Why Some People Need More Omega-3 Than Others, Explained by FADS1

Most of the omega-3 in a typical diet, whether it comes from flaxseed, walnuts, or canola oil, arrives as ALA, a plant-based fatty acid your body has to convert into the two forms that actually matter for heart and brain health: EPA and DHA. Variants in the FADS1 and FADS2 genes control the enzymes that do that conversion, and people with certain variants convert ALA at a lower rate. That means the "just eat more flaxseed" advice doesn't work the same way for everyone.

ALA has to be converted, it isn't used as-is

ALA (alpha-linolenic acid) is the omega-3 found in plant sources like flaxseed, chia, walnuts, and canola oil. It isn't biologically inert, but most of its documented health effects, the ones tied to heart and brain outcomes, come from EPA (eicosapentaenoic acid) and DHA (docosahexaenoic acid), the long-chain omega-3s found preformed in fatty fish and algae oil.

To turn ALA into EPA and DHA, your body runs it through a chain of desaturase and elongase enzymes. The two rate-limiting steps in that chain are controlled by the FADS1 and FADS2 genes (fatty acid desaturase 1 and 2). A 2025 study of Brazilian adults published in Metabolites found that FADS1 and FADS2 polymorphisms measurably change omega-3 and omega-6 fatty acid levels in red blood cells, and the authors described this as "a significant gene-diet interaction" between what people ate and how their variants processed it (Batista et al., 2025). In practice, that means two people eating identical amounts of flaxseed oil can end up with different blood levels of EPA and DHA, purely because of which version of these genes they carry.

What a "slow converter" FADS1/FADS2 variant actually means

If you carry FADS1 or FADS2 variants linked to lower enzyme activity, your body converts a smaller fraction of dietary ALA into usable EPA and DHA. You aren't unable to make any, the pathway still runs, it's just less efficient. Over time, on a diet that leans on plant-based omega-3 without much fish or algae oil, that inefficiency can translate into lower circulating EPA and DHA than someone with a more efficient variant eating the exact same diet.

This is where individual variation in supplement response comes from too. In a 2024 trial published in Nutrients, 76 adults with obesity were split into an omega-3 group (1.5 grams of n-3 fatty acids per day) and a placebo group (1.5 grams of sunflower oil per day), and the researchers linked FADS1 genetic variation to differences in how much red blood cell fatty acid composition shifted after supplementation (Reyes-Pérez et al., 2024). Same dose, same number of weeks, different genetic starting point, different result.

Genetics isn't the only lever here. A 2022 study of US Naval Academy athletes in Nutrients set out to see whether a personalized omega-3 dose, informed partly by molecular genetic testing, could get participants to an Omega-3 Index (a blood measure of EPA and DHA as a share of red blood cell fatty acids) of 8% or higher, a level generally considered protective (Rittenhouse et al., 2022). The point of that study wasn't that genetics alone determines your omega-3 status, it was that a one-size-fits-all dose doesn't get everyone to the same target, and factoring in the individual (genetics included) is one way to close that gap.

Should you prioritize EPA/DHA sources over ALA?

If you eat fish or take a fish oil or algae oil supplement regularly, your conversion efficiency matters less, because you're getting EPA and DHA directly and skipping the enzyme bottleneck entirely. Conversion genetics matters most for people who rely mainly on plant sources of omega-3, vegetarians, vegans, or anyone who mostly gets omega-3 from flax, chia, or walnuts rather than fish.

For a slow-converter genotype eating a plant-heavy diet, the practical options are the same options anyone has, just more relevant: eat fatty fish (salmon, sardines, mackerel) a couple of times a week, or use an algae-oil supplement, which delivers preformed DHA and EPA without needing the FADS pathway at all.

ALA sources vs. direct EPA/DHA sources

Source	Omega-3 form	Needs FADS1/FADS2 conversion?
Flaxseed, chia, walnuts, canola oil	ALA	Yes
Salmon, sardines, mackerel, anchovies	EPA + DHA	No, already preformed
Fish oil supplements	EPA + DHA	No
Algae oil supplements	DHA (some also EPA)	No

What Biome's panel reports on this

Biome sells a DNA test and a whole genome test, and the DNA panel includes an "Omega-3 conversion" result based on the FADS1 markers rs174537, rs174546, and rs174547, plus the FADS2 marker rs174575, with a moderate evidence tier. That result reflects the same conversion pathway described above: it doesn't diagnose an omega-3 deficiency, it flags whether your genetic variants are associated with less efficient ALA-to-EPA/DHA conversion, which is one input (not the whole picture) for deciding whether to lean more on direct EPA/DHA sources.

FAQ

What's the difference between ALA and EPA/DHA omega-3? ALA is the plant-based omega-3 in foods like flaxseed and walnuts. EPA and DHA are the long-chain forms found in fatty fish and algae oil, and most of the researched heart and brain benefits of omega-3 are tied to EPA and DHA specifically, not ALA itself.

Can I get enough omega-3 from flaxseed or walnuts alone? It depends partly on your FADS1/FADS2 variants. Everyone converts some ALA into EPA and DHA, but people with less efficient variants convert a smaller share, so relying only on plant sources may leave them with lower EPA/DHA levels than someone with a more efficient conversion genotype eating the same diet.

Do FADS1/FADS2 variants matter more for vegetarians and vegans? Yes. If fish or algae oil is already part of your diet, you're getting EPA and DHA directly and the conversion step matters less. If plant sources are your main or only omega-3 intake, your conversion efficiency has more influence on your actual EPA/DHA status.

Does taking more ALA supplement fix a slow-converter genotype? Increasing ALA intake can help somewhat, but it doesn't remove the bottleneck. Since the enzymes encoded by FADS1 and FADS2 are the limiting step, going straight to a food or supplement that already contains EPA and DHA sidesteps the conversion issue instead of working around it.

Does Biome test for omega-3 conversion genetics? Biome's DNA panel reports on "Omega-3 conversion" using the FADS1 markers rs174537, rs174546, rs174547 and the FADS2 marker rs174575, at a moderate evidence tier. Check the specific report's evidence notes for how to interpret the result alongside your actual diet.