What’s the Deal With Seed Oils?

In the United States, chronic illnesses and health problems largely attributed to diet represent the most serious threat to public health.  

Obesity increases the risk for many serious noncommunicable diseases, such as cardiovascular disease (CVD), diabetes, and certain cancers, all of which are some of the leading causes of preventable, premature death each year.

From 1999-2000 through 2017-2018, the prevalence of obesity increased from 30.5% to 42.4%. Over this period, numerous changes have taken place in the food environment to contribute to the rise. 

Generally speaking, the issue with the modern food environment stems from excessive access to hyper-palatable, energy-dense foods for a low cost. These items provide “empty calories,” overstimulate the reward system of the brain and generate little satiety, driving overconsumption. 

While it’s clear that there is a broad overarching issue, many have tried to pinpoint a specific change within the food supply as the most responsible for the widespread regression in health. One emerging theory revolves around vegetable oils.

The advent of the oil-seed processing industry at the beginning of the 20th century significantly raised the total intake of vegetable fat.

In the United States, during the 90-year period from 1909 to 1999, a significant increase in the use of vegetable oils occurred. Specifically, the per capita consumption of salad and cooking oils increased by 130%.

After the market introduction in 1986, the estimated per capita consumption of canola oil increased 167-fold in 13 years from 0.01 to 0.8 kg. The estimated per capita consumption of soybean oil increased from 0.009 kg in 1909 to 11.64 in 1999. Correspondingly, vegetable oils became the 4th major contributor of calories by the late 20th century.

Vegetable oils are rich in linoleic acid (LA), which is an 18-carbon omega-6 polyunsaturated fatty acid (PUFA). It is considered an essential fatty acid because the body cannot endogenously synthesize it (i.e., it must be consumed in the diet). 

As a direct result of consuming more energy from vegetable oils, there has been an increase in the average intake of LA. From 1909 to 1999, the percentage of energy intake increased from 2.79% to 7.21%.

This trend has been reflected in other metrics as well. In one review examining changes in the LA concentration of subcutaneous adipose tissue, it was found that from 1959 to 2008, there was an increase from ~9.1% to ~21.5%.

Unsurprisingly, the ratio of omega-6 to omega-3 PUFA in the diet has also increased. In comparison to our hunter-gatherer ancestors, whose diet contained a ratio of roughly 2-3:1, the current American diet has skewed to 10:1.

A large part of the concern over an increase in dietary LA derives from the theoretical consequences of an unfavorable omega-6 to omega-3 ratio.

The omega-3 and omega-6 PUFA, alpha-linolenic acid (ALA), and LA, respectively, compete for the same enzyme sites involved in the metabolism of the essential fatty acids.

In the body, LA is converted to arachidonic acid (AA) and by the same machinery, ALA can be converted to eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA), which are long-chain omega-3 PUFA typically referred to as “fish oil.”

AA, EPA, and DHA are precursors to potent lipid mediator signaling molecules termed “eicosanoids.” Eicosanoids derived from AA are generally considered pro-inflammatory, while eicosanoids generated from EPA and DHA promote anti-inflammatory activities.

The concern surrounding a high intake of LA is two-fold. Firstly, a large amount of LA could prompt the excessive formation of AA and subsequent synthesis of pro-inflammatory eicosanoids. 

Elevated pro-inflammatory eicosanoid generation could drive up other markers of inflammation such as interleukin-6 (IL-6), tumor necrosis factor (TNF), and C-reactive protein (CRP) that are associated with an increased incidence of disease.

Second, there is the possibility that high LA intake will lead to decreased conversion of ALA to EPA and/or DHA due to competition between LA and ALA for the same enzyme sites. This could further exacerbate inflammation and increase the risk of disease by reducing the formation of anti-inflammatory eicosanoids that are derived from EPA and DHA.

While these points lend good reason to study the effects of increased LA intake on human health, it’s important to understand that we’re talking about mechanisms. What looks good on paper doesn’t always lead to meaningful clinical outcomes. 

A good example of this is the carbohydrate-insulin model of obesity, which theorizes that diets high in carbohydrates are particularly fattening due to their propensity to elevate insulin secretion. Insulin has a major role in regulating the activity of several enzymes that promote the uptake, retention, and net storage of fat in adipose tissue.

It is speculated that since carbohydrates have a robust effect on insulin secretion, a high-carbohydrate diet will suppress the release of fatty acids from adipose tissue and direct circulating fat toward adipose storage and away from being used by metabolically active tissues such as the heart, muscle, and liver for energy. 

Sounds pretty darn good, right? However, controlled feeding studies show that when diets are matched for total calories and protein, the ratio of energy from fats and carbohydrates has no effect on fat loss.

Physiological underpinnings give us a good place to start, but we can’t automatically assume that the hypotheses generated will automatically pan out simply because they’re rational. We need direct research on the topic to determine if there is any truth to these ideas.

With that being said, let’s dive into our first concern regarding whether or not a high intake of LA increases inflammation and the risk of disease. To address this point, we’ll start with intervention trials that evaluated the impact of increasing LA intake on relevant biomarkers and follow-up with research assessing the relationship between LA and AA and disease.

The “Risks” of High LA Intake

Over the past decade, a collection of review articles examining the relationship between LA intake and inflammation have been published. In one such meta-analysis, results were pooled from 30 randomized controlled trials to investigate the effect of LA on inflammatory markers (e.g., IL-6, TNF, CRP). 

Within these trials, LA intake was increased through the consumption of sunflower oil in nine studies. Safflower and soybean oil were used in six and three studies, respectively. The remaining studies chose corn, sesame, and blended oils. The control groups utilized fats or oils low in LA such as flaxseed oil, canola oil, olive oil, or palm oil.

It was found that increasing dietary LA intake did not significantly affect blood concentrations of 11 inflammatory markers, including TNF, IL-6, and fibrinogen. In further analysis, it was found that very high LA intakes may slightly increase CRP concentrations.

These findings have been corroborated by an earlier review on the topic, which reported that “virtually no data exist to suggest that dietary LA increases inflammatory markers among healthy, free-living human beings older than age 1 year.”

In a more recent review of human intervention trials, the impact of LA consumption on CVD risk in healthy individuals was examined. The primary focus was the effect of LA consumption on lipid levels, including total cholesterol, triglycerides (TG), low-density lipoprotein cholesterol (LDL-C), and apoB (associated with LDL-C).

It was reported that LA consumption primarily decreased total cholesterol and produced mixed results on TG concentrations, whereas consumption of EPA and DHA more consistently decreased TGs. Also, LA consumption decreased LDL-C and apoB.

Further expanding on the question of whether high levels of LA and AA are associated with an increased risk of disease, there are a couple of massive review articles to lean on.

In a recent analysis, 76,356 fatty acid measurements from 68,659 participants in 30 prospective studies from 13 countries were examined to directly evaluate the effect of AA and LA levels on the risk of CVD events.

The studies utilized in this analysis measured fatty acids in different compartments, including plasma phospholipids, erythrocytes, plasma, serum, cholesterol esters, and adipose tissue.

Biomarker measurements are crucial for studying the effects of AA because they are free of the faults associated with self-reported dietary estimates, such as memory errors, recall bias, or inaccuracies of food databases. Also, variations in dietary LA have little effect on circulating AA levels, making these measurements a much more objective way to assess risk.

The results showed that higher levels of LA were associated with a lower risk of CVD events, in particular, CVD mortality and stroke. Also, AA levels were not associated with higher risk. In fact, in some analyses, AA levels were associated with lower CVD risk.

Another extensive review looked at the association between LA and AA biomarkers with the incidence of type 2 diabetes. In this article, data on 39,740 adults from 20 cohorts in ten countries were examined. 

The results indicated that biomarker levels of LA were inversely associated with the incidence of type 2 diabetes. High LA levels were associated with a 43% lower relative risk of type 2 diabetes, whereas levels of AA were not associated with diabetes.

These outcomes fall in line with the findings from a meta-analysis of randomized controlled feeding trials, which reported that the upper tertile of omega-6 PUFA intake (≥ 9% of total energy intake) led to the largest reductions in fasting insulin and HOMA-IR.

Together, the above data suggests that not only does LA not independently increase levels of inflammation, but the ability of PUFA to reduce CVD and type 2 diabetes risk is at least partially related to the effects of LA, rather than omega-3 PUFA alone.

Competition Between PUFA

Transitioning to our second area of concern, does a higher intake of LA counteract or reduce the positive effects of omega-3 PUFA?

As evidenced by the above, LA may very well be protective against many diseases, but there could be diminishing returns or a point where intake gets high enough that it starts to inhibit the beneficial properties of omega-3 PUFA. 

To address this point, it is first important to mention that, while higher omega-6 PUFA intake may inhibit the conversion of ALA to long-chain omega-3 PUFA, such conversion is already quite low. As such, it’s unlikely to have much impact on disease risk, and observational research supports this. 

In an investigation of the association between different patterns of PUFA intake and incident of coronary heart disease among 45,722 men in the Health Professionals Follow-up Study, it was shown that a modest dietary intake of long-chain omega-3 PUFA (i.e., DHA and EPA) was associated with a lower risk of coronary heart disease and a 40-50% lower risk of sudden death. Also, this outcome was not impacted by the background intake of omega-6 PUFA. 

In addition, a study on participants in the Framingham Offspring cohort showed that those with the highest red blood cell levels of EPA and DHA (Omega-3 Index) had a 34% lower risk of death from any cause and 39% lower risk for incident CVD. Moreover, exploratory analyses displayed omega-6 PUFA levels did not affect this outcome nor was it affected when replacing the Omega-3 Index for the omega-6 to omega-3 ratio. 

Similar results were found in the Women’s Health Initiative Memory Study cohort, where the highest Omega-3 Index values were associated with a 22% lower risk of death compared to the lowest, and neither LA nor AA was related to mortality.

In aggregate, these studies suggest that omega-6 PUFA do not counteract the numerous benefits and improved longevity associated with omega-3 PUFA. A very high LA intake may affect ALA uptake to a trivial degree, which could be an important consideration for certain populations (e.g., vegans), but in the context of consuming a sufficient amount of preformed EPA and DHA, it’s a moot point.

They also bring attention to a potentially more important issue. Rather than focusing on decreasing omega-6 PUFA intake, there should be a greater emphasis on increasing omega-3 PUFA intake.

Omega-3 PUFA are known to have beneficial effects on a variety of risk factors, including reductions in serum TG levels, blood pressure, inflammatory markers, plaque vulnerability, and improved endothelial function.

Many studies have documented reduced CVD and total mortality risk associated with higher omega-3 PUFA intakes and/or circulating levels. 

For those truly interested in reducing their risk of disease and prolonging their lifespan, the focus should be placed on increasing total PUFA intake, with an emphasis on omega-3 PUFA, specifically, as most people consume more than enough omega-6 PUFA in their diet.


Quite simply, if seed oils were the culprit for the universal deterioration in metabolic health, those with higher levels of LA and AA would display unfavorable lipid levels, markers of glucose metabolism, and inflammatory markers, and ultimately, exhibit a greater incidence of disease. Yet, the data consistently points in the opposite direction.

In the proposal that vegetable oil consumption needs to be reduced because of its high LA content, it seems that many people have failed to fully appreciate that AA and LA are involved in anti-inflammatory signaling pathways as well. 

While AA is the precursor to potentially pro-inflammatory eicosanoids, it is also the main precursor to key anti-inflammatory metabolites, such as omega-6 oxylipin, as well as other mediators that actively resolve inflammation. 

It’s a bit more complex than “omega-6 PUFA = proinflammatory = bad.” The current evidence does not support the hypothesis that omega-6 PUFA are detrimental to health in large quantities or antagonize the beneficial effects of omega-3 PUFA.

Despite the popularity of the omega-6/omega-3 ratio, due in large part to its appeal to the dietary patterns of our hunter-gatherer ancestors, it possesses little value and distracts us from perhaps a more important issue, increasing the intake of omega-3 PUFA. 

Overall, while increasing omega-3 PUFA levels seems to reduce the risk of CVD, it does not follow that decreasing omega-6 levels will do the same. In fact, high intakes of both omega-3 and omega-6 PUFA seem to provide for the lowest levels of inflammation and risk of total mortality.

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