Objective::This study aimed to explore the causal link between olive intake and the occurrence of coronary heart disease (CHD) using Mendelian randomization (MR).Methods::In this study, genome-wide association study data from IEU OpenGWAS were employed. A 2-sample MR analysis was used to determine the causal association of olive intake with CHD and cardiovascular outcomes (myocardial infarction, heart failure, stroke, and death due to cardiac causes). The data for olive intake included 64,949 samples and 9,851,867 single nucleotide polymorphisms (SNPs), the data for CHD included 361,194 samples and 13,295,130 SNPs; The data for myocardial infarction included 361,194 samples and 12,640,541 SNPs, the heart failure include 208,178 samples and 16,380,422 SNPs, the data for stroke included 361,194 samples and 12,404,026 SNPs, and the data for death due to cardiac causes included 361,194 samples and 10,071,648 SNPs. Additionally, a 2-step, 2-sample MR approach was used for mediation analysis to determine whether lipid traits mediate the causal association between olive intake and CHD. The data for total cholesterol, low-density lipoprotein cholesterol, high-density lipoprotein cholesterol, apolipoprotein B, and apolipoprotein A1 included 115,078 samples and 12,321,875 SNPs, while the data for triglycerides included 21,545 samples and 11,871,391 SNPs. Cochran’s Q test was applied to examine potential heterogeneity, and the MR-Egger method was used to assess horizontal pleiotropy among SNPs. Leave-one-out analysis was performed as a sensitivity analysis to evaluate the robustness of the results. Results::For each standard deviation increase in olive intake, the risk of CHD decreased by a substantial 1.9% (odds ratio (OR) = 0.981, 95% confidence interval (CI): 0.963 to 0.998, P = 0.031), the risk of myocardial infarction was significantly reduced by 1.6% (OR = 0.984, 95% CI: 0.969 to 0.999, P = 0.032), and the risk of heart failure declined by 62.1% (OR = 0.379, 95% CI: 0.192 to 0.746, P = 0.005). Furthermore, mediation analysis with MR indicated that lipid traits did not mediate the causal relationship between olive intake and CHD. Conclusion::There is a negative correlation between olive intake and the incidence of CHD, and this relationship is not mediated by lipid traits. Olive intake was also negatively associated with some cardiovascular outcomes, suggesting that increasing olive intake holds significant value in preventing the onset and progression of CHD.

Objective::This study aimed to explore the causal link between olive intake and the occurrence of coronary heart disease (CHD) using Mendelian randomization (MR).Methods::In this study, genome-wide association study data from IEU OpenGWAS were employed. A 2-sample MR analysis was used to determine the causal association of olive intake with CHD and cardiovascular outcomes (myocardial infarction, heart failure, stroke, and death due to cardiac causes). The data for olive intake included 64,949 samples and 9,851,867 single nucleotide polymorphisms (SNPs), the data for CHD included 361,194 samples and 13,295,130 SNPs; The data for myocardial infarction included 361,194 samples and 12,640,541 SNPs, the heart failure include 208,178 samples and 16,380,422 SNPs, the data for stroke included 361,194 samples and 12,404,026 SNPs, and the data for death due to cardiac causes included 361,194 samples and 10,071,648 SNPs. Additionally, a 2-step, 2-sample MR approach was used for mediation analysis to determine whether lipid traits mediate the causal association between olive intake and CHD. The data for total cholesterol, low-density lipoprotein cholesterol, high-density lipoprotein cholesterol, apolipoprotein B, and apolipoprotein A1 included 115,078 samples and 12,321,875 SNPs, while the data for triglycerides included 21,545 samples and 11,871,391 SNPs. Cochran’s Q test was applied to examine potential heterogeneity, and the MR-Egger method was used to assess horizontal pleiotropy among SNPs. Leave-one-out analysis was performed as a sensitivity analysis to evaluate the robustness of the results. Results::For each standard deviation increase in olive intake, the risk of CHD decreased by a substantial 1.9% (odds ratio (OR) = 0.981, 95% confidence interval (CI): 0.963 to 0.998, P = 0.031), the risk of myocardial infarction was significantly reduced by 1.6% (OR = 0.984, 95% CI: 0.969 to 0.999, P = 0.032), and the risk of heart failure declined by 62.1% (OR = 0.379, 95% CI: 0.192 to 0.746, P = 0.005). Furthermore, mediation analysis with MR indicated that lipid traits did not mediate the causal relationship between olive intake and CHD. Conclusion::There is a negative correlation between olive intake and the incidence of CHD, and this relationship is not mediated by lipid traits. Olive intake was also negatively associated with some cardiovascular outcomes, suggesting that increasing olive intake holds significant value in preventing the onset and progression of CHD.