September 3, 2026
Research
The Omega-3 Index: The Blood Test Worth Knowing About
October 9, 2026 · 7 min read
The average British adult sits at 5.6%
The Omega-3 Index in the UK Biobank averages 5.58%, with a standard deviation of 2.35. The figure most often proposed as a target is 8% or above. That gap is the whole reason this test exists.
The index is the combined EPA and DHA content of your red blood cell membranes, as a percentage of all the fatty acids in them. Red cells live about 120 days. So the number reflects what you have been eating for a season, not last Tuesday's salmon.
The UK Biobank figure comes from a 2023 analysis of about 117,000 adults aged 40 to 70. One caveat: the values were estimated from plasma NMR data using a prediction equation, not measured in red cells directly. Treat 5.58% as a good approximation rather than a lab result.
Remember the gap, because the rest of this piece asks how much it matters and how to close it, if you choose to.
What the number measures, and what it ignores
Blood plasma omega-3 swings with your last meal. Red cell membranes do not. That is the point of the index. It smooths out the noise and gives you a longer view.
It counts EPA plus DHA and nothing else. It does not include ALA from flax or walnuts, and it says nothing about the rest of your diet. It is also not a diagnostic test for anything.
The commonly cited zones, from a 2004 review by Harris and von Schacky, are below 4% as low, 4 to 8% as intermediate and above 8% as the target range. Those cut-points were proposed, not handed down by a regulator. Neither the NHS nor NICE uses them.
If you take one thing from this section, take this: the index tells you about your recent intake of long-chain omega-3. Nothing more, and nothing less.
What predicts a low result
In the UK Biobank analysis, oily fish intake was the strongest predictor. Fish oil supplement use came next. Being female and being older both pushed the number up. Smoking, a larger waist and a higher BMI pushed it down.
Here is the catch. All the measured predictors together explained only about 20.5% of the variation in the index. Oily fish alone explained 7%. So two people eating the same diet can land a long way apart.
Even among people who took fish oil and ate oily fish twice a week or more, only 35.7% reached 8% or above. If you eat salmon on Sundays and assume you are fine, the data say you might be. They also say you might not.
That is the practical case for measuring rather than guessing. Your own number is the only way to know where you are.
What the risk data show, and how far to trust them
The strongest published signal comes from the Framingham Offspring Cohort. McBurney and colleagues followed 2,240 adults, mean age mid-60s and free of cardiovascular disease at baseline, for about 11 years. They tested whether red-cell fatty acids improved prediction of all-cause mortality.
Key Study: Red-Cell Fatty Acids and Mortality
In 2,240 adults followed for 11 years, a model built on red-cell fatty acids, including the Omega-3 Index, predicted all-cause mortality as well as the standard risk factors it was compared with (C-statistic 0.778 versus 0.777). Adding smoking and diabetes raised it to 0.790. The authors' own press framing likened a low index to smoking in effect on life expectancy, a comparison that goes beyond what the C-statistics alone show.
Source: McBurney et al., American Journal of Clinical Nutrition, 2021 (n=2,240).
A C-statistic of 0.78 means decent discrimination, not a crystal ball. And it is a prediction study. It shows the index carries information. It does not show that raising your own number lowers your own risk.
The older work is more dramatic. A review by von Schacky reported roughly a ten-fold difference in sudden cardiac death risk between low and high EPA and DHA levels in the Seattle study and the Physicians' Health Study. That is a large gap. It is also a gap between groups of people who differ in many other ways, such as diet, exercise and smoking.
Why 8% is a proposal, not a law
Be careful with the target. It rests mainly on observational data and on populations such as Japan, where mean indices run around 8 to 9% and where people also eat very differently from us in many other respects.
A 2025 analysis of 3,826 US adults with cardiovascular disease, from NHANES, found that people in the top fifth for total dietary omega-3 had lower all-cause mortality than those in the bottom fifth (HR 0.77, 95% CI 0.60 to 0.99). But EPA, DHA and DPA individually were not significantly associated with mortality. That is a dietary-recall study, not a blood-level one, so it does not test the index directly. It does show how quickly a clean story gets messier.
Our view: the index is a useful measurement and a reasonable thing to know. It is not an outcome. Nobody has shown that taking your index from 5.6% to 8% changes what happens to you, and anyone who claims otherwise is ahead of the trials.
If you want a rule of thumb, treat 8% as a direction of travel and not a pass mark.
What moves your number
Dose is the dominant lever. In a randomised, double-blind trial of 115 healthy adults, Flock and colleagues gave daily EPA plus DHA at 0, 300, 600, 900 or 1,800 mg for about five months. The index rose in step with dose.
Key Study: A Dose-Response Trial
Across 115 adults, the EPA+DHA dose alone explained 68% of the variability in how much the index rose. Dose per kilogram of body weight explained 70%. Adding baseline index, age, sex and physical activity brought the total to 78%.
Source: Flock et al., Journal of the American Heart Association, 2013 (n=115).
Two practical points follow. First, body weight matters. A 95 kg man and a 60 kg woman on the same capsule will not move by the same amount. Second, your starting point matters. People who begin low tend to rise further.
Harris's 2008 review puts the time course at four to six months before the index plateaus. So a test six weeks after you start something is measuring a half-finished process.
For the doses tested and the label-claim context, our piece on how much DHA you need per day sets out the numbers. For the over-50 picture, see Omega-3 After 50: Priorities and Dosage.
How to test, and when to retest
Most home kits use a finger-prick dried blood spot, posted to a lab. Check one thing before you buy: that it reports the red-cell index. Plasma-only results respond within days and cannot be compared with the 8% figure.
Test once as a baseline, ideally after your usual diet has been stable for a few months. If you change your diet or start a supplement, wait four to six months and test again. Testing in between mostly measures noise and impatience.
A few cautions. Keep the testing company's commercial interest in mind: a lab that sells the kit and the supplement has reasons to like a low result. Ask whether the lab uses a standardised method. And if you take anticoagulants or have a heart condition, talk to your GP before changing your omega-3 intake.
The result is one data point among several. If you are also tracking inflammation, our guide to the hs-CRP marker covers a second number worth putting beside it.
What to do with the result
Below 4% usually means very little oily fish and no supplement. Between 4 and 8% is where most people sit, including the average UK Biobank participant. Above 8% means your recent intake has been high.
If you land below 8% and want to move, you have two routes. Food: eating oily fish more often raises the index, though by how much varies from person to person. Supplement: a measured daily EPA and DHA dose, with body weight in mind. If you eat no fish at all, algae-derived DHA is an option, and our Omega-3 DHA capsule gives a stated amount per serving.
Then retest at five to six months and compare. Judge it on your own trend. The population averages are only the backdrop.
Finally, keep the claim honest. A higher index is a measure of what you have been taking in. It is not a promise about your heart, brain or lifespan, and no trial has shown it to be one for you.
References
- Schuchardt JP, Tintle N, Westra J, Harris WS (2023). "Estimation and predictors of the Omega-3 Index in the UK Biobank." British Journal of Nutrition, 130(2), 312-322. doi:10.1017/S0007114522003282
- McBurney MI, Tintle NL, Vasan RS, Sala-Vila A, Harris WS (2021). "Using an erythrocyte fatty acid fingerprint to predict risk of all-cause mortality: the Framingham Offspring Cohort." American Journal of Clinical Nutrition, 114(4), 1447-1454. doi:10.1093/ajcn/nqab195
- Flock MR, Skulas-Ray AC, Harris WS, Etherton TD, Fleming JA, Kris-Etherton PM (2013). "Determinants of erythrocyte omega-3 fatty acid content in response to fish oil supplementation: a dose-response randomized controlled trial." Journal of the American Heart Association, 2(6), e000513. doi:10.1161/JAHA.113.000513. PMID 24252845
- von Schacky C (2010). "Omega-3 Index and Sudden Cardiac Death." Nutrients, 2(3), 375-388.
- Harris WS (2008). "The omega-3 index as a risk factor for coronary heart disease." American Journal of Clinical Nutrition, 87(6), 1997S-2002S. PMID 18541601
- Harris WS, von Schacky C (2004). "The Omega-3 Index: a new risk factor for death from coronary heart disease?" Preventive Medicine, 39(1), 212-220. PMID 15208005
- Yan Y, et al. (2025). "Association of dietary omega-3 fatty acids intake with all-cause and cardiovascular disease-specific mortality among individuals with cardiovascular disease." Scientific Reports, 15, 37279.
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