Emerging adulthood (ages 18–25) is the developmental peak for delayed sleep and circadian timing and a period of risk for psychopathology. The current study compared two chronotherapeutic interventions targeting delayed sleep timing in emerging adults with no-to-moderate depression. Study 1 (N = 21, ages 18–22, 43 = 15, ages 18–25, 86
Previous studies have reported associations between restless legs syndrome (RLS) and perinatal depressive symptoms. However, no study has used diagnostic instruments to examine changes in RLS status during pregnancy in relation to the incidence of perinatal depression. This study aimed to investigate whether time-varying RLS status is associated with an increased risk of incident perinatal depression. This prospective cohort study analyzed data from 2435 Japanese pregnant women in the control group of a randomized controlled trial on perinatal depression. Time-varying RLS status was assessed using data obtained in the second and third trimesters with the short form of the Cambridge–Hopkins diagnostic questionnaire. Incident major depressive episodes and depressive symptoms from the second trimester to 3 months postpartum were assessed using the self-administered World Health Organization Composite International Diagnostic Interview 3.0 and the Edinburgh Postnatal Depression Scale (EPDS), respectively. Associations were examined using Cox proportional hazards models with time-varying covariates. The prevalence of RLS was 40 (1.6
The role of oxidative stress in central sleep apnea (CSA) remains unknown. We examined whether “oxygen overshoot burden”—a measure of cumulative oxygen saturation levels above baseline—is associated with major adverse cardiovascular events (MACE) in CSA. We analyzed 7530 participants from the Sleep Heart Health Study (SHHS; age 64 years; 47.0
Obstructive sleep apnea (OSA) is a common disorder characterized by repetitive collapse of the upper airway during sleep. Given that excess adiposity is a known risk factor for OSA, we aimed to descriptively assess the association of tirzepatide, a GIP/GLP-1 receptor agonist, with changes in AHI, hypoxic burden, body weight, and blood pressure in different patient populations based on baseline characteristics such as age, sex, BMI, AHI, and neck circumference. These post hoc analyses examined data from two Phase 3 randomized, double-blind studies evaluating maximum tolerated dose (MTD) tirzepatide (10 mg or 15 mg) compared with placebo in adults with moderate-to-severe OSA (AHI ≥ 15 events/h) and obesity (BMI ≥ 30 kg/m2) over a 52-week period. Baseline subgroup analyses were conducted in participants with non-missing relevant baseline measurements. Generally, participants treated with tirzepatide showed greater improvements in OSA outcomes compared with placebo, regardless of baseline subgroup. Participants treated with tirzepatide experienced reductions in AHI across subgroups, regardless of baseline age (-27.7 to -34.1 events/h), sex (-19.8 to -32.6 events/h), AHI severity (-12.1 to -52.2 events/h), BMI (-25.2 to -34.4 events/h), and neck circumference (-23.9 to -30.8 events/h). Additionally, improvements were observed in body weight, systolic blood pressure, and sleep apnea-specific hypoxic burden across baseline subgroups. Overall, most participants experienced an improvement in AHI severity category with tirzepatide treatment (68
To estimate the prevalence of insomnia disorder and insomnia symptoms, explore risk factors for insomnia disorder, and characterize sleep at 6 weeks postpartum. Following IRB approval, adults who delivered a live infant at two academic US hospitals were prospectively recruited with a pre-specified cross-sectional analysis planned at 6 weeks postpartum, evaluating new sleep disturbance (SD) and sleep-related impairment (SRI) surveys. Participants were invited to complete surveys (Bergen Insomnia Scale (BIS), PROMIS SD, and SRI), and a structured clinical interview for sleep disorders (SCISD-R, the diagnostic standard), at 6 weeks postpartum, until 150 interviews were completed. Demographic and clinical variables were collected. Primary outcome was prevalence of insomnia disorder by SCISD-R; secondary outcomes were sleep characteristics and survey scores, clinical and sociodemographic factors associated with insomnia disorder, and exploratory evaluation of the diagnostic accuracy of BIS, PROMIS SD, and SRI for insomnia disorder identified by SCISD-R. Associations were assessed using univariate odds ratios and 95
This study examined associations among concussion history, multidimensional sleep health, physical activity, and serious cognitive difficulty in a nationally representative sample of US adolescents. Cross-sectional data from adolescents aged 12–17 years participating in the 2022–2024 National Survey of Children’s Health were analyzed. Sequential multivariable models accounting for complex sampling examined associations among concussion history, short sleep duration, bedtime inconsistency, sports participation, physical activity, and serious cognitive difficulty. Sensitivity analyses evaluated alternative bedtime consistency operationalizations and interaction effects. In fully adjusted models, concussion history (aOR = 2.07, 95
This study aimed to determine the accuracy and feasibility of utilizing a photoplethysmography-based home sleep apnea test (PPG-HSAT) in children ages 2 to 6 years. Fifty children aged 2 to 6 years referred for polysomnography (PSG) for evaluation of obstructive sleep apnea (OSA) were prospectively enrolled to wear the SleepImage PPG-HSAT concurrently during in-lab PSG. This is a ring-worn PPG-HSAT scored using proprietary SleepImage software. Thirty-nine participants completed testing. A “limited PSG” dataset was created by trimming PSG data to match periods when PPG-HSAT data were available. The apnea–hypopnea index (AHI) and presence of OSA were compared between methods. Device-related issues (e.g., detachment, intolerance, user setup error) that precluded successful data collection occurred in 11
Abstract Introduction Treatment initiation or intensification to prevent exacerbation of chronic obstructive pulmonary disease (COPD) is based on the identification of patients with high exacerbation risk. The commonly used high-risk category of at least 2 moderate or 1 severe exacerbation within the prior 12 months has limited supporting evidence. We aimed to test the discriminative accuracy and assess the clinical utility of various COPD exacerbation categories for predicting future exacerbations. Methods In the COPDGene and NOVELTY cohorts, for each 1-year and 2-year recall periods, we estimated 6 distinct categories of exacerbation frequencies: ≥1 moderate (M1), ≥2 moderate (M2), ≥1 severe (S1), ≥1 moderate and ≥1 severe (M1andS1), ≥1 moderate or ≥ 1 severe (M1orS1), and ≥2 moderate or ≥ 1 severe (M2orS1), each ascertained in 3 ways: within 1 year, in each of 2 consecutive years (suffix E), and over a rolling combined 2-year period (suffix R). We used the area under the receiver operating characteristic curve (AUC) and decision curve analysis to evaluate the discriminative accuracy and clinical utility of these 18 categories for predicting the occurrence of M2orS1 (current standard) in the subsequent year. Results In COPDGene (n = 3,035), for the prediction of future M2orS1, baseline M1orS1R had the highest AUC (0.69, 95%CI 0.67-0.71) vs. baseline M2orS1 (0.66, 95%CI 0.64-0.67; Δ = 0.03;p<0.001). In NOVELTY (n = 3,080), M1orS1R category had the highest AUC (0.87, 95%CI 0.85-0.88) vs. M2orS1 (0.75, 95%CI 0.72-0.77, Δ = 0.12;p<0.001). Decision curve analysis demonstrated that the two-year rolling patterns provided the highest clinical utility across a clinically relevant treatment threshold range of 5% to 30% (Figure). M1orS1R also had the highest AUC for predicting any exacerbation (M1orS1) in both COPDGene (AUC = 0.68, 95%CI 0.66-0.70) and in NOVELTY (AUC = 0.86, 95%CI 0.85-0.88). Conclusions At least 1 moderate or 1 severe exacerbation over the previous 2 years has the highest discrimination and confers the highest clinical utility for predicting high COPD exacerbation risk. Overall, the combination of higher performance of various exacerbation history patterns in terms of their statistical (AUC) and clinical utility (net benefit) indicates that using a two-year recall and a lower threshold for high-risk classification (any moderate/severe events) is superior to the current standard of care. This abstract is funded by: This work was supported by NHLBI R01 HL151421 (SPB and AN), U01 HL089897 and U01 HL089856, by NIH contract 75N92023D00011, and by a Team Grant from the Canadian Institutes of Health Research (PHT 178432). COPDGene is also supported by the COPD Foundation through contributions made to an Industry Advisory Board that has included AstraZeneca, Bayer Pharmaceuticals, Boehringer Ingelheim, Genentech, GlaxoSmithKline, Novartis, Pfizer, and Sunovion. The NOVELTY study was funded by AstraZeneca.
Obstructive sleep apnea (OSA) is a sleep disorder that causes recurrent airway obstruction and sleep fragmentation and increases cardiometabolic, cognitive, and mortality risk. Although slow-wave activity (SWA) and sleep homeostasis (SH) are central to restorative sleep and synaptic regulation, the extent to which SH is disrupted across OSA severity remains unclear. In this population-based cohort study, we analyzed 945 polysomnography (PSG) studies from adults with mild, moderate, severe OSA, or no OSA. Sleep parameters including apnea–hypopnea index (AHI) and slow wave activity (SWA 0.5–4 Hz) from electroencephalography (EEG) in non-rapid eye movement (NREM) sleep were extracted. SH was assessed with overnight decay of SWA, slopes of slow waves, and change in SWA with wake after sleep onset (WASO). Liner regression models were used to identify independent predictors of SH measures. SWA decay across successive NREM episodes was attenuated in severe OSA group. Higher AHI (p < 0·001) and greater WASO (p < 0·001) were associated with a flatter decay of SWA. For a given level of SWA decay, males exhibited higher AHI than females (p < 0·0001). Slope of slow waves decreased from the first to last hour of NREM sleep in all groups (p < 0.01) except severe OSA. Multivariable models revealed that diabetes, use of antidepressant, anti-anxiety, antihypertensive, and sedative medications and high caffeine intake independently predicted impaired SH, whereas greater N3 sleep percentage was associated with preserved SWA decline. These data demonstrate SH is disrupted in OSA but additionally modulated by metabolic and pharmacologic factors. Targeting SH may represent a strategy to mitigate neurocognitive and physiological consequences of OSA. Obstructive sleep apnea (OSA) is associated with adverse health outcomes including hypertension, cardiovascular complications, cognitive decline as well as mortality. Impaired sleep homeostasis in OSA may represent a mechanistic link between sleep-disordered breathing and adverse health outcomes as slow wave activity is critical for synaptic downscaling, memory consolidation, and metabolic regulation. OSA is known to impair sleep homeostasis though it is unknown if OSA severity matters. Our data suggested that severe OSA impaired sleep homeostasis but clinical factors should be considered as they can impact sleep homeostasis as well. Future research should evaluate whether therapeutic interventions for OSA can reverse all these impairments and whether treatments should also be directed towards correcting sleep homeostasis impairment as well.
Sleep and obesity are tightly interconnected, with bidirectional relationships that influence cardiometabolic health and the development and progression of sleep disorders. In this review, we synthesize current evidence linking insufficient sleep, insomnia, obstructive sleep apnea (OSA), and other sleep disorders with obesity, with a focus on pathophysiology, clinical implications, and emerging therapeutic strategies. Insufficient sleep is consistently associated with weight gain through hormonal, behavioral, and metabolic mechanisms, whereas the relationship between insomnia and obesity appears weaker and more heterogeneous. Obesity is a major driver of OSA via effects on upper airway anatomy, respiratory mechanics, and ventilatory control, though reciprocal effects of OSA on weight remain less clear. Recent advances in obesity pharmacotherapy, particularly incretin-based therapies such as dual GIP/GLP-1 receptor agonists, will likely reshape treatment paradigms. Clinical trial data demonstrate meaningful improvements in both weight and OSA severity, highlighting the potential for integrated management of comorbid obesity and OSA (COBOSA); however, traditional therapies—including continuous positive airway pressure (CPAP), exercise, and lifestyle modification—remain foundational components of care. We also review obesity hypoventilation syndrome and other sleep disorders associated with obesity, emphasizing shared and distinct mechanisms. Despite substantial progress, key knowledge gaps remain regarding optimal treatment integration, heterogeneity of treatment response, and long-term outcomes. Overall, effective management of obesity is increasingly central to sleep medicine, underscoring the need for multidisciplinary, patient-centered approaches and further research. Likewise, promoting adequate sleep should be considered an important component of weight management and overall health.
We examined the psychometric properties of the Pittsburgh Sleep Quality Index (PSQI) in a large sample of young women in Soweto, South Africa, to assess its reliability and structural validity in this context. Data were collected from 7182 women enrolled in the Bukhali randomized controlled trial, part of the Healthy Life Trajectories Initiative (HeLTI). Sociodemographic information and PSQI data were collected through interviewer-administered surveys. Internal consistency was assessed using Cronbach’s alpha, McDonald’s omega and item-level correlations. Confirmatory factor analysis (CFA) evaluated the original one-factor and established two- and three-factor multidimensional models. Model fit was examined using Root Mean Square Error of Approximation (RMSEA), Comparative Fit Index (CFI), and Tucker–Lewis Index (TLI). Most women (57.4
To evaluate the effects of acceptance and commitment therapy (ACT) for insomnia compared with waitlist/standard control conditions and cognitive behavioral therapy for insomnia (CBT-I). A systematic review and meta-analysis of randomized controlled trials was conducted. We searched on PubMed, Embase, and the Cochrane Library for studies comparing ACT or ACT-based interventions with non-ACT conditions in patients with insomnia. Continuous outcomes were pooled using a restricted maximum likelihood random-effects model on R. ACT showed moderate-to-large improvement in insomnia symptom severity compared with waitlist/standard controls (SMD − 0.67, 95
The purpose of this cross-sectional observational study was to describe the geographic distribution of utilization of polysomnography (PSG) among children enrolled in Medicaid/Child Health Insurance Program from 2017 to 2019. The data source was the Transformed Medicaid Information System (T-MSIS) research analytic files. PSG among children ages 0 to 18 years was identified from the claims data. All children enrolled in Medicaid with at least one service utilization claim formed the denominators for calculation of age-adjusted rates per 10,000 children at the US Census Bureau Division, state and local levels. Geographic patterns were visualized with maps and plots. PSG rates were modeled by Rural–Urban Commuting Area (RUCA) classification and race-ethnicity composition at the ZIP code level. Data quality concerns resulted in exclusion of Rhode Island and Vermont. There were 478,568 PSGs identified among eligible children in the claims data, resulting in a national rate of 50.1 PSGs per 10,000 Medicaid enrolled children per year. There was a fourfold difference in rates at the state level, ranging from 23 PSGs per 10,000 person-years (Kansas) to 93 per 10,000 (Michigan). New England and the Great Lakes regions had the highest local levels, while the Pacific and West South Central divisions had the lowest. ZIP codes with higher percent White population (> 90
To synthesize current evidence on how sleep deprivation, impaired sleep architecture, and circadian misalignment affect cardiovascular and metabolic regulation across autonomic, hormonal, inflammatory, and behavioral pathways, and to highlight remaining research gaps in cardiometabolic sleep medicine. A structured literature search was conducted using PubMed, Scopus, and Google Scholar to identify peer‑reviewed primary and review articles published within the past decade, using chronobiological and cardiometabolic search terms. Reference lists of retrieved articles were screened to identify additional relevant studies. Experimental and epidemiologic data consistently link short or disturbed sleep with increased incidence of hypertension, coronary artery disease, stroke, obesity, type 2 diabetes, and metabolic syndrome. Sleep loss activates the sympathetic nervous system and elevates cortisol, while suppressing growth hormone, thereby promoting vasoconstriction, endothelial dysfunction, and cardiac remodeling. Parallel disruption of leptin, ghrelin, and endocannabinoid signaling increases hunger, caloric intake, and preference for energy‑dense foods, driving weight gain, visceral adiposity, and insulin resistance. Circadian misalignment from shift work and social jet lag further amplifies inflammatory signaling and metabolic risk across the lifespan. Limited interventional data suggest that sleep extension can improve appetite regulation, blood pressure, and some glycemic indices, but mechanistic and long‑term outcomes remain underexplored. Sleep deprivation and circadian disruption mediate cardiometabolic disease through converging neuroendocrine, autonomic, inflammatory, and behavioral pathways. Future research should employ longitudinal designs and integrated multi- “omics” approaches combined with sleep phenotyping to clarify causal mechanisms and identify novel biomarkers and therapeutic targets in clinical sleep medicine.
