Potential causal associations between leisure sedentary behaviors, physical activity, sleep traits, and myopia: a Mendelian randomization study
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SUBMITTER: Zhang X
PROVIDER: S-EPMC10913247 | biostudies-literature | 2024 Jan
REPOSITORIES: biostudies-literature
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Project description:BackgroundObservational studies have suggested that sedentary behaviors and sleep status are associated with frailty. However, it remains unclear whether these associations are causal.MethodsUsing summary statistics from genome-wide association studies, we evaluated the causal effect of modifiable risk factors, including leisure sedentary behaviors and sleep status on the frailty index (FI) using two-sample univariable and multivariable Mendelian randomization (MR) analyses. Genetic correlations were tested between the correlated traits.ResultsWe identified potential causal associations between the time spent watching television (β = 0.26, 95% confidence interval [CI]: 0.21-0.31, P = 3.98e-25), sleep duration (β = -0.18, 95%CI: -0.26, -0.10; P = 6.04e-06), and daytime napping (β = 0.29, 95%CI: 0.18-0.41, P = 2.68e-07) and the FI based on the inverse-variance-weighted method. The estimates were consistent across robust and multivariate MR analyses. Linkage disequilibrium score regression detected a genetic correlation between the time spent watching television (Rg = 0.43, P = 6.46e-48), sleep duration (Rg = -0.20, P = 5.29e-10), and daytime napping (Rg = 0.25, P = 3.34e-21) and the FI.ConclusionsGenetic predispositions to time spent watching television and daytime napping were positively associated with the FI, while sleep duration was negatively associated with the FI. Our findings offer key insights into factors influencing biological aging and suggest areas for interventions to promote healthy aging and slow down the aging process.
| S-EPMC10874533 | biostudies-literature
Project description:Previous observational studies have observed a correlation between sedentary behavior and osteoporosis. However, conclusions from these studies have been contradictory. To explore the potential causal relationship between sedentary behavior and osteoporosis, we conducted a Mendelian randomization analysis. A two-sample Mendelian randomization was adopted to explore the causal relationship of leisure sedentary behavior with osteoporosis. We employed 5 methods to estimate the causal associations between leisure sedentary behavior and osteoporosis. Univariable Mendelian randomization results provided evidence for the causal relationship of the time spent on computer-use with the bone mineral density estimated by heel quantitative ultrasound (eBMD) (inverse variance weighted [IVW]: β (95% confidence interval [CI]) - 0.150 (-0.270 to -0.031), P = .013; weighted median: β (95%CI) - 0.195 (-0.336 to -0.055), P = .006). Similar associations were observed in the driving forearm bone mineral density (FABMD) (IVW: β (95%CI) - 0.933 (-1.860 to -0.007), P = .048) and driving lumbar spine bone mineral density (IVW: β (95%CI) - 0.649 (-1.175 to -0.124), P = .015). However, we did not find a significant causal relationship between the time spent on watching TV and bone mineral density. Research showed that there was a causal relationship between the time spent on computer use and driving time and eBMD, FABMD, and lumbar spine bone mineral density.
| S-EPMC10956994 | biostudies-literature
Project description:BackgroundThe 2019 coronavirus disease pandemic (COVID-19) poses an enormous threat to public health worldwide, and the ensuing management of social isolation has greatly decreased opportunities for physical activity (PA) and increased opportunities for leisure sedentary behaviors (LSB). Given that both PA and LSB have been established as major influencing factors for obesity, diabetes and cardiometabolic syndrome, whether PA/LSB in turn affects the susceptibility to COVID-19 by disrupting metabolic homeostasis remains to be explored. In this study, we aimed to systematically evaluate the causal relationship between PA/LSB and COVID-19 susceptibility, hospitalization and severity using a Mendelian randomization study.MethodsData were obtained from a large-scale PA dataset (N = 377,000), LSB dataset (N = 422,218) and COVID-19 Host Genetics Initiative (N = 2,586,691). The causal effects were estimated with inverse variance weighted, MR-Egger, weighted median and MR-PRESSO. Sensitivity analyses were implemented with Cochran's Q test, MR-Egger intercept test, MR-PRESSO, leave-one-out analysis and the funnel plot. Risk factor analyses were further conducted to investigate the potential mediators.ResultsGenetically predicted accelerometer-assessed PA decreased the risk for COVID-19 hospitalization (OR = 0.93, 95% CI 0.88-0.97; P = 0.002), while leisure television watching significantly increased the risk of COVID-19 hospitalization (OR = 1.55, 95% CI 1.29-1.88; P = 4.68 × 10-6) and disease severity (OR = 1.85, 95% CI 1.33-2.56; P = 0.0002) after Bonferroni correction. No causal effects of self-reported moderate to vigorous physical activity (MVPA), accelerometer fraction of accelerations > 425 milligravities, computer use or driving on COVID-19 progression were observed. Risk factor analyses indicated that the above causal associations might be mediated by several metabolic risk factors, including smoking, high body mass index, elevated serum triglyceride levels, insulin resistance and the occurrence of type 2 diabetes.ConclusionOur findings supported a causal effect of accelerometer-assessed PA on the reduced risk of COVID-19 hospitalization as well as television watching on the increased risk of COVID-19 hospitalization and severity, which was potentially mediated by smoking, obesity and type 2 diabetes-related phenotypes. Particular attention should be given to reducing leisure sedentary behaviors and encouraging proper exercise during isolation and quarantine for COVID-19.
| S-EPMC9100292 | biostudies-literature
Project description:BackgroundIncreasing evidence shows that leisure sedentary behaviors (LSB) and physical activity (PA) are associated with various musculoskeletal disorders. However, the causality between LSB/PA and musculoskeletal health remained unknown. In this study, we aimed to evaluate the causal relationships between LSB/PA and lower back pain (LBP), intervertebral disc disorder (IVDD), rheumatoid arthritis (RA), and bone mineral density (BMD) by using a two-sample Mendelian randomization method.MethodsThe exposure data were obtained from large-scale genome-wide association studies (GWAS), including the PA dataset (self-reported PA, n = 377,234; accelerometer-assessed PA, n = 91,084) and LSB dataset (n = 422,218). The outcome data were derived from the FinnGen LBP dataset (n = 248,528), FinnGen IVDD dataset (n = 256,896), BMD GWAS dataset (n = 56,284), and RA GWAS dataset (n = 58,284). The causal relationships were estimated with inverse variance weighted (IVW), MR-Egger, and weighted median methods. Sensitivity analyses were performed with Cochran's Q test, MR-Egger intercept test, and leave-one-out analysis to estimate the robustness of our findings.ResultsGenetically predicted leisure television watching increased the risk of LBP (OR = 1.68, 95% CI 1.41 to 2.01; P = 8.23×10-9) and IVDD (OR = 1.62, 95% CI 1.37 to 1.91; P = 2.13 × 10-8). In addition, this study revealed a potential causal relationship between computer use and a reduced risk of IVDD (OR = 0.60, 95% CI 0.42 to 0.86; P = 0.005) and RA (OR = 0.28, 95% CI 0.13 to 0.60; P = 0.001).ConclusionsOur results suggest that leisure television watching is a risk factor for LBP and IVDD, whereas leisure computer use may act as a protective factor against IVDD and RA. These findings emphasized the importance of distinguishing between different sedentary behaviors in musculoskeletal disease studies.
| S-EPMC10019723 | biostudies-literature
Project description: Not available
| S-EPMC11224541 | biostudies-literature
Project description:AimsPrevious studies investigated the associations between sleep traits and cardiac diseases, but the evidence for the causal inferences was unclear. This study aimed to explore the causal relationship between sleep and cardiac diseases by virtue of Mendelian randomization (MR).Methods and resultsSummary-level data for exposure variables (sleep duration, chronotype, and insomnia) and outcome variables (ischaemic heart disease, atrial fibrillation, myocardial infarction, and heart failure) were derived from UK Biobank. Data from the FinnGen consortium was used as a robustness check. In MR analysis, the inverse variance weighted (IVW) method was applied to infer causality between exposure and outcome. MR-Egger regression was used to identify pleiotropy, and MR-PRESSO outlier test was used to remove the pleiotropy of the genetic instruments. Based on UK Biobank, MR analysis suggested that sleep duration was weakly associated with atrial fibrillation (OR = 0.9999, 95% CI: 0.9998-0.9999) and ischaemic heart disease (OR = 0.9997, 95% CI: 0.9995-0.9998). Insomnia was associated with ischaemic heart disease (OR = 1.0117, 95% CI: 1.0051-1.0183) and myocardial infarction (OR = 1.0049, 95% CI: 1.0019-1.0079). No associations were found between chronotype and cardiac diseases (P > 0.05). We did not find pleiotropy except for insomnia with ischaemic heart disease and myocardial infarction using MR-Egger regression, and MR-PRESSO analysis consistent with IVW. Finally, we obtained the same direction as with UK Biobank using the FinnGen data.ConclusionsSleep duration and insomnia might be the potential causal risk factors of cardiac diseases. As the OR was small, these associations are probably not clinically relevant. Further validation studies are needed.
| S-EPMC9715768 | biostudies-literature
Project description:BackgroundEmerging evidence suggests bidirectional causal relationships between sleep disturbance and psychiatric disorders, but the underlying mechanisms remain unclear. Understanding the bidirectional causality between sleep traits and brain imaging-derived phenotypes (IDPs) will help elucidate the mechanisms. Although previous studies have identified a range of structural differences in the brains of individuals with sleep disorders, it is still uncertain whether grey matter (GM) volume alterations precede or rather follow from the development of sleep disorders.ResultsAfter Bonferroni correction, the forward MR analysis showed that insomnia complaint remained positively associated with the surface area (SA) of medial orbitofrontal cortex (β, 0.26; 95% CI, 0.15-0.37; P = 5.27 × 10-6). In the inverse MR analysis, higher global cortical SA predisposed individuals less prone to suffering insomnia complaint (OR, 0.89; 95%CI, 0.85-0.94; P = 1.51 × 10-5) and short sleep (≤ 6 h; OR, 0.98; 95%CI, 0.97-0.99; P = 1.51 × 10-5), while higher SA in posterior cingulate cortex resulted in a vulnerability to shorter sleep durations (β, - 0.09; 95%CI, - 0.13 to - 0.05; P = 1.21 × 10-5).ConclusionsSleep habits not only result from but also contribute to alterations in brain structure, which may shed light on the possible mechanisms linking sleep behaviours with neuropsychiatric disorders, and offer new strategies for prevention and intervention in psychiatric disorders and sleep disturbance.
| S-EPMC10544625 | biostudies-literature
Project description:ObjectivesThis study aims to investigate the relationship between five sleep traits (insomnia, sleep duration, getting up in morning, snoring, and daytime nap) and temporomandibular disorders (TMD) using bi-directional Mendelian randomization.MethodsThe bi-directional Mendelian randomization study was conducted in two stages. Initially, sleep traits were examined as exposures while TMD was evaluated as an outcome, whereas the second step was reversed. The inverse variance weighted (IVW) method and other Mendelian randomization methods were used for analysis. Furthermore, we performed the MR-Egger intercept, MR-PRESSO, Cochran's Q test, and "Leave-one-out" to assess the levels of pleiotropy and heterogeneity.ResultsThe IVW method indicates that getting up in the morning reduces the risk of developing TMD (OR = 0.50, 95% CI 0.30-0.81, p = 0.005), while insomnia may increase the risk of TMD (OR = 2.05, 95% CI 1.10-3.85, p = 0.025). However, other sleep traits are not associated with the risk of TMD, and having TMD does not alter an individual's sleep traits. After removing outliers, the results remained robust, with no pleiotropy detected.ConclusionGenetically determined difficulty in getting up in the morning and insomnia can increase the risk of TMD. By optimizing sleep, the risk of developing TMD can be reduced. This underscores the importance of sleep in preventing TMD.
| S-EPMC11303139 | biostudies-literature
Project description:BackgroundEvidence for a causal relationship between sarcopenia and obstructive sleep apnea (OSA) is scarce. This study aimed to investigate the causal association between sarcopenia-related traits and OSA utilizing Mendelian randomization (MR) analyses.MethodsMR analyses were conducted using genetic instruments for sarcopenia-related traits, including hand grip strength, muscle mass, fat mass, water mass, and physical performance. Data from large-scale genome-wide association studies (GWAS) were utilized to identify genetic variants associated with these traits. Causal associations with OSA were assessed using various MR methods, including the inverse variance-weighted (IVW) method, MR-Egger, and weighted median approaches. Pleiotropy and heterogeneity were evaluated through MR-PRESSO and other sensitivity analyses.ResultsLow hand grip strength in individuals aged 60 years and older exhibited a positive correlation with the risk of OSA (IVW, OR = 1.190, 95% CI = 1.003-1.413, p = 0.047), while no significant causal effects were observed for grip strength in the left and right hands. Muscle mass, fat mass, and water mass were significantly associated with OSA, even after adjusting for multiple testing. Notably, higher levels of body fat percentage, trunk fat percentage, and limb fat percentage were strongly correlated with increased risk of OSA. Physical performance indicators such as walking pace demonstrated an inverse association with OSA, while a higher risk of OSA was observed with increased log odds of falling risk and greater frequency of falls in the last year. Additionally, a causal effect was found between long-standing illness, disability, or infirmity and OSA.ConclusionsThis comprehensive MR analysis provides evidence of a significant causal relationship between characteristics associated with sarcopenia, including low hand grip strength, muscle mass, fat mass, and physical performance, and the risk of OSA. These findings underscore the importance of addressing sarcopenia-related factors in the management and prevention of OSA.
| S-EPMC11889072 | biostudies-literature
Project description:PurposeTo investigate the genetic correlation and causal links between sleep traits (including sleep duration, chronotype, and insomnia) and myopia.MethodsSummary data on three sleep traits (sleep duration, chronotype and insomnia) and myopia from FinnGen (n = 214,211) and UK Biobank (n = 460,536) were analyzed using linkage disequilibrium score regression (LD Score), univariable and multivariable mendelian randomization (MR) experiments and Causal Analysis Using Summary Effect (CAUSE) estimation.ResultsLD Score regression detected candidate genetic correlation between sleep traits and myopia, such as sleep duration, chronotype (Genetic Correlation Z-score >10.00, h2_observed_p < 0.005, Lambda GC > 1.05, p > 0.05). Univariable MR analyses indicated that increased sleep duration has a promotional effect on the occurrence of myopia (p = 0.046 < 0.05, P_FDR = 0.138 < 0.2, OR = 2.872, 95% CI: 1.018-8.101). However, after accounting for potential confounding factors, multivariable MR and CAUSE analysis did not provide evidence for a causal effect of the three sleep traits on myopia.ConclusionThere may be a potential genetic correlation between sleep duration, chronotype and myopia. However, neither of sleep duration, chronotype or insomnia had causal effect on myopia.
| S-EPMC11263174 | biostudies-literature