AA:EPA Test

If you could see one number that captures how much of a pro-inflammatory tilt your body is carrying, your AA:EPA ratio (arachidonic acid to eicosapentaenoic acid) would be a strong candidate. This ratio compares two types of fat that compete for the same machinery inside every cell: AA, an omega-6 fat that drives inflammation, and EPA, an omega-3 fat that helps resolve it. A high ratio means your cells are loaded with more inflammatory raw material and less of the calming kind.

What makes this test especially useful is that it picks up risk your standard cholesterol panel misses. In a study of over 3,100 Japanese adults followed for about five years, people with lower EPA relative to AA had about 50% higher risk of cardiovascular disease, but only when their inflammation was already elevated. Standard lipids did not capture that conditional risk. This ratio tells you something different from LDL or triglycerides: it tells you about the inflammatory environment inside your arteries.

What This Ratio Measures

Both AA and EPA are long-chain polyunsaturated fatty acids, meaning they are long fat molecules with multiple flexible bends in their structure. They sit in the outer walls of your cells. When your body needs to mount an immune response or heal an injury, enzymes pull these fats out of cell walls and convert them into signaling molecules. AA gets converted into molecules that ramp up inflammation, pain, and clotting. EPA gets converted into molecules that cool inflammation down and promote tissue repair.

The AA:EPA ratio reflects which team has more players on the field. A high ratio (lots of AA, little EPA) means your body's default signaling leans heavily toward inflammation. A low ratio means you have more raw material for resolution and repair. Your ratio is shaped primarily by what you eat: diets heavy in red meat, processed food, and vegetable oils (corn, soybean) push AA up, while regular fish or omega-3 supplementation pushes EPA up.

Heart Disease and Coronary Plaque

The cardiovascular evidence for this ratio is the strongest and most consistent. In a community study of over 3,100 adults (the Hisayama Study), those in the lowest quarter of EPA relative to AA had about 50% higher risk of cardiovascular disease compared to the highest quarter, after adjusting for blood pressure, diabetes, cholesterol, BMI, medications, smoking, and alcohol. That risk was concentrated in people who also had elevated hs-CRP (high-sensitivity C-reactive protein, a marker of systemic inflammation at or above 1.0 mg/L). When inflammation was low, the ratio mattered less.

The ratio also predicts what your arteries look like on the inside. In 193 people without known coronary artery disease, those with lower EPA relative to AA were more likely to have dangerous, rupture-prone plaque on coronary CT scans. In 370 statin-treated patients with known heart disease, those with ratios below 0.4 (EPA/AA) had more fat-filled plaques loaded with immune cells called macrophages and cholesterol crystals, the kind most likely to trigger a heart attack, even though their LDL cholesterol was controlled.

What this means for you: if your standard cholesterol numbers look fine but you eat little fish, have elevated hs-CRP, or carry other cardiovascular risk factors, this ratio can reveal a hidden inflammatory tilt that standard lipids miss.

Heart Failure and Peripheral Artery Disease

The ratio's reach extends beyond coronary arteries. Among 577 hospitalized heart failure patients, those with lower EPA/AA had significantly higher cardiac mortality, independent of how well their heart was pumping (measured by ejection fraction) and standard lab values. In 132 patients with peripheral artery disease (blocked leg arteries) who underwent procedures to restore blood flow, those with EPA/AA at or below 0.30 had substantially more limb events and higher death rates over follow-up.

Cancer Risk

In a community cohort of about 3,100 Japanese adults followed for nearly 10 years, those in the lowest quarter of EPA/AA had roughly twice the risk of dying from cancer compared to the highest quarter (about 1.9 times the risk after full adjustment). The association was strongest for liver cancer. Separately, tumor tissue from patients with metastatic colorectal cancer showed markedly higher AA/EPA compared to non-metastatic tumors, alongside higher levels of inflammation-driving enzymes.

A pilot study of lung cancer patients treated with the immunotherapy drug pembrolizumab found that those with higher EPA/AA before treatment had significantly better overall survival. While this is preliminary, it suggests the ratio may also reflect how well your immune system can fight cancer when given the right support.

Stroke and Brain Health

In 269 ischemic stroke patients, higher EPA/AA at admission correlated with less severe strokes and better outcomes. After adjusting for age, BMI, prior cardiovascular disease, lipids, and smoking, higher EPA/AA independently predicted lower risk of death and recurrent vascular events over about 2.3 years of follow-up.

In Alzheimer's disease, a randomized trial of DHA (docosahexaenoic acid, another omega-3 fat) supplementation in 414 patients found that the ability to raise EPA/AA and DHA/AA depended heavily on APOE genotype (a gene variant linked to Alzheimer's risk). Carriers of the protective APOE 2/3 variant showed larger increases in EPA/AA and less shrinkage of the hippocampus (the brain's memory center). Carriers of two copies of the risk variant APOE 4 showed smaller ratio increases and continued brain shrinkage.

Depression and Kidney Health

In about 2,500 Japanese adults, higher AA relative to EPA was associated with more depressive symptoms, but again, only among those with elevated systemic inflammation. When CRP was low, the ratio did not predict depression. This reinforces a pattern: the ratio matters most when inflammation is already present.

For kidney health, a study of 444 community-dwelling adults found that lower EPA/AA independently predicted microalbuminuria (small amounts of protein leaking into urine, an early sign of kidney damage) after adjusting for blood pressure, blood sugar, and CRP.

Atrial Fibrillation: A Trade-Off Worth Knowing

Not every association with higher EPA/AA is favorable. In a study of 673 older patients (age 65 and above) who underwent ablation for atrial fibrillation (an irregular heart rhythm), those with higher EPA/AA had more atrial fibrillation recurrence after the procedure. At the same time, they had fewer major cardiovascular events like heart attack and stroke. The RESPECT-EPA randomized trial of nearly 3,900 coronary disease patients also found that high-dose EPA supplementation, while reducing coronary events, increased new cases of atrial fibrillation.

This is not a reason to avoid improving your ratio, but it is a reason to be aware. If you have a history of atrial fibrillation or are at high risk for it, discuss this trade-off with a cardiologist before starting high-dose EPA supplementation.

Reference Ranges

No major Western guideline has established universal clinical cutpoints for AA:EPA. Most thresholds come from Japanese cardiovascular studies using serum fatty acids measured by specialized laboratory methods. The numbers below are research-derived orientation, not universal targets. Your lab may report the ratio differently (some labs report EPA/AA, some report AA/EPA, and the units can vary). Always compare your results within the same lab over time.

One Japanese treatment study proposed an EPA/AA target above 1.2 for secondary prevention in coronary disease patients receiving high-dose EPA, based on a threshold that predicted lower all-cause mortality. This is an aggressive target, achievable mainly with prescription-strength EPA, and should not be treated as a population-wide goal. For most people focused on prevention, moving your ratio from the bottom third into the middle or upper third is a meaningful and achievable improvement.

When Results Can Be Misleading

Your AA:EPA ratio is relatively stable compared to markers like glucose or cortisol, because it reflects fatty acids embedded in cell walls, which turn over slowly. Still, several factors can distort a single reading.

• Recent dietary changes: A single large fish meal will not meaningfully shift your ratio overnight, but starting or stopping fish oil supplements for a few weeks can. If you recently changed your omega-3 intake, wait at least 4 to 6 weeks before testing for a reading that reflects your new steady state.
• Blood sample type: Serum, plasma, and whole blood (dried blood spot) can give different absolute numbers. Most research uses serum measured by specialized laboratory methods. If your lab uses a different method, the numbers may not match published thresholds exactly.
• Active inflammation or illness: Acute infections, surgery, or inflammatory flares can temporarily shift fatty acid profiles. Test when you are feeling well and have been in your usual routine for several weeks.
• Statin use: Common statins like rosuvastatin and pitavastatin do not appear to change the AA:EPA ratio by themselves in clinical studies, so you do not need to account for them when interpreting your result.

Tracking Your Trend

A single AA:EPA reading gives you a snapshot of your inflammatory fat balance. A series of readings, spaced over months, tells you whether your diet and supplement strategy is actually working. This is where the ratio earns its keep as a tracking tool.

Get a baseline reading before making changes. If you start eating more fatty fish or begin omega-3 supplementation, retest in 3 to 4 months to see how much your ratio has moved. Omega-3 supplementation reliably lowers the AA:EPA ratio in both healthy people and those with coronary disease, but the magnitude of change varies by dose, formulation (EPA-only vs EPA+DHA), and individual metabolism. Seeing your own before-and-after numbers removes the guesswork.

After you have confirmed a shift in the right direction, retest at least annually to make sure your levels are holding. If you stop supplementation, the ratio tends to drift back toward its prior level, so tracking keeps you honest.

What to Do With an Abnormal Result

If your AA:EPA ratio is elevated (EPA/AA below about 0.30), the first step is to pair it with hs-CRP. The cardiovascular risk from a high ratio is most pronounced when systemic inflammation is also elevated. If both are unfavorable, the combination points to an inflammatory profile that standard lipid panels would not have flagged.

Consider ordering a full omega-3 panel (Omega-3 Index, EPA, DHA, and the Omega-6:Omega-3 ratio) if you have not already. This broader picture tells you whether the issue is low omega-3 intake, high omega-6 intake, or both. For cardiovascular risk assessment, pair with ApoB and Lp(a) to see whether you also have particle-level lipid risk.

If your ratio is very low and you have known coronary disease, heart failure, or peripheral artery disease, share this result with a cardiologist or lipidologist. High-dose EPA therapy (icosapent ethyl, 1.8 g/day or more) has been studied specifically in patients with low EPA/AA and existing cardiovascular disease, and a specialist can weigh the benefits against the atrial fibrillation trade-off. For someone without established disease, dietary changes and standard-dose omega-3 supplementation are reasonable first steps, with a retest in 3 to 4 months to confirm improvement.