Chronic Insufficient Sleep Research Articles

Sleep Health among Community-Recruited Opioid-Using People Who Inject Drugs in Los Angeles, CA and Denver, CO.

Chronic insufficient and poor-quality sleep are linked to hypertension, diabetes, depression, heart attack, and stroke. While studies on substance use and sleep typically focus on people in or entering treatment, there is a lack of research on sleep health among community-recruited people who inject drugs (PWID). To address this literature gap, we examined factors associated with insufficient and poor-quality sleep among community-recruited PWID. We recruited and interviewed 472 active opioid-using PWID (injected within the last 30days) in Los Angeles, CA and Denver, CO between 2021 and 2022. Participants completed computer-assisted interviews covering demographics, subsistence measures, drug use patterns, injection-related behaviors, health risks, and sleep duration and quality in the last 3months. Descriptive statistics were used to analyze all variables for subjects with complete responses to sleep items (n = 464). Bivariate analyses determined factors associated with sleep measures using chi-square and t-tests. Collinear variables were removed, and binomial linear multivariable regression calculated risk ratios (RR) for insufficient and poor-quality sleep in the last 3months. Participants exhibited low sleep duration (mean = 4.99, standard deviation (SD) = 2.70), with 76% reporting insufficient sleep and 62% poor-quality sleep. Bivariate analyses associated both sleep measures with drug use, high subsistence scores, violent victimization, and poor health outcomes. Multivariable analyses showed a high subsistence score predicting insufficient (RR = 1.31) and poor-quality sleep (RR = 1.69) compared to low subsistence. Poor sleep health is common among structurally vulnerablecommunity-recruited PWID, asmeasured by subsistence index associated with adverse sleep outcomes. Further research on structural interventions to address sleep and subsequent health outcomes among PWID is imperative.

Abstract P523: Circulating Endothelial-Cell Derived Microvesicles Associated With Insufficient Sleep Impairs Cerebral Microvascular Fibrinolytic Capacity

Chronic insufficient sleep (< 7 hour/night) is associated with increased risk of ischemic stroke. Endothelial cell dysfunction, specifically impairment endothelial release of tissue-type plasminogen activator (t-PA), represents an important mechanism underlying cerebrovascular events such as ischemic stroke. Endothelial cells are the primary site of synthesis and release of t-PA, the plasminogen activator in fibrinolysis and, thus, a key regulator of endogenous thrombolysis. We have previously demonstrated that insufficient sleep is associated with impaired endothelial capacity to release t-PA, however the mechanisms for the sleep-related fibrinolytic impairment are not well understood. Clinical interest in endothelial cell-derived microvesicles (EMVs) has intensified due to their involvement in the development of endothelial dysfunction and, in turn, cardiovascular and cerebrovascular events. The aim of this study was to determine, in vitro, the effects of circulating EMVs isolated from adults with chronic insufficient sleep on brain endothelial cell t-PA release. Considering EMVs are known to cross the blood brain barrier and are associated with ischemic stroke incidence, severity and outcome; circulating EMVs associated with insufficient sleep may be a mediator of stroke risk. Twenty-four healthy, non-obese, normotensive, sedentary adults (age: 23-69 years) were studied: 12 normal nightly sleep duration (7M/5F; age: 47±5 yr; nightly sleep: 7.4±0.1 hour/night) and 12 with short nightly sleep duration (9M/3F; 53±4 yr; 5.9±0.2 hour/night). EMV identification (CD144+) and isolation from peripheral blood was performed by flow cytometry. Human cerebral microvascular endothelial cells (hCMECs) were cultured and separately treated with EMVs from each subject. Cultured hCMECs were treated with EMVs in the absence and presence of thrombin (1 unit/mL) for 24 hours. Intracellular expression of t-PA was significantly lower (~30%) in hCMECs treated with EMVs from adults with insufficient sleep (31±3 AU) compared with cells treated with EMVs from normal sleep adults (40±3 AU). Although the effect of EMVs on basal t-PA release was not different between the groups; thrombin-stimulated t-PA release was significantly lower in cells treated with EMVs from adults with insufficient sleep (from 57±3 to 59±4 ng/mL) compared with EMVs from adults with normal sleep (from 53±3 to 66±4 ng/mL). The capacity of hCMECs to release t-PA in response to thrombin was ~75% lower when treated with EMVs from adults with insufficient sleep. These results indicate that circulating EMVs associated with chronic insufficient sleep diminishes brain endothelial cell t-PA production and impairs t-PA release. Circulating EMVs represent a mechanistic factor in insufficient sleep-related fibrinolytic dysfunction and ischemic stroke risk.

Sleep insufficiency, circadian rhythms, and metabolomics: the connection between metabolic and sleep disorders.

US adults who report experiencing insufficient sleep are more likely to suffer from metabolic disorders such as hyperlipidemia, diabetes, and obesity than those with sufficient sleep. Less is understood about the underlying molecular mechanisms connecting these phenomena. A systematic, qualitative review of metabolomics studies exploring metabolic changes in response to sleep insufficiency, sleep deprivation, or circadian disruption was conducted in accordance with PRISMA guidelines. An electronic literature review in the PubMed database was performed considering publications through May 2021 and screening and eligibility criteria were applied to articles retrieved. The following keywords were used: "metabolomics" and "sleep disorders" or "sleep deprivation" or "sleep disturbance" or "circadian rhythm." After screening and addition of studies included from reference lists of retrieved studies, 16 records were identified for review. Consistent changes in metabolites were observed across studies between individuals experiencing sleep deprivation compared to non-sleep deprived controls. Significant increases in phosphatidylcholines, acylcarnitines, sphingolipids, and other lipids were consistent across studies. Increased levels of amino acids such as tryptophan and phenylalanine were also noted. However, studies were limited to small samples of young, healthy, mostly male participants conducted in short inpatient sessions, limiting generalizability. Changes in lipid and amino acid metabolites accompanying sleep deprivation and/or circadian rhythms may indicate cellular membrane and protein breakdown underlying the connection between sleep disturbance, hyperlipidemia, and other metabolic disorders. Larger epidemiological studies examining changes in the human metabolome in response to chronic insufficient sleep would help elucidate this relationship.

Neighborhood Stress Predicts Fear of Sleep Independently of Posttraumatic Stress Disorder

ABSTRACT Background Chronic insufficient sleep is linked to a variety of adverse health outcomes, and African Americans have been found to have poorer sleep than their non-Hispanic White counterparts. African Americans disproportionately live in low-income disordered neighborhoods which increases their risk of trauma exposure and adversely affects their sleep. Fear of sleep is a construct linked to posttraumatic stress disorder (PTSD). We have reported a relationship between fear of sleep and insomnia in urban residing African Americans. Our objective is to report the relative contributions of neighborhood stress along with PTSD to fear of sleep. Methods The present study features a nonclinical sample of 117 African Americans (ages 18–35) who reside in DC. Results After controlling for gender, hierarchical linear regression analyses revealed that PTSD severity and perceptions of the neighborhood environment accounted for approximately 32% of the variance in sleep-related fears (∆R2 = .320, p < .001). Regression coefficients suggest that perceptions of the neighborhood (β = .360) predict sleep-related fears to a similar degree as PTSD severity (β = .368). Conclusion Results from this study have implications for interventions to help African Americans to cope with their neighborhood environments effect on their sleep.

Blunted heart rate recovery to spontaneous nocturnal arousals in short-sleeping adults.

Chronic insufficient sleep is a common occurrence around the world and results in numerous physiological detriments and consequences, including cardiovascular complications. The purpose of the present study was to assess the relationship between habitual total sleep time (TST) measured objectively via at-home actigraphy and heart rate (HR) reactivity to nocturnal cortical arousals. We hypothesized that short habitual TST would be associated with exaggerated cardiac reactivity to nocturnal cortical arousals. Participants included 35 healthy individuals [20 men, 15 women, age: 24 ± 1 yr, body mass index (BMI): 27 ± 1 kg/m2], and were split using a median analysis into short-sleeping (SS; n = 17) and normal-sleeping (NS; n = 18) adults based on a minimum of 7 days of at-home actigraphy testing. All participants underwent a full overnight laboratory polysomnography (PSG) testing session, including continuous HR (electrocardiogram, ECG) sampling. HR reactivities to all spontaneous cortical arousals were assessed for 30 cardiac cycles following the onset of the arousal in all participants. Baseline HR was not significantly different between groups (P > 0.05). Spontaneous nocturnal arousal elicited an augmented HR response in the SS group, specifically during the recovery period [F(5.261,163.08) = 3.058, P = 0.01, ηp2 = 0.09]. There were no significant differences in HR reactivity between sexes [F(3.818,118.368) = 1.191, P = 0.318]. These findings offer evidence of nocturnal cardiovascular dysregulation in habitual short sleepers, independent from any diagnosed sleep disorders.NEW & NOTEWORTHY Short habitual sleep is associated with poor cardiovascular outcomes, but mechanisms remain equivocal. The present study used objectively measured habitual sleep via wrist actigraphy, and reports that habitual short sleepers have augmented heart rate recovery responses to spontaneous arousals as determined by gold-standard polysomnography. There were no reported sex differences. The augmented heart rate recovery to spontaneous cortical arousals may be an important mechanism contributing to the associations between insufficient sleep and cardiovascular risk.

Self-reported sleep and sleep deficiency: Results from a large initiative of sailors attached to U.S. Navy warships.

SummaryChronic insufficient sleep is known to lead to a broad range of negative consequences (e.g. poor health and cognitive performance). While insufficient sleep and associated fatigue are present in many diverse populations, it is of special concern in high‐risk military environments, where a mishap can result in catastrophic outcomes. Although many studies have been conducted to characterise sleep in general military populations, relatively few have been conducted using a large representative sample of sailors assigned to United States Naval warships. The present cross‐sectional study characterises self‐reported sleep parameters in sailors (N = 11,738) and explores the role of possible contributors to insufficient sleep. The results indicate that sailors, across a variety of different subgroups, do not obtain the amount of sleep that they report requiring for feeling well‐rested. Of the many potential factors thwarting sleep, workload and an uncomfortable mattress are the most promising candidates to target for improvement.

Associations between insufficient sleep and prescription opioid misuse among high school students in the United States

The aim of this study was to estimate the association between insufficient sleep and prescription opioid misuse among US high school students. Participants were 6,884 high school students who self-reported on sleep duration and prescription opioid misuse in the 2019 Youth Risk Behavior Survey. Sleep duration was categorized by the Youth Risk Behavior Survey according to the American Academy of Sleep Medicine guidelines as follows: recommended sleep duration (8-9 hours) vs insufficient sleep (< 8 hours). Participants also reported whether they had any prescription opioid misuse during their lifetime and whether they had prescription opioid misuse within the past 30 days. Most (79.4%) participants reported sleeping less than 8 hours per night. Among all youth, 12.9% reported lifetime prescription opioid misuse and 6.2% reported current prescription opioid misuse. Prevalence of both lifetime and current opioid medication misuse was higher among those also reporting insufficient sleep compared to those reporting recommended sleep duration (14.3% vs 7.7%, P < .0001 for lifetime misuse and 6.6% vs 4.3%, P = .0091 for current misuse). In multivariate models, insufficient sleep was associated with an increased odds of lifetime prescription opioid misuse (adjusted odds ratios = 1.4; 95% confidence interval, 1.1-1.2; P = .006); however, we did not find an association between sleep duration and current prescription opioid misuse in multivariate analysis. Sleep duration is associated with lifetime opioid misuse among US youth. Longitudinal studies are needed to test whether causal relationships exist, and to understand biobehavioral mechanisms that underlie associations between sleep deficiency and opioid misuse in adolescents. Groenewald CB, Rabbitts JA, Tham SW, Law EF, Palermo TM. Associations between insufficient sleep and prescription opioid misuse among high school students in the United States. J Clin Sleep Med. 2021;17(11):2205-2214.

Sleep duration trajectory during the transition to adolescence and subsequent risk of non-suicidal self-harm.

Non-suicidal self-harm (NSSH) and chronic insufficient sleep are both major health problems during the transition from childhood to adolescence. We examined to identify sleep duration trajectories from childhood to adolescence and their associations with subsequent risk of NSSH. A cohort of children around the period of pubertal onset (7-9years old) were followed from 2013 over 6years. Group-based trajectory modeling was recruited to identify sleep duration trajectories derived from 5 repeated measures. Association between sleep duration trajectories with the risk of NSSH was examined using multivariate logistic regression model. Nonlinear dose-response associations between sleep duration and NSSH risk were also assessed using restricted cubic spline models. Of the 1973 participants included in the study (mean ± SD, 8.1 ± 0.9years age at baseline, 41.1% female). Three sleep duration trajectories were identified: persistent sleeping ≥ 8h/day (27.7%), moderately decreasing (60.8%) and rapidly decreasing (11.5%) sleep duration groups. After multivariable adjustment for covariates, compared with the persistent sleeping ≥ 8h/day group, the odds ratio of NSSH was 2.58 (95% CI 1.92, 3.45) for the moderately decreasing group, and 4.16 (2.86, 6.04) for rapidly decreasing group. In dose-response analysis, sleep duration was associated with NSSH risk in a non-linear fashion (χ2 = 25.16, Pnonlinearity < 0.001). When compared with the reference (sleep duration = 8h), the ORs (95% CI) for NSSH risks were 3.20 (1.93, 5.29), 2.37 (1.64, 3.41), 1.75 (1.39, 2.20) and 1.30 (1.18, 1.44) for sleep duration at 4 to 7h, respectively. Also, we found sleep duration at 9h [0.82 (0.75, 0.89)] and at 10h [0.72 (0.57, 0.91)] significantly associated with decreased risk of NSSH. Longitudinal sleep duration patterns may assist in identification of adolescents at greatest risk of NSSH in the future, which could lead to improved targeting of prevention and intervention strategies. The findings also highlight a non-linear relationship between sleep duration and NSSH during the transition to adolescence.

Modeling of chronic sleep restriction for translational studies

To develop of a chronic sleep restriction model in rats by repeated sleep deprivation using an orbital shaker and to determine whether this model leads to disturbances in sleep homeostatic mechanisms. Male Wistar rats (7-8 months old) underwent sleep restriction for five consecutive days: 3 h of sleep deprivation and 1 h of sleep opportunity repeating throughout each day. Polysomnograms were recorded telemetrically throughout the day before sleep restriction (baseline), on the 1st, 3rd, 5th day of sleep restriction and 2 days after the end of sleep restriction (recovery period). During the period of sleep restriction, the total amount of slow-wave sleep (SWS) and rapid eye movement (REM) sleep decreased by 61% and 55%, respectively, compared to baseline. On the first day of recovery, amount of SWS increased mainly in the dark (active) phase of the day, while REM sleep increased in both light and dark phases; there was no marked rebound of daily SWS amount, while REM sleep increased by 30% from baseline. On the first day of recovery, an elevation of EEG beta and sigma power in sleep states was observed mainly in the light phase of the day. The loss of deep SWS throughout the sleep restriction period increased from 50% on 1st day to 75% on 5th day. The level of deep SWS remained below the baseline by 15-20% on the two subsequent days of recovery. The findings suggest that homeostatic mechanisms of SWS are persistently impaired after 5-day chronic sleep restriction. Besides, a decline of wakefulness accompanied by an increase of SWS in the active phase of the recovery period indicates a disruption in circadian rhythm. The proposed model leads to the disruption of sleep homeostatic mechanisms, which, in turn, impede compensation of SWS loss caused by chronic insufficient sleep.

0333 Electronic Media Use is Associated with Poor Sleep In 3-6 Year-Old Children

Abstract Introduction Recent surveys estimate that electronic media use among young children is increasing and that behavioral sleep problems are prevalent. In this study, we employed assessments of sleep and media use and tested the hypothesis that poor sleeping children would be more likely to engage with media than good sleeping children. Methods Participants were 44 children from two different cohorts: (1) Healthy, good sleepers (n=26, 13 males, 4.3±0.4 years) who reportedly obtained ≥10.5 hours per night and had no behavioral sleep problems and (2) Poor sleepers (n=18, 9 males, 5.5±0.7 years) who reportedly obtained chronic insufficient sleep ≤9 hours per night and/or had behavioral sleep problems for ≥6 months. Sleep duration and sleep onset latency (SOL) were quantified through 7 nights of actigraphy and verified with sleep diaries. Media use, defined as any electronic device involving screen time that engages children, was assessed across 2 weekdays and 2 weekend days through a parental media diary. Independent t-tests compared the duration of media use and actigraphy variables between groups. Results Poor sleeping children on average had longer SOL (28.6±17.9 vs. 17.3±8.66 minutes, t=-2.5, p&amp;lt;0.05) and shorter sleep duration (589.6±37.5 vs. 627.4±27.4 minutes, t=3.7, p&amp;lt;0.01) compared to good sleeping children. Additionally, average daily media use (125.1±88.5 vs. 66.5±48.3 minutes, t=-2.6, p&amp;lt;0.05), evening media use (22.0±21.3 vs. 4.2±10.4 minutes, t=-3.3, p&amp;lt;0.01), and weekend media use (154.4±105.9 vs. 79.8±55.6 minutes, t=-2.7, p&amp;lt;0.05) duration was higher in poor than good sleepers. Conclusion Our findings indicate that media use duration and timing likely play an important role in early childhood sleep health. Young children who use more evening media are more likely to take longer to fall asleep and have shorter sleep duration overall. Time displacement (time spent using media instead of sleeping), psychological stimulation, and the effects of screen light on circadian timing are potential mechanisms underlying these associations. Support NIH R01-MH086566 and R21-MH110765 to MKL

Abstract P545: Insufficient Sleep and Nitric Oxide-Mediated Endothelium-Dependent Vasodilation in Adults With Elevated Blood Pressure

Elevated blood pressure (BP ≥130/80 mmHg) is associated with increased risk for myocardial infarction, heart failure, stroke and vascular disease. Insufficient nightly sleep (&lt;7 h/night) has been linked not only to the etiology of elevated blood pressure but is a prevalent, often ignored, comorbidity. Indeed, short sleep duration is now considered to be a plausible risk factor for elevated blood pressure and a harbinger of increased cardiovascular risk. A high prevalence of insufficient nightly sleep has been reported in adults with elevated blood pressure. The influence of insufficient sleep on endothelial vasodilator function in adults with elevated blood pressure is unknown. We tested the hypotheses that chronic insufficient sleep is associated with diminished nitric oxide (NO)-mediated endothelium-dependent vasodilation in adults with elevated blood pressure. Moreover, the insufficient sleep-related reduction in endothelial vasodilator function is due, at least in part to increased oxidative stress. Thirty-five middle-aged and older adults with elevated blood pressure were studied: 15 with normal nightly sleep duration (11M/4F; age: 58±2 yr; BP: 136/82±1/2 mmHg; sleep: 7.6±0.2 h/night) and 20 with short nightly sleep duration (14M/6F; 58±1 yr; BP: 138/84±1/1 mmHg; sleep: 6.0±0.1 h/night). Forearm blood flow (FBF) responses to intra-arterial infusion of acetylcholine (ACh), in the absence and presence of the endothelial NO synthase inhibitor N G -monomethyl-L-arginine (L-NMMA) and the antioxidant vitamin C were determined by venous occlusion plethysmography. The FBF response to ACh was significantly lower (~20%) in the short sleep (from 3.8±0.2 to 11.0±0.6 ml/100 ml tissue/min) compared with the normal sleep duration group (from 4.2±0.2 to 13.6±0.6 ml/100 ml tissue/min). L-NMMA significantly reduced (~25%) the FBF response to ACh in the normal sleep but not the short sleep group. Vitamin C markedly increased (~35%; P&lt;0.05) the vasodilator response to ACh in short sleepers only. In summary, habitual short sleep duration worsens NO-mediated endothelium-dependent vasodilation in adults with elevated blood pressure. Furthermore, the sleep-related diminishment in endothelial vasodilator function is due, in part, to increased oxidative stress.

Abstract 28: Regular Aerobic Exercise Counteracts Endothelial Vasomotor Dysfunction Associated With Insufficient Sleep

Insufficient sleep, defined as chronic short sleep duration (&lt;7 h/night), is an independent risk factor for cardiovascular disease (CVD). We have previously demonstrated that insufficient sleep is associated with reduced endothelium-dependent vasodilation and enhanced endothelin (ET)-1-mediated vasoconstrictor tone. Impaired endothelial vasomotor regulation is thought to contribute mechanistically to the increased risk of atherosclerotic vascular disease incurred with chronic insufficient sleep. Regular aerobic exercise is an effective lifestyle strategy for improving endothelial function and, in turn reducing cardiovascular risk. It is currently unknown if regular aerobic exercise can counteract the negative impact of insufficient sleep on endothelial vasomotor regulation. We tested the hypotheses that regular aerobic exercise would: 1) improve endothelial vasodilation; and 2) decrease ET-1-mediated vasoconstrictor tone in middle-aged adults who chronically sleep less than 7 h/night. We studied 36 healthy, middle-aged adults: 16 with normal sleep duration (10M/6F; age: 57±2 yr; sleep duration: 7.4±0.1 h/night) and 20 with short sleep duration (11M/9F; 56±1 yr; sleep duration: 6.2±0.1 h/night). The 20 short sleepers completed a 3-month aerobic exercise training intervention. Forearm blood flow (FBF; plethysmography) was determined in response to intra-arterial doses of acetylcholine (ACh), sodium nitroprusside (SNP), BQ-123 (ET A receptor antagonist) and ACh + BQ-123 in both groups and after the exercise intervention in the short sleepers. As expected, forearm vasodilator responses to ACh were lower (20%; P&lt;0.05) in the short (from 4.2±0.2 to 10.5±0.6 mL/100 mL tissue/min) vs normal (4.2±0.2 to 12.7±0.6 mL/100 mL tissue/min) sleepers. FBF responses to SNP were comparable between the groups. In response to BQ-123, short sleep group had a greater increase in resting FBF than normal sleep group (~25% vs ~8%; P&lt; 0.05). ACh+BQ-123 resulted in an ~25% increase in the ACh-vasodilation in the short sleep group only. After exercise training, although nightly sleep duration was not affected (6.4±0.1 h/night), ACh-mediated vasodilation was ~20% higher (P&lt;0.05), ET-1-mediated vasoconstriction was ~90% lower (P&lt;0.05) and vasodilator response to ACh was not significantly increased with ET A receptor blockade. These results indicate that regular aerobic exercise can reverse the negative influence of insufficient sleep on endothelial vasomotor function, independent of changes in nightly sleep duration.

What is the role of sleep in physician burnout?

The occurrence of physician burnout is widespread among clinicians and academic faculty, who report indicators such as low quality of life and poor work-life balance. Chronic insufficient sleep, whether due to extended work hours, circadian misalignment, or unrecognized sleep disorders, is a critically important risk factor for burnout that is overlooked and under-studied, and interventions to promote healthy sleep may reduce burnout susceptibility among attending physicians. While strategies to reduce burnout among resident and attending physicians have been under-evaluated, evidence suggests a need to address burnout at both individual and organizational levels. Solutions have been offered that are applicable to many stakeholders, including employers; payers; licensing and certification boards; state and federal regulatory agencies; and physicians and researchers. As more studies are undertaken to evaluate how these approaches impact burnout, two questions need to be addressed: (1) What is the role of sleep in the crisis of burnout, specifically among attendings, who are particularly under-studied? (2) Is restoration of healthy sleep the fundamental mechanism by which burnout interventions work? It is essential for key stakeholders to consider the role of sleep, sleepiness, and sleep disorders in order to optimize any efforts to mitigate the present crisis in physician burnout, particularly among attending physicians, an understudied group.

Parent–child relationship quality and sleep among adolescents: modification by race/ethnicity

BackgroundBoth parent–child relationship quality (PCRQ) and sleep are important for health and development, but few studies have examined links between PCRQ and adolescent sleep and potential interactions by race/ethnicity or sex. MethodsWe used cross-sectional data from 6,019 participants (mean = 15.9 years; 50% male; 66% non-Hispanic White, 16% non-Hispanic Black, 5% Hispanic all races) from the National Longitudinal Study of Adolescent to Adult Health, a nationally representative sample of U.S. adolescents. Our exposure was current adolescent-rated PCRQ score. Outcomes were adolescents’ reports of chronic insufficient sleep, sleep duration (mins), and frequency of insomnia symptoms (i.e., trouble falling or staying asleep “almost every day”/“every day” versus “never”/“just a few times”/“about once a week”). ResultsAdjusting for demographic characteristics, each 1-point increase in PCRQ score was associated with lower odds of insomnia symptoms (odds ratio [OR] = 0.92, 95% confidence interval [CI]: 0.90, 0.94), chronic insufficient sleep (OR = 0.93, 95% CI: 0.91, 0.95), and longer sleep duration (B = 2.56, 95% CI: 1.90, 3.22). After adjustment for depressive symptoms, the association with insomnia symptoms was no longer statistically significant. Race/ethnicity moderated the association between PCRQ and chronic insufficient sleep such that the magnitude of the association was greater in Hispanics vs. Whites and Blacks. There were no interactions of PCRQ with sex. ConclusionsAmong adolescents, better PCRQ was associated with better sleep, and this association varied by race/ethnicity for perceived chronic insufficient sleep. Longitudinal studies with objective and subjective sleep measures are needed to further understand these associations.

Erratum to: Identifying and validating blood mRNA biomarkers for acute and chronic insufficient sleep in humans: a machine learning approach.

Acute and chronic insufficient sleep are associated with adverse health outcomes and risk of accidents. There is therefore a need for biomarkers to monitor sleep debt status. None are currently available. We applied Elastic-net and Ridge regression to entire and pre-filtered transcriptome samples collected in healthy young adults during acute total sleep deprivation and following 1 week of either chronic insufficient (< 6 h) or sufficient sleep (~8.6 h) to identify panels of mRNA biomarkers of sleep debt status. The size of identified panels ranged from 9-74 biomarkers. Panel performance, assessed by leave-one-subject-out cross-validation and independent validation, varied between sleep debt conditions. Using between-subject assessments based on one blood sample, the accuracy of classifying ‘Acute sleep loss’ was 92%, but only 57% for classifying ‘Chronic sleep insufficiency’. A reasonable accuracy for classifying ‘chronic sleep insufficiency’ could only be achieved by a within-subject comparison of blood samples. Biomarkers for sleep debt status showed little overlap with previously identified biomarkers for circadian phase. Biomarkers for acute and chronic sleep loss also showed little overlap but were associated with common functions related to the cellular stress response, such as heat shock protein activity, the unfolded protein response, protein ubiquitination and endoplasmic reticulum associated protein degradation, and apoptosis. This characteristic response of whole blood to sleep loss can further aid our understanding of how sleep insufficiencies negatively affect health. Further development of these novel biomarkers for research and clinical practice requires validation in other protocols and age groups.

Genome-wide association analysis of self-reported daytime sleepiness identifies 42 loci that suggest biological subtypes

Excessive daytime sleepiness (EDS) affects 10–20% of the population and is associated with substantial functional deficits. Here, we identify 42 loci for self-reported daytime sleepiness in GWAS of 452,071 individuals from the UK Biobank, with enrichment for genes expressed in brain tissues and in neuronal transmission pathways. We confirm the aggregate effect of a genetic risk score of 42 SNPs on daytime sleepiness in independent Scandinavian cohorts and on other sleep disorders (restless legs syndrome, insomnia) and sleep traits (duration, chronotype, accelerometer-derived sleep efficiency and daytime naps or inactivity). However, individual daytime sleepiness signals vary in their associations with objective short vs long sleep, and with markers of sleep continuity. The 42 sleepiness variants primarily cluster into two predominant composite biological subtypes - sleep propensity and sleep fragmentation. Shared genetic links are also seen with obesity, coronary heart disease, psychiatric diseases, cognitive traits and reproductive ageing. A main symptom of chronic insufficient sleep is excessive daytime sleepiness. Here, Wang et al. report 42 genome-wide significant loci for self-reported daytime sleepiness in 452,071 individuals from the UK Biobank that cluster into two biological subtypes of either sleep propensity or sleep fragmentation.

Associations of longitudinal sleep trajectories with risky sexual behavior during late adolescence.

The current study examines longitudinal sleep patterns in relation to risky sexual behaviors in a racially/ethnically diverse sample of adolescents. The sample comprises 1,850 youth (mean age at first wave = 16.21; 57% female). Sleep duration, sleep variability (difference between weekend and weekday sleep duration), and sleep quality were collected over four annual assessments from 2013 to 2017. Risky sexual behaviors (i.e., sex without condom use or sex after using drugs or alcohol) were examined at the fourth follow-up assessment when youth were 19 years old. Longitudinal latent class analysis characterized patterns of individual sleep dimensions over time, as well as the combination of sleep dimensions, and examined how emergent sleep classes associated with subsequent risky sexual behavior, after adjustment for sociodemographics and mental health. After covariate adjustment, persistent "short" weekend sleepers were 2.2 times more likely to engage in risky sexual behaviors, compared to youth with sufficient weekend sleep duration. Contrary to expectations, adolescents with more consistent weekend/weekday sleep were 1.6-2 times more likely to engage in risky sexual behaviors, compared to those with greater variability; however, lack of variability may be an indicator of chronic insufficient sleep, both weekdays and weekends. There were no significant differences in risky sexual behavior according to classes of weekday sleep duration or quality. In the combined class model, those with persistently short and poor-quality sleep were at marginally greater risk for engaging in risky sexual behaviors. Insufficient sleep in adolescents may increase risk for sexual risk-taking and may set the stage for accelerated health risk trajectories into adulthood. (PsycINFO Database Record (c) 2019 APA, all rights reserved).

Identifying and validating blood mRNA biomarkers for acute and chronic insufficient sleep in humans: a machine learning approach.

Acute and chronic insufficient sleep are associated with adverse health outcomes and risk of accidents. There is therefore a need for biomarkers to monitor sleep debt status. None are currently available. We applied elastic net and ridge regression to transcriptome samples collected in 36 healthy young adults during acute total sleep deprivation and following 1 week of either chronic insufficient (<6 hr) or sufficient sleep (~8.6 hr) to identify panels of mRNA biomarkers of sleep debt status. The size of identified panels ranged from 9 to 74 biomarkers. Panel performance, assessed by leave-one-subject-out cross-validation and independent validation, varied between sleep debt conditions. Using between-subject assessments based on one blood sample, the accuracy of classifying “acute sleep loss” was 92%, but only 57% for classifying “chronic sleep insufficiency.” A reasonable accuracy for classifying “chronic sleep insufficiency” could only be achieved by a within-subject comparison of blood samples. Biomarkers for sleep debt status showed little overlap with previously identified biomarkers for circadian phase. Biomarkers for acute and chronic sleep loss also showed little overlap but were associated with common functions related to the cellular stress response, such as heat shock protein activity, the unfolded protein response, protein ubiquitination and endoplasmic reticulum-associated protein degradation, and apoptosis. This characteristic response of whole blood to sleep loss can further aid our understanding of how sleep insufficiencies negatively affect health. Further development of these novel biomarkers for research and clinical practice requires validation in other protocols and age groups.

Incorporating sleep medicine content into medical school through neuroscience core curricula.

To present (1) justification for earmarking sleep medicine education as an essential component of all medical school curricula and (2) various avenues to incorporate sleep medicine exposure into medical school curricula through (primarily) neuroscience and neurology courses. Per consensus of a team of leading neurology and sleep medicine educators, an evidence-based rationale for including sleep medicine across a 4-year medical school curriculum is presented along with suggested content, available/vetted resources, and formats for delivering sleep medicine education at various points and through various formats. Growing evidence has linked sleep disorders (e.g., sleep-disordered breathing, chronic insufficient sleep) as risk factors for several neurologic disorders. Medical educators in neurology/neuroscience are now strongly advocating for sleep medicine education in the context of neurology/neuroscience pre and post graduate medical education. Sleep medicine education is also a critical component of a proactive strategy to address physician wellness and burnout. The suggested curriculum proposes a sleep educational exposure time of 2-4 hours per year in the form of lectures, flipped-classroom sessions, clinical opportunities, and online educational tools that would result in a 200%-400% increase in the amount of sleep medicine exposure that US medical schools currently provide. The guidelines are accompanied by the recommendation for use of technological education, to facilitate more seamless curricular incorporation. Even in this era with limited flexibility to add content to an already packed medical school curriculum, incorporating sleep medicine exposure into the current medical school curriculum is both justified and feasible.

Chronic Insufficient Sleep Has a Limited Impact on Circadian Rhythmicity of Subjective Hunger and Awakening Fasted Metabolic Hormones.

The study was registered as clinical trial #NCT01581125.