Are Seed Oils Poisoning Our Food Supply?

by Ashley Hamer Pritchard
July 7, 2026

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For most of human history, people cooked with animal fat. Lard, tallow, and butter greased our pans, filled our baked goods, and fried our potatoes. Then, in the mid 20th century, that all changed. Concerns about heart disease and saturated fat led the American Heart Association and a generation of physicians to recommend replacing animal fats with vegetable oils.

But now, 60 years later, a growing movement says we got it backwards: the oils we adopted in the name of heart health are themselves the source of a chronic disease epidemic. They say these oils cause inflammation, disrupt our metabolism, and, in essence, are poisoning our food. The skepticism of seed oils has been building since the 1970s, and it’s traveled through academic papers and mainstream bestseller lists to arrive at the US Department of Health and Human Services, where Secretary RFK Jr. has declared that seed oils are driving the obesity epidemic.

Did we get it all wrong? Are seed oils actually worse for us than animal fats? To understand, we’ll have to examine each pillar of the case against them, one by one.

What Are Seed Oils?

The oils critics are after are those extracted from plant seeds, as opposed to those extracted from fruits, like olive oil and avocado oil. They’re what they call the “Hateful Eight”: canola, soybean, corn, sunflower, safflower, cottonseed, grapeseed, and rice bran oils. Critics use “seed oils” and “vegetable oils” interchangeably, and this episode will too.

Seed oils are extracted in two ways. Cold-pressed oils retain more flavor but have a short shelf life and low smoke point, which is why most seed oils on shelves today are chemically refined instead.

The most common chemical solvent used in this process is hexane, which can be toxic at certain levels, especially in its aerosolized form. But the amount left after processing is, to quote the US government, “toxicologically insignificant,” and even that amount is likely to evaporate once you heat your oil to cook with it.

While animal fats and tropical oils like coconut and palm oil are high in saturated fat, which can raise cholesterol and increase heart disease risk, seed oils are high in polyunsaturated fat, which is generally associated with positive health effects.

Specifically, seed oils are high in omega-6 and omega-3 fatty acids.

The Claims Against Seed Oils

The ratio of those two fatty acids in seed oils is the main target for critics. Seed oils tend to contain much more omega-6 than omega-3: for example, soybean oil contains around 7 grams of omega-3 and 51 grams of omega-6 per 100 grams of oil. Other seed oils have even higher ratios.

The argument goes that once you consume linoleic acid, the most common type of omega-6 fatty acid, your body converts it into another type of omega-6 called arachidonic acid. Arachidonic acid is a building block for compounds that cause inflammation. Therefore, critics say, seed oils cause chronic inflammation, which causes chronic disease.

They say humans evolved eating a 1:1 ratio of omega-3 to omega-6 fatty acids, and because of the skewed ratio in seed oils, modern Western diets now average 15:1 or higher. We were never meant to consume this many omega-6s, they say.

And there’s even evidence of a coverup: two major studies from the 1960s and 70s found no cardiovascular benefit, and in some cases harm, from replacing saturated fats with seed oils. These studies lay unpublished because they contradicted dominant medical beliefs — and critics say that public health has suffered as a result.

Let’s take these claims one by one.

Claim 1: Inflammation

The idea that linoleic acid is converted to arachidonic acid, which leads to inflammation, sounds simple enough — but biology is anything but simple. For one thing, arachidonic acid doesn’t just increase inflammation. It’s a precursor for both pro- and anti-inflammatory hormones — it does a little of each. What’s more, the body only converts a tiny fraction of dietary linoleic acid to arachidonic acid, and that tiny fraction is tightly regulated: consuming more omega-6s doesn’t increase levels of arachidonic acid in the body.

But does consuming more linoleic acid increase inflammation in practice? The direct evidence says no. A 2017 meta-analysis of randomized controlled trials found that increasing dietary linoleic acid had no significant effect on the concentration of inflammatory markers in the blood. A more recent analysis of the Framingham Offspring Study, which measured ten different inflammation-related biomarkers in nearly 2,800 people, found that linoleic acid was linked with lower levels of several inflammatory markers — the associations were weak, but statistically significant. That’s the opposite of what seed oil critics predict.

Eating more omega-6s is associated with better health on top of that, too. A 2019 paper that pooled data from nearly 70,000 people across 30 prospective studies found that higher blood levels of linoleic acid were linked to a lower risk of death from cardiovascular causes. That’s partly due to the fact that linoleic acid reduces levels of harmful LDL cholesterol, a finding that’s been replicated across dozens of studies.

Claim 2: The Omega Ratio

The idea that humans have historically consumed omega-6 and omega-3 fatty acids in a 1:1 ratio feels right — it invokes the idea that our diets used to be balanced, and any imbalance is a product of our modern, over-industrialized culture. But the idea had to come from somewhere.

And figuring out where is harder than it should be. The trail runs through a series of papers by S. Boyd Eaton and Melvin Konner, going back to a 1985 paper in the New England Journal of Medicine that’s largely cited as the founding document of the paleo diet movement. But that paper only contains a ratio the authors calculated for how much polyunsaturated fat to saturated fat they believe was present in the paleolithic diet — not the ratio of these two types of polyunsaturated fatty acids.

Eaton’s team did eventually cite an omega-6 to omega-3 ratio in a 1997 follow-up paper — they said it varied from 4:1 to 1:1. But that was a figure they attributed to other researchers, and they admitted that there isn’t good data to calculate this figure reliably. But none of the papers they cite for this range are the original source. The trail gets murkier from there.

What you find, in other words, is not a single foundational study that calculated humanity’s ancestral omega ratio. Instead, you find paper citing paper citing paper in a chain that gets thinner and less certain the further back you go. It dissolves into estimates, ranges, and acknowledgments that the data just wasn’t good enough to support a precise number.

The 1:1 figure didn’t come from a single calculation. It’s more of a legend than a scientific fact.

And this makes intuitive sense: Paleolithic humans didn’t eat a standardized diet. Depending on their environment, one group might eat a lot of red meat, another might eat mostly vegetarian. Even if you just look at one food, like fish, you find that its omega-3 content varies across species and climate. It’s not possible to make a single blanket claim about the nutrition of the paleolithic diet because the paleolithic diet isn’t one thing.

Claim 3: The Unpublished Trial Data

The strongest claim against seed oils is also the most dramatic. In 1968, the Minnesota Coronary Experiment was devised to test whether replacing saturated fat with polyunsaturated fats reduces heart attacks by lowering cholesterol. The experiment found something surprising: while participants given a diet high in omega-6 fatty acids had lower cholesterol than the control group, they didn’t have a lower mortality risk — in fact, their risk may have been higher than the group eating mostly animal fats.

Meanwhile, halfway across the world in Sydney, Australia, a similar study began in 1966. It also found that omega-6 lowered cholesterol but increased mortality risk.

Neither study made much noise at the time. The Minnesota results sat on a shelf for 16 years until a paper was finally published — one that didn’t really offer much detail. The Sydney study fared a little better: a 1978 paper did report that the omega-6 group had higher overall mortality, but it left out a breakdown of exactly how those people actually died.

Decades later, NIH researcher Christopher Ramsden tracked down the original data from both studies and ran the full analysis for the first time. His analysis confirmed and sharpened the same counterintuitive results the original researchers had already found. To critics of seed oils, this looks damning: real evidence, sidelined for decades, while public health agencies kept telling people to swap butter for corn oil.

The problem is that the original data wasn’t very good.

In Minnesota, researchers gave both the intervention and control groups more fat than dietary guidelines recommend, and for the intervention, they created fake meat, cheese, and milk by removing most of the other types of fat and replacing it with corn oil — meaning any existing omega-3 fats would have been replaced almost entirely with omega-6s. They also created a special corn-oil margarine that, while lower in trans fat than regular margarine, likely contained certain types of trans fats with dangerous health effects that wouldn’t have been understood by 1970s era scientists.

The Minnesota study also suffered from severe attrition: 83% of the participants were lost to follow-up and kept out of the data analysis, which would have inflated the perceived effect sizes, especially if some of those lost participants had died.

The Sydney experiment had its own issue: The control group wasn’t given any guidelines to follow. As a result, some of the control participants started swapping butter for margarine on their own, which made the “control” diet anything but.

Two old, flawed trials testing an extreme, artificial diet on a narrow population aren’t strong evidence for what happens when ordinary people cook with vegetable oil. For that, we have better evidence: large meta-analyses of dozens of cleaner randomized trials, and decades of data tracking hundreds of thousands of people eating their normal diets. That’s where the real picture of omega-6 and heart health comes into focus.

The Real Culprit: Our Diets

The critics are right about one thing: seed oils are in virtually all of the quick, convenient, highly palatable food we eat these days: chips, frozen dinners, packaged baked goods, fast food. Diets heavy in these convenience foods are associated with worse health outcomes: higher rates of heart disease, obesity, type 2 diabetes, and cancer.

But pointing at a single ingredient in this range of foods is missing everything that’s going along with them. Seed oils are paired with refined carbohydrates, added sugars, excess sodium, and a near-total absence of fiber. Multiple medical authorities and independent researchers have made the same point: Seed oils are not the likely driver of our health problems. Our diets are.

Conclusion

The case against seed oils is based on real research — it’s just research that gets less convincing the closer you look.

The inflammation story sounds reasonable until you check whether omega-6s actually raise inflammation in people — they don’t. The 1:1 ratio sounds like ancestral wisdom until you trace it back and find a citation chain that goes nowhere. And the unpublished trial data sounds like a cover-up until you read the actual study designs and find two narrow, poorly controlled experiments that can’t tell us what happens in a regular person’s kitchen.

What’s left is the one piece of the critics’ case that holds up: a diet built around chips, frozen dinners, and fast food really is making people sicker, and seed oils really are in almost all of it. But that’s an argument against the food, not against the oil itself. Swapping canola oil for beef tallow doesn’t touch the sugar, the refined starch, or the missing fiber that are doing the actual damage. It just changes which ingredient gets to play villain.

Seed oils aren’t poison. They’re a normal, well-studied part of a healthy diet that got caught up in a more legitimate argument about everything else on the shelf next to them.

By Ashley Hamer Pritchard