GWAS-Based Multivariate Mendelian Randomization Analysis of Causal Effects of Lipoproteins on Coronary Artery Disease

2018 ◽  
Author(s):  
Yuande Tan
Keyword(s):  
Coronary Artery Disease ◽  
Coronary Artery ◽  
Mendelian Randomization ◽  
Causal Effects ◽  
Mendelian Randomization Analysis ◽  
Artery Disease ◽  
Randomization Analysis

scholarly journals Mendelian randomization analysis to characterize causal association between coronary artery disease and COVID-19

2020 ◽  
Author(s):  
Lang Wu ◽  
Jingjing Zhu ◽  
Chong Wu
Keyword(s):  
Coronary Artery Disease ◽  
Coronary Artery ◽  
Observational Studies ◽  
Mendelian Randomization ◽  
Causal Association ◽  
Mendelian Randomization Analysis ◽  
Log Odds ◽  
Individual Decisions ◽  
Artery Disease ◽  
Randomization Analysis

AbstractObservational studies have suggested that having coronary artery disease increases the risk of Coronavirus disease 2019 (COVID-19) susceptibility and severity, but it remains unclear if this association is causal. Inferring causation is critical to facilitate the development of appropriate policies and/or individual decisions to reduce the incidence and burden of COVID-19. We applied Two-sample Mendelian randomization analysis and found that genetically predicted CAD was significantly associated with higher risk of COVID-19: the odds ratio was 1.29 (95% confidence interval 1.11 to 1.49; P = 0.001) per unit higher log odds of having CAD.

scholarly journals Mendelian Randomization Analysis of Hemoglobin A1cas a Risk Factor for Coronary Artery Disease

Diabetes Care ◽  
2019 ◽  
Vol 42 (7) ◽  
pp. 1202-1208 ◽  
Author(s):  
Aaron Leong ◽  
Ji Chen ◽  
Eleanor Wheeler ◽  
Marie-France Hivert ◽  
Ching-Ti Liu ◽  
...  
Keyword(s):  
Coronary Artery Disease ◽  
Risk Factor ◽  
Coronary Artery ◽  
Mendelian Randomization ◽  
Mendelian Randomization Analysis ◽  
Artery Disease ◽  
Randomization Analysis

scholarly journals Mendelian randomization analysis supports the causal role of dysglycaemia and diabetes in the risk of coronary artery disease

2015 ◽  
Vol 36 (23) ◽  
pp. 1454-1462 ◽  
Author(s):  
Stephanie Ross ◽  
Hertzel C. Gerstein ◽  
John Eikelboom ◽  
Sonia S. Anand ◽  
Salim Yusuf ◽  
...  
Keyword(s):  
Coronary Artery Disease ◽  
Coronary Artery ◽  
Mendelian Randomization ◽  
Causal Role ◽  
Mendelian Randomization Analysis ◽  
Artery Disease ◽  
Randomization Analysis

scholarly journals Genetically Predicted Type 2 Diabetes Mellitus Liability, Glycated Hemoglobin and Cardiovascular Diseases: A Wide-Angled Mendelian Randomization Study

Genes ◽  
2021 ◽  
Vol 12 (10) ◽  
pp. 1644
Author(s):  
Bowen Liu ◽  
Amy M. Mason ◽  
Luanluan Sun ◽  
Emanuele Di Angelantonio ◽  
Dipender Gill ◽  
...  
Keyword(s):  
Cardiovascular Disease ◽  
Coronary Artery Disease ◽  
Coronary Artery ◽  
Cardiovascular Diseases ◽  
General Population ◽  
Mendelian Randomization ◽  
Causal Effects ◽  
Disease Outcomes ◽  
Artery Disease ◽  
Diagnosed Diabetes

(1) Aim: To investigate the causal effects of T2DM liability and glycated haemoglobin (HbA1c) levels on various cardiovascular disease outcomes, both in the general population and in non-diabetic individuals specifically. (2) Methods: We selected 243 variants as genetic instruments for T2DM liability and 536 variants for HbA1c. Linear Mendelian randomization analyses were performed to estimate the associations of genetically-predicted T2DM liability and HbA1c with 12 cardiovascular disease outcomes in 367,703 unrelated UK Biobank participants of European ancestries. We performed secondary analyses in participants without diabetes (HbA1c < 6.5% with no diagnosed diabetes), and in participants without diabetes or pre-diabetes (HbA1c < 5.7% with no diagnosed diabetes). (3) Results: Genetically-predicted T2DM liability was positively associated (p < 0.004, 0.05/12) with peripheral vascular disease, aortic valve stenosis, coronary artery disease, heart failure, ischaemic stroke, and any stroke. Genetically-predicted HbA1c was positively associated with coronary artery disease and any stroke. Mendelian randomization estimates generally shifted towards the null when excluding diabetic and pre-diabetic participants from analyses. (4) Conclusions: This genetic evidence supports causal effects of T2DM liability and HbA1c on a range of cardiovascular diseases, suggesting that improving glycaemic control could reduce cardiovascular risk in a general population, with greatest benefit in individuals with diabetes.

scholarly journals Causal effects of serum levels of n-3 or n-6 polyunsaturated fatty acids on coronary artery disease: Mendelian randomization study

2020 ◽  
Author(s):  
Sehoon Park ◽  
Soojin Lee ◽  
Yaerim Kim ◽  
Yeonhee Lee ◽  
Min Woo Kang ◽  
...  
Keyword(s):  
Coronary Artery Disease ◽  
Fatty Acids ◽  
Linoleic Acid ◽  
Coronary Artery ◽  
Polyunsaturated Fatty Acids ◽  
Lower Risk ◽  
Mendelian Randomization ◽  
Causal Effects ◽  
Weighted Median ◽  
Artery Disease

AbstractBackgroundAdditional studies on the causal effects of 3-n and 6-n polyunsaturated fatty acids (PUFAs) on the risk of coronary artery disease (CAD) are warranted.MethodsThis Mendelian randomization (MR) study utilized a genetic instrument developed from previous genome-wide association studies for various serum 3-n and 6-n PUFA levels. First, we calculated the allele scores for genetic predisposition of PUFAs in individuals of European ancestry in the UK Biobank data (N=337,129). The allele score-based MR was obtained by regressing the allele scores to CAD risks. Second, summary-level MR was performed with the CARDIoGRAMplusC4D data for CAD (N=184,305). The inverse variance-weighted or Wald ratio method was the main analysis for the summary-level MR, and when multiple single nucleotide polymorphisms were utilized (e.g., linoleic acid), MR-Egger and weighted median methods were implemented as sensitivity analyses.ResultsHigher genetically predicted eicosapentaenoic acid and dihomo-gamma-linolenic acid levels were significantly associated with a lower risk of CAD both in the allele-score-based and summary-level MR analyses. Higher allele scores for linoleic acid level were significantly associated with lower CAD risks, and in the summary-level MR, the causal estimates by the MR-Egger and weighted median methods also indicated that higher linoleic acid levels cause a lower risk of CAD. Arachidonic acid was the 6-n PUFA that showed significant causal estimates for a higher risk of CAD. Higher docosapentaenoic acid and adrenic acid levels showed inconsistent findings in the MR analysis results.ConclusionsThis study supports the causal effects of certain 3-n and 6-n PUFA types on the risk of CAD.

scholarly journals Causal Effects of Serum Levels of n-3 or n-6 Polyunsaturated Fatty Acids on Coronary Artery Disease: Mendelian Randomization Study

Nutrients ◽  
2021 ◽  
Vol 13 (5) ◽  
pp. 1490
Author(s):  
Sehoon Park ◽  
Soojin Lee ◽  
Yaerim Kim ◽  
Yeonhee Lee ◽  
Min Woo Kang ◽  
...  
Keyword(s):  
Coronary Artery Disease ◽  
Fatty Acids ◽  
Linoleic Acid ◽  
Coronary Artery ◽  
Polyunsaturated Fatty Acids ◽  
Lower Risk ◽  
Mendelian Randomization ◽  
Causal Effects ◽  
European Ancestry ◽  
Artery Disease

We aimed to investigate the causal effects of n-3 and n-6 polyunsaturated fatty acids (PUFAs) on the risk of coronary artery disease (CAD) through Mendelian randomization (MR) analysis. This MR study utilized a genetic instrument developed from previous genome-wide association studies for various serum n-3 and n-6 PUFA levels. First, we calculated the allele scores for genetic predisposition of PUFAs in individuals of European ancestry in the UK Biobank data (N = 337,129). The allele score-based MR was obtained by regressing the allele scores to CAD risks. Second, summary-level MR was performed with the CARDIoGRAMplusC4D data for CAD (N = 184,305). Higher genetically predicted eicosapentaenoic acid and dihomo-gamma-linolenic acid levels were significantly associated with a lower risk of CAD both in the allele-score-based and summary-level MR analyses. Higher allele scores for linoleic acid level were significantly associated with lower CAD risks, and in the summary-level MR, the causal estimates by the pleiotropy-robust MR methods also indicated that higher linoleic acid levels cause a lower risk of CAD. Arachidonic acid showed significant causal estimates for a higher risk of CAD. This study supports the causal effects of certain n-3 and n-6 PUFA types on the risk of CAD.

scholarly journals Physical activity, sedentary behavior and risk of coronary artery disease, myocardial infarction and ischemic stroke: a two-sample Mendelian randomization study

2021 ◽  
Author(s):  
Martin Bahls ◽  
Michael F. Leitzmann ◽  
André Karch ◽  
Alexander Teumer ◽  
Marcus Dörr ◽  
...  
Keyword(s):  
Physical Activity ◽  
Myocardial Infarction ◽  
Coronary Artery Disease ◽  
Ischemic Stroke ◽  
Coronary Artery ◽  
Sedentary Behavior ◽  
Mendelian Randomization ◽  
Disease Risk ◽  
Cardiovascular Disease Risk ◽  
Artery Disease

Abstract Aims Observational evidence suggests that physical activity (PA) is inversely and sedentarism positively related with cardiovascular disease risk. We performed a two-sample Mendelian randomization (MR) analysis to examine whether genetically predicted PA and sedentary behavior are related to coronary artery disease, myocardial infarction, and ischemic stroke. Methods and results We used single nucleotide polymorphisms (SNPs) associated with self-reported moderate to vigorous PA (n = 17), accelerometer based PA (n = 7) and accelerometer fraction of accelerations > 425 milli-gravities (n = 7) as well as sedentary behavior (n = 6) in the UK Biobank as instrumental variables in a two sample MR approach to assess whether these exposures are related to coronary artery disease and myocardial infarction in the CARDIoGRAMplusC4D genome-wide association study (GWAS) or ischemic stroke in the MEGASTROKE GWAS. The study population included 42,096 cases of coronary artery disease (99,121 controls), 27,509 cases of myocardial infarction (99,121 controls), and 34,217 cases of ischemic stroke (404,630 controls). We found no associations between genetically predicted self-reported moderate to vigorous PA, accelerometer-based PA or accelerometer fraction of accelerations > 425 milli-gravities as well as sedentary behavior with coronary artery disease, myocardial infarction, and ischemic stroke. Conclusions These results do not support a causal relationship between PA and sedentary behavior with risk of coronary artery disease, myocardial infarction, and ischemic stroke. Hence, previous observational studies may have been biased. Graphic abstract

Sign in / Sign up

Export Citation Format

Share Document