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Association Between Dietary Fiber Intake and COPD: A Two-Stage Epidemiological and Clinical Cohort Study

Sep 2026 · International Journal of COPD · Vol 21 · 0 citations · 55 references
Medicine

Abstract

Background Chronic obstructive pulmonary disease (COPD) is a major cause of morbidity and mortality worldwide. This study aims to investigate the associations of dietary fiber intake with COPD, systemic inflammatory markers, and circulating lipopolysaccharide (LPS). Methods Data from the National Health and Nutrition Examination Survey (NHANES) 2013–2018 were analyzed. Dietary fiber intake was evaluated as the primary exposure, whereas dietary protein and carbohydrate intakes were included as dietary comparators. White blood cell (WBC), neutrophil, and lymphocyte counts were assessed as inflammatory markers in exploratory mediation analyses, and COPD status was the primary outcome. Multivariable logistic regression, mediation, stratified, and sensitivity analyses were conducted. In parallel, a retrospective clinical cohort of 331 participants (158 COPD patients and 173 non-COPD controls) was evaluated to compare dietary patterns, lung function, systemic inflammatory markers, and serum LPS levels. Results In the NHANES analysis, higher energy-adjusted dietary fiber intake was associated with lower COPD prevalence after adjustment for major confounders. In contrast, dietary protein and carbohydrate intakes showed no significant associations with COPD. WBC and neutrophil counts showed statistically significant but modest indirect associations, accounting for approximately 1.36% and 4.22%, respectively, of the observed association between dietary fiber intake and COPD. In the clinical cohort, among participants with COPD, higher dietary fiber intake was associated with lower levels of inflammatory markers and circulating LPS. Higher levels of these markers and LPS were associated with lower FEV1% predicted. Conclusion Higher dietary fiber intake was associated with lower COPD prevalence and reduced levels of systemic inflammatory markers and circulating LPS. These observational findings do not establish causal relationships or mediating pathways. Prospective longitudinal studies and intervention trials are needed to clarify the causal relationships and underlying mechanisms.

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