ArticleTranslational vision science & technology2025
Unraveling the Link Between Obesity and Keratoconus Risk Based on Genetic Evidence.
Article in Translational vision science & technology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
3 citing papers in PubMed.
- Obesity and Eye Diseases.Nutrients · 2026Review
- Obesity and Keratoconus: A Mediation Study Based on the Chinese Keratoconus Cohort.Translational vision science & technology · 2026Article
- Identification and risk-factor analysis for individuals at high risk for keratoconus via machine learning and logistic regression.PloS one · 2026Article
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Authors and funding
12 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Purpose: Keratoconus (KCN) is a progressive corneal disorder leading to vision impairment. While genetic and environmental factors contribute to its development, the role of obesity in KCN risk remains unclear. This study aimed to estimate the causal effect between obesity, measured by body mass index (BMI) and waist-to-hip ratio (WHR), and the risk of KCN. Methods: This two-sample Mendelian randomization (MR) case-control study used genome-wide association study data from GIANT, MRC-IEU UK Biobank, and FinnGen. BMI and WHR were used to estimate general and central obesity, respectively. Data from 311 KCN cases and 209,287 controls were analyzed. Causal effect estimates of BMI, WHR, and obesity-related chronic diseases on KCN risk were calculated. Results: Genetically predicted higher BMI was significantly associated with increased KCN risk (odds ratio [OR] = 2.003; 95% confidence interval [CI], 1.203-3.335; P = 0.008), as determined using European genetic databases. Consistent results were observed with the weighted median, MR-Egger, and MR-pleiotropy residual sum and outlier methods. No significant causal effect was found between WHR and KCN risk (OR = 0.578; 95% CI, 0.196-1.705; P = 0.321). Sensitivity analyses showed no evidence of pleiotropy, and no significant causal effect was observed between obesity-related chronic diseases and KCN risk. Conclusions: Using European genetic databases, general obesity was identified as a strong, independent causal effect contributor to KCN, while central obesity showed no association. These findings provide new insights into obesity's role in KCN development and may inform future preventive strategies. Translational Relevance: This study suggests that general obesity is a causal risk factor for keratoconus, suggesting that obesity management could help prevent or mitigate KCN progression.
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