NEW research employing Mendelian randomisation (MR) analysis has identified a potential causal relationship between lipid metabolism and chronic obstructive pulmonary disease (COPD), with apolipoprotein A-I (apoA-I) emerging as a protective factor.
The study utilised genome-wide association study data from 112,583 European participants with COPD from the MRC-IEU, alongside extensive lipid profile data from the UK Biobank. Measurements for low-density lipoprotein cholesterol (LDL-C), high-density lipoprotein cholesterol (HDL-C), triglycerides (TG), total cholesterol (TC), apoA-I, and apolipoprotein B (apoB) were included from cohorts ranging from 187,365–441,016 individuals. MR analyses were conducted using the inverse-variance weighted method to determine causal relationships between lipid levels and COPD, with sensitivity analyses performed to ensure robustness.
The primary inverse-variance weighted analysis identified significant associations between COPD and LDL-C (odds ratio [OR]: 0.994, 95% CI: 0.989–0.999, P=0.019), TG (OR: 1.005, 95% CI: 1.002–1.009, P=0.006), and apoA-I (OR: 0.995, 95% CI: 0.992–0.999, P=0.008), while no causal link was found with HDL-C, TC, or apoB. Sensitivity analysis confirmed the reliability of these findings. However, after multivariate MR and multiple testing correction, only apoA-I retained its significance as a protective factor against COPD (OR: 0.994, 95% CI: 0.990–0.999, P=0.008), while LDL-C and TG were no longer associated with COPD risk.
These findings highlight the potential role of lipid metabolism in COPD and emphasise the protective effect of apoA-I, offering significant implications for disease prevention and management strategies.
Ada Enesco, EMJ
Reference
Huang P et al. Causal relationships between blood lipid levels and chronic obstructive pulmonary disease: a mendelian randomization analysis. Int J Chron Obstruct Pulmon Dis. 2025;20:83-93.
