Myth: Vegetable Oils Are Bad for You

In the nutrition world, few topics are currently as polarizing as vegetable oils! While mainstream health guidelines typically advocate for vegetable oil consumption due to their favorable effects on LDL cholesterol levels, concerns have also circulated about their inflammatory potential, high omega-6 content, susceptibility to oxidizing, chemical solvents used for extraction and processing, and more. And on the surface, some seemingly compelling mechanisms and observational trends seem to support these fears.

However, a closer look at the research—particularly in humans—paints a different picture. In this article, we’ll be reviewing the full scope of evidence to see what the science really says!

The concerns surrounding vegetable oils generally boil down to two main arguments:

1. problems associated with their high content of linoleic acid, and
2. problems associated with the way they’re processed (namely, the use of high heat and chemical solvents such as hexane).

Let’s break down these arguments piece by piece!

Linoleic Acid: A Primer

Linoleic acid is a polyunsaturated omega-6 fatty acid, and one of only two essential fatty acids for humans (the other being the omega-3 fatty acid alpha-linolenic acid). Linoleic acid plays a number of crucial roles in the body: for instance, various enzymes can oxidize linoleic acid to produce oxidized linoleic acid metabolites (also called OXLAMs), which are then involved in immune response, cell signaling, inflammation, and pain regulation. Linoleic acid can also bind to peroxisome proliferator-activated receptor alpha (or PPAR-α)—a transcription factor heavily involved in metabolic regulation. PPAR-α helps control the transport of fatty acids, inhibits fat formation (lipogenesis), and activates enzymes involved in fat breakdown and oxidation.

In nutrition science, linoleic acid’s major claim to fame is its potent cholesterol-lowering effects. Specifically, linoleic acid lowers LDL cholesterol by increasing bile acid production, enhancing cholesterol breakdown, upregulating the LDL receptor, moving LDL cholesterol out from the blood and into body tissues, and decreasing the conversion of very low density lipoprotein (VLDL) to LDL. For this reason, early research into linoleic acid (and subsequent nutrition recommendations) focused on its role in preventing heart disease.

So, why has this fat gotten a bad rap?

Here’s the plot twist! Along with its aforementioned functions, linoleic acid also serves as a precursor for all other omega-6 fats—including a very small amount (0.3 to 0.6%) getting converted to arachidonic acid. Arachidonic acid is an omega-6 fat that, in excess, has been implicated in a number of chronic diseases due to its inflammatory potential. So here’s the argument…

More specifically, arachidonic acid can be converted into bioactive lipid mediators called eicosanoids, including prostaglandins (which are synthesized in damaged tissue and help generate the inflammatory response), leukotrienes (which are involved in asthmatic and allergic reactions, and help sustain inflammatory responses in general), and thromboxane (which is released from blood platelets and causes them to aggregate—AKA clump together). Although these lipid mediators are important for normal metabolic function, their over-production has been linked to a higher risk of cancer and other inflammation-related conditions. So, the fact that linoleic acid can potentially increase the body’s arachidonic acid pool and lead to greater production of eicosanoids has sparked some concern!

On top of this, linoleic acid competes with omega-3 fats for the same conversion enzymes in the body. This is why we often hear about the importance of a balanced ratio between omega-6 and omega-3 fats: too much dietary omega-6 relative to omega-3 could interfere with omega-3 metabolism, potentially inhibiting their beneficial anti-inflammatory effects. (Spoiler alert: We also don’t need to worry about the ratio of omega-6s to omega-3s in our diets; more on that below!)

In addition to competition for enzymes, linoleic acid has been shown to decrease the incorporation of omega-3 fats into phospholipid membranes. In fact, some research suggests increased consumption of linoleic acid could be contributing to the lower concentrations of omega-3 fats observed in human tissue over time. In regions where vegetable oil intake is high and fatty fish intake is relatively low (such as the United States), the amount of linoleic acid in fat tissue has increased by an estimated 130%, with a simultaneous drop in the proportion of omega-3s. This has potential implications for cell signaling, gene expression, membrane protein function, and more.

As a polyunsaturated fat, linoleic acid is also more susceptible to oxidation than saturated and monounsaturated fats. This is due to the multiple (“poly”) double bonds in its molecular structure, which are less stable and more reactive to oxygen than single bonds. This has stirred up some fear that linoleic acid-rich vegetable oil is not only partly oxidized by the time we bring it home from the store, but that the linoleic acid we ingest makes cells in our bodies more prone to oxidizing, too—including our LDL particles. That spells trouble for heart disease.

Lastly, due to increased vegetable oil production over the last century, the average linoleic acid intake has risen from about 1 to 2% of calories prior to the late 1930s, up to over 7% of calories today. This dramatic increase seems to have occurred in tandem with chronic disease rates, implicating linoleic acid (and vegetable oils at large) as potential agents in everything from cardiovascular disease to diabetes to cancer. While correlation can’t prove causation here, this observational trend does seem alarming in the context of plausible mechanisms linking linoleic acid with inflammation and oxidation.

Whew! That looks like a lot of strikes against linoleic acid, huh? There’s just one problem… when we look at the research in humans, these fears simply don’t pan out!

Linoleic Acid Research: Cell vs. Animal vs. Human

The main evidence against vegetable oils comes from animal and in vitro research, which show specific, isolated mechanisms by which linoleic could cause harm. It’s easy to selectively choose from these studies to build a case against linoleic acid (in fact, the same could be done for nearly any nutrient!).

However, while these types of studies are useful for giving direction to better-quality research (and helping us understand the mechanisms behind observed phenomena), they’re categorically inferior to studies conducted in humans. Differences in physiology between animals and humans, as well as the controlled but artificial conditions of in vitro experiments, limit how applicable their findings are to the complex inner workings of the human body.

Where linoleic acid is concerned, what ultimately matters isn’t what happens in a mouse or test tube, but what happens in the human body after consumption. Luckily, we have plenty of research to shed light on that topic! (And as a result, no need to rely on lower-quality animal or in vitro research to make our claims.)

Linoleic Acid, Arachidonic Acid, and Inflammation

Given that linoleic acid has the potential to be converted into arachidonic acid and subsequent inflammatory mediators, the next question is: does eating it actually do these things in humans? Let’s look at what the research here shows!

First of all, while the conversion pathway definitely exists, it’s not clear that linoleic acid intake (or vegetable oil intake in general) actually alters arachidonic acid levels in any meaningful way. For example, a 2011 systematic review of clinical trials found no impact of linoleic acid intake on arachidonic acid levels in the body, even when linoleic acid intake was decreased by as much as 90% or increased by as much as 600%. A randomized controlled trial from 2023 likewise found that among overweight or obese women, lowering linoleic acid intake had no independent effects on plasma arachidonic acid levels. And, a 2017 cross-sectional study found that higher intakes of polyunsaturated fat-rich cooking oils had no association with plasma arachidonic acid levels (red meat intake, however, did).

Second of all, even when it is produced, arachidonic acid hasn’t been consistently linked to pro-inflammatory effects or adverse health outcomes. A 2021 review of randomized controlled trials concluded that increasing arachidonic acid intake (up to 1500 mg/day) had no negative effects on markers of inflammation, immune function, platelet aggregation, or blood clotting, but that it might even benefit muscle and cognitive performance. A 2019 analysis of 30 prospective observational studies found that the highest versus lowest quintile of arachidonic acid levels (used as biomarkers for intake) were associated with an 8% lower risk of cardiovascular disease.

In addition, while some of the eicosanoids produced by arachidonic acid are inflammatory, others are anti-inflammatory (such as such as prostacyclin, lipoxin A4,11, and epoxyeicosatrienoic acids, say that five times fast!). So, even when small amounts of linoleic acid get converted into arachidonic acid, an inflammatory outcome isn’t guaranteed!

But, could linoleic acid be pro-inflammatory through any other avenues? Spoiler alert: it’s a “no” here, too! In fact, the evidence in humans overwhelmingly shows that linoleic acid consumption, as well as linoleic acid levels in the body, are either neutrally or inversely associated with inflammation. For example:

• A 2012 systematic review, encompassing 15 randomized controlled trials of healthy non-infant populations, investigated the effects of dietary linoleic acid on inflammatory biomarkers. None of the studies found any significant effects of linoleic acid on indicators of inflammation—including C-reactive protein, plasminogen activator inhibitor type 1, fibrinogen, soluble vascular adhesion molecules, cytokines, or tumor necrosis factor-α. The study authors stated, “We conclude that virtually no evidence is available from randomized, controlled intervention studies among healthy, noninfant human beings to show that addition of LA [linoleic acid] to the diet increases the concentration of inflammatory markers.”
• A 2003 study of healthy adults found that those with the highest intakes of both omega-6 and omega-3 fats had the lowest levels of inflammation. Overall, omega-6 intake didn’t inhibit the anti-inflammatory effects of omega-3 fats, but actually seemed to enhance those effects!
• A 2009 study of Japanese adults found that among men, intake of linoleic acid and alpha-linolenic acid were both significantly inversely associated with CRP concentrations—suggesting that each of these fats had beneficial effects on systemic inflammation. (In women, neither fat showed a significant relationship with CRP levels.)

In other words, there’s virtually no line of evidence in humans to suggest that linoleic acid increases inflammation. Instead, linoleic acid has either a neutral effect or it lowers inflammation!

…Let’s Not Forget About Dihomogamma Linolenic Acid!

The conversion pathway that produces arachidonic acid from linoleic acid also produces a highly beneficial (and less frequently discussed!) omega-6 fat: dihomogamma linolenic acid, or DGLA. Specifically, the enzyme delta-6-desaturase first converts linoleic acid into gamma linolenic acid (GLA), which can then undergo a two-carbon chain elongation by elongase to become DGLA.

DGLA has demonstrated a number of beneficial effects in the body. For example, it gets metabolized into anti-inflammatory signaling molecules such as prostaglandins of series 1 (PGE1) and thromboxane A1, which can enhance vasodilation (the widening of blood vessels), prevent platelet aggregation (AKA the clumping together of platelets in the blood), and reduce inflammation.

DGLA has also been shown to inhibit some critical processes involved in atherosclerosis—including monocyte migration, modified LDL uptake, foam cell formation, and inflammatory cytokine production. Similarly, DGLA metabolites can reduce blood pressure, enhance blood vessel dilation, and inhibit smooth muscle cell proliferation (a component of atherosclerotic plaque formation). Some research has even linked higher red blood cell levels of DGLA to significantly lower risk of stroke, heart attack, and death among people with existing cardiovascular disease (per a 2017 study, people with the highest versus lowest DGLA levels had a 43% lower risk of these three endpoints over the course of seven years!). Likewise, a 2021 clinical trial found that among elderly patients who recently had a heart attack, higher levels of DGLA in the blood were associated with a 46 – 53% lower risk of death over the course of the next two years.

Whether linoleic acid ultimately produces more arachidonic acid or DGLA is determined by a number of dietary, metabolic, and genetic factors. For one, zinc, magnesium, vitamin C, vitamin B3, and vitamin B6 all serve as cofactors for the enzymes involved in synthesizing DGLA from GLA, so being low in these nutrients can limit how much DGLA we can form. (In fact, the ratio of linoleic acid to DGLA in the blood is sometimes used to assess the presence of zinc deficiency!) Likewise, the omega-3 fat EPA has been shown to block delta-5-desaturase activity (the final enzymatic step in arachidonic acid synthesis), leading to higher blood levels of DGLA and lower levels of arachidonic acid and its inflammatory metabolites. As usual, omega-3s for the win! On top of that, genetic variations within the fatty acid desaturase (FADS) gene cluster can alter how much GLA gets converted into DGLA versus arachidonic acid, altering the ratio of these end-products by up to a three-fold difference.

So, while the potentially harmful conversion products of linoleic acid often steal the spotlight (needlessly so, as we’ve seen), this fat can also produce some very beneficial DGLA. And, whether it does so is largely a matter of eating a micronutrient-replete, omega-3 rich diet, a.k.a. Nutrivore, and with a dash of genetic variation thrown in!

Gamma Linolenic Acid

Gamma linolenic acid (GLA) is a polyunsaturated omega-6 fatty acid that may reduce symptoms of some chronic inflammatory diseases, particularly rheumatoid arthritis and atopic dermatitis. It may also benefit menstrual issues, diabetic neuropathy, cardiovascular health, and cancer—particularly via its conversion into other fatty acids and metabolites. Along with coming from food, it can be produced from another fat, linoleic acid.

Read moreGamma Linolenic Acid

What About Oxidation?

Another argument against linoleic acid involves its susceptibility to oxidation—not just going rancid in the bottle, but also increasing oxidation in our body due to its incorporation into cell membranes (which then become more vulnerable to free radical damage). This includes making our LDL particles more susceptible to oxidizing, which could play a role in the development of atherosclerosis. In addition, oxidized linoleic acid metabolites—called OXLAMs—have been associated with a number of diseases, adding even more fuel to the anti-linoleic-acid fire!

As with other arguments against this fat, we can find mechanistic studies that seem to confirm it. For example, an experiment from 1993 found that after feeding participants (in this case, people with mildly elevated cholesterol levels) diets high in either linoleic acid or monounsaturated oleic acid, LDL particles isolated from the linoleic acid group oxidized more quickly (as tested by exposure to copper, a strong oxidant). Several additional experiments from the early 1990s showed similar effects when linoleic acid and oleic acid were tested against each other.

However, even here, the research is inconsistent and requires some cherry-picking to ensure linoleic acid looks bad! While linoleic acid feeding creates more LDL-prone particles compared to oleic acid (again, in isolated controlled settings outside the body, and in a small number of available studies), its effects are actually similar to that of dietary saturated fat. A 1996 experiment included feeding participants different diets high in saturated fat (from butter and palm oil), high in long-chain omega-3 fats (from fatty fish), high in linoleic acid (from sunflower oil), and high in oleic acid (from olive oil), instead of testing only linoleic acid versus oleic acid. Lo and behold, this study found that diets high in saturated fat, linoleic acid, and omega-3 fats all produced LDL particles with similar resistance to oxidation; oleic acid still fared the best. (Interestingly, the high omega-3 diet also produced the greatest monocyte adhesion to endothelial cells, which typically suggests increased atherogenic risk. Given the overwhelming research linking long-chain omega-3s to better heart health, this is a great example of why these types of experimental studies aren’t always predictive of what happens in real-world settings!)

In fact, as more experiments of this type were conducted, the evidence began mounting that linoleic acid isn’t uniquely harmful among the fats, but that that oleic acid is uniquely beneficial!

What’s more, dietary fat modulation has a relatively small impact on LDL oxidation susceptibility relative to other dietary and lifestyle factors. Vitamin E intake, in particular, is a critical factor in how readily LDL particles oxidize—with even small (e.g., 25 mg per day) increases in vitamin E intake significantly reducing the susceptibility of LDL to oxidize. Although research here is extremely limited, some studies have tried to determine just how much our vitamin E requirements go up in order offset the increases in oxidation, with estimates landing around 0.6 mg of alpha-tocopherol per gram of dietary linoleic acid.

In addition, the body is a far more complex system than the controlled setting of these oxidation experiments. What ultimately matters is whether consuming more linoleic acid actually results in the disease outcomes that oxidized LDL could be linked to. As we’ll see shortly, that isn’t the case!  

Omega-6/Omega-3 Ratio: Important Balance, or Red Herring?

Apart from the specific effects of linoleic acid, another argument against omega-6-rich vegetable oils is their ability to drive up the overall omega-6/omega-3 ratio of the diet. The concern here involves the competition between these two fats in the body: linoleic acid and alpha-linolenic acid require the same enzymes (delta-6-desaturase and delta-5-desaturase) for conversion into their long-chain forms (arachidonic acid and EPA/DHA, respectively), and also compete for placement in cell membranes. So, in theory, excessive intake of omega-6 fats could interfere with the body’s use of omega-3s.

Adding to this argument is the fact that our modern diets feature a vastly skewed omega-6/omega-3 ratio compared to historical levels. For most of our past, the human diet had an estimated 1:1 ratio of omega-6 to omega-3 fats, whereas the modern Western diet has a ratio of 15 to 20:1 or higher!

So, it seems reasonable to suspect that vegetable oils could be harming us due to their excessive contribution of omega-6 fats relative to our omega-3 intake. Once again, though, we must ask: what does the research in humans show?

It turns out, the evidence for the omega-6/omega-3 ratio mattering in human health is much less compelling than once thought! In fact, many studies show that higher levels of linoleic acid and omega-3 fatty acids are both protective against all-cause mortality, disease-specific mortality, and some chronic health conditions; generally, omega-3s are just the more protective of the two. This suggests that as long as omega-3 levels are adequate, higher omega-6 intake (and the ratio it creates with omega-3 fats) may be of lesser concern, if not beneficial.

For example, a 2015 population-based cohort of 4,232 Swedish older adults found that serum levels of linoleic acid and very-long-chain omega-3 fats (partly reflective of vegetable oil and fish oil intake, respectively) were all independently, inversely associated with total mortality. In fact, linoleic acid was slightly more protective—27% lower risk for higher versus lower levels, compared to 19% for EPA and 20% for DHA!

A 2021 analysis of National Health and Nutrition Examination Survey (NHANES) data, tracking 4,132 participants with a mean follow-up of almost seven years, found that serum levels of linoleic acid and individual omega-3 fats (alpha-linolenic acid, EPA, and DHA) were all associated with significant reductions in all-cause mortality. Again, this supports the idea that while more omega-3 fats are great, it doesn’t need to be at the expense of lowering omega-6 intake!

A 2014 multicenter study of 2,792 participants free from cardiovascular disease at baseline found that higher circulating levels of linoleic acid were significantly protective of both total mortality and cardiovascular disease mortality. In a follow-up comment, the authors noted finding little evidence of any interaction between linoleic acid and omega-3 fats—but rather, that the benefit of linoleic acid was additive, with participants having the greatest risk reduction when both their linoleic acid levels and omega-3 levels were highest.

A 2012 cross-sectional study of 2,451 adults found that intake of omega-3 fats (as alpha-linolenic acid) and total omega-6 fats were both inversely associated with metabolic syndrome; in fact, participants in the highest versus lowest quartile of omega-6 intake had a 47% lower prevalence of metabolic syndrome. What’s more, participants consuming at least the median intake of alpha-linolenic acid (1084 mg per day) had lower rates of metabolic syndrome regardless of what their omega-6 intake was. In other words, omega-6 consumption had no impact on metabolic syndrome risk as long as omega-3 intake was high enough, and the ratio of omega-6 to omega-3 had no effect on metabolic syndrome risk!

A 2013 analysis of the Multi-Ethnic Study of Atherosclerosis, encompassing 2,837 adults, found that higher levels of EPA and DHA (both from the diet and in the blood) were associated with lower cardiovascular disease incidence, while omega-6 fats (linoleic acid and arachidonic acid) bore no relationship to cardiovascular disease risk. Interestingly, alpha-linolenic acid was also unassociated with cardiovascular disease risk in this study. This supports the idea that long-chain omega-3 fats are independently beneficial, regardless of omega-6 status.

And, here’s a great example of why reading the actual study (and not just the headline) is important! A 2024 population-based cohort study, encompassing more than 85,000 participants from the UK Biobank, was published with the title “Higher ratio of plasma omega-6/omega-3 fatty acids is associated with greater risk of all-cause, cancer, and cardiovascular mortality.” While this finding was technically true, there’s much more to the story! When these fats were assessed independently (rather than as a ratio), it turned out that high levels of omega-6 fats and omega-3 fats were both associated with a lower risk of death; omega-3 fats were just more strongly protective. Specifically, participants with the highest omega-6 levels had a 23% lower risk of dying from any cause, while those with the highest omega-3 levels had a 31% lower risk. The greater protection offered by omega-3s explains why a high omega-6 to omega-3 ratio was linked to harm, even though both fats were beneficial.

It’s also worth noting that while omega-3 fats typically demonstrate superior benefits compared to omega-6 fats, this isn’t always the case! Some studies have found that when both omega-6 and omega-3 fats are evaluated, omega-6 fats end up being the more protective of the two.

For example, a 2016 observational study of patients with acute decompensated heart failure found that the over the course of follow-up (a median of 560 days), those who had higher red blood cells levels of omega-6 fats were significantly less likely to experience either a worsening of their heart failure, or death from any cause. Meanwhile, red blood cell levels of omega-3 offered no protection against the risk of these adverse events.

Likewise, a 2022 study tracked the health outcomes of 8,537 patients with cardiometabolic disease (including cardiovascular disease and type 2 diabetes) for a median follow-up time of 10.3 years. The results showed that those in the highest versus lowest tertile of linoleic acid intake had a 14% lower risk of death from all causes. Interestingly, this association was non-linear, with the risk reduction plateauing when linoleic acid was 7.5% of total energy. Meanwhile, consumption of the omega-3 fats EPA and DHA had no significant protective effect here!

In other words, the common narrative that “omega-3 = good, omega-6 = bad” is not only oversimplified, it’s actually fundamentally wrong. A better way to look at it is this: For the majority of health outcomes, omega-6 fats range from neutral to beneficial, while omega-3 fats range from beneficial to extremely beneficial! Nowhere does the science support the claim that omega-6 fats are innately, independently harmful; nor does their ratio with omega-3 fats appear to be important, once absolute intakes of both fats are accounted for.

All that being said, even if we found evidence that the omega-6/omega-3 ratio is an important driver of disease risk, there’s an easy fix that doesn’t involve avoiding vegetable oils: eating more omega-3 rich foods! Yep, it’s really that simple. (And excellent advice in general!)

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A Note on FADS Genotype

While the polyunsaturated fat levels in our bodies are strongly influenced by diet, there’s another component here that deserves attention: genetics!

Specifically, there’s considerable genetic variation in the activity of the enzymes that convert short-chain omega fats (linoleic acid or alpha-linolenic acid) into their long-chain forms (arachidonic acid or EPA/DHA, respectively). These enzymes are encoded by two genes, FADS1 and FADS2, located on chromosome 11 in humans. Within these genes, a number of variants (called single nucleotide polymorphisms, or SNPs) exist, significantly impacting the activity and efficiency of these enzymes. As a result, some people have genetically enhanced conversion of linoleic acid into arachidonic acid, and of alpha-linoleic acid into EPA and DHA; meanwhile, other people have less efficient conversion.

Scientists believe these variants emerged due to selective pressure to adapt to agricultural diets higher in plant-based omega fats (e.g., from seeds and grains) and lower in animal-based or marine fats (such from as seafood). Supporting this hypothesis is the fact that FADS genotype has strong associations with ethnicity. For example, about 80% of people of African descent carry two copies of a major FADS SNP associated with higher arachidonic levels, compared to 46% of those with European ancestry, and virtually no one of Native American ancestry.

Along with influencing the conversion of the short-chain omega fats we consume, FADS variants have been shown to affect a number of risk markers for disease, as well as sometimes correlating with actual disease incidence. For example, the same SNPs that are associated with higher arachidonic acid levels are also associated with greater eicosanoid (inflammatory mediator) production, prostaglandin excretion (a marker for heart disease risk), LDL cholesterol, triglycerides, total cholesterol levels, C-reactive protein, and coronary artery disease risk.

Adding one more variable into the mix, some evidence suggests that genetic differences in the FADS gene cluster have stronger effects on omega-6 fats than omega-3 fats. For example, certain variants are associated with higher levels of arachidonic acid, but show no association with EPA and DHA—suggesting that the conversion of linoleic acid is more heavily impacted by these variants than alpha-linoleic acid. However, these findings could also be due to individual differences in omega-3 fat intake, which has more variation than omega-6 intake in Western diets. Due to limitations in the studies we have so far, we can’t tell for sure one way or another. Clearly, much more research is needed!

So, all this brings us to the question: could FADS variants impact how our bodies respond to eating linoleic acid? There’s some evidence for a “yes” here, but it comes with caveats!

A small number of human trials have been conducted to test the effects of linoleic acid consumption on people with different FADS variants. Although the results haven’t been totally consistent, some of them found a small but statistically significant increase in inflammation (as measured by C-reactive protein) for people with FADS variants associated with higher enzyme activity, but not for people with lower enzyme activity. While intriguing, the results weren’t generally dramatic enough to be clinically significant. Again, more research, with larger sample sizes, is needed to explore this topic!

What we can say for sure is that regardless of FADS genotypes, consuming more omega-3 fats (especially long-chain DHA and EPA) is protective. Even for individuals with genetically greater desaturase enzyme activity, the magnitude of any impact on inflammation appears small enough to be offset by other dietary components.

A Spotlight on Canola Oil

While canola oil gets lumped under the general “vegetable oil” umbrella (and therefore subject to the same critiques as other oils here), it actually has some properties that make it highly unique! In particular, its impressive fatty acid profile and high content of phytosterols make it one of the healthier plant oil options out there.

Canola oil traces its roots to an ancient crop from the Brassica genus (yep, it’s technically related to famous cruciferous vegetables like broccoli, cauliflower, cabbage, kale, and more!). Its “parent” plant, rapeseed, has been cultivated in India for at least 4000 years, and in China and Japan for 2000 years. Canola oil was bred from two rapeseed cultivars (Brassica napus and Brassica rapa) in the early 1970s, to produce a variety with seeds low in erucic acid (a monounsaturated fat that can be harmful at very high intakes) and bitter glucosinolates. The word “canola” comes from a combination of “Canada” (where this oil was first developed) and “ola,” based on the Latin word for oil.

One of canola oil’s standout features is its fatty acid profile. Unlike other vegetable oils, canola oil has relatively lower levels of linoleic acid (about 20% of total fat), and instead contains a predominance of monounsaturated fat (up to 66% of total fat). Nearly all of this comes from oleic acid—the same fat abundant in olive oil. In fact, in its upper range, the amount of oleic acid in canola oil is comparable to that in olive oil (which contains about 60 – 80% oleic acid, depending on the olive cultivar)!

Canola oil is also unusually high in the omega-3 fat alpha-linolenic acid, which comprises about 7 – 15% of its total fat composition (depending on the canola oil source and analysis). This makes it one of the highest omega-3 cooking oils out there!

Among the common cooking oils, canola oil has one of the highest contents of sterols—naturally occurring compounds found in the cell membranes of plants, which have a structure similar to that of cholesterol (which allows them to block the absorption of dietary cholesterol in the intestines). Although sterols are most famous for selectively lowering LDL cholesterol levels, they also exhibit anti-cancer, anti-inflammatory, antibacterial, and antifungal activities!

A 2019 analysis looked at the phytosterol content of 13 different oils: rapeseed (canola) oil, peanut oil, soybean oil, sesame oil, olive oil, camellia oil, corn oil, sunflower oil, flaxseed oil, rice bran oil, walnut oil, peony oil, and grapeseed oil. Of these, canola oil contained the third highest quantity of phytosterols (893 mg per 100 grams of oil), behind only rice bran oil and corn oil. (By comparison, this analysis found that olive oil contained 288 mg of phytosterols per 100 grams of oil.)

The phytosterol content of canola oil included 137 mg of brassicasterol, which demonstrates anti-cancer activity against liver cancer and bladder cancer, antiviral properties against hepatitis B and herpes simplex virus type 1 (HSV-1), antifungal activity against Mycobacterium tuberculosis (the bacteria responsible for tuberculosis infection), and angiotensin-converting enzyme (ACE) inhibiting activity (giving it a role in reducing hypertension)—and there’s still plenty more research to be done! Canola oil contains a number of other phytosterols as well, including 267 mg of campestanol, 394 mg of β-sitosterol, 41 mg of delta-5-avenasterol, 25 mg of stigmasterol, and smaller amounts of cycloartenol, methylene-cycloartanol, and egrosterol,

In controlled trials that compare the two side-by-side, canola oil sometimes demonstrates even more significant health benefits than olive oil—arguably the most uncontroversial oil out there! For example, a 2021 randomized controlled trial found that in women with PCOS, 10 weeks of canola oil consumption (25 grams daily) led to greater improvements than olive oil (as well as sunflower oil) when it came to lipid profiles and and insulin resistance (as measured by HOMA-IR). Specifically, canola oil had the biggest effect on reducing triglycerides, the total cholesterol/HDL ratio, and the triglyceride/HDL ratio. (Both canola oil and olive oil also reduced the severity of non-alcoholic fatty liver disease among the participants).

A 2020 systematic review and meta-analysis of 42 controlled clinical trials found that compared to other edible oils (including olive oil, saturated fats, and sunflower oil), canola oil consumption led to the greatest improvements in cardiometabolic risk factors. This included significantly reducing total cholesterol, LDL cholesterol, the LDL/HDL ratio, the total cholesterol/HDL ratio, apolipoprotein B (Apo B) levels, and the Apo B/Apo A-1 ratio. A dose-response analysis of the data showed that optimal effects on blood lipids occurred when consuming 15% of total calories as canola oil (specifically, when these calories displaced other dietary oils).

All this isn’t to say olive oil is bad; just that canola oil holds its own against well-established healthy foods! So, when it comes to vegetable oils, canola might deserve an extra special place at the table.

What About the High Heat and Hexane?!

Another argument against vegetable oils is the way they’re processed, which typically involves a mixture of high heat and chemical solvents. The proposed risk is twofold: fatty acid oxidation from the heat, and potentially toxic compounds remaining in the oil after extraction.

Although both of these points sound scary, they don’t hold up to scrutiny!

For one, while high temperatures may indeed used during extraction, it’s also done under high pressure—which means no oxygen (and therefore, no potential for oxidation)! Not only that, but lipid peroxidation is measured as part of the quality control for all oils that are on the store shelves. In other words, if you’re purchasing a commercially prepared oil, regulations are in place to ensure you’re not carrying home already-oxidized oil.

As far as toxic compounds involved in processing? Here’s the full scoop on how vegetable oils are made, and why the fear here is unfounded, too!

To make vegetable oil from plants, first the plant parts that are used to make the oil are harvested, deshelled, hulled, and cleaned. If the seed is used to make the oil, it is crushed or broken up into smaller pieces. Sometimes a first-press oil is made by mechanical extraction, basically squeezing these tiny pieces until oils comes out (a.k.a. cold pressing), and then a second-press oil is made from solvent extraction.

During solvent extraction, hexane is added to the crushed plant parts and then briefly heated, which causes a chemical reaction to allow the oil from the plant to separate out. The heat also causes hexane to evaporate—most vegetable oils have no detectable hexane residues. In one study, the highest concentration of hexane detected was 0.4 milligrams per kilogram (1.1 liters) of oil. The provisional chronic reference dose of hexane is 0.06 milligrams per kilogram bodyweight per day—so, a 70-kg person (154 pounds) would have to consume over 11 liters of this highest-hexane-detected vegetable oil every day to ingest enough hexane to worry! That would add up to about 97,000 calories worth of oil every day, not recommendable for a multitude of reasons, least of which is hexane! (By the way, hexane is used in the production of a number of other foods and supplements, including collagen powder!)

Once the oil is extracted, it’s then bleached using bleaching clay—not the bleach you use to clean—to remove any coloring pigments like carotenoids or chlorophyll which can make the oil more susceptible to oxidation in response to light. It’s then deodorized to remove any odor and off-flavors, and contaminants (pesticides, polycyclic aromatic hydrocarbons, etc.). Finally, it is filtered to remove any residual solvents, leaving the oil in its final state, which is packaged and sold. The refining process gives vegetable oil its light color, makes it flavorless and odorless, and makes it more stable with a longer shelf life. The claim that refining vegetable oil makes it more likely to go rancid is untrue. In fact, refining vegetable oil reduces the likelihood of rancidity!

In addition, expeller-pressed (cold-pressed) options for most vegetable oils exist and are easy to find at the grocery store, so you have plenty of options if you want to avoid refined vegetable oils.

Bottom Line

While we can build a case against vegetable oils from a mechanistic perspective, it just doesn’t hold up within living, real-world human bodies. The evidence is far more compelling in favor of consuming adequate omega-3-rich foods than keeping our vegetable oil intake low—especially in the context of a diverse, nutrient-dense diet!