Low EPA, DPA, and DHA: What It Means and How to Fix It

Low levels of EPA (eicosapentaenoic acid), DPA (docosapentaenoic acid), and DHA (docosahexaenoic acid) signal that your body is short on the long-chain omega-3 fatty acids it needs for resolving inflammation, maintaining brain and eye function, and protecting cardiovascular health. These three fats are not interchangeable with the plant-based omega-3 (ALA) found in flax and walnuts, because humans convert very little ALA into EPA and even less into DHA. The practical upshot is that if a blood test or dietary assessment flags you as low, the fix almost always involves eating more seafood or taking a marine-origin supplement, not adding more seeds to your smoothie.

What EPA, DPA, and DHA Actually Do

EPA and DHA sit in the membranes of your cells, where they influence how fluid and responsive those membranes are to signals from the rest of the body.¹ Their most studied role involves inflammation. When your body encounters injury or infection, it generates signaling molecules from whatever fatty acids are available in cell membranes. If arachidonic acid (an omega-6 fat) dominates, you get more pro-inflammatory signals. When EPA is abundant, the signaling molecules it generates tend to be less potent at ramping up inflammation. Both EPA and DHA are also precursors to a class of compounds called resolvins and protectins, which actively help shut down inflammation once it has served its purpose.² Think of it as having both a weaker accelerator and a stronger brake on the inflammatory response.

DHA has an additional job that sets it apart. It concentrates heavily in brain tissue and the retina, where it supports neuronal signaling, memory formation, and photoreceptor function.³ No other fatty acid accumulates in these tissues to the same degree, which is part of the reason that DHA gets so much attention in discussions of brain health and infant development.

DPA is the least studied of the three, but research is catching up. A supplementation trial with highly pure DPA suggested it serves as a storage depot that the body can convert into EPA or, to a lesser extent, DHA as needed. Lab and animal studies have also linked DPA directly to reduced platelet clumping, improved fat metabolism, and better endothelial cell migration, which matters for blood vessel repair.⁴ Separate research has connected dietary DPA with improvements in cardiovascular and metabolic risk markers, including insulin sensitivity and plasma lipid levels.⁵ In short, DPA is not just a bystander between EPA and DHA on the metabolic pathway; it appears to pull its own weight.

Why Your Levels Might Be Low

The most obvious reason is diet. EPA, DPA, and DHA are found almost exclusively in seafood, with fatty fish like salmon, mackerel, sardines, herring, and anchovies being the richest sources. If you rarely eat fish or shellfish, your intake of all three will be minimal. The Western diet compounds the problem because it is typically heavy in omega-6-rich vegetable oils (soybean, corn, sunflower), and high omega-6 intake competes with omega-3s in the body’s metabolic pathways. That imbalance pushes the system toward a more pro-inflammatory state.⁶

People who eat plant-based diets sometimes assume that flaxseed, chia seeds, hemp seeds, and walnuts cover their omega-3 needs. These foods are excellent sources of ALA, the short-chain omega-3. But the human body converts ALA to EPA at a rate of only about 6%, and to DHA at roughly 4% or less, depending on the background diet.⁷ Women of reproductive age seem to convert ALA to DHA somewhat more efficiently than men, likely because of estrogen’s effect on the conversion enzymes, but even that advantage does not close the gap.⁸ Relying solely on ALA-rich foods to maintain adequate EPA and DHA status is, for most people, a losing strategy.

Genetics also plays a role. Variations in the FADS1 and FADS2 genes, which encode the desaturase enzymes that help convert shorter-chain fatty acids into longer ones, differ across individuals and populations. People who carry certain common variants in these genes tend to have lower circulating levels of EPA and DHA even when their diets are similar to those of non-carriers.⁹ These polymorphisms are common enough that they contribute meaningfully to the range of omega-3 levels seen in any large group of people eating roughly the same diet.¹⁰ You cannot change your genotype, but knowing about it helps explain why two people eating the same amount of fish can end up with different blood levels, and why some people may need higher intakes or supplementation to reach the same target.

How Low Levels Are Measured

The most widely used clinical marker is the omega-3 index, which measures the combined percentage of EPA and DHA in the membranes of red blood cells. Because red blood cells turn over roughly every 120 days, the omega-3 index reflects your average intake over the previous three to four months rather than what you ate last night.¹¹ An index below about 4% is considered high risk, while 8% or above is associated with the lowest cardiovascular risk.¹² Most Americans and Europeans who do not regularly eat fish or supplement fall somewhere in the 4–5% range. DPA is not always reported on standard panels, but its levels generally track with EPA and DHA because it shares the same dietary sources.

You can get the test through some direct-to-consumer lab companies or through a physician who orders a specialized fatty acid profile. The test uses a dried blood spot or a small vial of blood, and results usually come back within a couple of weeks. It is not part of a routine lipid panel, so you will need to ask for it specifically.

Cardiovascular Risks of Running Low

The cardiovascular connection is the most studied consequence of low omega-3 status. A pooled analysis of ten cohort studies found that people in the highest quintile of the omega-3 index (median around 8.3%) had meaningfully lower risk of fatal coronary heart disease compared with those in the lowest quintile (median around 4.2%). Each standard-deviation increase in the combined EPA, DPA, and DHA level was associated with a 15% lower risk of dying from coronary heart disease.¹² The omega-3 index has been proposed as an independent risk factor for cardiovascular events, alongside more familiar markers like cholesterol and blood pressure.¹³

These are observational associations, not proof that raising your omega-3 index will prevent a heart attack. But the relationship has held up across diverse populations and study designs, and the underlying biology is plausible: EPA and DHA lower triglycerides, reduce inflammatory signaling in arterial walls, and modestly decrease blood pressure and heart rate. The effect sizes are not enormous on a population level, but for someone with a very low omega-3 index, raising it from 4% toward 8% is one of the more straightforward dietary levers available.

Brain Health and Cognitive Decline

DHA is the dominant omega-3 in the brain, so it makes sense that low DHA status has been linked with cognitive problems. A large evidence synthesis incorporating 48 longitudinal studies and over 100,000 participants found moderate-to-high evidence that dietary omega-3 intake was associated with roughly a 20% lower risk of dementia or cognitive decline. DHA intake specifically carried a relative risk of about 0.82, meaning an 18% risk reduction. Each additional 0.1 grams per day of DHA or EPA was linked with an 8–10% lower risk of cognitive decline.¹⁴ Blood markers showed a similar pattern: higher plasma EPA and higher red blood cell DHA were both associated with lower cognitive decline risk.

This does not mean omega-3 supplements cure or reliably prevent Alzheimer’s disease. Clinical trials in people who already have significant cognitive impairment have generally been disappointing. The benefit appears to be more about maintaining brain health over years and decades rather than reversing damage that has already occurred, and it is strongest when omega-3 status starts out low.

Pregnancy and Early Development

Pregnant women with low DHA intake or low DHA blood levels face a higher risk of preterm birth and early preterm birth.¹⁵ An evidence review by the International Society for the Study of Fatty Acids and Lipids confirmed that adequate omega-3 intake in early pregnancy, particularly DHA and EPA, is associated with longer gestation in singleton pregnancies and that women who are low in omega-3 fatty acids benefit the most from supplementation.¹⁶ An exploratory analysis from a randomized controlled trial reinforced this: women with low total omega-3 status early in pregnancy had higher risk of early preterm birth and were the group most likely to benefit from supplementation.¹⁷

DHA also accumulates rapidly in fetal brain tissue during the third trimester, making maternal DHA status especially consequential during late pregnancy and breastfeeding. Many prenatal vitamins now include DHA, but the doses vary widely. If you are pregnant or planning to become pregnant and eat very little fish, checking your omega-3 status and supplementing if needed is a reasonable step that lines up with current nutritional guidelines.

Inflammation, Joint Disease, and Dry Eyes

Because EPA and DHA directly shape the body’s inflammatory signaling, low levels have implications beyond the heart and brain. In rheumatoid arthritis, clinical studies have found that omega-3 supplementation can modulate disease activity, particularly reducing the number of swollen and tender joints.¹⁸ The effect is not large enough to replace standard medications, but it may reduce the need for anti-inflammatory drugs in some patients.

Dry eye syndrome, another condition driven partly by surface inflammation, also responds to omega-3 supplementation. A meta-analysis of randomized controlled studies found that omega-3 supplementation improved tear break-up time and Schirmer’s test results (a standard measure of tear production) compared to placebo.¹⁹ If you spend long hours staring at screens and deal with chronically dry, irritated eyes, persistently low omega-3 intake could be one factor worth addressing, though it is rarely the only cause.

Children and ADHD Symptoms

The developing brain’s appetite for DHA extends into childhood, and researchers have investigated whether omega-3 supplementation can help children with attention and behavior difficulties. A systematic review and meta-analysis found that omega-3 supplementation produced a small but statistically significant improvement in ADHD symptoms, and that higher EPA content in the supplement correlated with greater benefit.²⁰ A separate review found favorable effects across 13 studies, including improvements in hyperactivity, impulsivity, attention, visual learning, and working memory.²¹

The effect sizes are small compared with stimulant medications, so omega-3s are not a substitute for standard ADHD treatment. But for children whose diets are clearly low in omega-3s, correcting that deficiency is a low-risk intervention that may modestly improve attention and behavior alongside other approaches.

How to Raise Your Levels

The most effective way to increase EPA, DPA, and DHA is to eat fatty fish two to three times per week. Salmon, mackerel, sardines, herring, and anchovies are the richest sources, each providing roughly 1,000–2,000 milligrams of combined EPA and DHA per serving. Shellfish like mussels and oysters are moderate sources. White fish like cod and tilapia contain much less. DPA occurs naturally alongside EPA and DHA in these same seafood sources, so you generally do not need to seek it out separately.

If fish is not an option due to taste preference, allergy, dietary restrictions, or concerns about contaminants, supplements are the next best approach. A dose-response trial found that the omega-3 index increased in direct proportion to the dose of EPA and DHA given, with dose alone accounting for about 68% of the variation in response.²² That means the amount you take matters more than most other variables, though individual factors like body weight and baseline status also play a role.

Not all supplements are created equal. The main forms you will see on shelves include fish oil (in triglyceride or ethyl ester form), krill oil (naturally rich in phospholipid-bound omega-3s), and algal oil (derived from microalgae, suitable for vegetarians and vegans). A network meta-analysis found that krill oil formulations rich in phospholipids offered superior absorption compared with standard triglyceride-based fish oil.²³ Meanwhile, a clinical trial comparing microalgal oil to fish oil found that the algal source was statistically noninferior in terms of raising plasma EPA and DHA levels.²⁴ For people avoiding animal products entirely, algal oil is the only direct source of preformed DHA and EPA, and the evidence suggests it works about as well as fish oil.

A few practical notes on supplements: take them with a meal that contains some fat, since omega-3s are fat-soluble and absorb better alongside dietary fat. Fish oil capsules sometimes cause fishy burps, which you can minimize by choosing enteric-coated capsules or keeping them in the freezer. High-dose fish oil (above about 3 grams per day of combined EPA and DHA) can thin the blood, so if you are on anticoagulant medication, talk to your doctor before starting. At standard doses of 1–2 grams per day, side effects are usually limited to mild digestive discomfort.

What About Reducing Omega-6 Intake

Raising omega-3 intake is half the equation. The other half, which gets less attention, involves the omega-6 fatty acids that compete for the same enzymes. Modern diets are flooded with linoleic acid from soybean oil, corn oil, sunflower oil, and the processed foods made with them. High omega-6 consumption competes with omega-3s for incorporation into cell membranes and tilts the balance of inflammatory signaling molecules toward pro-inflammatory pathways.⁶

You do not need to eliminate omega-6 fats, which are essential nutrients in their own right. But swapping some of the high-linoleic-acid oils in your kitchen for olive oil, avocado oil, or even butter changes the ratio in a favorable direction. Reducing fried and ultra-processed foods, which tend to be cooked in cheap seed oils, has a similar effect. The goal is not zero omega-6 but a more balanced ratio, which amplifies whatever omega-3 you are consuming.

DHA, Seafood, and the Human Brain’s Evolutionary History

There is an interesting evolutionary angle to why humans seem so dependent on a dietary source of DHA. The human brain is unusually large relative to body size, and its growth during our species’ evolution required enormous quantities of DHA. Fossil evidence and molecular biology both point to early humans exploiting lakeside and coastal food webs at the time the brain was expanding most rapidly.²⁵ The savanna environment, by contrast, offers almost no preformed DHA, which has led researchers to argue that the transition from archaic to modern humans depended on access to the land-water interface where DHA-rich food was abundant.²⁶

This is not just a neat historical footnote. It helps explain why human biology never developed an efficient internal pathway for making DHA from plant-based precursors. If your ancestors had plentiful DHA from fish and shellfish, there was no evolutionary pressure to get better at synthesizing it from scratch. That legacy means we are essentially stuck relying on dietary sources, and in a modern food environment where seafood is expensive and seed oils are cheap, many people end up chronically undersupplied.