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 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 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 Circulating folate concentrations and risk of coronary artery disease: a prospective cohort study in Chinese adults and a Mendelian randomization analysis

2020 ◽  
Vol 111 (3) ◽  
pp. 635-643 ◽  
Author(s):  
Pinpin Long ◽  
Xuezhen Liu ◽  
Jun Li ◽  
Shiqi He ◽  
Huiting Chen ◽  
...  
Keyword(s):  
Coronary Artery Disease ◽  
Coronary Artery ◽  
Mendelian Randomization ◽  
Causal Relation ◽  
Serum Folate ◽  
European Ancestry ◽  
Inverse Association ◽  
Chinese Adults ◽  
Chinese Populations ◽  
Artery Disease

ABSTRACT Background The association between circulating folate concentrations and risk of coronary artery disease (CAD) has been evaluated in Western populations with inconsistent results; however, the observational and causal associations in Chinese populations with relatively low folate concentrations remain unclear. Objectives We aimed to examine the association of circulating folate concentrations with incident CAD in Chinese adults, and further evaluated the causal relation using Mendelian randomization (MR) analysis. Methods We measured baseline serum folate in 1605 incident CAD cases and 1605 age- and sex-matched controls nested within the Dongfeng-Tongji (DFTJ) cohort, which recruited 27,009 individuals with a mean age of 63.6 y in 2008–2010 and followed up until the end of 2013 (mean: 4.4 y). We quantified the observational association between folate and incident CAD using conditional logistic regression models. A 2-sample MR analysis was performed using summary statistics obtained for genetic variants identified from a genome-wide association study (GWAS) of circulating folate concentrations in participants of European ancestry (n = 37,341) and from the CardiogramplusC4D 1000 genomes–based GWAS meta-analysis (n = 184,305). We also conducted 1-sample MR among 1545 incident CAD cases and 1444 controls with genotyping data in the DFTJ cohort. Results In the DFTJ cohort, higher serum folate concentrations were associated with a lower risk of CAD: the OR (95% CI) across sex-specific quartiles of folate (from lowest to highest concentrations) was 1.00 (reference), 0.78 (0.63, 0.97), 0.77 (0.61, 0.97), and 0.75 (0.60, 0.95), respectively (P-trend = 0.01). In the MR analysis, the OR of CAD per SD increase in genetically predicted serum folate was 1.00 (0.88, 1.14) and 0.88 (0.59, 1.32) for European and Chinese populations, respectively. Conclusions We found an inverse association between circulating folate concentrations and incident CAD among Chinese populations. However, we confirmed that there was no genetic evidence to support the causal relation in both European and Chinese populations.

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