The AA : EPA ratio explained
If the omega-6 : omega-3 ratio is a marker of dietary pattern, the AA : EPA ratio is the most direct biochemical readout of where your body sits on the pro- versus anti-inflammatory eicosanoid spectrum.
What it measures
The AA : EPA ratio is arachidonic acid (AA, a 20-carbon omega-6) divided by eicosapentaenoic acid (EPA, a 20-carbon omega-3). Both fatty acids compete for the same enzymes that produce eicosanoids — short-lived signalling molecules that drive inflammation, vasoconstriction and platelet aggregation.
AA-derived eicosanoids (PGE2, LTB4, TXA2) tend to be pro-inflammatory. EPA-derived eicosanoids (PGE3, LTB5) are weakly inflammatory at most, and EPA is also the precursor for the resolvins and protectins that actively switch off inflammation when it has done its job.
Why this is more direct than the omega-6 : omega-3 ratio
The total omega-6 : omega-3 ratio includes linoleic acid (LA), the precursor sitting upstream of AA. LA itself does not directly drive eicosanoid biology — it has to be desaturated and elongated through several steps to become AA. The conversion is slow, regulated and varies dramatically between individuals.
The AA : EPA ratio measures the actual building blocks downstream — the molecules your enzymes are choosing between in real time. It is a cleaner signal of inflammatory tone, which is why Calder (Biochem Soc Trans, 2017) and the foundational Endres et al. paper (NEJM, 1989) lean on it as the more biologically meaningful marker.
What the ratio looks like in practice
What drives a high AA : EPA ratio
- Low EPA intake — primarily low fish consumption with no supplementation.
- High intake of animal fats and refined seed oils together (the typical Australian processed-food pattern).
- Genetic FADS variants that more efficiently convert LA → AA, pushing the omega-6 side of the ratio up.
- Inflammatory conditions, obesity and insulin resistance, all of which up-regulate the desaturases that produce AA.
What lowering it actually does
EPA-derived eicosanoids — PGE3, LTB5, the resolvins, the protectins — compete with AA-derived ones (PGE2, LTB4, TXA2) for the same enzymes and receptors. Raising EPA shifts the substrate pool and pushes the downstream signalling balance toward resolution rather than escalation.
Clinical trials in rheumatoid arthritis (Goldberg & Katz Pain, 2007 meta-analysis), inflammatory bowel disease and several other chronic inflammatory conditions show consistent symptomatic benefit once the AA : EPA ratio drops below roughly 10 : 1.
The fastest way to lower it
EPA-specific supplementation. EPA-dominant fish oils — or naturally EPA-rich species like sardines and anchovies — move the ratio faster than DHA-dominant products. Algae-based products are increasingly EPA-rich; older algae products were DHA-only and are not the best choice if AA : EPA is the marker you are trying to move.
What improvement looks like over time
- Starting at around 20 : 1 with no supplement, roughly 1,500 mg/day of an EPA-dominant supplement can typically move you to around 10 : 1 within 3–4 months.
- Starting at around 8 : 1, the same dose can usually bring you into the optimal band (~3 : 1) in a similar timeframe.
- Red blood cell turnover is roughly four months, so a 3–4 month retest cadence is the standard.
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Order Plus Ratios →References: Endres S et al. The effect of dietary supplementation with n-3 polyunsaturated fatty acids on the synthesis of interleukin-1 and tumor necrosis factor. N Engl J Med. 1989. · Calder PC. Omega-3 fatty acids and inflammatory processes. Biochem Soc Trans. 2017. · Goldberg RJ, Katz J. A meta-analysis of the analgesic effects of omega-3 polyunsaturated fatty acid supplementation for inflammatory joint pain. Pain. 2007.