Cold-pressed oil from flax seed, roughly half to 55% alpha-linolenic acid — the plant omega-3. It contains no EPA and no DHA.
Flaxseed oil is frequently sold as a vegetarian substitute for fish oil, and the biochemistry does not support that framing. Humans convert alpha-linolenic acid to EPA at something like 5–8%, and to DHA at well under 1% in most measurements, with conversion further suppressed by the high linoleic acid intake typical of Western diets. Taking flax oil raises blood ALA and modestly raises EPA; it does not meaningfully raise DHA. That does not make it useless — ALA has its own observational associations with cardiovascular risk — but it is not the same intervention as a marine oil, and the whole seed additionally supplies fibre and lignans that the oil does not.
Sold as
Cold-pressed liquid oil, Softgel, High-lignan oil
Standardised to
Typically 50–58% alpha-linolenic acid — a product without this marker may not resemble what was studied.
Also known as
Linseed oil, Alpha-linolenic acid oil, Flax oil
Regulation: Sold as a dietary supplement or a food oil with no pre-market efficacy review. EFSA permits a claim that ALA contributes to maintenance of normal blood cholesterol at 2 g/day.
What the research used
The amounts, forms and durations published trials of Flaxseed oil (ALA) actually administered.
These are the amounts published trials administered — not a recommendation, and not a dose to copy. Trial participants were screened, supervised and given a characterised preparation. What is in a retail bottle is frequently not what was studied, and the amount that suits one person is not general advice.
One tablespoon of flaxseed oil supplies roughly 7–8 g of ALA. Effects on lipids in trials are small and less consistent than those seen with whole ground flaxseed, which also delivers fibre.
Studied for Adequate Intake reference for ALA
1.1–1.6 g
Moderate
ALA daily from all dietary sources
The US Adequate Intake figures for alpha-linolenic acid — 1.1 g/day for women and 1.6 g/day for men. An intake reference, not a supplement dose.
This is general information about food, not medical advice. It cannot diagnose, treat or replace guidance from a clinician who knows your history.
When it was taken
Each window says whether a trial compared it against an alternative, or whether it is convention and pharmacology. Most timing advice is the second kind.
None of the timings below were directly compared in a trial. They reflect how the research happened to dose, or what the pharmacology implies — which is not the same as a timing being better.
🕐Any time
Not enough
No trial has compared timing. Flaxseed oil is a food fat and is absorbed as one; the practical constraint is heat and light, since it oxidises quickly and should not be cooked with.
Timing was not directly compared. This reflects convention or how the compound behaves in the body, not a trial showing this window works better.
The evidence in depth
Best supported: Limited
What each association actually rests on, and the papers behind it. A rating describes the state of the research, not how promising the supplement sounds. How we rate evidence.
Meta-analyses of flaxseed report small reductions in LDL cholesterol, with the effect clearer for whole or ground seed than for the oil alone — which points to the fibre and lignans rather than the ALA. Effects on triglycerides are much weaker than with EPA and DHA.
Limited evidence. Early human work, or mostly lab and animal research.
Observational cohorts associate higher ALA intake with lower cardiovascular risk, but randomised trials of ALA supplementation have not shown event reductions, and the conversion of ALA to the long-chain omega-3s studied in cardiovascular trials is minimal in humans.
What may be going on: ALA is converted to EPA at roughly 5–8% and to DHA at well under 1%, with the desaturase steps competing with linoleic acid from the same enzymes.
Limited evidence. Early human work, or mostly lab and animal research.
Some trials of flaxseed report modest reductions in blood pressure, most notably a trial in peripheral arterial disease using milled seed rather than oil. Results across the wider literature are inconsistent and the oil-only trials are weaker.
Limited evidence. Early human work, or mostly lab and animal research.
Deep research mode adds each paper’s own conclusion and stated limitations.
Things to know
Interactions, contraindications and dose limits, most serious first. Concentrated extracts interact with medication in ways the whole plant does not, so this section carries more weight here than it does on a food page.
Worth knowing
Not a replacement for EPA and DHA
Conversion of ALA to EPA is limited and conversion to DHA is negligible in most people. Anyone taking flaxseed oil in place of a marine or algal omega-3 for a DHA-dependent purpose — pregnancy, for example — is not achieving the same thing.
Worth knowing
Oxidises rapidly
Flaxseed oil is one of the least stable edible oils. It should be refrigerated, kept away from light, used well within its date and never heated. Rancid flax oil smells of paint and delivers oxidation products rather than intact ALA.
Interaction
Possible additive effect with blood thinners
Interacts withWarfarin, direct oral anticoagulants, antiplatelet drugs
Reports of prolonged bleeding time with high ALA intake exist, and the theoretical additive effect with anticoagulant and antiplatelet drugs is usually flagged even though the human interaction data are thin.
Worth knowing
Hormone-sensitive conditions and the lignan question
High-lignan flaxseed oils and whole flaxseed contain phytoestrogenic lignans. Human evidence of harm is absent and some data are reassuring, but people with hormone-sensitive cancers are usually advised to discuss it rather than assume.
In the food catalogue
The whole-food form, where one exists. The evidence for a concentrated extract rarely transfers to the food, or the other way round — these are cross-links, not equivalents.