scholarly journals Associations Between Measures of Sarcopenic Obesity and Risk of Cardiovascular Disease and Mortality: A Cohort Study and Mendelian Randomization Analysis Using the UK Biobank

Author(s):  
Ruth E. Farmer ◽  
Rohini Mathur ◽  
A. Floriaan Schmidt ◽  
Krishnan Bhaskaran ◽  
Ghazaleh Fatemifar ◽  
...  
Author(s):  
Muktar Ahmed ◽  
Anwar Mulugeta ◽  
S. Hong Lee ◽  
Ville-Petteri Mäkinen ◽  
Terry Boyle ◽  
...  

2021 ◽  
Author(s):  
Jie Chen ◽  
Xuejie Chen ◽  
Ying Xie ◽  
Yuhao Sun ◽  
Xiaoyan Wang ◽  
...  

Abstract Background: IBS and Migraine are two diseases featuring high prevalence. Previous studies have suggested a relationship between Irritable Bowel Syndrome (IBS) and migraine, although the causal association remains unclear. We sought to explore the causal association between IBS and migraine, and to prove the importance of migraine prevention in IBS patients.Methods: This study used a two-sample Mendelian-randomization analysis to explore the association of IBS with migraine. Genetic association with migraine were acquired from the UK Biobank (UKB) genetic databases (cases: 1,072; controls: 360,122). We performed estimation using Inverse Variance Weighting (IVW), along with Maximum Likelihood, MR-RAPS, MR-Egger and Weighted Median for sensitivity analysis. Considering possible bias, we also conducted polymorphism, heterogeneity, and directional analysis.Results: The IVW estimation genetically predicted the causal association between IBS and migraine (OR=1.09, 95%CI 1.01 to 1.17, p=0.03). Neither statistical horizontal pleiotropy (MR Egger p=0.42; MR-PRESSO p=0.78) nor possible heterogeneity (IVW Q = 26.15, p=0.80) was found. Reverse causation was also not detected (p steiger<0.01).Conclusion: Mendelian randomization analysis supported a positive-going causal association of IBS with migraine, providing enlightenment for disease prevention and control.


Nutrients ◽  
2021 ◽  
Vol 13 (7) ◽  
pp. 2218
Author(s):  
Shuai Yuan ◽  
Paul Carter ◽  
Amy M. Mason ◽  
Stephen Burgess ◽  
Susanna C. Larsson

Coffee consumption has been linked to a lower risk of cardiovascular disease in observational studies, but whether the associations are causal is not known. We conducted a Mendelian randomization investigation to assess the potential causal role of coffee consumption in cardiovascular disease. Twelve independent genetic variants were used to proxy coffee consumption. Summary-level data for the relations between the 12 genetic variants and cardiovascular diseases were taken from the UK Biobank with up to 35,979 cases and the FinnGen consortium with up to 17,325 cases. Genetic predisposition to higher coffee consumption was not associated with any of the 15 studied cardiovascular outcomes in univariable MR analysis. The odds ratio per 50% increase in genetically predicted coffee consumption ranged from 0.97 (95% confidence interval (CI), 0.63, 1.50) for intracerebral hemorrhage to 1.26 (95% CI, 1.00, 1.58) for deep vein thrombosis in the UK Biobank and from 0.86 (95% CI, 0.50, 1.49) for subarachnoid hemorrhage to 1.34 (95% CI, 0.81, 2.22) for intracerebral hemorrhage in FinnGen. The null findings remained in multivariable Mendelian randomization analyses adjusted for genetically predicted body mass index and smoking initiation, except for a suggestive positive association for intracerebral hemorrhage (odds ratio 1.91; 95% CI, 1.03, 3.54) in FinnGen. This Mendelian randomization study showed limited evidence that coffee consumption affects the risk of developing cardiovascular disease, suggesting that previous observational studies may have been confounded.


Nutrients ◽  
2021 ◽  
Vol 13 (12) ◽  
pp. 4283
Author(s):  
Katherine M. Livingstone ◽  
Gavin Abbott ◽  
Joey Ward ◽  
Steven J. Bowe

To examine associations of unhealthy lifestyle and genetics with risk of all-cause mortality, cardiovascular disease (CVD) mortality, myocardial infarction (MI) and stroke. We used data on 76,958 adults from the UK Biobank prospective cohort study. Favourable lifestyle included no overweight/obesity, not smoking, physical activity, not sedentary, healthy diet and adequate sleep. A Polygenic Risk Score (PRS) was derived using 300 CVD-related single nucleotide polymorphisms. Cox proportional hazard ratios (HR) were used to model effects of lifestyle and PRS on risk of CVD and all-cause mortality, stroke and MI. New CVD (n = 364) and all-cause (n = 2408) deaths, and stroke (n = 748) and MI (n = 1140) events were observed during a 7.8 year mean follow-up. An unfavourable lifestyle (0–1 healthy behaviours) was associated with higher risk of all-cause mortality (HR: 2.06; 95% CI: 1.73, 2.45), CVD mortality (HR: 2.48; 95% CI: 1.64, 3.76), MI (HR: 2.12; 95% CI: 1.65, 2.72) and stroke (HR:1.74; 95% CI: 1.25, 2.43) compared to a favourable lifestyle (≥4 healthy behaviours). PRS was associated with MI (HR: 1.35; 95% CI: 1.27, 1.43). There was evidence of a lifestyle-genetics interaction for stroke (p = 0.017). Unfavourable lifestyle behaviours predicted higher risk of all-cause mortality, CVD mortality, MI and stroke, independent of genetic risk.


2022 ◽  
Vol 97 (1) ◽  
pp. 110-121
Author(s):  
Irene Rodríguez-Gómez ◽  
Stuart R. Gray ◽  
Frederick K. Ho ◽  
Fanny Petermann-Rocha ◽  
Paul Welsh ◽  
...  

SLEEP ◽  
2022 ◽  
Author(s):  
Zheran Liu ◽  
Yaxin Luo ◽  
Yonglin Su ◽  
Zhigong Wei ◽  
Ruidan Li ◽  
...  

Abstract Study Objectives Sleep and circadian phenotypes are associated with several diseases. The present study aimed to investigate whether sleep and circadian phenotypes were causally linked with coronavirus disease 2019 (COVID-19)-related outcomes. Methods Habitual sleep duration, insomnia, excessive daytime sleepiness, daytime napping, and chronotype were selected as exposures. Key outcomes included positivity and hospitalization for COVID-19. In the observation cohort study, multivariable risk ratios (RRs) and their 95% confidence intervals (CIs) were calculated. Two-sample Mendelian randomization (MR) analyses were conducted to estimate the causal effects of the significant findings in the observation analyses. Beta values and the corresponding 95% CIs were calculated and compared using the inverse variance weighting, weighted median, and MR-Egger methods. Results In the UK Biobank cohort study, both often excessive daytime sleepiness and sometimes daytime napping were associated with hospitalized COVID-19 (excessive daytime sleepiness [often vs. never]: RR=1.24, 95% CI=1.02-1.5; daytime napping [sometimes vs. never]: RR=1.12, 95% CI=1.02-1.22). In addition, sometimes daytime napping was also associated with an increased risk of COVID-19 susceptibility (sometimes vs. never: RR= 1.04, 95% CI=1.01-1.28). In the MR analyses, excessive daytime sleepiness was found to increase the risk of hospitalized COVID-19 (MR IVW method: OR = 4.53, 95% CI = 1.04-19.82), whereas little evidence supported a causal link between daytime napping and COVID-19 outcomes. Conclusions Observational and genetic evidence supports a potential causal link between excessive daytime sleepiness and an increased risk of COVID-19 hospitalization, suggesting that interventions targeting excessive daytime sleepiness symptoms might decrease severe COVID-19 rate.


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