Causality between aging and interstitial lung disease: A bidirectional two-sample Mendelian randomization study

Objective Aging has been shown to be associated with adverse health outcomes in patients with interstitial lung disease. However, the causal relationship between them is not fully understood. In this study, two-sample Mendelian randomization was applied to analyze the causal relationship between aging phenotypes (facial aging and telomere length) and interstitial lung disease risk. Methods Data on single nucleotide polymorphisms were extracted from the pooled dataset of genome-wide association studies. Single nucleotide polymorphisms were used as instrumental variables. The causal association between aging phenotypes and interstitial lung disease risk was evaluated using inverse variance weighting, Bayesian weighted Mendelian randomization, Mendelian randomization–robust adjusted profile score, Mendelian randomization–Egger regression, and weighted median methods. Results Inverse variance weighting revealed that facial aging increased the risk of genetic susceptibility to interstitial lung disease (odds ratio: 2.336, 95% confidence interval: 1.256–4.342, p = 0.007). Telomere length was negatively correlated with interstitial lung disease risk (odds ratio: 0.632, 95% confidence interval: 0.523–0.765, p < 0.001). No reverse causality was found; interstitial lung disease had no significant effect on facial aging (odds ratio = 0.999, 95% confidence interval: 0.995–1.003, p = 0.664) or telomere length (odds ratio = 0.996, 95% confidence interval: 0.989–1.004, p = 0.328). Conclusion The results of this study show that facial aging significantly increases the risk of interstitial lung disease, while telomere length significantly reduces the risk. Anti-aging may be an effective strategy for the prevention and treatment of interstitial lung disease.