Research

Hormonal

Dietary omega-3 polyunsaturated fatty acids (specifically EPA) combined with aspirin or other NSAIDs generate novel anti-inflammatory lipid mediators (18R-HEPE, 5,12,18R-triHEPE, and 15-epi-LXA5) via transcellular processing involving COX-2 and leukocyte 5-lipoxygenase, which inhibit polymorphonuclear leukocyte (PMN) transendothelial migration and infiltration.

If you take omega-3 supplements (specifically EPA) and have inflammation (which upregulates COX-2), your body can convert these fats into potent anti-inflammatory signals, especially if you take aspirin or certain other NSAIDs. These signals actively stop immune cells from migrating to inflamed tissues. This suggests that the benefit of omega-3s is not just passive competition but active creation of anti-inflammatory mediators.

GoodSupportsHIGH confidence
These new compounds proved to be potent inhibitors of human polymorphonuclear leukocyte transendothelial migration and infiltration in vivo (ATL analogue 5,12,18R-triHEPE).
Charles N. Serhan et al. · The Journal of Experimental Medicine · 2000

Why this rating

The study uses rigorous biochemical identification (LC/MS/MS) and functional assays in human cells and murine models, though it is a mechanistic study rather than a large-scale clinical trial.

Source

Novel Functional Sets of Lipid-Derived Mediators with Antiinflammatory Actions Generated from Omega-3 Fatty Acids via Cyclooxygenase 2–Nonsteroidal Antiinflammatory Drugs and Transcellular Processing

Charles N. Serhan et al. · The Journal of Experimental Medicine · 2000

DOI 10.1084/jem.192.8.1197

mechanism_onlyCited 1,181×
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DOI resolved against Crossref · corpus check 2026-06-10

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