Introduction

“Seed oils” – rich in the omega-6 fat linoleic acid (LA) – have been accused of promoting inflammation, oxidative stress, and chronic disease. Internet anecdotes blame seed oils for everything from heart disease to diabetes, fueling a pseudoscientific backlash against soybean, corn, sunflower, and similar oils. In reality, these claims do not hold up under scientific scrutiny.

This analysis will unpack the main anti-seed oil arguments and evaluate them against the evidence. We’ll dissect the commonly cited older studies (Sydney Diet-Heart, Minnesota Coronary Experiment, LA Veterans trial) and contrast them with higher-quality human trials and meta-analyses. We’ll also address concerns about seed oil processing (extraction, refining, cooking stability, omega-6/omega-3 ratio).

The bottom line – supported by converging clinical evidence – is that linoleic-rich oils are not inherently harmful; in fact, replacing saturated fats with polyunsaturated fats (PUFAs) is beneficial for cardiovascular health​.

Let’s explore why.

Claim 1: “Seed Oils Cause Inflammation and Oxidative Stress”

A core argument of seed oil detractors is that LA (an omega-6 PUFA) metabolizes to arachidonic acid and pro-inflammatory molecules, supposedly leading to systemic inflammation, oxidative damage, and oxidized LDL. However, robust human experiments do not support this claim. A 2012 systematic review of 15 controlled trials found “virtually no evidence” that adding LA to the diet increases inflammatory markers in healthy people. None of the trials reported significant increases in C-reactive protein (CRP), interleukins, tumor necrosis factor, or other inflammation indicators with higher omega-6 intake.

Similarly, a 2024 evidence review highlighted the consistency among clinical trials in showing that increased LA intake does not increase markers of inflammation or oxidative stress. In fact, some trials indicate that high-LA diets either reduce inflammation or have no effect, especially when weight change is controlled.

It’s true that LA is biochemically prone to oxidation (it’s an unsaturated fat), and lab tests show LA in LDL can form oxidized byproducts. But in vivo, the body’s antioxidant systems and the cholesterol-lowering effect of LA appear to offset this. Notably, replacing saturated fat with PUFA lowers LDL-C levels, meaning there are fewer LDL particles available to oxidize.

Some controlled feeding studies have directly measured LDL oxidation and found that diets rich in polyunsaturates do not lead to higher oxidized LDL than saturated fat diets, especially when accompanied by dietary antioxidants (like vitamin E naturally present in vegetable oils). And increased LA intake does not worsen oxidative stress, as demonstrated in clinical trials.

Critics often point to a high ratio of omega-6 : omega-3 as a driver of inflammation. They typically mention that our evolutionary diet had a 1:1 ratio of omega-6 to omega-3, whereas modern diets might be 10:1 or 20:1, implying this imbalance causes inflammation. It’s true that many people get too little omega-3 (from fish, flax, etc.), and increasing omega-3 intake is important. However, fixating on the ratio can be misleading. The benefit does not come from omega-6 intake, but rather the key is to bring up omega-3 intake. Thus, the omega-6:omega-3 ratio concern is largely theoretical and should not distract from the proven benefits of PUFA.

In short, the biological outcome of consuming seed oils does not match the pro-inflammatory theory. Our bodies tightly regulate conversion of LA to arachidonic acid – only a small fraction (<1%) of dietary LA becomes tissue AA. On the contrary, many studies link higher omega-6 intake to lower inflammation and lower cardiovascular risk. Thus, the blanket claim that seed oils promote chronic inflammation or oxidative damage is not supported by the clinical literature.

Claim 2: “Seed Oils Drive Heart Disease and Chronic Illness”

Another popular claim is that LA-rich oils supposedly cause heart disease, obesity, or other chronic ills via the above mechanisms. This runs directly counter to decades of nutrition research. Large epidemiologic studies and randomized trials overwhelmingly support PUFA (including omega-6) as heart-healthy, not harmful.

Prospective cohort studies find that people who eat more LA have lower risk of coronary heart disease (CHD) in a dose-response manner. For example, an analysis of 11 cohort studies found that replacing 5% of calories from saturated fat with PUFA was associated with significantly reduced CHD events. And in a pooled analysis of 30 cohort studies, showed higher blood levels of LA were associated with lower risk of total CVD, cardiovascular mortality, and ischemic stroke. And even AA levels were not associated with higher risk of cardiovascular outcomes.

In addition to the epidemiology, randomized controlled trials (RCTs) consistently demonstrate cardiovascular benefit when saturated fats are swapped for PUFA. A landmark 2010 meta-analysis of RCTs (spanning ~1965–1986) found that increasing polyunsaturated fat intake in place of saturated fat reduced CHD events by 19% (see figure below). This corresponded to a ~10% reduction in risk for each 5% of energy exchanged from saturated to polyunsaturated fat​.

Beyond heart disease, higher PUFA intake has been linked to favorable outcomes like improved insulin sensitivity and lower Type 2 diabetes risk. Some controlled trials suggest omega-6 PUFA–rich diets can improve insulin resistance compared to saturated fat diets​. Consistently, cohort studies also find that people with higher LA intake or tissue levels have lower risk of developing Type 2 diabetes.

There is no credible evidence that consuming seed oils leads to obesity or other chronic illnesses independent of excess calories. In fact, traditional populations with high PUFA diets (e.g. certain Mediterranean or Asian diets using soybean, sesame, or sunflower oils) have low rates of heart disease and generally healthy inflammatory profiles. Taken together, the weight of scientific evidence indicates that LA from seed oils is neutral or beneficial for chronic disease risk – not a driver of disease.

Revisiting Three Commonly Cited Studies

Anti-seed oil proponents often cite a few older studies from the 1960s–70s that they claim “prove” omega-6 oils are harmful. Let’s critically evaluate the Sydney Diet-Heart Study, the Minnesota Coronary Experiment, and the LA Veterans Administration Study. These trials do not provide strong evidence against seed oils once we understand their methods and limitations.

Sydney Diet-Heart Study (1966–1973)

This trial involved 458 men (age 30–59) with established coronary artery disease, randomized in the late 1960s to two diets. The intervention group was instructed to replace saturated fats (from butter, milk, meat) with safflower oil (a very high-LA omega-6 oil with virtually no omega-3) and safflower polyunsaturated margarine​. The control group got no specific diet advice and ate their usual diet.

Notably, this was a secondary prevention trial (participants already had heart disease), and it was single-blinded – meaning participants knew if they were on the special diet or not, which can introduce bias. The study’s outcomes were not fully reported until decades later when researchers recovered the raw data and published a 2013 re-analysis by Ramsden et al., which is what is frequently cited by anti-seed oil advocates.

What Sydney found: The re-analysis reported that the safflower oil group had higher mortality than the control group after about 3–7 years. All-cause deaths were 17.6% in the omega-6 group vs 11.8% in controls (HR 1.62, P = 0.05)​. Deaths from cardiovascular causes were similarly higher (≈17% vs 11%, HR ~1.7)​. In other words, despite lowering serum cholesterol by about 13% on the safflower oil diet, participants did not see a benefit – paradoxically, they fared worse in terms of mortality. This outcome is often trumpeted as “proof” that seed oils cause harm.

However, there are critical confounders and flaws:

• The intervention provided “Miracle” brand safflower margarine. In the 1960s, margarines were made by partial hydrogenation, which produces trans fatty acids. The Miracle margarine used in Sydney Diet-Heart contained approximately 15% trans fat​. Trans fats are a well-known pro-atherogenic, pro-inflammatory fat, effectively increasing heart disease risk. Any harm observed in the safflower group could be due to these trans fats, not the linoleic acid per se. Today’s margarines and liquid oils are virtually trans-free, so the Sydney trial doesn’t reflect modern dietary advice.
• The experimental diet was pure omega-6 (safflower is ~75% LA) with negligible omega-3 fatty acids. We now understand that including omega-3 PUFAs (from fish or plant sources like flax) is important in a heart-healthy diet. Omega-3s yield anti-inflammatory eicosanoids and other benefits.
• All participants were men with prior coronary events, a group at very high short-term risk. By chance or other factors, the control group mortality was unusually low (only ~10% CHD mortality over 5 years, which is surprisingly favorable for 1970s medical care). The treated group’s 16% CHD mortality was closer to expected. With such small numbers, it’s conceivable the difference was due to chance variation or slight baseline imbalances.
• The fact that the original researchers did not publish the mortality outcomes at the time raises questions (perhaps they found the results puzzling or unreliable). This post-hoc resurrection of data, while valuable, means we lack some context (e.g. were there adherence issues? other differences in care?). It also means the findings should be viewed as hypothesis-generating rather than conclusive.

Given these limitations, the Sydney study does not provide robust evidence that LA is dangerous. If anything, it warns against trans-fat laden margarine – a point universally accepted now. Overall, Sydney Diet-Heart was an outlier study with serious confounders.

Minnesota Coronary Experiment (1968–1973)

The Minnesota Coronary Experiment (MCE) is another study often cited to claim “vegetable oils aren’t good for heart health”. MCE was a large RCT in state mental hospitals and a nursing home in the late 1960s. Over 9,400 institutionalized men and women (aged 20–97) were enrolled, making it one of the largest diet trials ever.

Participants were assigned to either a control diet (high in saturated fat from animal foods, typical American fare) or an intervention diet where saturated fat was sharply reduced and replaced with corn oil and corn oil polyunsaturated margarine (high in omega-6 LA).

The goal was an extreme PUFA intake – about 15% of calories from LA, which is well above today’s recommended range​. In fact, to achieve this, the researchers went to unusual lengths: they created “fake” foods like imitation milk, cheese, and meat that had the animal fat removed and replaced with corn oil​. This meant the intervention diet was very high in omega-6 and had minimal omega-3, since any n-3 present in the natural foods was largely removed by the fat substitution process​. They even formulated a special soft corn oil margarine that was meant to be lower in trans fat than typical margarines of the time​. (Even so, we now know that lightly hydrogenated oil can have higher levels of certain 18:2 trans isomers, which are particularly harmful trans fats​.)

What MCE found: The full results of MCE were not published until 2016 (another data “lost and found” situation). The intervention successfully lowered participants’ blood cholesterol by about 13% compared to controls​. However, this did not translate into fewer deaths or heart attacks in the intervention group during the study period. There was actually a hint that among older participants, those who had the largest cholesterol drops had higher mortality – a puzzling finding the original investigators struggled to interpret. The 2016 BMJ re-analysis (Ramsden et al.) concluded that there was no mortality benefit from the omega-6 diet, and questioned whether replacing saturated fat with LA is truly beneficial.

Key limitations of MCE:

• MCE was intended to run for many years, but it coincided with the deinstitutionalization movement (patients were being released from mental hospitals in the early 1970s). As Dr. Walter Willett noted: “The most serious problem with MCE is the very short duration – [they] lost nearly 75% of participants within the first year.”​ Many patients only stayed on the diets for a few months; only ~25% remained for 1 year, and perhaps only ~50% were on the diet for 3 years​. The median follow-up was around 1 year – far too short to assess heart disease outcomes, which develop over decades. The trial was essentially underpowered and truncated. Willett bluntly stated “the study was clearly a failure… it adds very minimal information, if any, about the long-term effects of diet on heart disease.”​
• The corn oil diet in MCE was an artificial diet that virtually no free-living population has ever consumed​. LA intake was pushed to ~15-20% of calories (double the AHA’s upper recommendation of 10%​). Achieving this required processed food replacements that, while carefully controlled, do not mirror typical dietary patterns.In effect, MCE tested a very specific hypothesis in a very controlled environment – but one that’s not relevant to normal diets.
• With the limited data, MCE did not show a significant difference in heart attack incidence or mortality between groups during follow-up. But given the short follow-up, this null finding is not shocking. When you graph the survival curves, they only start to diverge slightly towards the very end (by which time so many had dropped out that the data are hard to interpret). It’s a classic case of a trial “stopping too early” to capture a true effect. Interestingly, cholesterol was lowered (which normally predicts benefit), so the lack of observed benefit might simply be due to insufficient time – or the countervailing effect of trans fats or other factors in the institutional setting (infections, smoking rates, etc. could swamp any dietary effect over short periods).

In summary, MCE does not prove that seed oils are harmful or ineffective – if anything, it underscores how difficult long-term diet trials are. Current guidelines don’t advise eating 20% of calories as corn oil with zero omega-3s. They advise moderate increases in unsaturated fats in a balanced diet. MCE’s extreme conditions and execution problems make it a poor guide for modern diets.

Los Angeles Veterans Trial (1969)

The LA Veterans Administration Hospital Study (1969) was a multi-year trial in older men that actually did show cardiovascular benefits from replacing saturated fat with PUFA, but it’s sometimes misrepresented. Typically it is held up to claim that there is no mortality benefit from replacing saturated fat with PUFAs.

In this study, 846 male veterans living in a VA home were randomized for 8 years to either: a control diet (high in saturated fat and cholesterol, typical of the era) or an experimental diet where ~50% of the fat was replaced by corn oil (plus some corn oil margarine), resulting in a diet low in SFA and high in PUFA.

The participants’ average age was over 60, and about 30% had pre-existing cardiovascular disease​ (so it was a mix of primary and secondary prevention in an older cohort). Compliance was good since they were in a controlled institutional setting.

What LA Veterans found: The PUFA group’s cholesterol dropped ~13% relative to controls (plasma ~233→202 mg/dL)​. Over the 8-year period, the PUFA diet group experienced fewer heart attacks and fewer deaths from atherosclerotic causes. Specifically, the incidence of myocardial infarction and sudden cardiac death was 45 in the PUFA group vs 67 in controls (a 33% reduction, though with p≃0.06 it narrowly missed statistical significance on its own)​. When combining all cardiovascular events (including stroke), the difference became significant – 66 total events in the PUFA group vs 96 in controls (P=0.01)​. Likewise, fatal atherosclerotic events (deaths due to heart attack or stroke) were 48 in the PUFA group vs 70 in controls, a significant reduction (P < 0.05)​​. In fact, for all combined endpoints (heart events, stroke, etc.), 31.3% of the PUFA group had an event versus 47.7% of the control group – a notable 34% risk reduction​. By these measures, the corn oil diet improved cardiovascular outcomes.

However, total mortality between the groups ended up similar. Why? Largely because the PUFA group had more deaths from cancers and non-cardiac causes. This was not statistically significant in any single category, but when pooled over 8 years, the corn oil group had a slight excess of cancer cases (e.g. more new lung cancers, which isn’t shocking given many were heavy smokers).

A graph published later (shown below) showed higher cancer incidence in the PUFA group over time​. This has been seized upon by anti-seed oil writers to claim “seed oils cause cancer”.

In truth, the trial was not designed to study cancer, and the participants were elderly men (more prone to cancer in any case). The difference could well have been due to chance. Investigators themselves cautioned that the cancer finding was inconclusive. It’s important that no other controlled trial has ever replicated an increase in cancer from polyunsaturated fat. Large population studies also do not show higher cancer risk in people who consume more vegetable oils – if anything, some studies link higher PUFA to lower cancer mortality, likely because it often correlates with a healthier diet overall.

Thus, attributing the LA Veterans cancer observation to seed oils is speculative and not supported by broader evidence. A more likely explanation is that by preventing fatal heart attacks in some men, the PUFA diet allowed them to live long enough to be diagnosed with cancer (a classic competing risks scenario). Meanwhile, more men in the control group might have died earlier of heart disease, truncating their cancer risk window.

What Do These Three Trials Tell Us?

The Sydney, Minnesota, and LA Veterans studies were pioneering but imperfect. Sydney and Minnesota, especially, had major methodological issues (trans fats, no omega-3s, short follow-up) that render their results context-specific and not generalizable to typical diets​. The LA Veterans trial, the most robust of the three, actually found cardiovascular benefit from PUFA, with a quirk in cancer outcomes that hasn’t been seen elsewhere.

When weighed alongside all evidence, these older studies do not refute the lipid hypothesis or the benefits of replacing saturated fat with vegetable oils. At most, they suggest that an extreme pure-LA diet or inclusion of trans fats can negate benefits – which is already well-understood in nutrition science.

Evidence from Modern Trials and Meta-Analyses

To get the full picture, we must consider higher-quality, more recent evidence on PUFA, inflammation, and disease risk. Nutrition science has advanced, and many controlled trials and systematic reviews have evaluated the health effects of linoleic-rich oils. Let’s take a look at what the best evidence shows.

No Increase in Inflammation Markers

• As noted earlier, a comprehensive review of 15 RCTs concluded that increasing LA intake does not raise inflammatory biomarkers.
• In healthy adults, diets with up to 11% of calories from omega-6 (which is above average intake) showed no rise in CRP, IL-6, TNF-α, or other cytokines compared to lower-LA diets.
• Some trials even found slight decreases in certain inflammation markers on higher PUFA diets (likely due to concurrent improvements in metabolic health). For example, weight-controlled feeding studies have shown that high-PUFA diets can lower CRP relative to high saturated fat diets, especially in the context of weight loss.
• The AHA’s scientific advisory examined dozens of studies and stated: “at present, little direct evidence supports a net proinflammatory, proatherogenic effect of LA in humans”

Improved Lipid Profiles

• It is one of the most consistent findings in nutrition that replacing saturated fat with polyunsaturated fat lowers LDL cholesterol. A 2023 meta-analysis of 40 RCTs confirmed that higher dietary LA significantly reduces LDL-C levels (by ~3–4 mg/dL on average, and even more – ~8+ mg/dL – when replacing saturated fat directly).

Lower Risk of Heart Disease Events

Beyond biomarkers, we have clinical endpoint trials. We’ve discussed older ones, but also consider more recent large-scale interventions:

• For example, the Women’s Health Initiative (WHI) in the 2000s – while primarily a low-fat diet study – did achieve a modest increase in PUFA intake and decrease in saturates among ~48,000 women. Over 8 years, WHI did not show a significant drop in CHD, likely because the dietary changes were small. But in women who substantially increased PUFA intake, there were trends toward benefit. And certainly no increase in risk was seen.
• More clearly, the previosly mentioned pooled analysis of controlled trials (including Sydney, LA Veterans, MCE, and several others like the Oslo Diet-Heart Study and the Medical Research Council Soy Oil trial) found a significant ~24% reduction in coronary events in the PUFA groups vs controls​.
• The Oslo Diet-Heart Study (which gave a balanced PUFA diet including some omega-3 from fish) saw markedly lower heart attack recurrence in the intervention group (38% cardiac mortality reduction over 5 years). Note that this study was covered in detail in episode 505 of the podcast.
• The “Finnish Mental Hospital Study” – a crossover trial in two hospitals – found that shifting middle-aged patients from a high-SFA diet to a high-PUFA diet cut CHD incidence by 50–70% (especially in men) over 6 years.

These older trials, together with newer analyses, form a consistent picture: as long as trans fats are kept low and some omega-3 is included, PUFA-rich diets reduce cardiovascular risk.

No Adverse Effect on Diabetes or Metabolic Health

Critics sometimes claim seed oils cause insulin resistance or fatty liver. But RCTs contradict this.

• In a controlled trial where subjects were overfed either saturated fat or polyunsaturated fat, the saturated fat led to greater increases in liver fat and insulin resistance, whereas the PUFA led to more lean tissue gain and less liver fat accumulation.
• In a meta-analysis of feeding trials, higher intakes of PUFA (compared to carbohydrates, SFA or MUFA) led to improved glycaemia, insulin resistance, and insulin secretion capacity.

Omega-6 Intake and Overall Mortality

• As discussed in an excellent review published in the BJN in 2024, mega-cohort meta-analyses (with hundreds of thousands of participants) found that higher consumption of PUFAs, including LA, is associated with lower all-cause mortality.
• There’s no epidemiologic signal that people who use more vegetable oil die earlier – quite the opposite, they often have better health outcomes, likely because it’s a marker of replacing animal fats or refined carbs with healthier fats.

Key Point: High-quality human evidence shows that typical use of seed oils is safe and beneficial for cardiovascular health.

Multiple converging lines of evidence – metabolic ward studies, randomized trials, observational cohorts, and mechanistic research – all support the conclusion that omega-6 PUFA is cardioprotective when used in place of saturated fats

Addressing Common Concerns about Seed Oil Processing and Use

Beyond the metabolic effects, the anti-seed oil rhetoric brings up various food processing and cooking issues – often based on misunderstandings. Let’s tackle some of the frequent concerns, namely:

1. “Toxic Hexane” Extraction
2. Refining, Bleaching, Deodorizing (RBD)
3. Stability During Cooking

“Toxic Hexane” Extraction

It’s true that most commercial seed oils are extracted using the solvent n-hexane. Hexane is a volatile petroleum-derived solvent used to efficiently pull oil from crushed seeds. This sounds scary (“fuel in my food!”), but in practice almost all hexane is removed during production.

After extraction, the oil-hexane mixture is heated to evaporate hexane, which is then recycled. The pressed seed meal is also desolventized by heat and steam. By the end, residual hexane in the oil is extremely low – typically on the order of a few parts per million or less.

The European Union sets a maximum residue limit of 1 mg/kg (1 ppm) for hexane in food oils​, and reputable producers meet or fall below this. To put that in perspective, 1 ppm is one milligram per liter – an insignificant trace. Regulators (like EFSA) consider these trace levels safe; there’s no evidence that consuming oil with a few ppm of hexane poses any risk.

Hexane is far more of an occupational hazard (for factory workers inhaling vapors) than a dietary hazard. In short, the finished oils do not contain meaningful hexane. If one is still uncomfortable, cold-pressed or expeller-pressed oils are an alternative (they avoid solvent use, though they are more expensive). But from a health standpoint, the minute hexane residues in commercial oils are a non-issue and certainly not a reason to avoid seed oils.

Refining, Bleaching, Deodorizing (RBD)

Often people have concerns about products that are “refined”. However, when it comes to production of oils, refining is simply the process of removing the many types of impurities in the oils that affect their quality, taste and safety.

Crude seed oil contains various impurities such as free fatty acids, gums, pigments, odors, etc. Refining removes these through:

• Neutralization (to remove free fatty acids that could cause oxidation)
• Bleaching (using clays to remove pigments and some oxidation products)
• Deodorizing (steam distillation to remove volatile compounds and any residual solvent).

The end result is a neutral, stable oil with high purity. Far from making the oil toxic, these steps ensure the oil doesn’t spoil easily and has a high smoke point for cooking.

And while it is true that some of the natural vitamin E and antioxidants are reduced during refining, often antioxidants like tocopherols are added back to preserve shelf life. Most commercial vegetable oils do contain additives like TBHQ or citric acid to prevent oxidation. Thus, the notion that “refined = rancid” is false – refined oils are sold specifically for their bland taste and oxidative stability. Modern refined oils have peroxide values and oxidation measures well within safe limits.

Of course, all fats can form breakdown products if grossly abused (e.g. repeatedly heated to smoking), but fresh refined seed oil is not delivered to consumers full of toxins. It’s worth noting that refining also eliminates practically all trans fat (if any formed naturally in seeds or during processing) and removes allergens (proteins) – making refined oils very pure fat. Overall, the RBD process is there to ensure quality and safety, not to poison the oils.

Stability During Cooking

A legitimate point is that polyunsaturated oils are less heat-stable than saturated fats – they can oxidize at high temperatures to form aldehydes and peroxides if overheated or used repeatedly. However, this concern is often exaggerated. In typical home cooking (sautéing, baking, light frying at ~180°C or below), quality seed oils perform fine. They have high smoke points (often 230°C/446°F or above for refined oils) and don’t break down significantly in one-time use.

The problems occur with prolonged deep-frying or reusing oil many times, which can happen in commercial fryers. Even then, restaurants mitigate this by filtering oils and discarding after a set number of uses. If you’re pan-frying at home in corn or soybean oil and discard the excess, you’re not creating some uniquely dangerous concoction – you’ll mainly get some usual cooking volatiles (which any oil, even lard or butter, would produce when overheated).

The sensible practice is to cook within the oil’s temperature limits and avoid reusing frying oil excessively. Studies on deep-frying show that oils high in PUFA do produce more total polar compounds (TPCs) after repeated frying than oils high in monounsaturates​. But for one-off frying, differences are modest.

If you want maximum frying stability, high-oleic sunflower or peanut oil (with more monounsaturated fat) are great choices – but standard soybean or canola oil is still perfectly adequate for most uses. The evidence does not show that normal cooking with seed oils creates toxic levels of oxidation products that cause health damage. Populations that traditionally cook with seed oils (like many Asian countries using soybean/peanut oil, or Mediterranean using sunflower oil) do not show higher cancer or heart disease rates attributable to this.

In summary, use seed oils sensibly (don’t burn them, refresh oil when deep-frying, etc.) and they are safe for cooking. The concern is overblown when basic kitchen practices are followed.

Conclusions

After examining the claims and the relevant evidence, it is clear that the fear of seed oils and linoleic acid is not supported by the scientific literature. The anti-seed oil arguments cherry-pick anomalies (often from antiquated studies with confounders) while ignoring the much larger body of rigorous research. When we look at well-conducted human trials and nutritional epidemiology, the picture is consistent: Diets that include vegetable oils in place of saturated fats tend to improve cardiovascular health, without causing inflammation or other harm.

Nutrition professionals should feel assured that recommending seed oils (like canola, soybean, corn, sunflower, safflower, etc.) is evidence-based and in line with global dietary guidelines. Replacing butter or palm oil with these PUFAs helps lower LDL cholesterol and reduces heart disease risk, as demonstrated in clinical trials​.

Contrary to internet myths, seed oils are not “toxic” poisons. The human body evolved to handle a range of fat intakes, and moderate-to-liberal amounts of linoleic acid have been consumed in many healthy populations. What we see in research is that problems arise not from seed oils, but from industrial trans fats (now largely eliminated), excessive refined carb intake, and overall poor diet quality. Blaming seed oils is a distraction from the real issues.

In fact, the partial replacement of animal fats with vegetable oils has been one of the key contributors to the decline in cardiovascular mortality in the late 20th century. While that’s hard to quantify, it aligns with the evidence that higher PUFA intake correlates with lower heart disease incidence. This does not mean more is always better – pouring oil on everything is clearly not the recommendation. But within a balanced diet, PUFAs are a positive element, not a negative one.

In conclusion, labeling seed oils as “unsafe” or “inflammatory” is a modern myth not borne out by scientific data. Dismissing these oils outright is not only unnecessary, it could be harmful if people revert to using more saturated fats or avoid beneficial foods like nuts, which are rich in linoleic acid. The evidence-based view is that unsaturated plant oils, including those high in omega-6, can be healthful culinary fats. They should be used in moderation to replace sources of saturated fat as part of a varied, nutrient-rich diet. Such an approach is supported by decades of research and aligns with recommendations to improve cardiovascular outcomes.

Summary of Key Points

• Seed oils do not inherently cause chronic inflammation – controlled trials show no increase in inflammatory markers with high-LA diets​.
• Linoleic acid does not generate oxidative stress in the body – no rise in oxidative stress markers or oxidized LDL has been found with typical intakes.
• Replacing saturated fat with PUFA consistently lowers LDL-C and improves the cholesterol profile, which is strongly linked to reduced atherosclerosis risk​.
• Clinical trials and meta-analyses find that shifting to a higher-PUFA diet reduces coronary events (≈10–20% risk reduction or more, depending on the degree of change)​.
• The infamous older studies cited against seed oils have serious flaws (trans fats, short duration, extreme diets) and do not override the broader evidence of benefit.
• Concerns about processing (hexane, refining) are largely unfounded and based on a misunderstanding – final oils have negligible solvent residues​ and refining makes oils more stable and safe, not dangerous.
• Cooking with seed oils is safe when done properly; all oils can degrade if abused, but vegetable oils used within normal temperature ranges do not produce unique toxins beyond what any heated fat would produce.
• Omega-6/omega-3 balance is achieved by adding omega-3s, not eliminating omega-6s. Omega-6 PUFAs remain a valuable part of a healthy diet.

Recommended Resources

If you want to learn more about this topic, we have several related podcast episodes which you might enjoy (find Sigma Nutrition Radio on any podcast app):

• 502: Sydney Diet-Heart Study – Is Linoleic Acid Causing Heart Disease?
• 504: Vegetable Oil vs. Saturated Fat – Analysis of the LA Veterans Study
• 505: Oslo Diet-Heart Study: Cholesterol-lowering Diets & Cardiovascular Events
• 329: Diet & Inflammation

If you are interested in enhancing your ability to critique nutrition studies and develop confidence in reading and interpreting research, consider joining the next cohort of our Applied Nutrition Literacy course.