Do Seed Oils Cause Inflammation? An In-Depth Look at the Research by Team Kalorist

Do Seed Oils Cause Inflammation? An In-Depth Look at the Research

Seed oils like sunflower, soybean, corn, and canola have become one of the most argued-about topics in nutrition. The claim shows up everywhere: seed oils are inflammatory, they are driving chronic disease, they should be avoided entirely. It has moved well past wellness social media too, U.S. Health and Human Services Secretary Robert F. Kennedy Jr. has publicly described seed oils as harmful, and some restaurant chains have begun marketing “seed oil free” menus in response.

At Kalorist, we think food choices should be guided by the actual evidence, not by whichever claim is loudest. Here is a full look at where the seed oil concern comes from, what the research actually shows, and where a real, narrower nuance does exist.

Where the Claim Comes From

The biochemical argument goes like this: linoleic acid (LA), the main omega-6 fat in seed oils, can be converted in the body into arachidonic acid (AA). AA is a precursor to some pro-inflammatory signaling molecules, so more LA supposedly means more inflammation.

That mechanism is real as far as it goes, but it leaves out two important details. First, the conversion of LA to AA is carried out by a rate-limiting enzyme (delta-6-desaturase) that is tightly regulated by the body. Eating more LA does not simply scale up how much gets converted. Second, AA is not exclusively inflammatory. It is also the precursor to compounds involved in resolving inflammation, not just triggering it. A biochemical pathway existing on paper does not tell you what actually happens when real people eat real diets, which is exactly why the human trials below matter more than the pathway alone.

The Newest Direct Evidence: Blood, Not Food Diaries

Most nutrition research on this question relies on food diaries or questionnaires, which depend on people accurately remembering and reporting what they ate. A study led by Kevin C. Maki (Indiana University School of Public Health-Bloomington, and chief scientist at Midwest Biomedical Research) took a different approach.

In a cross-sectional analysis of nearly 1,900 adults, researchers measured linoleic acid directly in participants’ blood rather than asking what they ate. People with higher blood linoleic acid had lower hs-CRP (high-sensitivity C-reactive protein test), glycoprotein acetyls, and serum amyloid A, the actual clinical markers doctors use to assess inflammation. The same group also had lower glucose, lower insulin, and lower HOMA-IR, the standard measure of insulin resistance. Every marker moved opposite to what the popular claim would predict.

This was first presented at NUTRITION 2025, the flagship annual meeting of the American Society for Nutrition, and has since been published as a peer-reviewed paper (Maki et al., 2026).

It is worth being precise about what this study can and cannot tell us. It is cross-sectional and observational, so it shows a strong association, not proof of cause and effect in either direction. The authors themselves frame it as consistent with earlier observational work linking higher linoleic acid intake to lower risk of type 2 diabetes and cardiovascular disease, not as a single study that settles the question on its own.

This Isn’t an Outlier

The Maki study fits into a much larger body of evidence, not a lone contrarian finding.

Innes and Calder (2018) reviewed the existing trial evidence in healthy adults and found that increased intake of linoleic acid or arachidonic acid did not raise concentrations of inflammatory markers, and in some cases lowered them.

Jackson and colleagues (2024) published an update reviewing the cardiometabolic effects of linoleic acid, again finding evidence of benefit rather than harm.

The American College of Cardiology’s own Nutrition and Lifestyle Work Group published a review in early 2026 (Miller et al., 2026) sorting several controversial foods into three categories: evidence of harm, evidence lacking, and evidence of benefit. Seed oils and seafood landed in the “evidence of benefit” category. Notably, this is the same review that recommends limiting beef tallow due to its effect on LDL cholesterol, so the panel was not simply defending processed foods across the board.

Major health institutions have said the same thing. The American Heart Association (2024), Harvard T.H. Chan School of Public Health, Johns Hopkins Bloomberg School of Public Health, Stanford Medicine, and the Cleveland Clinic have all published statements concluding that current evidence does not support avoiding seed oils.

One source deserves a transparency note. A 2025 review reaching similar conclusions (Petersen et al.) was funded by the Soy Nutrition Institute Global and the United Soybean Board, industry groups with an obvious stake in the outcome. Its findings are consistent with the independently funded research above, but the funding source is worth knowing.

Where the Real Nuance Actually Is

None of this means seed oils are beyond any legitimate concern. Two real, narrower issues are worth understanding.

The omega-6 to omega-3 ratio matters, not just the absolute amount. Simopoulos (2006) documented that humans likely evolved eating a diet with an omega-6 to omega-3 ratio of roughly 1 to 1, while typical Western diets today run 15 to 1 or higher. A heavily skewed ratio, driven by high omega-6 intake alongside very low omega-3 intake, is a biologically plausible pro-inflammatory pattern.

However, this does not mean background omega-6 intake cancels out the benefits of omega-3. Mozaffarian and colleagues (2005) followed 45,722 men over 14 years and found that omega-3 intake reduced coronary heart disease risk regardless of how much omega-6 was also in the diet. The two fats are not simply canceling each other out in a straightforward tug of war.

How you cook with the oil matters. Seed oils are more polyunsaturated than oils like olive oil, which gives them a lower smoke point and makes them more prone to oxidation under high, repeated heat, think oil that gets reused for deep frying multiple times. Oxidized fat is a genuine, specific inflammatory trigger. This is a real reason to avoid reusing frying oil or cooking at excessively high temperatures, but it is a very different and much narrower claim than “the oil itself is inflammatory.”

Put together, the evidence suggests that for background omega-6 intake to actually create a pro-inflammatory state, you would need a genuinely extreme pattern: a diet built almost entirely around refined vegetable oil, heavy and repeated frying, and essentially no fish or other omega-3 sources at all. That is a far cry from someone who cooks with sunflower oil a few times a week and also eats some fish or takes a fish oil supplement.

So What Should You Actually Do?

Using seed oils for normal cooking, roasting, sauteing, or salad dressings is not the health risk the viral claim describes. The strongest current evidence, including blood-based studies, RCT reviews, and statements from major cardiology and public health institutions, points the other way.

What is worth actually paying attention to: avoid repeatedly reusing oil for deep frying, and make sure you are getting some omega-3s regularly, through fatty fish, walnuts, flaxseed, chia, or a supplement, so your overall ratio does not run wildly skewed. Both of these things can be true at once: the “seed oils are toxic” claim does not hold up, and how you cook and what else is in your diet still matter.

If you are tracking your meals and want your fats and oils logged with real specificity rather than lumped into a vague category, that level of detail is exactly what Kalorist’s food database is built for.

References

Innes, J. K., & Calder, P. C. (2018). Omega-6 fatty acids and inflammation. Prostaglandins, Leukotrienes and Essential Fatty Acids, 132, 41-48.

Jackson, K. H., Harris, W. S., Belury, M. A., Kris-Etherton, P. M., & Calder, P. C. (2024). Beneficial effects of linoleic acid on cardiometabolic health: an update. Lipids in Health and Disease, 23(1), 296.

Maki, K. C., Chen, X., Wilcox, M. L., Kirkpatrick, C. F., Guarneiri, L. L., Palacios, O. M., Beidelman, E. T., Macagno, A. L. M., & Allison, D. B. (2026). Inverse associations of serum total omega-6 polyunsaturated fatty acids and linoleic acid with biomarkers of inflammation: A cross-sectional analysis. The Journal of Nutrition, 156(6), 101471.

Miller, M., Aggarwal, M., Allen, K., Bhattacharya, R., Dastmalchi, L. N., Kris-Etherton, P. M., Klodas, E., Mozaffarian, D., Ostfeld, R. J., Petersen, K. S., Reddy, K. R., Ros, E., Vinaithirthan, V., & Freeman, A. M. (2026). A clinician’s guide for trending cardiovascular nutritional controversies in 2026. JACC: Advances, 5(3).

Mozaffarian, D., Ascherio, A., Hu, F. B., Stampfer, M. J., Willett, W. C., Siscovick, D. S., & Rimm, E. B. (2005). Interplay between different polyunsaturated fatty acids and risk of coronary heart disease in men. Circulation, 111(2), 157-164.

Simopoulos, A. P. (2006). Evolutionary aspects of diet, the omega-6/omega-3 ratio and genetic variation: Nutritional implications for chronic diseases. Biomedicine & Pharmacotherapy, 60(9), 502-507.