Changes in Serum, Red Blood Cell, and Colonic Fatty Acids in a Personalized Omega-3 Fatty Acid Supplementation Trial

Abstract

This study evaluated changes in fatty acids from sera, red blood cells, and colonic biopsies from a phase Ib clinical trial of personalized ω-3 fatty acid dosing in 47 healthy volunteers. The trial aimed to reduce colonic prostaglandin E₂ (PGE₂), a pro-inflammatory product of arachidonic acid (AA) oxidation. The personalized doses ranged 2–10 grams/day (54% eicosapentaenoic acid, EPA, 24% other ω-3 fatty acids). In colon, increases in ω-3 highly unsaturated fatty acids (HUFA) and EPA:AA ratios each were correlated with decreases in PGE₂. Changes in either colonic EPA:AA ratios or ω-3 HUFA were significantly correlated with changes in the same fatty acid measures in red blood cells or serum. The only blood-based measure significantly correlated with changes in colonic PGE₂ was change in red blood cell ω-3 HUFA (ρ = −0.39), and the increase in red blood cell ω-3 HUFA was significantly greater in participants who had at least a median reduction in colonic PGE₂ vs. those who did not. In summary, fatty acid changes in blood did reflect fatty acid changes in the colon, but additional factors will be needed for optimizing dosing models that seek to predict the anti-inflammatory effects of ω-3 fatty acids on the colon.

Acknowledgments

We thank the individuals who volunteered to participate in this study. Drs. Justin Colacino and Dave Bridges provided helpful discussions, and Kirk Herman was the clinical study coordinator.

Disclosure Statement

No potential conflict of interest was reported by the authors.

Author Contributions

Conceptualization, YS, AS, DTK, MTR, WLS, DEB, ZD; Data Acquisition, JR, GG; Data Analysis, YS, AS, ZD; Resources, DEB; Data Curation, YS, AS; Writing – Original Draft Preparation, YS, ZD, AS; Writing – Review & Editing, DKT, MTR, DEB, YS, ZD, AS; Supervision, WLS, DEB, ZD; Funding Acquisition, WLS, DEB.

Additional information

Funding

The study was supported by the National Cancer Institute (NCI) grant P50 CA130810, the Rogel Cancer Center grant P30 CA046592, the University of Michigan Clinical Research Center grant UL1 RR024986, the Michigan Diabetes Research Center (Chemistry Laboratory) grant P30 DK020572 from the National Institute of Diabetes and Digestive and Kidney Disease, the University of Michigan Rogel Cancer Center Clinical Translational Resource Allocation Committee, the Kutsche Family Memorial Endowment (to DEB), and the Rose and Lawrence C. Page Foundation (to DKT).