A longitudinal observational population-based study of brain volume associated with changes in sleep timing from middle to late-life

SLEEP ◽  
2020 ◽  
Author(s):  
Regina E Y Kim ◽  
Hyeon Jin Kim ◽  
Soriul Kim ◽  
Robert D Abbott ◽  
Robert J Thomas ◽  
...  

Abstract Study Objectives Sleep behaviors are related to brain structure and function, but the impact of long-term changes in sleep timing on brain health has not been clearly addressed. The purpose of this study was to examine the association of longitudinal changes in sleep timing from middle to late-life with gray matter volume (GMV), an important marker of brain aging. Methods We enrolled 1798 adults (aged 49–82 years, men 54.6%) who underwent magnetic resonance imaging (MRI) between 2011 and 2014. Midsleep time (MST) on free days corrected for sleep debt on workdays was adopted as a marker of sleep timing. Data on MST were available at the time of MRI assessment and at examinations that were given 9 years earlier (2003–2004). Longitudinal changes in MST over the 9-year period were derived and categorized into quartiles. Subjects in quartile 1 were defined as “advancers” (MST advanced ≥ 1 h) while those in quartile 4 were defined as “delayers” (MST delayed ≥ 0.2 h). Quartiles 2–3 defined a reference group (MST change was considered modest). The relationship of GMV with MST changes over 9 years was investigated. Results Nine-year change in MST were significantly associated with GMV. Compared to the reference group, advancers had smaller GMVs in the frontal and temporal regions. A delay in MST was also associated with smaller cerebellar GMV. Conclusions In middle-to-late adulthood, the direction of change in MST is associated with GMV. While advancers and delayers in MST tend to present lower GMV, associations appear to differ across brain regions.

2012 ◽  
Vol 42 (12) ◽  
pp. 2619-2629 ◽  
Author(s):  
E. Scafato ◽  
L. Galluzzo ◽  
S. Ghirini ◽  
C. Gandin ◽  
A. Rossi ◽  
...  

BackgroundDepression is recognized as being associated with increased mortality. However, there has been little previous research on the impact of longitudinal changes in late-life depressive symptoms on mortality, and of their remission in particular.MethodAs part of a prospective, population-based study on a random sample of 5632 subjects aged 65–84 years, with a 10-year follow-up of vital status, depressive symptoms were assessed by the 30-item Italian version of the Geriatric Depression Scale (GDS). The number of participants in the GDS measurements was 3214 at baseline and 2070 at the second survey, 3 years later. Longitudinal changes in depressive symptoms (stable, remitted, worsened) were examined in participants in both evaluations (n=1941). Mortality hazard ratios (MHRs) according to severity of symptoms and their changes over time were obtained by means of Cox proportional hazards regression models, adjusting for age and other potentially confounding factors.ResultsSeverity is significantly associated with excess mortality in both genders. Compared to the stability of depressive symptoms, a worsened condition shows a higher 7-year mortality risk [MHR 1.46, 95% confidence interval (CI) 1.15–1.84], whereas remission reduces by about 40% the risk of mortality in both genders (women MHR 0.55, 95% CI 0.32–0.95; men MHR 0.59, 95% CI 0.37–0.93). Neither sociodemographic nor medical confounders significantly modified these associations.ConclusionsConsistent with previous reports, the severity and persistence of depression are associated with higher mortality risks. Our findings extend the magnitude of the association demonstrating that remission of symptoms is related to a significant reduction in mortality, highlighting the need to enhance case-finding and successful treatment of late-life depression.


2021 ◽  
pp. 089198872098891
Author(s):  
Regina Eun Young Kim ◽  
Robert Douglas Abbott ◽  
Soriul Kim ◽  
Robert Joseph Thomas ◽  
Chang-Ho Yun ◽  
...  

This study aimed to evaluate the effect of sleep duration on brain structures in the presence versus absence of sleep apnea in middle-aged and older individuals. The study investigated a population-based sample of 2,560 individuals, aged 49-80 years. The presence of sleep apnea and self-reported sleep duration were examined in relation to gray matter volume (GMV) in total and lobar brain regions. We identified ranges of sleep duration associated with maximal GMV using quadratic regression and bootstrap sampling. A significant quadratic association between sleep duration and GMV was observed in total and lobar brain regions of men with sleep apnea. In the fully adjusted model, optimal sleep durations associated with peak GMV between brain regions ranged from 6.7 to 7.0 hours. Shorter and longer sleep durations were associated with lower GMV in total and 4 sub-regions of the brain in men with sleep apnea.


2017 ◽  
Vol 47 (5) ◽  
pp. 497-503 ◽  
Author(s):  
Anette Fischer Pedersen ◽  
Peter Vedsted

Aims: Negative cancer beliefs have been associated with late stage at cancer diagnosis. High levels of negative cancer beliefs have been found among individuals with low socioeconomic position and ethnic minority women, but the impact of cancer experience on cancer beliefs is unexamined. The aim of this study was to examine whether cancer beliefs are associated with cancer experience. Methods: This was a cross-sectional population-based study. Telephone interviews of 2992 Danish residents (30+) were carried out using the Awareness and Beliefs about Cancer Measure (ABC). Respondents reported whether they or someone close had been diagnosed with cancer and whether they agreed/disagreed with three positively and three negatively framed cancer beliefs. Results: Respondents with someone close diagnosed was reference group. Compared with these, respondents with no cancer experience (RRadj=0.91, 95% CI=0.84–0.98) or who had had cancer themselves (RRadj=0.87, 0.77–0.98) were less likely to believe that cancer treatment is worse than the cancer itself, and respondents with no cancer experience were less likely to believe that a diagnosis of cancer is a death sentence (RRadj=0.83, 0.70–0.98), but more likely to report that they did not want to know if they had cancer (RRadj=1.31, 1.01–1.71). Conclusions: The results suggest that cancer beliefs are sensitive to cancer experience. This is an important addition to previous results focusing on the association between cancer beliefs and static factors such as socioeconomic position and ethnicity. Since cancer beliefs may determine health-related behaviour, it is important that negative cancer beliefs are addressed and possibly reframed in population-based interventions.


2020 ◽  
Vol 22 (2) ◽  
pp. 113-126

This review summarizes studies on the neurobiological correlates of internet gaming disorder (IGD), presently the most direct approach to analyzing the impact of digital technology and the internet on brain mechanisms. Brain imaging studies have shown that IGD shares, to a large extent, neurobiological alterations that are typical for other addictions, such as: (i) activation in brain regions associated with reward, as evident from cue exposure and craving studies and neurotransmitter systems studies that indicate an involvement of dopamine-mediated reward mechanisms; (ii) reduced activity in impulse control areas and impaired decision making; and (iii) reduced functional connectivity in brain networks that are involved in cognitive control, executive function, motivation, and reward. Moreover, there are structural changes, mainly reduction in gray-matter volume and white-matter density. Comorbidity studies indicate that executive control networks in attention deficit-hyperactivity disorder (ADHD) may increase the susceptibility to develop IGD. Most importantly, this review also outlines findings that show the effects of excessive use of screens, here referring to the playing of computer games, which activate many brain regions associated with cognitive, motor, and sensory function and not directly involved in other forms of addiction. This review describes and summarizes comprehensively the neurobiological correlates of addictive internet use in adolescents and young adults.


Author(s):  
Priya Palta ◽  
Michael Griswold ◽  
Radhikesh Ranadive ◽  
Karen Bandeen-Roche ◽  
Aaron R Folsom ◽  
...  

Abstract Background We examined the relationship of midlife cardiovascular health (CVH) with late-life robustness among men and women and the impact of survivorship bias on sex-differences in robustness. Methods Prospective analysis of 15,744 participants aged 45-64 (Visit 1 median age: 54 years, 55% female, 27% Black) in 1987-1989 from the population-based ARIC Study. CVH was operationalized according to the Life’s Simple 7 (LS7) metric of health behaviors (smoking, weight, physical activity, diet, cholesterol, blood pressure, and glucose); each behavior was scored as ideal (2 points), intermediate (1 point), or poor (0 points) and summed. Late-life robust/pre-frail/frailty was defined at Visit 5 (2011-2013). Multinomial regression estimated relative prevalence ratios (RPR) of late-life robustness/pre-frailty/frailty/death across overall midlife LS7 score and components, for the full Visit 1 sample. Separate analyses considered Visit 5 survivors only. Results For each one-unit greater midlife LS7 score, participants had a 37% higher relative prevalence of being robust versus frail (overall RPR=1.37, [95% CI: 1.30-1.44]; women=1.45 [1.36-1.54]; men=1.24 [1.13-1.36]). Among the full Visit 1 sample, women had a similar one-level higher robustness category prevalence (RPR=1.35 [95% CI: 1.32-1.39]) than men (RPR=1.31 [95% CI: 1.27-1.35]) for every one-unit higher midlife LS7 score. Among survivors, men were more likely to be robust than women at lower LS7 levels; differences were attenuated and not statistically different at higher midlife LS7 levels. Conclusions Midlife CVH is positively associated with robustness in late-life among men and women. Accounting for mortality in part explains documented sex-differences in robustness across all levels of LS7.


2015 ◽  
Vol 45 (6) ◽  
pp. 1557-1565 ◽  
Author(s):  
Grégory Moullec ◽  
J. Mark FitzGerald ◽  
Roxanne Rousseau ◽  
Wenjia Chen ◽  
Mohsen Sadatsafavi ◽  
...  

Little is known about the potential synergistic effect of comorbid psychological distress (PD) and uncontrolled asthma (UA) on productivity loss. We estimated the productivity loss associated with the combination of these two potentially preventable conditions in employed adults with asthma.A population-based random sample of 300 adults with asthma in British Columbia, Canada, was prospectively recruited between Dec 2010 and Aug 2012. PD and productivity loss due to absenteeism and presenteeism was measured using validated instruments, and asthma control was ascertained using 2010 Global Initiative for Asthma management strategy. We used two-part regression models to study the contribution of UA and PD to productivity loss.Compared with reference group (controlled asthma (CA)+noPD), those with UA+noPD had CAD$286 (95%CI $276–297) weekly productivity loss, and those with CA+PD had CAD$465 ($445–485). Those with UA+PD had CAD$449 (437–462) in productivity loss. There was no significant interaction effect of PD with asthma control levels on productivity loss (p=0.22).In patients without PD, uncontrolled asthma was associated with a higher productivity loss than controlled asthma, but this was not the case in patients with PD. This finding can be explained by the fact that the contribution of PD to productivity loss is so large that there is no room for synergy with asthma control. Future studies should assess the impact of interventions that modify PD in patients with asthma.


2022 ◽  
Author(s):  
Michael N Weedon ◽  
Samuel E Jones ◽  
Jacqueline Lane ◽  
Jiwon Lee ◽  
Hanna M Ollila ◽  
...  

Rare variants in ten genes have been reported to cause Mendelian sleep conditions characterised by extreme sleep duration or timing. These include familial natural short sleep (ADRB1, DEC2/BHLHE41, GRM1 and NPSR1), advanced sleep phase (PER2, PER3, CRY2, CSNK1D and TIMELESS) and delayed sleep phase (CRY1). The association of variants of these genes with extreme sleep conditions were usually based on clinically ascertained families, and their effects when identified in the population are unknown. We aimed to determine the effects of these variants on sleep traits in large population-based cohorts. We performed genetic association analysis of variants previously reported to be causal for Mendelian sleep and circadian conditions. Analyses were performed using 191,929 individuals with data on sleep and whole-exome or genome-sequence data from 4 population-based studies: UK Biobank, FINRISK, Health-2000-2001, and the Multi-Ethnic Study of Atherosclerosis (MESA). We identified sleep disorders from self-report, hospital and primary care data. We estimated sleep duration and timing measures from self-report and accelerometery data. We identified carriers for 10 out of 12 previously reported pathogenic variants for 8 of the 10 genes. They ranged in frequency from 1 individual with the variant in CSNK1D to 1,574 individuals with a reported variant in the PER3 gene in the UK Biobank. We found no association of any of these variants with extreme sleep or circadian phenotypes. Using sleep timing as a proxy measure for sleep phase, only PER3 and CRY1 variants demonstrated association with earlier and later sleep timing, respectively; however, the magnitude of effect was smaller than previously reported (sleep midpoint ~7 mins earlier and ~5 mins later, respectively). We also performed burden tests of protein truncating (PTVs) or rare missense variants for the 10 genes. Only PTVs in PER2 and PER3 were associated with a relevant trait (for example, 64 individuals with a PTV in PER2 had an odds ratio of 4.4 for being "definitely a morning person", P=4x10-8; and had a 57-minute earlier midpoint sleep, P=5x10-7). Our results indicate that previously reported variants for Mendelian sleep and circadian conditions are often not highly penetrant when ascertained incidentally from the general population.


2019 ◽  
Vol 8 (5) ◽  
pp. 685 ◽  
Author(s):  
Chiara La Rosa ◽  
Marco Ghibaudi ◽  
Luca Bonfanti

Brain plasticity is important for translational purposes since most neurological disorders and brain aging problems remain substantially incurable. In the mammalian nervous system, neurons are mostly not renewed throughout life and cannot be replaced. In humans, the increasing life expectancy explains the increase in brain health problems, also producing heavy social and economic burden. An exception to the “static” brain is represented by stem cell niches leading to the production of new neurons. Such adult neurogenesis is dramatically reduced from fish to mammals, and in large-brained mammals with respect to rodents. Some examples of neurogenesis occurring outside the neurogenic niches have been reported, yet these new neurons actually do not integrate in the mature nervous tissue. Non-newly generated, “immature” neurons (nng-INs) are also present: Prenatally generated cells continuing to express molecules of immaturity (mostly shared with the newly born neurons). Of interest, nng-INs seem to show an inverse phylogenetic trend across mammals, being abundant in higher-order brain regions not served by neurogenesis and providing structural plasticity in rather stable areas. Both newly generated and nng-INs represent a potential reservoir of young cells (a “brain reserve”) that might be exploited for preventing the damage of aging and/or delay the onset/reduce the impact of neurological disorders.


Author(s):  
David Bergman ◽  
Hamed Khalili ◽  
Bjorn Roelstraete ◽  
Jonas F Ludvigsson

Abstract Background and Aims The association between microscopic colitis [MC] and cancer risk is unclear. Large, population-based studies are lacking. Methods We conducted a nationwide cohort study of 11 758 patients with incident MC [diagnosed 1990–2016 in Sweden], 50 828 matched reference individuals, and 11 614 siblings to MC patients. Data were obtained through Sweden´s pathology departments and from the Swedish Cancer Register. Adjusted hazard ratios [aHRs] were calculated using Cox proportional hazards models. Results At the end of follow-up [mean: 6.7 years], 1239 [10.5%] of MC patients had received a cancer diagnosis, compared with 4815 [9.5%] of reference individuals (aHR 1.08 [95% confidence interval1.02–1.16]). The risk of cancer was highest during the first year of follow up. The absolute excess risks for cancer at 5, 10, and 20 years after MC diagnosis were + 1.0% (95% confidence interval [CI] 0.4%-1.6%), +1.5% [0.4%-2.6%], and + 3.7% [-2.3–9.6%], respectively, equivalent to one extra cancer event in every 55 individuals with MC followed for 10 years. MC was associated with an increased risk of lymphoma (aHR 1.43 [1.06–1.92]) and lung cancer (aHR 1.32 [1.04–1.68]) but with decreased risks of colorectal (aHR 0.52 [0.40–0.66]) and gastrointestinal cancers (aHR 0.72 [0.60–0.85]). We found no association with breast or bladder cancer. Using siblings as reference group to minimise the impact of shared genetic and early environmental factors, patients with MC were still at an increased risk of cancer (HR 1.20 [1.06–1.36]). Conclusions This nationwide cohort study demonstrated an 8% increased risk of cancer in MC patients. The risk was highest during the first year of follow-up.


2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Shijia Li ◽  
Jie Song ◽  
Pengfei Ke ◽  
Lingyin Kong ◽  
Bingye Lei ◽  
...  

AbstractThe effect of the gut microbiome on the central nervous system and its possible role in mental disorders have received increasing attention. However, knowledge about the relationship between the gut microbiome and brain structure and function is still very limited. Here, we used 16S rRNA sequencing with structural magnetic resonance imaging (sMRI) and resting-state functional (rs-fMRI) to investigate differences in fecal microbiota between 38 patients with schizophrenia (SZ) and 38 demographically matched normal controls (NCs) and explored whether such differences were associated with brain structure and function. At the genus level, we found that the relative abundance of Ruminococcus and Roseburia was significantly lower, whereas the abundance of Veillonella was significantly higher in SZ patients than in NCs. Additionally, the analysis of MRI data revealed that several brain regions showed significantly lower gray matter volume (GMV) and regional homogeneity (ReHo) but significantly higher amplitude of low-frequency fluctuation in SZ patients than in NCs. Moreover, the alpha diversity of the gut microbiota showed a strong linear relationship with the values of both GMV and ReHo. In SZ patients, the ReHo indexes in the right STC (r = − 0.35, p = 0.031, FDR corrected p = 0.039), the left cuneus (r = − 0.33, p = 0.044, FDR corrected p = 0.053) and the right MTC (r = − 0.34, p = 0.03, FDR corrected p = 0.052) were negatively correlated with the abundance of the genus Roseburia. Our results suggest that the potential role of the gut microbiome in SZ is related to alterations in brain structure and function. This study provides insights into the underlying neuropathology of SZ.


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