Where the evidence diverges from the popular narrative is the cardiovascular endpoint question. The 2020 Cochrane review of 19 randomized trials with 6,461 participants found that increasing omega-6 polyunsaturated fat intake reduced cardiovascular events by a relative 9% (RR 0.91, 95% CI 0.81 to 1.02) — a directionally protective effect that just missed conventional statistical significance. That is genuinely not the picture that 'seed oils cause heart disease' implies.

The Minnesota Coronary Experiment reanalysis published in BMJ in 2016 is frequently cited on the other side. That trial did show that participants substituting corn oil for saturated fat experienced lower serum cholesterol but no mortality benefit, and possibly higher mortality in the over-65 subgroup. The trial was, however, conducted in psychiatric inpatients on highly controlled diets in the 1960s, and the reanalysis depends on incomplete recovered records. It is a data point, not a verdict.

The inflammation story is similarly mixed. The hypothesis is mechanistically reasonable: linoleic acid is a precursor to arachidonic acid, which feeds into prostaglandin and leukotriene synthesis. But the direct measurement studies — including the Johnson and Fritsche meta-analysis of 15 controlled feeding trials — have generally not found that increasing dietary linoleic acid raises circulating arachidonic acid or measurable inflammatory markers in healthy adults.

What does the honest synthesis look like? Industrial seed oils are not the metabolic catastrophe that the popular discourse claims. They are also not a health food, and the displacement of whole-food fat sources — olives, avocados, dairy, fatty fish, nuts — by ultra-processed-food formulations that happen to use seed oils as a cheap fat base is a real concern. The villain, on the evidence, is the ultra-processed matrix, not the linoleic acid molecule.