Dataset Information

Education Attainment, Intelligence and COVID-19: A Mendelian Randomization Study.

ABSTRACT:

Background

Evidence of socioeconomic inequality in COVID-19-related outcomes is emerging, with a higher risk of infection and mortality observed among individuals with lower education attainment. We aimed to evaluate the potential interventions against COVID-19 from the socioeconomic perspective, including improvement in education and intelligence.

Methods

With a two-sample Mendelian randomization approach using summary statistics from the largest genome-wide association meta-analysis, univariable analysis was adopted to evaluate the total causal effects of genetically determined education attainment and intelligence on COVID-19 outcomes. Multivariable analysis was performed to dissect the potential mechanisms.

Results

Genetic predisposition to higher education attainment by 1 SD (4.2 years) was independently associated with reduced risk of COVID-19 severity (OR = 0.508 [95% CI: 0.417-0.617]; p < 0.001). Genetically higher education attainment also lowered the risk of COVID-19 hospitalization (0.685 [0.593-0.791]; p < 0.001), but the association was attenuated after adjustment for beta estimates of intelligence in multivariable analysis. Genetically higher intelligence was associated with reduced risk of COVID-19 hospitalization (0.780 [0.655-0.930]; p = 0.006), with attenuation of association after adjustment for education attainment. Null association was observed for genetically determined education attainment and intelligence with SARS-CoV-2 infection.

Conclusion

Education may act independently and jointly with intelligence in improving the COVID-19 outcomes. Improving education may potentially alleviate the COVID-19-related health inequality.

SUBMITTER: Li GH

PROVIDER: S-EPMC8584527 | biostudies-literature |

REPOSITORIES: biostudies-literature

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Project description:Background: Low educational attainment has been reported as a risk factor for many diseases. However, conclusion on the association between educational attainment and endometrial cancer (EC) are inconsistent in previous observational studies. This study aims to explore the potential causal association between educational attainment and EC. Methods: A Mendelian Randomization analysis was performed using publicly summary-level data sets of genome-wide association studies (GWAS). A total of 306 single-nucleotide polymorphisms (SNPs) were extracted as instrumental variables for the exposure of educational attainment from the Social Science Genetic Association Consortium GWAS summary data of 1,131,881 participants of European ancestry. SNPs of EC were obtained from the Endometrial Cancer Association Consortium, the Epidemiology of Endometrial Cancer Consortium and the UK Biobank involving 121,885 people. We conducted inverse variance weighted (IVW) to estimate the causal effect as our primary outcome. And we perform several sensitivity analyses, including MR-Egger regression, weighted median method, MR-PRESSO (Mendelian Randomization Pleiotropy Residual Sum and Outlier) global test, and leave-one-out sensitivity analysis, to evaluate the effect of pleiotropism on the causal estimates. Results: Genetic predisposition towards 4.2 years of additional educational attainment was associated with 38% lower risk of EC. (odds ratio 0.72, 95% confidence interval 0.62 to 0.83; p = 1.65*10-5). The consistent results of sensitivity analyses indicated our causal estimates were reliable. Genetic predisposition towards longer educational attainment was associated with lower risk of obesity, high waist-to-hip ratio (WHR), and diabetes. Conclusion: This study indicated that low educational attainment was a causal risk factor for EC, especially for EC with endometrioid histology. Low educational attainment might lead to EC through the mediator of obesity, high WHR, and diabetes.