Self-reported Sleep Duration Research Articles

Sleep duration, sleep efficiency, and amyloid β among cognitively healthy later-life adults: a systematic review and meta-analysis

BackgroundAbnormal amyloid β (Aβ) deposits in the brain are a hallmark of Alzheimer’s disease (AD). Insufficient sleep duration and poor sleep quality are risk factors for developing AD. Sleep may play a role in Aβ regulation, but the magnitude of the relationship between sleep and Aβ deposition remains unclear. This systematic review examines the relationship between sleep (i.e., duration and efficiency) with Aβ deposition in later-life adults.MethodsA search of PubMed, CINAHL, Embase, and PsycINFO generated 5,005 published articles. Fifteen studies met the inclusion criteria for qualitative syntheses; thirteen studies for quantitative syntheses related to sleep duration and Aβ; and nine studies for quantitative syntheses related to sleep efficiency and Aβ.ResultsMean ages of the samples ranged from 63 to 76 years. Studies measured Aβ using cerebrospinal fluid, serum, and positron emission tomography scans with two tracers: Carbone 11-labeled Pittsburgh compound B or fluorine 18-labeled. Sleep duration was measured subjectively using interviews or questionnaires, or objectively using polysomnography or actigraphy. Study analyses accounted for demographic and lifestyle factors. Based on 13 eligible articles, our synthesis demonstrated that the average association between sleep duration and Aβ was not statistically significant (Fisher’s Z = -0.055, 95% CI = -0.117 ~ 0.008). We found that longer self-report sleep duration is associated with lower Aβ (Fisher’s Z = -0.062, 95% CI = -0.119 ~ -0.005), whereas the objectively measured sleep duration was not associated with Aβ (Fisher’s Z = 0.002, 95% CI = -0.108 ~ 0.113). Based on 9 eligible articles for sleep efficiency, our synthesis also demonstrated that the average association between sleep efficiency and Aβ was not statistically significant (Fisher’s Z = 0.048, 95% CI = -0.066 ~ 0.161).ConclusionThe findings from this review suggest that shorter self-reported sleep duration is associated with higher Aβ levels. Given the heterogeneous nature of the sleep measures and outcomes, it is still difficult to determine the exact relationship between sleep and Aβ. Future studies with larger sample sizes should focus on comprehensive sleep characteristics and use longitudinal designs to better understand the relationship between sleep and AD.

Shorter night-time sleep duration and later sleep timing from infancy to adolescence.

Here, we (a) examined the trajectories of night-time sleep duration, bedtime and midpoint of night-time sleep (MPS) from infancy to adolescence, and (b) explored perinatal risk factors for persistent poor sleep health. This study used data from 12,962 participants in the Avon Longitudinal Study of Parents and Children (ALSPAC). Parent or self-reported night-time sleep duration, bedtime and wake-up time were collected from questionnaires at 6, 18 and 30 months, and at 3.5, 4-5, 5-6, 6-7, 9, 11 and 15-16 years. Child's sex, birth weight, gestational age, health and temperament, together with mother's family adversity index (FAI), age at birth, prenatal socioeconomic status and postnatal anxiety and depression, were included as risk factors for persistent poor sleep health. Latent class growth analyses were applied first to detect trajectories of night-time sleep duration, bedtime and MPS, and we then applied logistic regressions for the longitudinal associations between risk factors and persistent poor sleep health domains. We obtained four trajectories for each of the three sleep domains. In particular, we identified a trajectory characterized by persistent shorter sleep, a trajectory of persistent later bedtime and a trajectory of persistent later MPS. Two risk factors were associated with the three poor sleep health domains: higher FAI with increased risk of persistent shorter sleep (OR = 1.20, 95% CI = 1.11-1.30, p < .001), persistent later bedtime (OR = 1.28, 95% CI = 1.19-1.39, p < .001) and persistent later MPS (OR = 1.30, 95% CI = 1.22-1.38, p < .001); and higher maternal socioeconomic status with reduced risk of persistent shorter sleep (OR = 0.99, 95% CI = 0.98-1.00, p = .048), persistent later bedtime (OR = 0.98, 95% CI = 0.97-0.99, p < .001) and persistent later MPS (OR = 0.99, 95% CI = 0.98-0.99, p < .001). We detected trajectories of persistent poor sleep health (i.e. shorter sleep duration, later bedtime and later MPS) from infancy to adolescence, and specific perinatal risk factors linked to persistent poor sleep health domains.

Brain-Derived Neurotrophic Factor is Associated with Self-Reported Quality of Sleep in Type 2 Diabetes Patients in Ghana.

Sleep disturbances are common in patients with type 2 diabetes (T2DM), and this exacerbates disease severity and results in poor quality of life. Brain-derived neurotrophic factor (BDNF) has been reported to mediate the association between T2DM and poor sleep health. The burden of self-reported poor sleep quality and duration in T2DM and their association with serum BDNF levels were investigated. In this case-control design, the Pittsburgh Sleep Quality Instrument was used to assess self-reported sleep quality and duration in 100 patients with T2DM and 80 nondiabetic controls. Sociodemographic data and medical history were collected from case notes and/or using a structured questionnaire. Fasting venous blood samples (5 mL) were collected to measure plasma lipid profile and serum BDNF levels. patients with T2DM had low levels of BDNF, poor sleep quality (61.9% vs 27.5%, p<0.001), and shorter sleep duration (6.1±2.2 vs 6.9±1.1 h, p=0.003). T2DM status was associated with doubling the odds of poor sleep quality [OR (95%CI)=2.06 (1.07-6.43), p=0.039] and 1.6 times the odds of short sleep duration [1.63 (1.03-3.79), p=0.028]. Multivariable logistic regression analysis revealed no association between serum BDNF levels and sleep status. However, there was a negative biological interaction between T2DM and BDNF levels on poor sleep quality, resulting in 0.28 relative excess risk due to the interaction and a 12% attributable proportion due to the interaction. In this study population, patients with T2DM had a high burden of self-reported poor quality of sleep and shorter sleep duration compared to the nondiabetic controls. T2DM interacts negatively with serum BDNF levels to affect sleep quality.

The association of self-reported sleep and circadian measures with glycemic control and diabetes complications among young adults with type 2 diabetes.

We aim to examine the association of sleep duration, sleep quality, late chronotype, and circadian misalignment with glycemic control and risk of complications in young adults with youth-onset type 2 diabetes followed in the Treatment Options for Type 2 Diabetes in Adolescents and Youth (TODAY) study. Self-reported sleep duration, quality, timing, and circadian misalignment were assessed via a modified Pittsburgh Sleep Quality Index (PSQI) questionnaire, and chronotype was assessed via the Morningness-Eveningness Questionnaire (MEQ). We examined diabetes complications including loss of glycemic control (defined as hemoglobin A1c ≥8%), hypertension, dyslipidemia, albuminuria, and diabetic peripheral neuropathy. Multivariable logistic regression models were constructed to assess associations between sleep and circadian measures with outcomes of interest, such as loss of glycemic control and diabetes complications. A total of 421 participants (34.2% male), mean age 23.6 ± 2.5 yr, mean body mass index (BMI) of 36.1 ± 8.3 kg/m2, and mean diabetes duration of 10.0 ± 1.5 yr were evaluated. Self-reported short sleep duration, daytime sleepiness, and sleep quality were not associated with loss of glycemic control or diabetes complications. Late self-reported bedtime (after midnight) on work/school nights, rather than self-expressed chronotype or circadian misalignment, was independently associated with loss of glycemic control. An association was seen between late bedtimes and albuminuria but was attenuated after adjusting for depression. In conclusion, late bedtime on work/school days, rather than short sleep duration, daytime sleepiness, or poor sleep quality, was independently associated with loss of glycemic control in this longitudinal cohort of young adults with youth-onset type 2 diabetes.NEW & NOTEWORTHY The prevalence of type 2 diabetes in youth is increasing at an alarming rate. Identifying potentially modifiable factors modulating glycemic control is critically important to reduce micro and macrovascular complications. In a large cohort of youth-onset type 2 diabetes, self-reported late bedtime on work/school days was independently associated with loss of glycemic control in this longitudinal cohort of young adults with youth-onset type 2 diabetes.

Neuropathologic changes at age 90+ related to sleep duration 19 to 40 years earlier: The 90+ Study.

We investigated the association between sleep duration and neuropathologic changes 19 to 40 years later in oldest-old (age 90+) participants of The 90+ Study. Participants self-reported sleep duration and underwent neuropathologic evaluation. We categorized sleep duration as<7, 7 to 8=reference,>8hours and dichotomized neuropathologic changes as present/absent. We estimated odds ratio (OR) and 95% confidence intervals (CI) using logistic regression. In 264 participants, mean age at sleep self-report was 69 years, mean age at autopsy was 98 years, and mean interval between sleep self-report and autopsy was 29 years (range: 19-40). Those reporting>8hours of sleep had lower likelihood of limbic-predominant age-related TDP-43 encephalopathy neuropathologic change (LATE-NC) inclusions (OR=0.18; CI=0.04-0.82) and amyloid beta deposits (OR=0.34; 95% CI=0.12-0.94). Long self-reported sleep is associated with lower odds of neurodegenerative neuropathologic changes 19 to 40 years later in the oldest-old, suggesting a potential role of sleep in accumulation of dementia-related neuropathologies. Association of self-reported sleep with non-Alzheimer's disease neuropathologic changes has not been explored. Whether sleep duration is related to dementia neuropathologic changes decades later is unclear. Long self-reported sleep is associated with lower odds of Alzheimer's disease neuropathologic change 19 to 40 years later in the oldest-old. Long self-reported sleep is associated with lower odds of limbic-predominant age-related TDP-43 encephalopathy neuropathologic change 19 to 40 years later in the oldest-old.

Suboptimal self-reported sleep efficiency and duration are associated with faster accumulation of brain amyloid beta in cognitively unimpaired older adults.

This study investigated whether self-reported sleep quality is associated with brain amyloid beta (Aβ) accumulation. Linear mixed effect model analyses were conducted for 189 cognitively unimpaired (CU) older adults (mean±standard deviation 74.0±6.2; 53.2% female), with baseline self-reported sleep data, and positron emission tomography-determined brain Aβ measured over a minimum of three time points (range 33.3-72.7 months). Analyses included random slopes and intercepts, interaction for apolipoprotein E (APOE) ε4 allele status, and time, adjusting for sex and baseline age. Sleep duration<6hours, in APOE ε4 carriers, and sleep efficiency<65%, in the whole sample and APOE ε4 non-carriers, is associated with faster accumulation of brain Aβ. These findings suggest a role for self-reported suboptimal sleep efficiency and duration in the accumulation of Alzheimer's disease (AD) neuropathology in CU individuals. Additionally, poor sleep efficiency represents a potential route via which individuals at lower genetic risk may progress to preclinical AD. In cognitively unimpaired older adults self-report sleep is associated with brain amyloid beta (Aβ) accumulation.Across sleep characteristics, this relationship differs by apolipoprotein E (APOE) genotype.Sleep duration<6hours is associated with faster brain Aβ accumulation in APOE ε4 carriers.Sleep efficiency< 65% is associated with faster brain Aβ accumulation in APOE ε4 non-carriers.Personalized sleep interventions should be studied for potential to slow Aβ accumulation.

Vicarious racism, ethnic/racial identity, and sleep among Asian Americans.

Vicarious racism-witnessing or hearing about other individuals of one's ethnic/racial group being the target of racism-has been salient among Asian Americans during the coronavirus disease (COVID-19) pandemic. There is emerging evidence that such experiences adversely impact several health-related outcomes, including sleep. The present study examines associations between vicarious racism and subjective sleep duration and quality, and the potential moderating role of ethnic/racial identity (ERI). Multivariable regression models assessed the association between vicarious racism, private regard, and centrality on self-reported sleep disturbance and duration. The sample consisted of an online sample of 600 Asian American adults (Mage = 38.55, SDage = 17.11; 65.17% female; 60% ≥ Bachelor's degree) recruited from May to June 2020. Vicarious racism was associated with compromised sleep quality and duration, including after adjustment for sociodemographic variables that have been linked to sleep. Private regard toward one's own ethnic/racial group and centrality of ethnicity/race to self-identity buffered the association between vicarious racism and sleep quality and duration. Adverse effects of high vicarious racism on sleep quality and duration were lessened among respondents reporting high levels of ERI private regard and centrality. Findings from this study extend research on racism and sleep by examining vicarious racism, an understudied facet of racism, and by focusing specifically on Asian Americans and in the context of the COVID-19 pandemic. Future research and practice should consider expanding research on discrimination to include a broader range of unjust experiences. Vicarious racism contributes to health hazards experienced by Asian Americans during the COVID-19 pandemic. (PsycInfo Database Record (c) 2024 APA, all rights reserved).

Abstract 2232: Association between sleep characteristics and cancer survival: Findings from the UK Biobank study

Abstract Background Sleep characteristics have been associated with patient outcomes after cancer. We aimed to appraise the causal relationship of chronotype, sleep duration, insomnia, and snoring with cancer survival. Methods This large prospective cohort study enrolled 38350 cancer survivors aged ≥40 years from the UK Biobank between 2004 and 2022. Habitual sleep characteristics were obtained from the self-reported baseline questionnaire, including chronotype, sleep duration, insomnia, and snoring. Cox proportional hazards regression models were applied to evaluate the association between sleep characteristics and cancer survival, then one sample Mendelian randomization (MR) analyses were further used to validate these causal relationships. In particular, restricted cubic splines (RCS) and non-linear MR analyses were applied to assess the possible nonlinear association between sleep duration and cancer survival. Results Among 38350 study participants (mean [SD] age, 59.8 [7.3] years; 24150 [63.0%] males; 35534 [92.7%] White individuals), 12671 (33.1%) reported evening preference chronotype; 9050 (23.6%) reported short and 3773 (9.8%) reported long sleep duration;12274 (32.0%) reported snoring; and 30426 (79.4%) reported experiencing insomnia sometimes or usually. During up to 18 years of follow-up, 6274 deaths occurred. Multivariable regression models showed that evening preference (HR = 1.09, 95% CI: 1.03 to 1.15), short (HR = 1.14, 95% CI: 1.07 to 1.21) and long sleep duration (HR = 1.37, 95% CI: 1.28 to 1.48), insomnia (HR = 1.14, 95% CI: 1.09 to 1.21) and snoring (HR = 0.83, 95% CI: 0.78 to 0.87) were associated with death among pan to cancer survivors. Restricted cubic splines suggested nonlinear associations between sleep duration and death after cancer (nonlinear P &amp;lt; 0.001). In the one-sample MR, genetically predicted sleep duration (HR = 0.71, 95% CI: 0.56 to 0.90) and snoring (HR = 1.18, 95% CI: 1.05 to 1.34) demonstrated a reversed cancer survival pattern compared to multivariable regressions. A nonlinear U-shape association between sleep duration and cancer survival was observed in restricted cubic spline analyses (P &amp;lt; 0.001) but not evident when evaluating by nonlinear MR (P &amp;gt; 0.05). Conclusions Evening preference chronotype, insomnia, snoring, and short sleep duration are likely to be causally associated with a higher risk of death among cancer survivors, whilst long sleep duration does not appear to be a causal factor. Citation Format: Jiajing Che, Jiali Lv, Keyu Pan, Tiantian Sun, Chao Cao, Shengxu Li, Tao Zhang, Fuzhong Xue, Lin Yang. Association between sleep characteristics and cancer survival: Findings from the UK Biobank study [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2024; Part 1 (Regular Abstracts); 2024 Apr 5-10; San Diego, CA. Philadelphia (PA): AACR; Cancer Res 2024;84(6_Suppl):Abstract nr 2232.

Abstract P540: Sleep Duration, Rapid Eye Movement Sleep, and Subclinical Myocardial Damage

Introduction: Sleep is strongly linked to clinical cardiovascular disease and was added in 2022 to the AHA’s Life’s Essential 8. Optimizing sleep duration and quality may reduce the risk of cardiovascular disease. Few studies have examined self-reported sleep duration and percent time in rapid eye movement (REM) sleep measured by single night in-home polysomnography with high sensitivity cardiac troponin T (hs-troponin T), a biomarker of subclinical cardiovascular disease. Methods: We conducted a cross-sectional study of adults without a history of cardiovascular disease who participated in both the Atherosclerosis Risk in Communities (ARIC) Study and the Sleep Heart Health Study (SHHS) in 1995-1998. We used linear regression with sleep duration and percentage time of REM sleep modeled as predictors with restricted cubic splines and examined associations with the outcome, hs-troponin T. We adjusted for age, sex, body mass index, waist-to-hip ratio, alcohol intake, smoking status, systolic blood pressure, hypertension medication use, diabetes, HDL- and LDL-cholesterol, and cholesterol-lowering medication use. Results: Among 1,587 participants (mean age 63, 54% female), the mean sleep duration was 7.3 hours, and mean % REM time was 20.7. Sleep duration was not associated with hs-troponin T ( Figure, Panel A ). However, percentage REM sleep was negatively associated with hs-troponin T, but with a threshold effect; there was a negative linear association of hs-troponin T with % REM sleep but only at values &lt;15% ( Figure, Panel B ). Conclusion: While self-reported sleep duration was not associated with TnT levels, there was evidence that low % REM sleep, a specific neurophysiological sleep state, was associated with subclinical cardiovascular disease. These findings suggest that multiple sleep dimensions should be considered in efforts to optimize cardiovascular health.

Nightly Sleep Predicts Next-Morning Expectations for Stress and Positive Experiences.

Abundant research has linked nightly sleep as an antecedent of daily psychosocial experiences; however, less is known about sleep's influence on daily expectations of these experiences. Therefore, this research examined the day-to-day associations of sleep quality, duration, and efficiency with next-day expectations for stress(ors) and positive experiences, as well as whether these expectations were related to end-of-day reports of physical symptoms. In Study 1, U.S. adults ( n = 354; ages 19 to 74) completed twice-daily diaries for 10 weekdays about sleep, expectations for encountering daily stressors and positive events, and physical symptoms. In Study 2, adults in Canada ( n = 246; ages 25 to 87) wore a sleep watch for 14 consecutive days and completed mobile surveys 5×/day about sleep, stressfulness and pleasantness expectations, and physical symptoms. Multilevel models indicated that self-reported sleep quality and duration, but not efficiency, were associated with lower next-day expectations for stressors (Study 1) and stressfulness (Study 2). Self-reported sleep quality (Study 1) and all sleep indices (Study 2) predicted greater next-day expectations for positive events and pleasantness, respectively. For actigraphy-assessed sleep (Study 2), only longer-than-usual actigraphic sleep duration was associated with lower stressfulness expectations, whereas both sleep duration and efficiency were positively linked with daily pleasantness expectations. Only pleasantness expectations (Study 2)-but not daily stressfulness and event expectations (Study 1)-predicted end-of-day physical symptoms. Findings suggest the importance of sleep on expectations of next-day stress and positive experiences, of which may have implications for daily physical health.

Genetic evidence for the causal effects of C–reactive protein on self-reported habitual sleep duration

Inflammatory responses to acute stimuli are proposed to regulate sleep, but the relationship between chronic inflammation and habitual sleep duration is elusive. Here, we study this relation using genetically predicted level of chronic inflammation, indexed by CRP and IL6 signaling, and self-reported sleep duration. By Mendelian randomization analysis, we show that elevated CRP level within <10 mg/L has a homeostatic effect that facilitates maintaining 7–8 h sleep duration per day — making short-sleepers sleep longer (p = 2.42 × 10−2) and long-sleepers sleep shorter (1.87 × 10−7); but it is not associated with the overall sleep duration (p = 0.17). This homeostatic effect replicated in an independent CRP dataset. We observed causal effects of the soluble interleukin 6 receptor and gp130 on overall sleep duration (p = 1.62 × 10−8, p = 2.61 × 10−58, respectively), but these effects disappeared when CRP effects were accounted for in the model. Using polygenic score analysis, we found that the homeostatic effect of CRP on sleep duration stems primarily from the genetic variants within the CRP gene region: when genetic variants outside of this region were used to predict CRP levels, the opposite direction of effect was observed. In conclusion, we show that elevated CRP level may causally facilitate maintaining an optimal sleep duration that is beneficial to health, thus updating our current knowledge of immune regulation on sleep.

The influence of sleep on subjective well-being: An experience sampling study.

Previous research has associated sleep with subjective well-being (SWB), but less is known about the underlying within-person processes. In the current study, we investigated how self-reported and actigraphy-measured sleep parameters (sleep onset latency, sleep duration, sleep satisfaction, social jetlag, and sleep efficiency) influence SWB (positive affect [PA], negative affect [NA], and life satisfaction [LS]) at the within- and between-person levels. Multilevel analyses of data from 109 university students who completed a 2-week experience sampling study revealed that higher within-person sleep satisfaction was a significant predictor of all three components of next day's SWB (ps < .005). Higher between-person sleep satisfaction was also related to higher levels of PA and LS (ps < .005), whereas shorter self-reported between-person sleep onset latency was associated with higher PA and LS, and lower NA (ps < .05). However, longer actigraphy-measured within-person sleep onset latency was associated with higher next day's LS (p = .028). When including within- and between-person sleep parameters into the same models predicting SWB, only within- and between-person sleep satisfaction remained a significant predictor of all components of SWB. Additionally, we found an effect of higher self-reported within-person sleep onset latency on PA and of shorter self-reported within-person sleep duration on LS (ps < .05). Our results indicate that the evaluative component of sleep-sleep satisfaction-is most consistently linked with SWB. Thus, sleep interventions that are successful in not only altering sleep patterns but also enhancing sleep satisfaction may stand a better chance at improving students' SWB. (PsycInfo Database Record (c) 2023 APA, all rights reserved).

Sleep and Risk of Pancreatic Cancer in the UK Biobank.

Light at night, which may cause circadian disruption, is a potential pancreatic cancer risk factor. However, evidence from related exposures such as poor sleep health and shift work remains inconclusive and sparsely investigated. We evaluated associations between self-reported typical sleep duration, chronotype, shift work, insomnia symptoms, snoring, and daytime sleeping and pancreatic ductal adenocarcinomas (PDAC) incidence among 475,286 UK Biobank participants. We used Cox proportional hazards models to estimate HRs and 95% confidence intervals (CI) adjusting for age, sex, body mass index, smoking status, duration, and frequency, alcohol intake, diabetes status, race, and employment/shift work. Over 14 years of follow-up, 1,079 adults were diagnosed with PDAC. There were no associations observed between sleep characteristics, including sleep duration [<7 vs. 7-<9 hours; HR, 1.03; 95% CI, 0.90-1.19; ≥9 hours; HR, 1.00 (0.81-1.24), evening chronotype ("definitely" an evening person vs. "definitely" a morning person; HR, 0.99 (0.77-1.29)], shift work, insomnia symptoms, snoring, or daytime sleep and PDAC risk. Self-reported typical sleep characteristics and shift work were not associated with PDAC risk. Considering the role of light at night and shift work in circadian disruption and cancer risk, it is plausible that poor sleep health among a general population may be related to cancer risk through similar sleep and circadian disrupting processes. This work may suggest that typical sleep characteristics and shift work are not associated with PDAC, although additional work is needed to confirm these findings.

Shorter self-reported sleep duration is associated with worse virtual spatial navigation performance in men.

Sleep has been shown to impact navigation ability. However, it remains unclear how different sleep-related variables may be independently associated with spatial navigation performance, and as to whether gender may play a role in these associations. We used a mobile video game app, Sea Hero Quest (SHQ), to measure wayfinding ability in US-based participants. Wayfinding performance on SHQ has been shown to correlate with real-world wayfinding. Participants were asked to report their sleep duration, quality, daytime sleepiness and nap frequency and duration on a typical night (n = 766, 335 men, 431 women, mean age = 26.5years, range = 18-59years). A multiple linear regression was used to identify which self-reported sleep variables were independently associated with wayfinding performance. Shorter self-reported sleep durations were significantly associated with worse wayfinding performance in men only. Other self-reported sleep variables showed non-significant trends of association with wayfinding performance. When removing non-typical sleepers (< 6 or > 9h of sleep on a typical night), the significant association between sleep duration and spatial navigation performance in men was no longer present. These findings from U.S.-based participants suggest that a longer self-reported sleep duration may be an important contributor to successful navigation ability in men.

An Emerging 21st-Century Midlife Sleep Crisis? Cohort Differences in Sleeping Patterns Among Americans in Midlife and Older Adulthood.

To descriptively document birth cohort differences in sleeping patterns, self-reported age-specific sleep duration, and insomnia symptoms among adults aged 50+ from the National Health Interview Survey (NHIS) and the Health and Retirement Study (HRS). We analyzed respondents aged 50+ (born 1920-1969) from the 2006-2018 NHIS (n = 162,400) and HRS (n = 28,918). We fit multinomial models among the NHIS sample predicting age-specific optimal sleep duration (optimal for age vs short for age, and optimal for age vs long for age). For the HRS sample, we fit growth curve models predicting age-based insomnia symptom trajectories. The models for both samples adjusted for age, gender, race/ethnicity, and educational attainment. Results regarding sleep duration in the NHIS, suggested that cohorts born in the 1950s and 1960s had significantly higher odds of reporting short sleep duration than cohorts before them. Results from the HRS similarly illustrated that cohorts born in the 1950s and 1960s had significantly higher levels of insomnia symptoms than those born before them. The worsening sleep among cohorts entering midlife was consistent regardless of alternative cohort specification, when age groups or periods were analyzed, and when more extensive covariates were modeled. We observe a pronounced decline in healthy sleeping patterns among American cohorts in midlife, with consistent and striking results across data sets, methods, and measures. These findings have important implications for the well-being and longevity of Americans who have entered midlife in the 21st century.

Sleep Duration Polygenic Risk and Phenotype: Associations with Biomarkers of Accelerated Aging in the Baltimore Longitudinal Study of Aging.

We sought to explore whether genetic risk for, and self-reported, short sleep are associated with biological aging and whether age and sex moderate these associations. Participants were a subset of individuals from the Baltimore Longitudinal Study of Aging who had complete data on self-reported sleep (n = 567) or genotype (n = 367). Outcomes included: Intrinsic Horvath age, Hannum age, PhenoAge, GrimAge, and DNAm-based estimates of plasminogen activator inhibitor-1 (PAI-1) and granulocyte count. Results demonstrated that polygenic risk for short sleep was positively associated with granulocyte count; compared to those reporting <6 hr sleep, those reporting >7 hr demonstrated faster PhenoAge and GrimAge acceleration and higher estimated PAI-1. Polygenic risk for short sleep and self-reported sleep duration interacted with age and sex in their associations with some of the outcomes. Findings highlight that polygenic risk for short sleep and self-reported long sleep is associated with variation in the epigenetic landscape and subsequently aging.

Officer-Involved Killings of Unarmed Black People and Racial Disparities in Sleep Health

Racial disparities in sleep health may mediate the broader health outcomes of structural racism. To assess changes in sleep duration in the Black population after officer-involved killings of unarmed Black people, a cardinal manifestation of structural racism. Two distinct difference-in-differences analyses examined the changes in sleep duration for the US non-Hispanic Black (hereafter, Black) population before vs after exposure to officer-involved killings of unarmed Black people, using data from adult respondents in the US Behavioral Risk Factor Surveillance Survey (BRFSS; 2013, 2014, 2016, and 2018) and the American Time Use Survey (ATUS; 2013-2019) with data on officer-involved killings from the Mapping Police Violence database. Data analyses were conducted between September 24, 2021, and September 12, 2023. Occurrence of any police killing of an unarmed Black person in the state, county, or commuting zone of the survey respondent's residence in each of the four 90-day periods prior to interview, or occurence of a highly public, nationally prominent police killing of an unarmed Black person anywhere in the US during the 90 days prior to interview. Self-reported total sleep duration (hours), short sleep (<7 hours), and very short sleep (<6 hours). Data from 181 865 Black and 1 799 757 White respondents in the BRFSS and 9858 Black and 46 532 White respondents in the ATUS were analyzed. In the larger BRFSS, the majority of Black respondents were between the ages of 35 and 64 (99 014 [weighted 51.4%]), women (115 731 [weighted 54.1%]), and college educated (100 434 [weighted 52.3%]). Black respondents in the BRFSS reported short sleep duration at a rate of 45.9%, while White respondents reported it at a rate of 32.6%; for very short sleep, the corresponding values were 18.4% vs 10.4%, respectively. Statistically significant increases in the probability of short sleep and very short sleep were found among Black respondents when officers killed an unarmed Black person in their state of residence during the first two 90-day periods prior to interview. Magnitudes were larger in models using exposure to a nationally prominent police killing occurring anywhere in the US. Estimates were equivalent to 7% to 16% of the sample disparity between Black and White individuals in short sleep and 13% to 30% of the disparity in very short sleep. Sleep health among Black adults worsened after exposure to officer-involved killings of unarmed Black individuals. These empirical findings underscore the role of structural racism in shaping racial disparities in sleep health outcomes.

Relationship Between Sleep Duration and Cognitive Function in Older Adults: Analysis of NHANES and UK Biobank GWAS Data.

To explore the relationship between sleep duration and cognitive functions in older adults using NHANES, a national US population study dataset, and to explore the causal association with Mendelian randomization (MR) using the UK Biobank. First, an observational study was conducted with the NHANES database with participants ≥60 years. Sleep duration was measured with accelerometers for 7 consecutive days. Participants were divided into habitual short sleep (<7h) and long sleep (>9h) groups. Cognitive functions were measured with the CERAD Word Learning sub-set, Animal Fluency, and Digit Symbol Substitution test (DSST). Multivariate regression models were used to explore relationships between sleep duration and cognitive functions. Second, bidirectional MR was conducted with data for self-reported sleep duration, which came from a genome-wide association study (GWAS) comprising 446,118 adults from the UK Biobank, and general cognitive performance, which was obtained from a recent GWAS study (N = 257,841). Inverse-variance weighted (IVW) was used as the primary estimation of the outcome. In the observational study, 2687 participants were included. Sleep duration was associated with cognitive functions in a non-linear way. Habitual long sleep (>9°h) was associated with lower scores on DSST (OR = 0.01, p = .003) in the fully-adjusted model. The association between habitual short sleep and cognitive functions was insignificant. For the MR, genetically predicted lower general cognitive performance was causally associated with a higher prevalence of habitual short sleep (OR = 0.97, p = 5.1 × 10-7) and long sleep (OR = 0.97, p = 8.87 × 10-16). Short and long sleep duration might be both causally associated with worse outcomes of cognitive functions in older adults, highlighting the importance of maintaining sleep health.

Sleep and 24-H Activity Rhythms and the Risk of Stroke: A Prospective Cohort Study

Introduction: Short and long self-reported sleep durations are associated with a higher risk of stroke, but the association between objective estimates of sleep and 24-h activity rhythms is less clear. We studied the association of actigraphy-estimated sleep and 24-h activity rhythms with the risk of stroke in a population-based cohort of middle-aged and elderly. Methods: We included 1,718 stroke-free participants (mean age 62.2 ± 9.3 years, 55.1% women) from the prospective, population-based Rotterdam Study. Actigraphy-estimated sleep (total sleep time, sleep efficiency, sleep onset latency, and wake after sleep onset) and 24-h activity rhythms (interdaily stability, intradaily variability, and onset of the least active 5 h) were measured during a median of 7 days (Q1–Q3: 6–7 days). The association of sleep and 24-h activity rhythms with risk of stroke was analyzed using Cox proportional hazards models. Results: During a mean follow-up of 12.2 years (SD: 3.2), 105 participants developed a stroke, of whom 81 had an ischemic event. Although there was no clear association between actigraphy-estimated sleep and the risk of stroke, a more fragmented 24-h activity rhythm was associated with a higher risk of stroke (hazard ratio [HR] per SD increase 1.28, 95% confidence interval [CI] 1.07–1.53). A less stable (HR per SD increase in stability 0.78, 95% CI: 0.63–0.97) and more fragmented (HR 1.28, 95% CI: 1.04–1.58) 24-h activity rhythm was also associated with a higher risk of ischemic stroke. Conclusions: Disturbed 24-h activity rhythms, but not sleep, are associated with a higher risk of stroke in middle-aged and elderly persons. This suggests that unstable and fragmented activity rhythms may play a more prominent role in the risk of stroke than sleep per se.

Short sleep duration is associated with worse quality of life in Parkinson's disease: A multicenter cross-sectional study

ObjectiveTo characterize sleep duration and investigate its association with quality of life among Parkinson's Disease (PD) patients. MethodsIn this multicenter cross-sectional study, 970 PD patients were divided into five groups based on self-reported sleep duration: <5, ≥5 to <6, ≥6 to <7, ≥7 to ≤8, and >8 h. The quality of life was evaluated using the 39-Item Parkinson's Disease Questionnaire (PDQ-39). Multivariable linear regression analysis, subgroup analysis, and mediation analysis were conducted to examine the association between sleep duration and quality of life. ResultsIn multivariable linear regression model, patients with sleep duration (<5 h) had significantly higher PDQ-39 scores (β = 8.132, 95 % CI: 3.99 to 12.266), especially in mobility, activities of daily living, emotional well-being, stigma, social support, cognition, communication, and bodily discomfort (p < 0.05). The association between sleep duration (<5 h) and worse quality of life was more pronounced in patients with higher HY stage, longer disease duration, and sleep disorders. Moreover, a significant indirect effect of sleep duration (<5 h) on quality of life was observed, with UPDRS I, UPDRS II, and UPDRS IV scores acting as mediators. ConclusionsShort sleep duration (<5 h) is associated with worse quality of life among PD patients. This association was stronger among patients with advanced PD and sleep disorders, while non-motor symptoms and motor complications were identified as significant mediators in this association. These findings highlight the significance of adequate sleep duration and suitable interventions for sleep may help improve quality of life.