Associations of Plasma Omega-3 Fatty Acids With Progression and Survival in Pulmonary Fibrosis.

BACKGROUND

Preclinical experiments suggest protective effects of omega-3 fatty acids and their metabolites in lung injury and fibrosis. Whether higher intake of omega-3 fatty acids is associated with disease progression and survival in humans with pulmonary fibrosis is unknown.

RESEARCH QUESTION

What are the associations of plasma omega-3 fatty acid levels (a validated marker of omega-3 nutritional intake) with disease progression and transplant-free survival in pulmonary fibrosis?

STUDY DESIGN AND METHODS

Omega-3 fatty acid levels were measured from plasma samples of patients with clinically diagnosed pulmonary fibrosis from the Pulmonary Fibrosis Foundation Patient Registry (n = 150), University of Virginia (n = 58), and University of Chicago (n = 101) cohorts. The N-3 index (docosahexaenoic acid + eicosapentaenoic acid) was the primary exposure variable of interest. Linear-mixed effects models with random intercept and slope were used to examine associations of plasma omega-3 fatty acid levels with changes in FVC and diffusing capacity for carbon monoxide over a period of 12 months. Cox proportional hazards models were used to examine transplant-free survival. Stratified analyses by telomere length were performed in the University of Chicago cohort.

RESULTS

Most of the cohort were patients with idiopathic pulmonary fibrosis (88%) and male patients (74%). One-unit increment in log-transformed N-3 index plasma level was associated with a change in diffusing capacity for carbon monoxide of 1.43 mL/min/mm Hg per 12 months (95% CI, 0.46-2.41) and a hazard ratio for transplant-free survival of 0.44 (95% CI, 0.24-0.83). Cardiovascular disease history, smoking, and antifibrotic usage did not significantly modify associations. Omega-3 fatty acid levels were not significantly associated with changes in FVC. Higher eicosapentaenoic acid plasma levels were associated with longer transplant-free survival among University of Chicago participants with shorter telomere length (P value for interaction = .02).

INTERPRETATION

Further research is needed to investigate underlying biological mechanisms and whether omega-3 fatty acids are a potential disease-modifying therapy.

Informations de copyright

Copyright © 2023 American College of Chest Physicians. Published by Elsevier Inc. All rights reserved.

Déclaration de conflit d'intérêts

Financial/Nonfinancial Disclosures The authors have reported to CHEST the following: J. M. O. reports fees and support from BI, Roche, Lupin and Gatehouse Bio and DMC for Genentech, Endeavor BioMedicines and Novartis. A. A. has received research grants from the Pulmonary Fibrosis Foundation, the American College of Chest Physicians, and the National Institutes of Health for the conduct of studies in pulmonary fibrosis and served on a pulmonary fibrosis educational forum for Boehringer Ingelheim, as well as consultancy for Roche Pharmaceuticals, Boehringer Ingelheim, Inogen, and Medscape. M. E. S. reports grant support from Galapagos and personal fees from Fibrogen. Reports grant, personal fees, and non-financial support from Boehringer-Ingelheim. All of these are outside the scope of submitted work. I. N. reports personal fees from Boehringer Ingelheim, Genentech, and Confo. All of these are outside the submitted work. In addition, Dr. Noth has a patent transcriptomic prognostics in IPF pending. None declared (J. S. K., S.-F. M., J. Z. M., Y. H., C. A. B., K. R. F., E. S., I. U., J. J. M., S. G., K. M.).