Singh, Rupsha; Atha, Raegan; Lenker, Kristina P; Calhoun, Susan L; Liao, Jiangang; He, Fan; Vgontzas, Alexandros N; Liao, Duanping; Bixler, Edward O; Jackson, Chandra L; Fernandez-Mendoza, Julio
Study ObjectivesTo examine differences in the longitudinal prevalence of childhood insomnia symptoms across black/African American, Hispanic/Latinx, and non-Hispanic white groups.MethodsParticipants 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 ± 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.ResultsBlack/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.ConclusionsThe 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 InformationN/A; Not a clinical trial.
Silva, Samuel; Hayden, Jill A; Mendes, Gabriel; Verhagen, Arianne P; Pinto, Rafael Z; Silva, Andressa
doi: 10.1093/sleep/zsae023pmid: 38300526
Sleep problems are common in individuals with low back pain (LBP) and sleep restriction seems to be associated with impaired pain processing. Our objective was to investigate whether sleep is associated with future LBP outcomes (i.e. pain intensity, disability, and recovery) in adults. We conducted a systematic review of prospective cohort studies and secondary analyses of randomized controlled trials (registration—PROSPERO CRD42022370781). In December 2022, we searched the MEDLINE, Embase, CINAHL, and PsycINFO databases. Fourteen studies, totaling 19 170 participants were included. Thirteen studies were rated as having high risk of bias (QUIPS tool). We used vote-counting and meta-analysis approaches to synthesize the data. We found associations between baseline sleep with future pain intensity, recovery, and between changes in sleep with changes in pain intensity, changes in disability, and recovery. We further synthesized outcomes as “overall LBP improvement” outcomes. Baseline poor sleep was moderately associated with non-improvement in LBP in the long-very long term (OR 1.55, 95% CI: 1.39 to 1.73; three studies providing unadjusted effect sizes), and non-improvement in sleep was largely associated with non-improvement in LBP in the short-moderate term (OR 3.45, 95% CI: 2.54 to 4.69; four studies providing unadjusted effect sizes). We found no association between baseline sleep with future disability and overall LBP improvement in the short-moderate term. Therefore, sleep may be a prognostic factor for pain intensity and recovery from LBP. All findings were supported by low to very low-quality evidence. Better-conducted studies are needed to strengthen our certainty about the evidence.
Spira, Adam P; Liu, Fangyu; Zipunnikov, Vadim; Bilgel, Murat; Rabinowitz, Jill A; An, Yang; Di, Junrui; Bai, Jiawei; Wanigatunga, Sarah K; Wu, Mark N; Lucey, Brendan P; Schrack, Jennifer A; Wanigatunga, Amal A; Rosenberg, Paul B; Simonsick, Eleanor M; Walker, Keenan A; Ferrucci, Luigi; Resnick, Susan M
doi: 10.1093/sleep/zsae037pmid: 38381532
Study ObjectivesTo compare sleep and 24-hour rest/activity rhythms (RARs) between cognitively normal older adults who are β-amyloid-positive (Aβ+) or Aβ− and replicate a novel time-of-day-specific difference between these groups identified in a previous exploratory study.MethodsWe studied 82 cognitively normal participants from the Baltimore Longitudinal Study of Aging (aged 75.7 ± 8.5 years, 55% female, 76% white) with wrist actigraphy data and Aβ+ versus Aβ− status measured by [11C] Pittsburgh compound B positron emission tomography. RARs were calculated using epoch-level activity count data from actigraphy. We used novel, data-driven function-on-scalar regression analyses and standard RAR metrics to cross-sectionally compare RARs between 25 Aβ+ and 57 Aβ− participants.ResultsCompared to Aβ− participants, Aβ+ participants had higher mean activity from 1:00 p.m. to 3:30 p.m. when using less conservative pointwise confidence intervals (CIs) and from 1:30 p.m. to 2:30 p.m. using more conservative, simultaneous CIs. Furthermore, Aβ+ participants had higher day-to-day variability in activity from 9:00 a.m. to 11:30 a.m. and lower variability from 1:30 p.m. to 4:00 p.m. and 7:30 p.m. to 10:30 p.m. according to pointwise CIs, and lower variability from 8:30 p.m. to 10:00 p.m. using simultaneous CIs. There were no Aβ-related differences in standard sleep or RAR metrics.ConclusionsFindings suggest Aβ+ older adults have higher, more stable day-to-day afternoon/evening activity than Aβ− older adults, potentially reflecting circadian dysfunction. Studies are needed to replicate our findings and determine whether these or other time-of-day-specific RAR features have utility as markers of preclinical Aβ deposition and if they predict clinical dementia and agitation in the afternoon/evening (i.e. “sundowning”).
Fechner, Julia; Contreras, María P; Zorzo, Candela; Shan, Xia; Born, Jan; Inostroza, Marion
doi: 10.1093/sleep/zsae061pmid: 38452190
Study ObjectivesSleep supports systems memory consolidation through the precise temporal coordination of specific oscillatory events during slow-wave sleep, i.e. the neocortical slow oscillations (SOs), thalamic spindles, and hippocampal ripples. Beneficial effects of sleep on memory are also observed in infants, although the contributing regions, especially hippocampus and frontal cortex, are immature. Here, we examined in rats the development of these oscillatory events and their coupling during early life.MethodsEEG and hippocampal local field potentials were recorded during sleep in male rats at postnatal days (PD)26 and 32, roughly corresponding to early (1–2 years) and late (9–10 years) human childhood, and in a group of adult rats (14–18 weeks, corresponding to ~22–29 years in humans).ResultsSO and spindle amplitudes generally increased from PD26 to PD32. In parallel, frontocortical EEG spindles increased in density and frequency, while changes in hippocampal ripples remained nonsignificant. The proportion of SOs co-occurring with spindles also increased from PD26 to PD32. Whereas parietal cortical spindles were phase-locked to the depolarizing SO-upstate already at PD26, over frontal cortex SO-spindle phase-locking emerged not until PD32. Co-occurrence of hippocampal ripples with spindles was higher during childhood than in adult rats, but significant phase-locking of ripples to the excitable spindle troughs was observed only in adult rats.ConclusionsResults indicate a protracted development of synchronized thalamocortical processing specifically in frontocortical networks (i.e. frontal SO-spindle coupling). However, synchronization within thalamocortical networks generally precedes synchronization of thalamocortical with hippocampal processing as reflected by the delayed occurrence of spindle-ripple phase-coupling.
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