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Updated: Jul 4, 2025
Surgical Models of Gastroesophageal Reflux with Mice
Published on: August 25, 2015
Modifiable risk factors mediate the effect of gastroesophageal reflux disease on stroke and subtypes: A Mendelian
Shixuan Chen1, Zhenzhen Chen2, Xia Jiang1
1Department of Rehabilitation Medicine, Zhejiang University of Traditional Chinese Medicine Affiliated Wenzhou City Hospital of Integrated Western and Traditional Chinese Medicine, China.
Objectives:
Previous observational studies have suggested that gastroesophageal reflux disease (GERD) increases the risk of stroke, but the specific underlying mechanisms are unclear. We investigated the causal associations of GERD with stroke and its subtypes using Mendelian randomization (MR), and evaluated the potential mediating effects of modifiable stroke risk factors in the causal pathway.
Methods:
Genetic instrumental variables for GERD were extracted from the latest genome-wide association study (GWAS) summary level data. We initially performed two-sample MR to examine the association of GERD with stroke and its subtypes, including ischemic stroke, intracranial hemorrhage, and the major subtypes of ischemic stroke. Two-step MR was further employed to investigate the mediating effect of 15 risk factors in the causal pathway.
Results:
We found significant causal associations of genetically predicted GERD with increased risk of stroke (OR: 1.22 95% CI: 1.126-1.322), ischemic stroke (OR: 1.19 95% CI: 1.098-1.299), and large-artery stroke (OR: 1.49 95% CI: 1.214-1.836). Replication and sensitivity analyses yielded consistent effect directions and similar estimates. Further mediation analyses indicated that hypertension (HTN), systolic blood pressure (SBP), and type 2 diabetes (T2D) mediated 36.0%, 9.0%, and 15.8% of the effect of GERD on stroke; 42.9%, 10.8%, and 21.4% for ischemic stroke, and 23.3%; 7.9%, and 18.7% for large-artery stroke, respectively.
Conclusions:
This study supports that GERD increases susceptibility to stroke, ischemic stroke, and large-artery stroke, and is partially mediated by HTN, SBP, and T2D.
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