Extended Summary
Vegetable oils constitute an assortment of culinary oils derived from a number of plant sources, such as sunflower seeds, rapeseeds, soybeans, and even wheat kernels. These oils typically differ from animal-derived oils in that they primarily consist of unsaturated fatty acids (typically, linoleic acid) instead of saturated fatty acids. This difference in fatty acid composition is understood to affect serum concentrations of low-density lipoproteins (LDL) in humans and influence the risk of cardiovascular disease, which we have discussed previously in our misinformation article titled “Saturated Fat Does Not Cause Heart Disease”.
To provide initial evidence opposing the claim that vegetable oils cause heart disease, a comprehensive 2018 meta-analysis showed that linoleic acid was associated with a borderline significant 12 % decrease in the risk of heart attacks in randomised controlled trials. Only two of the included trials were reasonably well-powered, and only one was particularly well-designed; nevertheless, nearly the same magnitude of benefit is observed for cardiovascular disease mortality when aggregating data from prospective cohort studies which look at dietary intake (or biomarkers of intake) of linoleic acid.
Likely the best human intervention trial investigating the use of vegetable oils in the primary prevention of cardiovascular disease was the LA Veterans trial back in the 1960s. This randomised controlled inpatient trial entailed a strict, double-blinded substitution of vegetable oils for saturated animal fats. And again, in opposition to predictions of the claim that vegetable oils cause heart disease, the trial found a 36 % reduction in the risk of cardiovascular events and a 33 % reduction in cardiovascular-related death among those in the vegetable oil group.
However, some authors challenge the notion that vegetable oils are indeed cardioprotective. The most concise account of such a hypothesis can be found in the 2018 narrative review paper by DiNicolantonio and O’Keefe. In fact, these authors actually go a step further by affirming that vegetable oils increase the risk of cardiovascular disease in humans. They conclude the increase in risk is mediated by the oxidation of the same unsaturated fats we discussed a moment ago, namely the omega-6 fatty acid: linoleic acid. Specifically, the authors argue that linoleic acid oxidation produces compounds such as malondialdehyde (MDA) which oxidatively modify LDL particles and initiate the atherosclerotic process. The authors recommend reducing vegetable oil intake for this reason.
But although the linoleic acid oxidation hypothesis seems intuitively plausible, if not compelling at first glance, it suffers from a fatal flaw. That is, holding to the hypothesis that something increases the risk of cardiovascular disease if, and only if, that something facilitates the oxidative modification of LDL particles, leads one to affirm the absurd position that omega-3 fatty acids, such as alpha-linolenic acid, must also be atherogenic and increase cardiovascular disease risk. Evidence for this flaw is that not only do omega-3 fatty acids also produce MDA when oxidised, they actually produce more MDA than linoleic acid. So why do DiNicolantonio and O’Keefe declare in their review that omega-3 fatty acids are cardioprotective? (which they are). This straightforwardly entails a contradiction of their hypothesis, leaving them with a position that affirms it both is and is not the case that omega-3 fatty acids protect against cardiovascular disease. And it should go without saying that a hypothesis that entails a contradiction should not be given much credence.
Beyond that, there are additional issues with the oxidised linoleic acid hypothesis, such as the utter incompatibility with the prevailing understanding of cardiovascular disease pathophysiology. The oxidative modification of LDL particles is indeed a necessary step in facilitating atherogenesis; however, the consequences of LDL’s relative susceptibility to oxidise are often overstated. The simple reason is that, based on the most well-defended explanation for atherogenesis (the response-to-retention hypothesis), simply binding to certain protein structures within the arterial wall will massively increase LDL oxidation rates. Regardless of factors such as the linoleic acid content of LDL and its relative susceptibility to oxidation, once LDL enters the arterial wall, the chance of oxidation is high. In support of this, we note that not only has mechanistic research upheld predictions of the response-to-retention hypothesis, but human trials generally fail to support LDL oxidation as a useful target for cardiovascular disease prevention. We must remember that evidence is just another word for that which meets the expectations of a hypothesis, and different hypotheses often make different predictions about what to expect from observation and intervention. With that in mind, the oxidised linoleic acid hypothesis predicts that, 1) consuming more vegetable oil increases the risk of cardiovascular disease, and 2) therapies targeting a reduction in LDL oxidation should decrease cardiovascular disease risk. However, the bulk of strong evidence is not consistent with such predictions.
