https://orcid.org/0000-0002-1073-3254
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Abstract
Purpose
Observational studies have reported that autoimmune diseases are closely related to sarcopenia, but the causalities of autoimmune diseases with sarcopenia have not been established. We conducted this Mendelian randomization (MR) study to reveal the causal associations of overall autoimmune disease and five common autoimmune diseases with sarcopenia-related traits.
Methods
The publicly available summary-level data of autoimmune diseases and three sarcopenia-related traits were used for analysis. The causal effects of autoimmune diseases on sarcopenia-related traits were first identified in discovery samples using the inverse-variance-weighted method as the primary method, and the robustness of results was examined by additional sensitivity analyses. Replication MR analyses were then conducted using replication samples of five autoimmune diseases. Finally, the possibility of reverse causation was assessed by reverse MR analyses.
Results
In both the discovery and replication samples, we identified potential causal effects of rheumatoid arthritis (RA) on appendicular lean mass (ALM) and low grip strength (OR = 0.979, 95% CI: 0.964–0.995 for ALM; OR = 1.042, 95% CI: 1.013–1.072 for low grip strength), but not on walking pace. We also found that inflammatory bowel disease (IBD) and type 1 diabetes (T1D) were only causally negatively associated with ALM in the discovery stage (OR = 0.986, 95% CI: 0.974–0.999 for IBD; OR = 0.987, 95% CI: 0.975–0.999 for T1D), whereas systemic lupus erythematosus, multiple sclerosis, and overall autoimmune disease were not associated with any of the three sarcopenia-related traits. Additionally, reverse MR analysis only found an association between walking pace and overall autoimmune disease, but this association did not remain in the weighted-median method.
Conclusion
This study demonstrates that RA is causally associated with low grip strength and reduced ALM, and that IBD and T1D may be causally negatively related to ALM.
Data Sharing Statement
The original contributions presented in the study are included in the article/ Supplementary Material. Further inquiries can be directed to the corresponding authors.
Ethics Statement
Our study was based on publicly available GWAS summary-level data and all original studies have been approved by their Institutional Review Boards or local ethics committees. Besides, our study did not involve individual-level data and was deemed not to require ethical approval after consultation with the Ethics Committee of Wenzhou Medical University.
Acknowledgments
The authors gratefully acknowledge all researchers and participants who provided publicly available GWAS summary data.
Author Contributions
All authors made a significant contribution to the work reported, whether is in conception, study design, execution, acquisition of data, analysis and interpretation, or all these areas, took part in drafting, revising, or critically reviewing the article, gave final approval to the version to be published, have agreed on the journal to which the article has been submitted, and agree to be accountable for all aspects of the work.
Disclosure
The authors report no conflicts of interest in this work.