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 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.

We-P14:465 The association of polyunsaturated fatty acids and blood pressure in men with coronary artery disease

2006 ◽  
Vol 7 (3) ◽  
pp. 449
Author(s):  
M. Stolyhwo Gofron ◽  
J. Bellwon ◽  
W. Sobiezewski ◽  
D. Ciecwierz ◽  
A. Rynkiewicz ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Coronary Artery Disease ◽  
Fatty Acids ◽  
Coronary Artery ◽  
Polyunsaturated Fatty Acids ◽  
Artery Disease

scholarly journals Causal associations of insulin resistance with coronary artery disease and ischemic stroke: a Mendelian randomization analysis

2020 ◽  
Vol 8 (1) ◽  
pp. e001217 ◽  
Author(s):  
Weiqi Chen ◽  
Shukun Wang ◽  
Wei Lv ◽  
Yuesong Pan
Keyword(s):  
Myocardial Infarction ◽  
Coronary Artery Disease ◽  
Ischemic Stroke ◽  
Coronary Artery ◽  
Mendelian Randomization ◽  
Artery Occlusion ◽  
Small Artery ◽  
Small Artery Occlusion ◽  
Weighted Median ◽  
Artery Disease

IntroductionThe relationship between insulin resistance (IR) and cardiovascular diseases is unclear. We aimed to examine the causal associations of IR with cardiovascular diseases, including coronary artery disease, myocardial infarction, ischemic stroke and its subtypes, using Mendelian randomization.Research design and methodsDue to low sample size for gold standard measures and in order to well reflect the underlying phenotype of IR, we used 53 single nucleotide polymorphisms associated with IR phenotypes (ie, fasting insulin, high-density lipoprotein cholesterol and triglycerides) from recent genome-wide association studies (GWASs) as instrumental variables. Summary-level data from four GWASs of European individuals were used. Data on IR phenotypes were obtained from meta-analysis of GWASs of up to 188 577 individuals and data on the outcomes from GWASs of up to 446 696 individuals. Mendelian randomization (MR) estimates were calculated with inverse-variance weighted, simple and weighted-median approaches and MR-Egger regression was used to explore pleiotropy.ResultsGenetically predicted 1-SD increase in IR phenotypes were associated with a substantial increase in risk of coronary artery disease (OR=1.79, 95% CI: 1.57 to 2.04, p<0.001), myocardial infarction (OR=1.78, 95% CI: 1.54 to 2.06, p<0.001), ischemic stroke (OR=1.21, 95% CI: 1.05 to 1.40, p=0.007) and the small-artery occlusion subtype of stroke (OR=1.80, 95% CI: 1.30 to 2.49, p<0.001), but not associated with the large-artery atherosclerosis and cardioembolism subtypes of stroke. There was no evidence of pleiotropy. Results were broadly consistent in sensitivity analyses using simple and weighted-median approaches accounting for potential genetic pleiotropy.ConclusionsThis study provides evidence to support that IR was causally associated with risk of coronary artery disease, myocardial infarction, ischemic stroke and the small-artery occlusion subtype of stroke.

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