Actigraphy measures show sleep improvement after parathyroidectomy for primary hyperparathyroidism.

IMPORTANCE: The symptoms of primary hyperparathyroidism are often subtle, such as fatigue, mood changes, and sleep disturbances. After parathyroidectomy, patients often report improvement in sleep and mood; however, objective data supporting these improvements is lacking. OBJECTIVE: This prospective study uses standard measures to objectively and subjectively assess sleep in patients with primary hyperparathyroidism before and after parathyroidectomy. DESIGN: A longitudinal prospective study was conducted over three one-week-long periods: pre-parathyroidectomy, 1-week post-parathyroidectomy, and three months post-parathyroidectomy. During each time point, patients wore an actigraphy device, recorded a sleep diary, and completed the Pittsburgh Sleep Quality Index (PSQI), Insomnia Severity Index (ISI), and Depression Anxiety Stress Scale (DASS). Statistical analysis was performed using repeated measures models to compare the average measures among the three time points and test for trends over time. SETTING: Single institution, tertiary care center. PARTICIPANTS: Patients with primary hyperparathyroidism from ages 18 to 89 years old. EXPOSURE: Parathyroidectomy between September 2020 and January 2024. MAIN OUTCOMES AND MEASURES: Actigraphy data, consensus sleep diary, Pittsburgh Sleep Quality Index (PSQI), Insomnia Severity Index (ISI), Depression Anxiety Stress Scales - 21 Items (DASS). RESULTS: Thirty-six patients were enrolled, and 34 patients completed the study. Actigraphy data showed a significant negative trend in average sleep latency (p = 0.045) and average time in bed (p = 0.046). Sleep diary data showed additional differences in the number of awakenings (p = 0.002), wake after sleep onset (p < 0.001), sleep quality (p < 0.001), and sleep efficiency (p = 0.02) among the three time points and/or as a significant negative trend. PSQI and ISI scores were significantly different among the three time points (p = 0.002 and p < 0.001, respectively) and also declined significantly over time (p = 0.008 and p = 0.007, respectively). DASS depression, anxiety, and stress scores were significantly different among the three time points (p < 0.001, p = 0.01, and p < 0.001, respectively), and stress also declined significantly over time (p = 0.005). CONCLUSION AND RELEVANCE: This study represents the most extensive prospective study demonstrating objective and subjective sleep and mood improvement in patients with primary hyperparathyroidism after parathyroidectomy.

Edward O. Bixler, PhD: from the Apollo project and chimpanzees to sleep epidemiology.

What an honor to write about Dr. Edward O. Bixler's contributions to the sleep field. In 1967, Dr. Bixler published a case report on a chimpanzee with implanted brain electrodes while working at an Air Force base in New Mexico. A few years later, in 1971, he published on the sleep effects of flurazepam in individuals with insomnia together with Dr. Anthony Kales, data that he had collected when the Sleep Research & Treatment Center (SRTC) was housed at the University of California Los Angeles. Dr. Bixler, a meticulous scientist, learned from Dr. Kales, a devoted clinician, to study "the whole patient, and all aspects of sleep," a legacy that continued when the SRTC moved to Penn State in Hershey. Indeed, Dr. Bixler's tenure at Penn State from 1971 until 2019 kept the science of the SRTC focused on that premise and helped translate scientific evidence into clinical care. He not only contributed early to the pharmacology of sleep and the effects of hypnotics, but he was also a pioneer in "sleep epidemiology." His "Prevalence of sleep disorders in the Los Angeles metropolitan area" study of 1979 was the first rigorous epidemiological study on sleep disturbances. Starting in 1990, he established the Penn State Adult Cohort to estimate the prevalence and natural history of sleep-disordered breathing and other sleep disorders in adults. Inspired by life-course epidemiology, he established in 2001 the Penn State Child Cohort to estimate the same phenomena in children. This Living Legend paper captures and highlights Dr. Bixler's enduring legacy to sleep science.

A meta-analysis of the association between insomnia with objective short sleep duration and risk of hypertension.

The aim of this meta-analysis was to examine the association between insomnia with objective short sleep duration (ISSD) with prevalent and incident hypertension in cross-sectional and longitudinal studies, respectively. Data were collected from 6 cross-sectional studies with 5914 participants and 2 longitudinal studies with 1963 participants. Odds ratios (ORs) for prevalent and risk ratios (RRs) for incident hypertension were calculated through meta-analyses of adjusted data from individual studies. Compared to normal sleepers with objective normal sleep duration (NNSD), ISSD was significantly associated with higher pooled OR for prevalent hypertension (pooled OR = 2.67, 95%CI = 1.45-4.90) and pooled RR for incident hypertension (pooled RR = 1.95, 95%CI = 1.19-3.20), respectively. Compared to insomnia with objective normal sleep duration, ISSD was associated with significantly higher pooled OR of prevalent hypertension (pooled OR = 1.94, 95%CI = 1.29-2.92) and pooled RR for incident hypertension (pooled RR = 2.07, 95%CI = 1.47-2.90), respectively. Furthermore, normal sleepers with objective short sleep duration were not associated with either prevalent (pooled OR = 1.21, 95%CI = 0.84-1.75) or incident (pooled RR = 0.97, 95%CI = 0.81-1.17) hypertension compared to NNSD. Our findings suggest that ISSD is a more severe phenotype of the disorder associated with a higher risk of hypertension. Objective short sleep duration might be a valid and clinically useful index of insomnia's impact on cardiovascular health.

Short-term stability and night-to-night variability of sleep parameters in nightmares comorbid with chronic insomnia Disorder across multiple nights of polysomnography.

STUDY OBJECTIVES: The purpose of this study was to examine the degree of short-term stability of polysomnographic (PSG) measured sleep parameters and the overall differences between individuals with comorbid nightmares and insomnia compared to those with chronic insomnia disorder alone or good sleeping controls across four nights in the sleep lab. METHODS: A total of 142 good sleeping controls, 126 chronic insomnia alone, and 24 comorbid insomnia/nightmare participants underwent four consecutive nights of 8-hour PSG recordings. Outcomes included sleep continuity, architecture, and REM-related parameters across nights one through four. Intraclass correlation coefficients with mixed-effect variances and repeated-measure analysis of covariance were used, respectively, to determine short-term stability as well as between-participants and time-by-group interaction effects. RESULTS: Wake after sleep onset and stage 1 showed "poor stability" in the comorbid insomnia/nightmare group compared to "moderate stability" in the good sleeping controls and chronic insomnia alone group. Significant between-group effects (all ps < .05) showed that the comorbid insomnia/nightmare group took longer to fall asleep and had a greater first-night-effect in stage 1 compared to good sleeping controls and chronic insomnia alone group; in addition, the comorbid insomnia/nightmare and insomnia alone groups slept shorter, with fewer awakenings and REM periods, compared to the good sleeping controls. CONCLUSIONS: Nightmares are associated with abnormal sleep above and beyond REM disruption, as sleep continuity was the primary aspect in which poor stability and group differences emerged. The greater inability to fall asleep and instability of sleep fragmentation in those with comorbid insomnia/nightmares compared to chronic insomnia alone may be attributed to the impact of presleep anticipatory anxiety and nightmare-related distress itself. CLINICAL TRIAL INFORMATION: The data analyzed in this study does not come from any current or previous clinical trials. Therefore, there is no clinical trial information to report.

Insomnia with objective but not subjective short sleep duration is associated with incident cardiovascular and/or cerebrovascular disease.

STUDY OBJECTIVES: Insomnia with objective short sleep duration (ISSD) has been associated with cardiometabolic outcomes i.e., hypertension or diabetes. We examined whether ISSD, based on objective or subjective sleep measures are associated with more serious health problems such as incident cardiovascular and/or cerebrovascular disease (CBVD). METHODS: 1,258 men and women from the Penn State Adult Cohort (56.9% women, 48.3±12.95 years) without CBVD at baseline were followed up for 9.21±4.08 years. The presence of CBVD was defined as a history of diagnosis or treatment of heart disease and/or stroke. Insomnia was defined as a complaint of insomnia with a duration ≥ 1 year. Poor sleep was defined as a complaint of difficulty falling asleep, staying asleep, nonrestorative sleep or early morning awakening. Objective short sleep duration was defined as <6-hours sleep based on polysomnography. Subjective short sleep duration was based on the median self-reported percentage of sleep time (i.e., <7 hours). RESULTS: Compared to normal sleepers with normal sleep duration, the highest risk of incident CBVD was in the ISSD group (OR=2.46, 95%CI=1.04-5.79), and the second highest in normal sleepers with short sleep duration (OR=1.68, 95%CI=1.11-2.54). The risk for incident CBVD was not significantly increased in poor sleepers or those with insomnia with normal sleep duration (INSD). Finally, insomnia with subjective short sleep duration, was not associated with increased incident CBVD. CONCLUSIONS: These data add to the cumulative evidence that ISSD, based on objective but not subjective measures, is the more severe biological phenotype of the disorder associated with incident CBVD.

Racial/ethnic disparities in the trajectories of insomnia symptoms from childhood to young adulthood.

STUDY OBJECTIVES: To examine differences in the longitudinal prevalence of childhood insomnia symptoms across black/African American, Hispanic/Latinx, and non-Hispanic white groups. METHODS: Participants were 519 children from the Penn State Child Cohort (baseline [V1] from 2000-2005) who were followed up 8 years later as adolescents (V2) and 15 years later as young adults (S3). Mean age at S3 was 24.1 ±â€…2.7 years. Approximately, 76.5% identified as non-Hispanic white, 12.9% as black/African American, 7.1% as Hispanic/Latinx, and 3.5% as "other" race/ethnicity. Insomnia symptoms were defined as parent-reported (childhood) or self-reported (adolescence and young adulthood) moderate-to-severe difficulties initiating/maintaining sleep. Longitudinal trajectories of insomnia symptoms were identified across three-time points and the odds of each trajectory were compared between racial/ethnic groups, adjusting for sex, age, overweight, sleep apnea, periodic limb movements, psychiatric/behavioral disorders, and psychotropic medication use. RESULTS: Black/African Americans compared to non-Hispanic whites were at significantly higher odds of having a childhood-onset persistent trajectory through young adulthood (OR = 2.58, 95% CI [1.29, 5.14]), while Hispanics/Latinx were at nonsignificantly higher odds to have the same trajectory (OR = 1.81, 95% CI [0.77, 4.25]). No significant racial/ethnic differences were observed for remitted and waxing-and-waning trajectories since childhood or incident/new-onset trajectories in young adulthood. CONCLUSIONS: The results indicate that disparities in insomnia symptoms among black/African American and, to a lesser extent, Hispanic/Latinx groups start early in childhood and persist into young adulthood. Identifying and intervening upon upstream determinants of racial/ethnic insomnia disparities are warranted to directly address these disparities and to prevent their adverse health sequelae. CLINICAL TRIAL INFORMATION: N/A; Not a clinical trial.

Circadian misalignment impacts the association of visceral adiposity with metabolic syndrome in adolescents.

STUDY OBJECTIVES: Although insufficient sleep is a risk factor for metabolic syndrome (MetS), the circadian timing of sleep (CTS) is also involved in cardiac and metabolic regulation. We examined whether delays and deviations in the sleep midpoint (SM), a measure of CTS, modify the association between visceral adipose tissue (VAT) and MetS in adolescents. METHODS: We evaluated 277 adolescents (median 16 years) who had at least 5 nights of at-home actigraphy (ACT), in-lab polysomnography (PSG), dual-energy X-ray absorptiometry (DXA) scan, and MetS score data. Sleep midpoint (SM), sleep irregularity (SI), and social jetlag (SJL) were examined as effect modifiers of the association between VAT and MetS, including waist circumference, blood pressure, insulin resistance, triglycerides, and cholesterol. Linear regression models adjusted for demographics, ACT-sleep duration, ACT-sleep variability, and PSG-apnea-hypopnea index. RESULTS: The association between VAT and MetS was significantly stronger (p-values for interactions < 0.001) among adolescents with a schooldays SM later than 4:00 (2.66 [0.30] points increase in MetS score), a SI higher than 1 hour (2.49 [0.30]) or a SJL greater than 1.5 hours (2.15 [0.36]), than in those with an earlier SM (<3:00; 1.76 [0.28]), lower SI (<30 minutes; 0.98 [0.70]), or optimal SJL (<30 minutes; 1.08 [0.45]). CONCLUSIONS: A delayed sleep phase, an irregular sleep-wake cycle, and greater social jetlag on schooldays identified adolescents in whom VAT had a stronger association with MetS. Circadian misalignment is a risk factor that enhances the impact of visceral obesity on cardiometabolic morbidity and should be a target of preventative strategies in adolescents.

Age-related differences in the association of mild-to-moderate sleep apnea with incident cardiovascular and cerebrovascular diseases.

BACKGROUND: Mild-to-moderate obstructive sleep apnea (mmOSA) is highly prevalent in the general population. However, studies on its association with incident cardiovascular and/or cerebrovascular disease (CBVD) are limited. We examined the association between mild-to-moderate OSA and incident cardiovascular and/or cerebrovascular (CBVD) in a general population sample, and whether age modifies this association. METHODS: A total of 1173 adults from the Penn State Adult Cohort (20-88 years) without CBVD or severe OSA at baseline were followed-up after 9.2 (±4.1) years. Incident CBVD was defined based on a self-report of a physician diagnosis or treatment for heart disease and/or stroke. Logistic regression examined the association of mild-to-moderate OSA (AHI 5-29.9) with incident CBVD and the combined effect of mmOSA and MetS on incident CBVD after adjusting for multiple confounders. RESULTS: Age significantly modified the association between mmOSA with incident CBVD (p-interaction = 0.04). Mild-to-moderate OSA was significantly associated with incident CBVD in adults aged <60 years (OR = 1.74, 95%CI = 1.06-2.88, p = 0.029), but not in adults aged ≥60 years (OR = 0.71, 95%CI = 0.39-1.27, p = 0.247). Even mild OSA (AHI 5-14.9) carried a significant risk for incident CBDV in adults aged <60 years (OR = 1.86, 95%CI = 1.05-3.28, p = 0.032). An additive effect was found between mmOSA and MetS with incident CBVD in those aged <65 years (OR = 3.84, 95%CI = 1.95-7.56, p<0.001). CONCLUSIONS: The risk of incident CBVD is increased in young and middle-aged but not older adults with mmOSA, which may affect the way we currently diagnose and treat this highly prevalent sleep-related breathing disorder.

Berry Consumption and Sleep in the Adult US General Population: Results from the National Health and Nutrition Examination Survey 2005-2018.

INTRODUCTION: Poor sleep is associated with numerous adverse health outcomes. Berries are rich in micronutrients and antioxidants that may improve sleep quality and duration. We determined the association of berry consumption and sleep duration and sleep difficulty among adult participants in NHANES. METHODS: We analyzed the diet of US adults aged ≥ 20 y using two non-consecutive 24 h recalls from the National Health and Nutrition Examination Survey 2005 to 2018 (N = 29,217). Poor sleep quality was measured by sleep duration (short sleep duration: <7 h), long sleep (≥9 h), and reported sleep difficulty. The relative risk of poor sleep outcomes for berry consumers vs. nonconsumers was modelled using population weight-adjusted multivariable general logistic regression. RESULTS: About 46% of participants reported inadequate sleep duration, and 27% reported sleep difficulties. Twenty-two percent reported consuming berries. Berry consumers had a 10-17% decreased risk of short sleep. The findings were consistent for specific berry types including strawberries and blueberries (p < 0.05). No significant associations with long sleep were found for total berries and any berry types. A decreased risk of sleep difficulties was found to be linked to blackberry consumption (adjusted OR = 0.63, 95% CI: 0.40-0.97; p = 0.036) but not for other berries. CONCLUSIONS: US adult berry consumers had a decreased risk of reporting short sleep compared to nonconsumers. Berries are underconsumed foods in the US adult population, and increased berry consumption may improve sleep quality.

Objective and subjective measures of sleep initiation are differentially associated with DNA methylation in adolescents.

INTRODUCTION: The onset of puberty is associated with a shift in the circadian timing of sleep, leading to delayed sleep initiation [i.e., later sleep onset time (SOT)] due to later bedtimes and/or longer sleep onset latency (SOL). Several genome-wide association studies (GWAS) have identified genes that may be involved in the etiology of sleep phenotypes. However, circadian rhythms are also epigenetically regulated; therefore, epigenetic biomarkers may provide insight into the physiology of the pubertal sleep onset shift and the pathophysiology of prolonged or delayed sleep initiation. RESULTS: The gene-wide analysis indicated differential methylation within or around 1818 unique genes across the sleep initiation measurements using self-report, actigraphy (ACT), and polysomnography (PSG), while GWAS-informed analysis yielded 67 genes. Gene hits were identified for bedtime (PSG), SOL (subjective, ACT and PSG) and SOT (subjective and PSG). DNA methylation within 12 genes was associated with both subjective and PSG-measured SOL, 31 with both ACT- and PSG-measured SOL, 19 with both subjective and ACT-measured SOL, and one gene (SMG1P2) had methylation sites associated with subjective, ACT- and PSG-measured SOL. CONCLUSIONS: Objective and subjective sleep initiation in adolescents is associated with altered DNA methylation in genes previously identified in adult GWAS of sleep and circadian phenotypes. Additionally, our data provide evidence for a potential epigenetic link between habitual (subjective and ACT) SOL and in-lab SOT and DNA methylation in and around genes involved in circadian regulation (i.e., RASD1, RAI1), cardiometabolic disorders (i.e., FADS1, WNK1, SLC5A6), and neuropsychiatric disorders (i.e., PRR7, SDK1, FAM172A). If validated, these sites may provide valuable targets for early detection and prevention of disorders involving prolonged or delayed SOT, such as insomnia, delayed sleep phase, and their comorbidity.

Cognitive Disengagement Syndrome (CDS) (Formerly Sluggish Cognitive Tempo), Autism, and Insomnia Symptoms in Childhood Predict CDS in Adolescence: A Longitudinal Population-Based Study.

Our study is the first using multiple variables to compare concurrent with longitudinal predictors of cognitive disengagement syndrome (CDS). The population-based sample comprised 376 youth (mean baseline age 8.7 and follow-up 16.4 years) rated by parents on the Pediatric Behavior Scale. The baseline CDS score was the strongest predictor of follow-up CDS. Baseline autism and insomnia symptoms also predicted follow-up CDS above and beyond baseline CDS. Autism, insomnia, inattention, somatic complaints, and excessive sleep were concurrently related to CDS at baseline and follow-up. Additionally, follow-up depression was associated with follow-up CDS, and baseline hyperactivity/impulsivity was negatively associated with baseline CDS. Oppositional defiant/conduct problems and anxiety were nonsignificant. Age, sex, race, and parent occupation were unrelated to CDS, and correlations between baseline CDS and 15 IQ, achievement, and neuropsychological test scores were nonsignificant. Results indicate childhood CDS is the strongest risk factor for adolescent CDS, followed by autism and insomnia symptoms.

Mild-to-moderate obstructive sleep apnea and mortality risk in a general population sample: The modifying effect of age and cardiovascular/cerebrovascular comorbidity.

About 5.4%-45.7% of the general population has mild-to-moderate obstructive sleep apnea (mmOSA), which is highly comorbid with cardiovascular and/or cerebrovascular diseases (CBVD). We examined the association between mmOSA and all-cause mortality and the modifying effect of age and CBVD. A total of 1681 adults 20-88 years old from the Penn State Adult Cohort (PSAC) (41.9% male) were followed up for 20.1 ± 6.2 years for all-cause mortality. Mild and moderate OSA were defined as an apnea/hypopnea index (AHI) 5-14.9 and 15-29.9 events/hour, respectively. CBVD was defined as a report of a physician diagnosis or treatment for heart disease and/or stroke. Cox proportional hazards regression models were used to estimate all-cause mortality adjusted for confounders. All-cause mortality risk was significantly increased in the mmOSA group in young and middle-aged adults (<60 years) (HR = 1.59, 95%CI 1.08-2.04) but not in older adults (≥60 years) (HR = 1.05, 95%CI 0.80-1.39). A synergistic effect between mmOSA and CBVD was stronger in those <60 years (HR = 3.82, 95%CI 2.25-6.48 in <60 years vs 1.86 95%CI 1.14-3.04 in ≥60 years). There was an additive effect between moderate OSA and hypertension in <60 but not in those ≥60 years. Mild OSA was associated with all-cause mortality only in the presence of CBVD. Mortality risk is increased in young and middle-aged adults with moderate OSA, whereas the mortality risk associated with mild OSA is elevated only, regardless of age, in the presence of comorbid CBVD. AHI cut-offs warranting treatment of mmOSA may need to be adjusted based on age and comorbidities.

Insomnia nosology: a systematic review and critical appraisal of historical diagnostic categories and current phenotypes.

Insomnia nosology has significantly evolved since the Diagnostic and Statistical Manual (DSM)-III-R first distinguished between 'primary' and 'secondary' insomnia. Prior International Classification of Sleep Disorders (ICSD) nosology 'split' diagnostic phenotypes to address insomnia's heterogeneity and the DSM nosology 'lumped' them into primary insomnia, while both systems assumed causality for insomnia secondary to health conditions. In this systematic review, we discuss the historical phenotypes in prior insomnia nosology, present findings for currently proposed insomnia phenotypes based on more robust approaches, and critically appraise the most relevant ones. Electronic databases PsychINFO, PubMED, Web of Science, and references of eligible articles, were accessed to find diagnostic manuals, literature on insomnia phenotypes, including systematic reviews or meta-analysis, and assessments of the reliability or validity of insomnia diagnoses, identifying 184 articles. The data show that previous insomnia diagnoses lacked reliability and validity, leading current DSM-5-TR and ICSD-3 nosology to 'lump' phenotypes into a single diagnosis comorbid with health conditions. However, at least two new, robust insomnia phenotyping approaches were identified. One approach is multidimensional-multimethod and provides evidence for self-reported insomnia with objective short versus normal sleep duration linked to clinically relevant outcomes, while the other is multidimensional and provides evidence for two to five clusters (phenotypes) based on self-reported trait, state, and/or life-history data. Some approaches still need replication to better support whether their findings identify true phenotypes or simply different patterns of symptomatology. Regardless, these phenotyping efforts aim at improving insomnia nosology both as a classification system and as a mechanism to guide treatment.

Dopamine D1 Agonists: First Potential Treatment for Late-Stage Parkinson's Disease.

Current pharmacotherapy has limited efficacy and/or intolerable side effects in late-stage Parkinson's disease (LsPD) patients whose daily life depends primarily on caregivers and palliative care. Clinical metrics inadequately gauge efficacy in LsPD patients. We explored if a D1/5 dopamine agonist would have efficacy in LsPD using a double-blind placebo-controlled crossover phase Ia/b study comparing the D1/5 agonist PF-06412562 to levodopa/carbidopa in six LsPD patients. Caregiver assessment was the primary efficacy measure because caregivers were with patients throughout the study, and standard clinical metrics inadequately gauge efficacy in LsPD. Assessments included standard quantitative scales of motor function (MDS-UPDRS-III), alertness (Glasgow Coma and Stanford Sleepiness Scales), and cognition (Severe Impairment and Frontal Assessment Batteries) at baseline (Day 1) and thrice daily during drug testing (Days 2-3). Clinicians and caregivers completed the clinical impression of change questionnaires, and caregivers participated in a qualitative exit interview. Blinded triangulation of quantitative and qualitative data was used to integrate findings. Neither traditional scales nor clinician impression of change detected consistent differences between treatments in the five participants who completed the study. Conversely, the overall caregiver data strongly favored PF-06412562 over levodopa in four of five patients. The most meaningful improvements converged on motor, alertness, and functional engagement. These data suggest for the first time that there can be useful pharmacological intervention in LsPD patients using D1/5 agonists and also that caregiver perspectives with mixed method analyses may overcome limitations using methods common in early-stage patients. The results encourage future clinical studies and understanding of the most efficacious signaling properties of a D1 agonist for this population.

Sleep health dimensions and shift work as longitudinal predictors of cognitive performance in the UK Biobank cohort.

STUDY OBJECTIVES: The long-term effects of sleep health and shift work on cognitive performance are unclear. In addition, research has been limited by small sample sizes and short follow-up periods. We conducted one of the largest examinations of the longitudinal influence of sleep health dimensions and shift work on cognitive performance in people of middle and old age using data from the UK Biobank. The hypothesis was that poor sleep health and shift work would predict lower cognitive performance. METHODS: Self-reported sleep duration, daytime sleepiness, insomnia symptoms, chronotype, and shift work status were assessed as predictors at baseline. Cognitive performance was operationalized by a touchscreen test battery at follow-up between 7.4 ±â€…2.2 and 9.0 ±â€…0.9 years after baseline assessment, depending on the specific task. Models were performed for each cognitive domain including relevant confounders (e.g. depression). The alpha level was set at p < 0.01 for all analyzes. RESULTS: The study sample comprised 9394 participants for the reasoning task, 30 072 for the reaction time task, 30 236 for the visual memory task, 2019 for the numeric memory task, and 9476 for the prospective memory task. Shift work without night shifts (ß = -2.0 × 10-1 ± 6.5 × 10-2, p = 0.002) and with night shifts (ß = -1.9 × 10-1 ± 7.2 × 10-2, p = 0.010) predicted a significantly reduced performance in the reasoning task. Short sleep duration (ß = -2.4 × 10-1 ± 7.9 × 10-2, p = 0.003) and shift work without night shifts (ß = -3.9 × 10-1 ± 1.2 × 10-1, p = 0.002) predicted a significantly lower performance in the task probing prospective memory. CONCLUSIONS: Our results suggest that, after controlling for confounding variables, shift work, and short sleep duration are important predictors for cognitive performance in people of middle and old age. Further work is required to examine causal mechanisms of the observed associations.

Insomnia with objective, but not subjective, short sleep duration is associated with increased risk of incident hypertension: the Sleep Heart Health Study.

STUDY OBJECTIVES: Insomnia with objective short sleep duration has been associated with higher risk of cardiometabolic morbidity. In this study, we examined the association between insomnia with objective short sleep duration, also based on subjective sleep duration, with incident hypertension in the Sleep Heart Health Study. METHODS: We analyzed data from 1,413 participants free of hypertension or sleep apnea at baseline from the Sleep Heart Health Study, with a median follow-up duration of 5.1 years. Insomnia symptoms were defined based on difficulty falling asleep, difficulty returning to sleep, early morning awakening, or sleeping pill use more than half the days in a month. Objective short sleep duration was defined as polysomnography-measured total sleep time < 6 hours. Incident hypertension was defined based on blood pressure measures and/or use of antihypertensive medications at follow-up. RESULTS: Individuals with insomnia who slept objectively < 6 hours had significantly higher odds of incident hypertension compared to normal sleepers who slept ≥ 6 hours (odds ratio = 2.00, 95% confidence interval = 1.09-3.65) or < 6 hours (odds ratio = 2.00, 95% confidence interval = 1.06-3.79) or individuals with insomnia who slept ≥ 6 hours (odds ratio = 2.79, 95% confidence interval = 1.24-6.30). Individuals with insomnia who slept ≥ 6 hours or normal sleepers who slept < 6 hours were not associated with increased risk of incident hypertension compared to normal sleepers who slept ≥ 6 hours. Finally, individuals with insomnia who self-reported sleeping < 6 hours were not associated with significantly increased odds of incident hypertension. CONCLUSIONS: These data further support that the insomnia with objective short sleep duration phenotype based on objective, but not subjective measures, is associated with increased risk of developing hypertension in adults. CITATION: Dai Y, Chen B, Chen L, et al. Insomnia with objective, but not subjective, short sleep duration is associated with increased risk of incident hypertension: the Sleep Heart Health Study. J Clin Sleep Med. 2023;19(8):1421-1428.

Circadian Misalignment Impacts the Association of Visceral Adiposity With Elevated Blood Pressure in Adolescents.

BACKGROUND: Although insufficient sleep has been shown to contribute to obesity-related elevated blood pressure, the circadian timing of sleep has emerged as a novel risk factor. We hypothesized that deviations in sleep midpoint, a measure of circadian timing of sleep, modify the association between visceral adiposity and elevated blood pressure in adolescents. METHODS: We studied 303 subjects from the Penn State Child Cohort (16.2±2.2 years; 47.5% female; 21.5% racial/ethnic minority). Actigraphy-measured sleep duration, midpoint, variability, and regularity were calculated across a 7-night period. Visceral adipose tissue (VAT) was measured with dual-energy X-ray absorptiometry. Systolic blood pressure (SBP) and diastolic blood pressure levels were measured in the seated position. Multivariable linear regression models tested sleep midpoint and its regularity as effect modifiers of VAT on SBP/diastolic blood pressure levels, while adjusting for demographic and sleep covariables. These associations were also examined as a function of being in-school or on-break. RESULTS: Significant interactions were found between VAT and sleep irregularity, but not sleep midpoint, on SBP (P interaction=0.007) and diastolic blood pressure (P interaction=0.022). Additionally, significant interactions were found between VAT and schooldays sleep midpoint on SBP (P interaction=0.026) and diastolic blood pressure (P interaction=0.043), whereas significant interactions were found between VAT and on-break weekdays sleep irregularity on SBP (P interaction=0.034). CONCLUSIONS: A delayed and an irregular sleep midpoint during school and during free-days, respectively, increase the impact of VAT on elevated blood pressure in adolescents. These data suggest that deviations in the circadian timing of sleep contribute to the increased cardiovascular sequelae associated with obesity and that its distinct metrics require measurement under different entrainment conditions in adolescents.

Short-term and intermediate-term fine particulate air pollution are synergistically associated with habitual sleep variability in adolescents - A cross-sectional study.

BACKGROUND: Both air pollution and poor sleep have been associated with increased risk of cardiovascular diseases. However, the association between air pollution and sleep health, especially among adolescents, is rarely investigated. METHODS: To investigate the association between fine particulate (PM2.5) air pollution and habitual sleep patterns, we analyzed data obtained from 246 adolescents who participated in the Penn State Child Cohort follow-up examination. We collected their individual-level 24-h (short-term) PM2.5 concentration by using a portable monitor. We estimated their residential-level PM2.5 concentration during the 60-day period prior to the examination (intermediate-term) using a kriging approach. Actigraphy was used to measure participants' sleep durations for seven consecutive nights. Habitual sleep duration (HSD) and sleep variability (HSV) were calculated as the mean and SD of the seven-night sleep duration. Multivariable-adjusted linear regression models were used to assess the association between PM2.5 exposures and HSD/HSV. An interaction between short-term and intermediate-term PM2.5 was created to explore their synergistic associations with HSD/HSV. RESULTS: Elevated short-term and intermediate-term PM2.5 exposure were significantly (p < 0.05) associated with higher HSV, but not HSD. Specifically, the mean (95% CI) increase in HSV associated with 1 SD higher 24-h (26.3 µg/m3) and 60-day average (2.2 µg/m3) PM2.5 were 14.6 (9.4, 14.8) and 4.9 (0.5, 9.2) minutes, respectively. In addition, there was a synergistic interaction (p = 0.08) between short-term and intermediate-term PM2.5 exposure on HSV, indicative that the association between intermediate-term PM2.5 and HSV became stronger as short-term PM2.5 increases, and vice versa. CONCLUSION: Short-term individual-level and intermediate-term residential-level PM2.5 exposures are adversely and synergistically associated with increased sleep variability, an indicator of instability of sleep quantity, in adolescents. Through such an association with sleep pattern, PM2.5 air pollution may increase long-term cardiometabolic risks.

Sleep variability and regularity as contributors to obesity and cardiometabolic health in adolescence.

OBJECTIVE: Adolescence is a developmental stage of critical changes in sleep and its circadian timing when the contribution of abnormal sleep variability (amount) and sleep regularity (timing) to obesity and its associated adverse cardiometabolic health outcomes appears to increase. The aim of this study was to summarize findings from studies conducted in adolescents examining both sleep variability and regularity in relation to obesity and cardiometabolic health. Gaps in research and potential causal pathways that future studies should examine are highlighted. RESULTS: Nightly deviations in sleep duration and sleep midpoint appear to contribute to the development of obesity and associated adverse cardiometabolic outcomes in youth. Studies show that increased sleep variability and irregularity are associated with obesity, decreased physical activity, dysregulated eating and inadequate diet, metabolic dysfunction, impaired cardiac autonomic balance, and elevated blood pressure in adolescents. CONCLUSIONS: A stable circadian timing of sleep is essential to the overall physical well-being of youth. Emerging evidence supports that sleep variability and circadian misalignment, including sleep irregularity, contribute to adverse obesity-related health outcomes early on in adolescence. Future studies should focus on the underlying behavioral and biological mechanisms in the causal pathway between day-to-day deviations in the amount and timing of sleep and obesity.