration (BrAC) of 0.08 ± 0.02 g%; a non-alcohol mixer beverage was provided on the other night. Drinking occurred over 45 minutes ending one hour before lights out. Sleep recordings included EEG, EOG, EMG and HR from modified lead-I or II EKG placement. Sleep was scored in 30-sec epochs and matched to mean HR values.

Results
A statistically significant increase in HR following alcohol was found for N2 (t=5.24, p&lt; 0.000; alcohol HR=67.22 ± 5.29, mixer HR=61.68 ± 5.00); N3 (t=3.43, p=0.002; alcohol HR=68.81 ± 4.32, mixer HR=62.26 ± 4.54); and REM sleep (t=4.54, p&lt; 0.000; alcohol HR=70.00 ± 11.27, mixer HR=64.70 ± 6.53)

Conclusion
Overall, alcohol significantly increased HR in N2, N3, and REM sleep. We plan to examine whether this effect persists across three consecutive nights of pre-sleep alcohol and may vary with time of night.

Support (if any)
This study was funded under grant R01AA025593
0131 Sleep Deprivation Alters Two Physiological Systems' Responses to Repeated Stressors Differentially
Authors: Lundholm Kirsie , Delane Sara , James Stephen , Honn Kimberly , Hansen Devon , Van Dongen Hans , Satterfield Brieann 
Published: May 2023

Abstract

Introduction
The hypothalamic-pituitary-adrenal (HPA) and sympathetic-adrenal-medullary (SAM) axes activate in response to stressors. Real-world exposure to stressors often co-occurs with total sleep deprivation (TSD). The SAM response to a single stressor appears unchanged by TSD, but salivary alpha-amylase (sAA) has shown that TSD blunts the SAM response to repeated stressor exposure. Using salivary cortisol concentration (SCC), we investigated the HPA response to repeated stressors under well-rested and TSD conditions.

Methods
N=10 healthy adults (ages 28.3±5.78; 5f) completed a 4-day/3-night in-laboratory study with 38h TSD preceded and followed by 10h sleep opportunities. On day 2 (well-rested) and day 3 (TSD), participants completed two stressor sessions in a high-fidelity shooting simulator, separated by 30min. Acting as police officers, civilian participants verbally interacted with emergency response scenarios and decided whether to use (simulated) deadly force. Seven saliva samples were collected each day: pre-stressor, and 0min, 15min, and 30min after each session. Samples were assayed for SCC and normalized against each day’s pre-stressor sample.

Results
Mixed-effects ANOVA showed a significant effect of sample time (F[5,99]=19.85, p&lt; 0.001), with SCC peaking 15min after the first stressor session and steadily declining thereafter. The SCC peak was significantly blunted during TSD compared to well-rested (t[99]=2.84, p=0.006). Correlations with previously reported, simultaneously assessed sAA concentrations, which peaked right after the first stressor session, were not significant (p&gt;0.2). Additionally, whereas sAA showed a second peak after the second stressor session when participants were well-rested, no second peak was found in SCC.

Conclusion
The SCC response after one stressor session with simulated emergency response scenarios was blunted during TSD, unlike the sAA response. However, while sAA peaked twice in response to repeated stressor exposure when participants were well-rested (though not during TSD), SCC continued to decline after the first stressor exposure, potentially indicating a HPA refractory mechanism or habituation. Also, over participants there was no significant relationship between the magnitude of the stressor response between SCC and sAA. Taken together, our results suggest fundamentally distinct SAM and HPA axis responsivity to repeated acute stressors, with differential impact of TSD.

Support (if any)
ONR N00014-13-1-0302, PRMRP W81XWH-20-1-0442.
0158 Preliminary Study of the Links Between Adverse Childhood Experiences and Actigraphy-Measured Sleep Characteristics in Young Adults
Authors: Zucker Anna , Schwager Laura , Hart Thomas , Flores Mark , Moon Chooza , Thomas Emily , Jenkins Nathaniel 
Published: May 2023

Abstract

Introduction
Adverse Childhood Experiences (ACEs) are highly stressful events during the first 18 years of life that have been linked with adverse adult health outcomes. Sleep is an important behavioral risk factor for a myriad of health outcomes that have been linked to ACE exposure. A growing body of evidence indicates that ACEs are associated with low self-reported sleep durations, but these findings should be verified using objectively measured sleep characteristics. The purpose of this study was to examine associations of ACE exposure with actigraphy-measured sleep duration, timing, and variability.

Methods
Methods: In twenty-four young adults (20F/4M; mean±SD, age=24±5 y), we assessed ACE exposure using the 10-item ACE scale and measured sleep characteristics over a ≥6 day period using a wrist-worn actigraphy device. Participants with 0–1 ACEs were characterized as low-ACE (ACE-low, n=10) and participants with 2+ ACEs were characterized as moderate-high-ACE exposure (ACE-mh, n=14). Independent samples t-tests and Hedges’ g effect sizes were used to compare total sleep duration, bed-time, get-up time, time-in-bed, sleep onset latency and the standard deviation of bed time and total sleep duration between groups.

Results
Time-in-bed was greater in ACE-mh than in ACE-low (mean±SE difference=-60±25 min; p=0.027; g=-0.95), yet there was no difference in total sleep duration (-9±10 min; p=0.46; g=-0.37). This discrepancy was accompanied by a non-significant, but large-effect size difference between ACE-mh and ACE-low (-15±7 min; p=0.051; g=-0.83) in sleep onset latency. There were no differences between groups in either bed-time (p=0.34; g=0.39) or get-up time (p=0.35; g=-1.2), nor in either bed-time (p=0.84; g=-0.08) or total sleep duration (p=0.36; g=-0.37) variability.

Conclusion
In contrast to prior evidence based on self-report, our initial evidence indicates that ACE exposure is not linked with shorter sleep durations or higher sleep variability when measured using actigraphy. Instead, ACE exposure is linked to greater time in bed and greater sleep onset latencies, suggesting that individuals exposed to ACEs may have less efficient sleep.

Support (if any)
Support: Research reported in this publication was supported in part by the NCATS of the NIH (UL1TR002537) and by the Injury Prevention Research Center through the CDC (R49 CE003095).
0162 The neural bases of emotion dysregulation in rotating shift workers
Authors: Lee Kyung Hwa , Lee Ha Young , Jeon Jeong Eun , Lee Mi Hyun , Lee Jooyoung , Shin Jiyoon , Seo Min Cheol , Lee Yu Jin , Kim Seog Ju 
Published: May 2023

Abstract

Introduction
Shift work is known to be associated with sleep disturbance and circadian misalignment and may contribute to alterations in the brain implicated in emotion dysregulation. In this study, we examined 1) neural correlates of emotion dysregulation, including emotional reactivity and regulation in shift workers and 2) relationships between neural correlates of emotion dysregulation, sleep disturbance, and circadian misalignment.

Methods
Fifty-six rotating shift workers (SW, 42 females, 30.80 ± 6.94 years old) who had non-standard shift schedules and 52 healthy controls (HC, 36 females, 31.69 ± 7.86 years old) who did not work as shift schedules participated in this study. Both SW and HC completed self-reported measures of sleep and mood problems, and wrote sleep diary and wore actigraphy to assess sleep quality and circadian rhythms. They also underwent one night polysomnography and were scanned while they were performing the emotion regulation task. We analyzed group differences in mood, sleep, circadian rhythms, and neural bases of emotional reactivity and regulation, and examined relationships between these variables.

Results
SW showed significant differences in actigraphy-estimated sleep (i.e., lower sleep efficiency) and circadian rhythms (e.g., greater motor activity [M10] and lower interdaily stability) compared to HC. SW also exhibited increased anterior insula (AI) activation in response to negative pictures, but reduced activation in the dorsomedial prefrontal cortex (dMPFC) and AI-dMPFC functional connectivity during emotion regulation compared to HC. AI activation and AI-dMPFC functional connectivity were significantly associated with sleep disturbance (i.e., sleep diary-estimated sleep onset latency) and circadian misalignment (e.g., M10 and interdaily stability). Furthermore, a mediation analysis revealed that shift work was associated with increased motor activity during the most active 10-hour period, which then contributed to increased AI activation in response to negative pictures.

Conclusion
Our findings suggest that shift work may contribute to sleep disturbance and circadian misalignment, and neural alterations associated with emotional reactivity and regulation. Furthermore, the mediation result suggests that increased motor activity along with misaligned circadian rhythm may serve as a pathway, through shift work contributes to heightened emotional reactivity to negative information.

Support (if any)
National Research Foundation (No. 2022R1A2C2008417, NRF-2022R1A2C1008209) and Korea Institute for Advancement of Technology (No. 20009210).
0164 Move Your Feet and Sleep: A Longitudinal Dynamic Analysis of Physical Activity, Sedentary Behavior, and Insomnia Symptoms
Authors: Nielson Spencer , Boyle Julia , Perlis Michael , Dzierzewski Joseph 
Published: May 2023

Abstract

Introduction
Insomnia symptoms, which include sleep disturbances and daytime dysfunction, are associated with poor physical and mental health. Physical activity has been associated with good sleep while sedentary behavior has been associated with poor sleep. This study investigated whether physical activity and sedentary behavior are associated with insomnia symptoms both generally (i.e., between-persons, mean-level) and dynamically (i.e., within-persons, person-centered).

Methods
Participants (N=775) included adults (Mage=47.3 years,54.6% female) who completed an online longitudinal study investigating sleep and health across the lifespan at three time points (approximately 17-weeks apart). Participants reported: (a) their duration of moderate-to-vigorous physical activity per week (in minutes), (b) the percentage of their day spent sedentary, and (c) their insomnia symptoms via the Insomnia Severity Index which was scored according to traditional standards (i.e., total score) as well as proposed two factor scores: (1) Sleep Disturbance (items 1,2,3) and (2) Daytime Dysfunction (items 4,5,6,7). Multilevel modeling was used to examine the associations among physical activity, sedentary behavior, and insomnia symptoms at both between- and within-persons levels.

Results
No significant associations were observed among total ISI score or the factor scores, and minutes spent in moderate-to-vigorous physical activity (all p’s&gt;.05). Sedentary behavior, however, was significantly associated with total ISI score at both the between-person and within-person levels (β=.02, t=2.71, p=.007; β=0.03, t=2.62, p=.009, respectively). For the Sleep Disturbance factor, between-person sedentary behavior was not a significant predictor while within-person sedentary behavior was associated with higher sleep disturbance scores (β=0.01, t=1.16, p=.245; β=.01, t=2.06, p=.039, respectively). For the Daytime Dysfunction factor, both between-persons and within-person levels of sedentary behavior were associated with increased daytime dysfunction (β=.02, t=3.30, p=.001; β=.01, t=2.53, p=.012).

Conclusion
Sedentary behavior appears to be a more robust predictor of insomnia symptoms than physical activity. Further, the association between sedentary behavior and insomnia symptoms was observed to be dynamic in that when an individual reported being more sedentary than customary, they also reported more insomnia symptoms. Future analyses should consider demographic variables and comorbid conditions to identify subgroups in which these associations are most pronounced.

Support (if any)
National Institute on Aging of the National Institutes of Health under Award Number K23AG049955 (PI: Dzierzewski).
0165 The Relationships between Early Maternal Sleep and Mother-Infant Bonding, and Infant Bedtime Difficulty Later: A Path Analysis
Authors: Jiao Nana , Pituch Keenan , Whisner Corrie , Petrov Megan 
Published: May 2023

Abstract

Introduction
Infant sleep is influenced by biopsychosocial factors. However, the influences of early parental sleep quality and parent-infant bonding on infant sleep development are underexplored. This study aimed to examine the relationships between early maternal sleep quality and mother-infant bonding at 8 weeks postpartum, and infant bedtime difficulty at 3 months postpartum.

Methods
This study is a secondary analysis from the Snuggle Bug/Acurrucadito Study, an observational, longitudinal cohort study investigating the associations between 24-hr sleep-wake patterns, gut microbiome, and weight development among infants. Mothers (n=60, 31.5±5.4y, 66.3% married, 40.8% Hispanic, 41.5% &lt; bachelor’s degree) and their full-term (≥37wk), singleton infants without major complications were recruited from Phoenix, Arizona metropolitan area. At 3 and 8 weeks, and 3 months of infant age, mothers completed the Pittsburgh Sleep Quality Index (PSQI, range:0-21, higher scores indicate worse sleep quality), and reported on infant bedtime difficulty, using a 5-point Likert scale (range:1-5) with higher scores indicating greater bedtime difficulty. Mother-infant bonding was measured by the Postpartum Bonding Questionnaire (PBQ, range:0-125) at 8-week age, with higher scores indicating greater bonding problems. Based on the Transactional Model of Infant Sleep, path analyses were conducted to identify the direct effect of 8-week PSQI scores, and indirect effects of 8-week PBQ total scores and 8-week bedtime difficulty on 3-month bedtime difficulty, using z scores for all variables and the 3-week bedtime difficulty as a covariate.

Results
At 8 weeks postpartum, the means of PSQI, PBQ, and bedtime difficulty were 5.8±2.6, 5.3±4.7, and 2.4±1.0, respectively. Bedtime difficulty at 3 months was 2.0±1.0. After adjusting for the 3-week bedtime difficulty, the 8-week maternal sleep quality was not directly associated with 8-week (β=.005, 95%CI [-0.31, 0.32]) or 3-month infant bedtime difficulty (β=-0.14, 95%CI [-0.43, 0.14]), whereas 8-week mother-infant bonding significantly mediated the relationship between 8-week maternal sleep quality and 3-month infant bedtime difficulty (β=0.1, 95%CI [0.02, 0.22]).

Conclusion
This study highlighted that early maternal sleep may disrupt early mother-infant bonding, which, in turn, may increase infant bedtime difficulty later in development. Future research should investigate how best to support healthy family sleep and bonding relationships.

Support (if any)
NIH/NHLBI R01HL147931