# Causal Effects Between Genetically Determined Human Serum Metabolite Levels on the Risk of Idiopathic Pulmonary Fibrosis: A Mendelian Randomization Study

## TL;DR

This study uses genetic data to explore how blood metabolites may influence the risk of idiopathic pulmonary fibrosis, identifying several metabolites with potential causal links.

## Contribution

The study identifies 14 metabolite associations with IPF using Mendelian randomization, offering new insights into disease mechanisms.

## Key findings

- 23 metabolites showed a causal connection with IPF.
- 14 robust or potential causal associations were identified after sensitivity analysis.
- Six specific metabolites were linked to IPF through these associations.

## Abstract

The incidence of idiopathic pulmonary fibrosis (IPF) is increasing every year; however, the potential biological mechanisms have not been completely clarified. The objective of this study is to reveal the etiologic effects of circulating metabolites on IPF.

This research evaluated the causal relationship between serum metabolites and IPF utilizing two‐sample Mendelian randomization (MR) analysis. IVW served as the main method of analysis; concurrently, MR‐Egger, weighted median, and MR‐PRESSO acted as supplementary analyses. Sensitivity analyses were performed with Cochran's Q test, MR‐Egger's intercept test, and leave‐one‐out method of analysis. All statistical analyses were accomplished in R software.

Our results showed that 23 metabolites have a causal connection with IPF. Following sensitivity analysis, 2 robust and 12 potential causal association pairs were identified among the known metabolites. These 14 causal pairs concerned six metabolites.

This study presents a novel perspective on potential mechanisms involved in IPF with important significance for screening, prevention, and treatment.

The objective of this study is to reveal the etiologic effects of circulating metabolites on IPF. This research evaluated the causal relationship between serum metabolites and IPF utilizing two‐sample Mendelian randomization (MR) analysis. This study presents a novel perspective on potential mechanisms involved in IPF with important significance for screening, prevention, and treatment.