Clinical and Translational Research
Copyright ©The Author(s) 2024. Published by Baishideng Publishing Group Inc. All rights reserved.
World J Clin Cases. Jun 6, 2024; 12(16): 2789-2795
Published online Jun 6, 2024. doi: 10.12998/wjcc.v12.i16.2789
Causal association between 25-hydroxyvitamin D status and cataract development: A two-sample Mendelian randomization study
Chun-Hui Wang, Zhi-Kun Xin
Chun-Hui Wang, Zhi-Kun Xin, Department of Ophthalmology, Aviation General Hospital, Beijing 100010, China
Author contributions: Wang CH contributed to research design, data collection, interpretation, analysis, and manuscript drafting; Xin ZK contributed to result interpretation and critical revision of the manuscript; all authors approved the final version and agree to be accountable for all aspects of the work.
Conflict-of-interest statement: There is no conflict of interest related to the manuscript.
Open-Access: This article is an open-access article that was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution NonCommercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See: https://creativecommons.org/Licenses/by-nc/4.0/
Corresponding author: Zhi-Kun Xin, BMed, Chief Physician, Department of Ophthalmology, Aviation General Hospital, No. 3 Anwai Beiyuan Courtyard, Anli Road, Chaoyang District, Beijing 100010, China. xzkavic@163.com
Received: March 10, 2024
Revised: April 23, 2024
Accepted: April 28, 2024
Published online: June 6, 2024
Processing time: 79 Days and 23.9 Hours
Abstract
BACKGROUND

Vitamin deficiencies are linked to various eye diseases, and the influence of vitamin D on cataract formation has been noted in prior research. However, detailed investigations into the causal relationship between 25-(OH)D status and cataract development remain scarce.

AIM

To explore a possible causal link between cataracts and vitamin D.

METHODS

In this study, we explored the causal link between 25-(OH)D levels and cataract development using Mendelian randomization. Our analytical approach included inverse-variance weighting (IVW), MR-Egger, weighted median, simple mode, and weighted mode methods. The primary analyses utilized IVW with random effects, supplemented by sensitivity and heterogeneity tests using both IVW and MR-Egger. MR-Egger was also applied for pleiotropy testing. Additionally, a leave-one-out analysis helped identify potentially impactful single-nucleotide polymorphisms.

RESULTS

The analysis revealed a positive association between 25-(OH)D levels and the risk of developing cataracts (OR = 1.11, 95%CI: 1.00-1.22; P = 0.032). The heterogeneity test revealed that our IVW analysis exhibited minimal heterogeneity (P > 0.05), and the pleiotropy test findings confirmed the absence of pleiotropy within our IVW analysis (P > 0.05). Furthermore, a search of the human genotype-phenotype association database failed to identify any potentially relevant risk-factor single nucleotide polymorphisms.

CONCLUSION

There is a potential causal link between 25-(OH)D levels and the development of cataracts, suggesting that greater 25-(OH)D levels may be a contributing risk factor for cataract formation. Further experimental research is required to confirm these findings.

Keywords: Cataract, 25-hydroxyvitamin D, Mendelian randomization, Single nucleotide polymorphism, Causal relationship

Core Tip: Previous studies have documented the role of vitamin D in cataract development, yet investigations into the causal relationship between 25-(OH)D status and cataract onset are still lacking. Using Mendelian randomization, our study established a significant association between elevated 25-(OH)D levels and increased cataract risk. Additionally, a search of the human genotype-phenotype association database revealed no potentially relevant risk-factor single nucleotide polymorphisms. These findings need to be verified by further experiments.