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A Bidirectional Mendelian Randomization Study of Selenium Levels and Ischemic Stroke.
Hui Fang1, Weishi Liu1, Luyang Zhang1
1Department of Neurology, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, China.
This Mendelian randomization study found no causal link between genetically predicted selenium levels and ischemic stroke (IS). The findings do not support selenium supplementation for IS prevention at the genetic level.
Area of Science:
- Nutritional Epidemiology
- Genetic Epidemiology
- Cardiovascular Disease Research
Background:
- Observational studies suggest an inverse association between selenium levels and ischemic stroke (IS).
- Causal relationships between selenium and IS remain unclear.
- Genetic epidemiology offers tools to investigate causality.
Purpose of the Study:
- To evaluate the causal links between circulating selenium levels and ischemic stroke (IS) and its subtypes.
- To utilize Mendelian randomization (MR) analysis for assessing causality.
- To determine if genetic predisposition to selenium levels influences IS risk.
Main Methods:
- Two-sample Mendelian randomization (MR) analysis was employed.
- Genetic variants (SNPs) associated with selenium levels were identified from a large genome-wide association study (GWAS) meta-analysis.
- The inverse variance-weighted (IVW) method was used to estimate causal effects.
Main Results:
- Four single nucleotide polymorphisms (SNPs) significantly associated with selenium levels were identified.
- MR analysis revealed no causal effect of selenium levels on ischemic stroke (IS) (OR = 0.968, P = 0.269).
- No evidence of a causal link was found for IS subtypes.
Conclusions:
- Genetically predicted selenium levels do not appear to causally influence ischemic stroke risk.
- The study provides no genetic evidence to support selenium supplementation for IS prevention.
- Further research may explore other mechanisms or populations.
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