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Your EPA/AA ratio compares the blood levels of two fatty acids that compete for the same biological machinery: EPA (eicosapentaenoic acid), an omega-3 fat from fish and supplements, and AA (arachidonic acid), an omega-6 fat your body produces from dietary sources. The ratio tells you which of these two molecules is winning the competition inside your cells, and that balance has real consequences for inflammation and cardiovascular risk.
This is not a general wellness marker. The EPA/AA ratio has shown its strongest value in people who already have heart disease or elevated inflammation. If you fall into one of those categories, this number can help you understand whether your current omega-3 intake is actually shifting your biology in a protective direction, or whether it is barely making a dent.
EPA and AA are both raw materials your body uses to produce signaling molecules called eicosanoids. Think of eicosanoids as local hormones: they do not travel far, but they powerfully influence inflammation, blood clotting, and blood vessel behavior right where they are made. The key detail is that EPA and AA use the same enzymes to get converted into these signals, so they are in direct competition.
The enzymes involved, called COX enzymes (cyclooxygenase), strongly prefer AA. COX-1 processes EPA at only about 10% of the efficiency it handles AA, and COX-2 is roughly 2 to 3 times more active with AA than EPA. This means AA-derived signals dominate by default. The signals AA produces tend to promote clotting and constriction of blood vessels. EPA-derived signals do the opposite: they inhibit platelet clumping, relax blood vessels, and reduce damage during cardiac events.
Your EPA/AA ratio captures this tug of war in a single number. A higher ratio means more EPA is available to compete with AA, tilting the balance of signaling molecules toward protection. A lower ratio means AA is running the show largely unopposed.
Most of the clinical evidence for this ratio comes from cardiovascular populations, particularly in Japan, where omega-3 intake and fatty acid testing are more routine. The findings are consistent: lower EPA/AA ratios track with worse cardiovascular outcomes, especially when inflammation is already present.
In a study of about 3,100 Japanese adults followed for roughly 5 years, a lower EPA/AA ratio predicted higher cardiovascular disease risk, but only in people whose high-sensitivity CRP (a general inflammation marker) was at or above 1.0 mg/L. In that inflamed subgroup, each small drop in the ratio (0.20 units) was associated with about a 1.5-fold increase in cardiovascular risk. Notably, this association was specific to coronary heart disease, not stroke, and was not seen with the DHA/AA ratio.
People experiencing acute coronary syndrome (a heart attack or unstable angina) tend to have lower EPA/AA ratios than those without. In one study, a ratio at or below 0.33 was associated with roughly 3 times the odds of acute coronary syndrome.
| Who Was Studied | What Was Compared | What They Found |
|---|---|---|
| About 3,100 Japanese adults with elevated CRP, followed roughly 5 years | Lower versus higher EPA/AA ratio | Each 0.20 drop in the ratio was linked to about 1.5 times higher coronary heart disease risk |
| Adults with and without acute coronary syndrome | EPA/AA ratio at or below 0.33 versus above | Low-ratio group had about 3 times the odds of acute coronary syndrome |
| Acute coronary syndrome patients with high triglycerides on lipid-lowering therapy | Those whose EPA/AA ratio increased 42% or more versus smaller changes | Greater ratio increases were linked to roughly half the rate of cardiovascular events over 3 years (6.0% vs 11.0%) |
| Statin-treated patients with coronary artery disease, imaged with optical coherence tomography | EPA/AA below 0.41 versus above | Lower ratio was associated with more vulnerable plaque features, even when LDL cholesterol was well controlled |
Sources: Hisayama Study (Ninomiya et al.); Nishizaki et al.; Inagaki et al.; Asakura et al.
What this means for you: if you have coronary artery disease or a history of a cardiac event, your EPA/AA ratio can tell you something that LDL cholesterol and standard lipid panels cannot. Even with good statin therapy and controlled LDL, a low EPA/AA ratio may signal that the inflammatory and clotting side of your risk profile is not being addressed.
The EPA/AA ratio responds primarily to EPA intake. Because your body does not efficiently convert plant-based omega-3s (like those in flaxseed) into EPA, the most direct way to raise this ratio is through marine sources or supplements.
EPA supplementation: The landmark JELIS trial established that an EPA/AA ratio above 0.75 was associated with significant reduction in coronary events. A follow-up study, the TREAT-CAD trial, suggested a more ambitious target: an EPA/AA ratio above 1.2 may be needed to reduce mortality in people with coronary artery disease. In that study, a post-treatment ratio of 1.23 showed strong accuracy for predicting survival (AUC of 0.85). EPA treatment in people starting with very low ratios (at or below 0.4) showed a trend toward reduced cardiovascular death.
EPA-to-DHA ratio in supplements matters: If your goal is to lower arachidonic acid and raise the EPA/AA ratio, the composition of your omega-3 supplement matters. A meta-analysis of 96 trials found that supplements with an EPA-to-DHA ratio of 1.0 or higher were most effective at reducing arachidonic acid levels. The EPA-to-DHA blood ratio was the single strongest predictor of how much AA dropped. In practical terms, this means choosing a supplement that emphasizes EPA over DHA if your primary goal is shifting the EPA/AA ratio.
Anti-inflammatory effects of raising the ratio: Both EPA and DHA reduce CRP, TNF-alpha, and IL-6, with the strongest effects in people who have dyslipidemia and elevated baseline CRP. However, a 2025 genetic study using Mendelian randomization found that higher total omega-3 levels may actually cause modest increases in CRP and another inflammatory marker called GlycA, which contradicts what observational studies have shown. This suggests the relationship between omega-3 fats and inflammation may be more complex than a simple "anti-inflammatory" label implies.
Important context on populations: Most of the target ratios and outcome data come from Japanese populations, who have substantially different baseline fatty acid profiles than Western populations. Japanese adults typically have higher baseline EPA/AA ratios due to higher fish consumption. Whether the same thresholds (0.75, 1.2) apply equally to Western populations with lower starting ratios is not fully established. The ratio's predictive value is strongest when combined with inflammatory markers like hs-CRP.