Seed oils

Sunflower, safflower, soybean, canola and corn oil have become an online villain, accused of driving inflammation and heart disease through their main fat, the omega-6 linoleic acid. The human evidence points the other way: people with more linoleic acid in their blood do better, controlled trials find no rise in inflammation, and the real problems are commercial deep-frying and the ultra-processed food these oils turn up in.

Don't fear seed oils in your own kitchen: use fresh oil at moderate heat, and use it in place of butter and other saturated fats. Avoid ultra-processed food and commercial deep-fried food instead, and don't chase an omega-6 to omega-3 ratio.

What seed oils are

Seed oils are vegetable oils pressed or extracted from seeds. Their dominant fat is linoleic acid (LA), the main omega-6 fat in the diet. Omega-6 and omega-3 are the two families of polyunsaturated fat, and both are essential nutrients: the body cannot make them. The case against seed oils is that linoleic acid feeds inflammation and heart disease; the case for them is that replacing saturated fat with polyunsaturated fat lowers heart risk.

People with more linoleic acid do better, not worse

A 2025 review pooling 150 cohort studies found higher omega-6 linked to lower death rates — about 12% lower for omega-6 in the diet (relative risk 0.88, 95% confidence interval 0.83–0.94; the interval is the range where the true effect most plausibly lies) — with the strongest and most consistent signals coming from blood measurements rather than diet questionnaires.[1] For dietary omega-6 the results were null for cardiovascular disease and for cancer overall, with one small signal of higher endometrial and ovarian cancer risk, and the certainty of the evidence ranged from very low to moderate. Read it as no overall harm plus a mortality benefit, not broad protection.

Blood measurements are more favourable still. Pooling 30 cohorts across 13 countries, 68,659 people and 15,198 events, those with the most linoleic acid in their blood had about 7% less cardiovascular disease, 22% lower cardiovascular death rates and 12% fewer ischaemic strokes than those with the least. The authors concluded the results "support a favorable role for LA in CVD prevention."[2] These are observational studies, so they show association, not proof.

Linoleic acid doesn't raise inflammation in trials

The inflammation claim is testable, and it has been tested. A systematic review of 15 randomised trials found that adding linoleic acid had no effect on C-reactive protein, fibrinogen, cytokines, adhesion molecules or tumour necrosis factor — the standard blood markers of inflammation.[3]

The benefit depends on what the oil replaces

The American Heart Association and most national authorities count replacing saturated fat with polyunsaturated fat as protective for the heart, and the Cochrane review of cutting saturated fat supports it (see Dietary fats).

Trials that simply raised omega-6 intake, usually in place of saturated or monounsaturated fat, are less impressive. Cochrane's separate review of them, covering 19 trials in 6,461 people, found that more omega-6 made little or no difference to deaths or cardiovascular events at low certainty, and no evidence that more omega-6 reduces cardiovascular outcomes other than heart attack.[4] The strongest case for seed oils is as a replacement for saturated fat.

The critiques that do hold up

They are about how the oil is used, not the molecule.

  • Commercial deep-frying. Fryers running for hours produce oxidised fats with measurable effects in humans, though the evidence concerns blood-vessel function rather than inflammation. In a controlled test in 10 men, a meal cooked in fat taken from a commercial fast-food fryer wiped out the arteries' ability to widen, while the identical meal cooked in fresh fat did not.[5] The claim that this oil is pro-inflammatory rests on animal and cell studies; no long-term human exposure trial exists.
  • Ultra-processed food. Refined oils are calorie-dense and turn up alongside refined sugar, white flour and additives, and that surrounding food is the more plausible cause of harm than linoleic acid itself. See Ultra-processed food.

The omega-6 to omega-3 ratio

The ratio argument starts from real biochemistry: the two families compete for the same enzymes that convert them into longer fats. The popular version runs from there to a body tipped towards inflammation, and that step does not survive the human data.

  • Eating more linoleic acid doesn't raise the inflammatory omega-6. Pooling 36 human trials that ranged from a 90% cut to a six-fold increase in dietary linoleic acid, intake showed no relationship with blood levels of arachidonic acid, the omega-6 that inflammatory signalling molecules are actually built from.[6]
  • The Western ratio is lower than claimed. US survey estimates run around 8:1 to 10:1, not the 15:1 or 20:1 that circulates.[7]

The ratio does predict death rates — for a reassuring reason. In a UK study of 85,425 adults, the fifth with the highest blood omega-6 to omega-3 ratio had about 26% higher death rates than the lowest fifth and 31% higher cardiovascular death rates; the 14% higher cancer figure was the weakest, with a range reaching down to no effect. But the same paper found that higher omega-6 on its own was protective — about 23% lower overall and 20% lower cancer death rates in the highest fifth versus the lowest. In its own plain-language summary, "both are protective"; the ratio predicts harm mainly because omega-3 protects more strongly.[8] That is an argument for adding omega-3, not for cutting linoleic acid.

A separate, larger UK analysis added the ratio to a standard European heart-risk calculator. Prediction improved, but barely — from 0.742 to 0.747 on a scale where 0.5 is a coin flip and 1.0 is perfect — which its authors call "modest from a clinical standpoint."[9]

No major authority sets a ratio target. A joint expert consultation of the UN's Food and Agriculture Organization and the World Health Organization found no rational basis for one, provided you get enough of each.[10] The Nordic recommendations, the European Food Safety Authority, the US Institute of Medicine, Japan and China likewise set absolute amounts and no ratio. The 1:1 to 4:1 figure that circulates online traces to a single review, which gave different ratios for different diseases rather than one target, not to any guideline.[11]

What to do

  1. Cook with seed oils at home without worry, using fresh oil at moderate heat.
  2. Use them instead of butter and other saturated fats, not on top of your current diet; that swap is where the benefit is.
  3. Avoid commercial deep-fried food and ultra-processed food. That is where the legitimate concerns lie.
  4. Skip the ratio. If you want to change it, eat more omega-3 — fatty fish twice a week, or see Omega-3 — rather than less omega-6.

Further reading

  • Marklund M et al. Biomarkers of Dietary Omega-6 Fatty Acids and Incident Cardiovascular Disease and Mortality. Circulation 2019.[12]
  • Sadeghi R et al. Dietary and circulating omega-6 fatty acids and their impact on cardiovascular disease, cancer risk, and mortality: a global meta-analysis of 150 cohorts and meta-regression. J Transl Med 2025.[13]
  • Hooper L et al. Omega-6 fats for the primary and secondary prevention of cardiovascular disease. Cochrane Database of Systematic Reviews 2018.[14]
  • Rett BS, Whelan J. Increasing dietary linoleic acid does not increase tissue arachidonic acid content in adults consuming Western-type diets: a systematic review. Nutr Metab (Lond) 2011.[15]
  • Zhang Y et al. Higher ratio of plasma omega-6/omega-3 fatty acids is associated with greater risk of all-cause, cancer, and cardiovascular mortality: A population-based cohort study in UK Biobank. eLife 2024.[16]
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