Can seed oils really be "toxic"? Science proves otherwise!

Seed oils have been caught in the crossfire of nutrition debates, with claims ranging from heart health benefits to concerns about inflammation, oxidation, and processing. But what does the evidence actually say? Our experts take a closer look at the science behind these claims and put them into context for advising patients on optimal cardiovascular health.

What are seed oils?

Oils that are extracted from seeds. Common ones used in the UK are rapeseed oil (also called canola oil) and sunflower oil, but there are others such as corn oil, sesame oil and flaxseed oil.

Are seed oils harmful?

Seed oils per se, when eaten in moderation and as part of a healthy balanced diet, are not harmful. In fact, the opposite, these oils have been shown to lower cholesterol and reduce the risk of cardiovascular disease (CVD) when compared to foods high in saturated fat.

BUT when they get used to make foods that are high in saturated fat, salt and sugar (think cakes, pastries, biscuits, etc) then that food becomes unhealthy.

Why the controversy?

Two main arguments given for seed oils being harmful is they cause inflammation and oxidation. Simply put, oils contain polyunsaturated fats (PUFAs) - in particular linoleic acid (LA) an omega-6 fatty acid (also an essential fatty acid – essential because our bodies can’t make it). Due to PUFAs chemical structure, it’s been argued that these oils are prone to oxidation and they promote inflammation. Then we’ve got the processing of seed oils which gets banded about as being harmful. All of this sounds pretty scary stuff. So, let’s do a deeper dive.

What’s the evidence for the negative health associations? 

There’s no human evidence that seed oils cause human harm!

 

Inflammation 

The theoretical argument for inflammation is that linoleic acid gets converted into another fatty acid called arachidonic acid (AA) in the body. AA then serves as the raw material to produce chemicals called eicosanoids, and these can then go onto promote inflammation. BUT there’s no human evidence that either increasing or decreasing LA alters levels of AA in the blood. That’s because this process is tightly regulated in the body.

A review of 36 human studies found that neither increasing LA levels by over 500% or decreasing levels by 90% altered AA in the blood¹. Another review of 15 human studies, which looked at the actual markers of inflammation, concluded there’s virtually no data from randomized, controlled studies, showing that adding LA to diets increases markers of inflammation in healthy adults². And yet another analysis of 83 controlled human studies, of people with and without inflammatory bowel disease, found that increasing omega-3, omega-6 or total PUFAs had either little or no effect on inflammatory markers or risk of disease³.

Oxidation 

And what about oxidation? Surely this is harmful?

One common claim given is that seed oils cause LDL-cholesterol (often referred to as ‘bad’ cholesterol) to become oxidised in the blood and this is harmful. Yet, there’s plenty of research available showing that what more accurately predicts risk of CVD is non-HDL-cholesterol, which includes all LDL-cholesterol⁴, whether oxidised or not⁵. Where oxidation happens is also important. The oxidation of LDL-cholesterol occurring within the artery wall is the problem, not the oxidised LDL-cholesterol in the blood. This is supported by trials using antioxidant supplements which found no benefits of antioxidant supplements reducing the risk of CVD⁶.

Heating

Another claim made is to do with the heating of oils causing the production of trans fats. While this may be the case for cooking at high temperatures, for long periods of time, there’s no evidence that cooking at common temperatures at home produces trans fats. This was shown in a review of 33 studies which concluded that heating edible oils to common cooking temperatures (≤200 ◦C) had minimal effect on trans fat generation whereas heating to higher temperatures can increase levels⁷.

Processing

All seed, nut, or fruit oils undergo processing to produce the final product. Chemical extraction is the primary method used, because there is simply no way that traditional methods of extracting oil from seeds or nuts could produce anything like the amounts required for our food supplies. To extract the oil, a solvent is added to the crushed seeds. However, once the solvent has separated the oil, it is heated to evaporate the solvent. Vegetable oils that make it onto our shelves have levels of solvent that are not detected. Or if there are some trace levels detected, they are far below the maximum residue level set for foods. There are further processes, to remove the chlorophyll content (otherwise the oils would be green!). "Deodorising" is a final step that involves heating and steam distilling the oil to remove impurities and odorous compounds in the oil, e.g., aldehydes and ketones. However, there is no detectable levels of any of these compounds in the final product that is of any concern to human health.

The final product is defined by its nutritional composition, not by the processing method and both the nutritional composition of seed oils, and the human outcome data using these oils, support benefits for health^8,9.

So how does this translate into hard clinical outcomes such as CVD and death? 

If seed oils are ‘toxic’ then surely, they must be deadly! In fact, the opposite.

An analysis of 30 studies, which involved thousands of people from all over the world, and followed-up for up to 32 years, looked at levels of LA in the body and found that people with higher levels of LA in their blood and fat stores, actually have a lower risk of CVD¹⁰.

Another analysis of 4 very well conducted studies found that reducing dietary saturated fat and replacing it with polyunsaturated vegetable oil (seed oils rich in LA) reduced the risk of heart disease by around 29%¹¹. And yet another analysis of 8 studies, including over 13,600 people, found that increasing polyunsaturated fats as a replacement for saturated fats reduced heart disease events by 19%¹².

One of the most robust, trustworthy assessment of the evidence comes from a Cochrane review published in 2020¹³. This included 15 controlled studies, with over 56,000 participants, and found that replacing saturated fat with unsaturated fat reduced the risk of cardiovascular events by 21%. The source of unsaturated fat used in these studies included seed oils!

Another recent review of the evidence concluded that increased consumption of PUFA (n-6 and n-3) rich food is associated with better cardiovascular prognosis and is in line with international guidelines¹⁴.

Yet what often gets referred to in the support of seed oils being harmful are a handful of studies conducted in the 1960s and 70s.   If you hear the Sydney Diet Heart Study and the Minnesota Coronary Experiment mentioned alarm bells should start ringing.   These studies have serious methodological flaws. For example: The type of processing used back then to make polyunsaturated margarines resulted in them in being high in trans-fats (at the time the harmful effects of trans fats were unknown). This type of fat we now know increases the risk of CVD and is why manufacturers have removed trans fats from spreads. It’s not surprising then that the group taking this polyunsaturated spread had a higher risk of CVD compared to the control group. It was nothing to do with the PUFAs, but the trans fats. Only measuring total cholesterol (which doesn’t give a good indication of risk). Did not take into account other dietary factors (which may have contributed to risk). Problems with the provision of the study diets. Weakness in the statistical analysis.

In summary

There is no human data to suggest that seed oils are harmful, in fact the opposite.

When seed oils are being cited as deadly or toxic, look at the evidence provided. If it’s not being cited, ask for it. Don’t rely on people’s anecdotes. If you are provided with the data, are these human studies and are they based on the totality of evidence? Or is it cherry picked data? Really scrutinise the data.

 

References

1. 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. 2011; 10:8:36. doi: 10.1186/1743-7075-8-36.

2. Johnson GH, Fritsche K. Effect of dietary linoleic acid on markers of inflammation in healthy persons: a systematic review of randomized controlled trials. J Acad Nutr Diet. 2012;112(7):1029-41,1041.e1-15. doi: 10.1016/j.jand.2012.03.029.

3. Ajabnoor, S.M., Thorpe, G., Abdelhamid, A. et al. Long-term effects of increasing omega-3, omega-6 and total polyunsaturated fats on inflammatory bowel disease and markers of inflammation: a systematic review and meta-analysis of randomized controlled trials. Eur J Nutr. 2021;60:2293–2316. doi: 10.1007/s00394-020-02413-y.

4. Ference BA, Ginsberg HN, Graham I, et al. Low-density lipoproteins cause atherosclerotic cardiovascular disease. 1. Evidence from genetic, epidemiologic, and clinical studies. A consensus statement from the European Atherosclerosis Society Consensus Panel. Eur Heart J. 2017;38(32):2459-2472. doi: 10.1093/eurheartj/ehx144.

5. Wu T, Willett WC, Rifai N, et al. Is plasma oxidized low-density lipoprotein, measured with the widely used antibody 4E6, an independent predictor of coronary heart disease among U.S. men and women? J Am Coll Cardiol. 2006;48(5):973-9. doi: 10.1016/j.jacc.2006.03.057.

6. Pellegrino D. Antioxidants and cardiovascular risk factors. Diseases. 2016;4(1):11. doi: 10.3390/diseases4010011.

7. Bhat S, Maganja D, Huang L, et al. Influence of heating during cooking on trans fatty acid content of edible oils: a systematic review and meta-analysis. Nutrients. 2022;14(7):1489. doi: 10.3390/nu14071489.

8. Schwingshackl L, Bogensberger B, Benčič A, et al. Effects of oils and solid fats on blood lipids: a systematic review and network meta-analysis. J Lipid Res. 2018;59(9):1771-1782. doi: 10.1194/jlr.P085522.

9. Christensen JJ, Arnesen EK, Rundblad A, et al. Dietary fat quality, plasma atherogenic lipoproteins, and atherosclerotic cardiovascular disease: An overview of the rationale for dietary recommendations for fat intake. Atherosclerosis. 2024;389:117433. doi: 10.1016/j.atherosclerosis.2023.117433

10. Marklund M, Wu JHY, Imamura F, et al. Biomarkers of dietary omega-6 fatty acids and incident cardiovascular disease and mortality: aAn individual-level pooled analysis of 30 cohort studies. Circulation. 2019;139(21):2422-2436. doi: 10.1161/CIRCULATIONAHA.118.038908.

11. Sacks FM, Lichtenstein AH, Wu JHY, et al. Dietary fats and cardiovascular disease: A presidential advisory from the American Heart Association. Circulation. 2017;136(3):e1-e23. doi: 10.1161/CIR.0000000000000510.

12. Mozaffarian D, Micha R, Wallace S. Effects on coronary heart disease of increasing polyunsaturated fat in place of saturated fat: a systematic review and meta-analysis of randomized controlled trials. PLoS Med. 2010;7(3):e1000252. doi: 10.1371/journal.pmed.1000252.

13. Hooper L, Martin N, Jimoh OF, et al. Reduction in saturated fat intake for cardiovascular disease. Cochrane Database of Systematic Reviews 2020, Issue 8. Art. No.: CD011737. DOI: 10.1002/14651858.CD011737.pub3.

14. Poli A, Agostoni C and Visioli F. Dietary fatty acids and inflammation: Focus on the n-6 series. Int J Mol Sci. 2023;24:4567. Doi: 10.3390/ijms24054567