REF-122 · Calder, 2017 · Biochemical Society Transactions, Vol. · Paper

Omega-3 Fatty Acids and Inflammatory Processes: From Molecules to Man

B+moderate evidenceMeasured on a mixed groupWritten before October 2026, being re-checked

Calder reviews the nutritional and metabolic biology of omega-6 and omega-3 fatty acids in inflammation.

EPA and DHA (from oily fish and fish-oil supplements) partly inhibit many aspects of inflammation: leucocyte chemotaxis, adhesion-molecule expression and leucocyte-endothelial adhesion, production of eicosanoids (prostaglandins, leukotrienes) from the omega-6 arachidonic acid, and production of pro-inflammatory cytokines.

EPA-derived eicosanoids are often less biologically potent than the arachidonic-acid-derived ones, and EPA and DHA give rise to inflammation-resolving mediators — resolvins, protectins and maresins.

Mechanisms include altered membrane phospholipid composition, disruption of lipid rafts, inhibition of the pro-inflammatory transcription factor NF-κB and activation of the anti-inflammatory PPARγ.

Animal models show benefit across inflammatory conditions; human trials show benefit of oral omega-3 in rheumatoid arthritis and in stabilizing advanced atherosclerotic plaques, and intravenous omega-3 may help critically ill patients. The review contains no athlete data, no doses and no percentages.

Key Findings

Anti-inflammatory actions of EPA/DHA: reduced leucocyte chemotaxis and adhesion, fewer arachidonic-acid eicosanoids, fewer pro-inflammatory cytokines.
Pro-resolution: EPA and DHA are precursors of resolvins, protectins and maresins.
Molecular mechanisms: membrane composition, lipid rafts, NF-κB inhibition, PPARγ activation.
Human evidence cited: rheumatoid arthritis, atherosclerotic plaque stabilization, critical illness (intravenous).

Practical Application

EPA and DHA damp several arms of inflammation — immune-cell migration and adhesion, arachidonic-acid eicosanoids, pro-inflammatory cytokines — and supply the resolvins, protectins and maresins that actively switch inflammation off; the human evidence in this review is clinical (rheumatoid arthritis, atherosclerosis, critical illness), not athletic.
Inference, not tested: training-induced inflammation is a necessary adaptive signal, so the relevance for athletes is helping resolution after hard blocks, not suppressing the response; this review does not test recovery, soreness or performance.
Not from this paper: for an omega-3 supplementation trial in trained people see REF-123 (Heileson 2023 — fish oil + resistance training).
Not from this paper; the base's own practice: we do not prescribe omega-3 doses from this review; any dose we suggest comes from the trial literature, and food sources (oily fish) are the default.

Limitations

Mechanistic review with clinical examples; no exercise, recovery or performance outcomes; no dose-response data in the abstract.
How this entry was checked and changed
Content correction 2026-09-27
"EPA inhibits chemotaxis 40-50%", "cytokines reduced 15-25%", "optimal EPA:DHA 2:1", "EPA 2.3 g + DHA 1.6 g daily", "salmon 3-4×/week", "recovery markers improve 10-15%" -> none of these figures is in the paper; all deleted. IL-6/TNF-α named as the cytokines -> the abstract says pro-inflammatory cytokines generally.
Added the abstract's mechanisms (NF-κB, PPARγ, lipid rafts, maresins) and its clinical human evidence; the training-recovery link relabelled as inference. Title changed to the paper's title.