Higher dietary inflammation linked to increased COPD risk in UK Biobank cohort
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Key Takeaway
Consider that higher dietary inflammation is associated with increased COPD risk, but causality is not established.
This prospective cohort study analyzed 167,440 participants from the UK Biobank over a median follow-up of 13.4 years. The primary exposure was the Dietary Inflammatory Index (DII) and the Energy-adjusted Dietary Inflammatory Index (E-DII), with the lowest quartile of scores serving as the comparator. The primary outcome was risk of chronic obstructive pulmonary disease (COPD).
The main results showed that each unit increase in DII was associated with a 5% higher COPD risk (HR: 1.05, 95% CI: 1.04–1.07). Each unit increase in E-DII was associated with a 20% higher risk (HR: 1.20, 95% CI: 1.16–1.25). Comparing the highest versus lowest quartile, DII was associated with a higher risk (HR: 1.27, 95% CI: 1.17–1.39), and E-DII was associated with a higher risk (HR: 1.42, 95% CI: 1.30–1.55). A total of 4,041 COPD cases occurred during follow-up.
Safety and tolerability data were not reported. A key limitation is population heterogeneity indicated in subgroup analyses. Mediation analyses suggest the association may be partially explained by systemic inflammation, specifically CRP and SII. Sensitivity analyses confirmed the robustness of the findings.
The practice relevance was not reported. These observational findings indicate an association between dietary inflammation and COPD risk, but they do not prove that reducing dietary inflammation prevents COPD. Clinicians should interpret these results cautiously, considering the study design and unmeasured confounding.
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View Original Abstract ↓
BackgroundChronic obstructive pulmonary disease (COPD) continues to pose a significant global burden, which may be exacerbated by pro-inflammatory diets. This study aimed to investigate the association between the Dietary Inflammatory Index (DII) and the Energy-adjusted Dietary Inflammatory Index (E-DII) and the risk of COPD.MethodsA total of 167,440 participants were recruited for a prospective analysis from the UK Biobank. Cox proportional hazards models were employed to analyze the associations of DII and E-DII with COPD. Restricted cubic spline (RCS) and subgroup analyses were also performed. Additionally, mediation analyses were conducted to explore the potential mediating role of inflammatory biomarkers between DII, E-DII and COPD risk.ResultsDuring a median follow-up of 13.4 years, 4,041 COPD cases occurred. After adjusting for covariates, each unit increase in DII and E-DII was associated with a 5% [HR: 1.05 (95% CI: 1.04–1.07)] and 20% [HR: 1.20 (95% CI: 1.16–1.25)] higher risk of COPD. Participants in the highest quartile of DII and E-DII scores had a higher risk of COPD compared to those in the lowest quartile, with HR = 1.27 (95% CI: 1.17–1.39) and HR = 1.42 (95% CI: 1.30–1.55). In mediation analyses, C-reactive protein (CRP) showed the highest proportion mediated for both DII and E-DII, followed by systemic immune-inflammation index (SII). Subgroup analyses indicated population heterogeneity, and sensitivity analyses confirmed the robustness of the findings.ConclusionBoth DII and E-DII are associated with an increased risk of COPD, and this association may be partially explained by systemic inflammation, particularly CRP and SII.
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