Seed (Vegetable) Oils

Our bodies have evolved to use fats from the animals and plants we encountered over millions of years. Today we tend to consume processed ingredients that are unnaturally high in easily absorbed sugars, starches, seed oils which our bodies are not adapted to. This has created an evolutionary mis-match between what we have evolved to consume and what we actually do consume.

A few years ago I concluded that seed oils and highly bioavailable carbohydrates may have contributed to my heart disease so I stopped consuming them. Because of my ongoing research, I’m now convinced that seed oils were a cause of my heart disease.

“…I’m now convinced that seed oils were a cause of my heart disease”

Common seed oils

Table 1 contains a list of common seed oils, their starting materials, and the ways they are commonly used [1].

Fats in nature we co-evolved with

It is hard to understand the damage caused by seed oils without using a little specialized terminology. Fats are more accurately referred to as fatty acids, of which there are three types in nature we have evolved to consume, absorb, and process healthily.

Saturated fatty acids (SFA)

SFA is the most common type of fat in nature. We are exposed to it from natural foods (e.g., meats, dairy, fish, coconut, and some nuts). Our body even manufactures its own SFA.

The word “saturated” is used in chemistry to denote a fatty acid characterized by carbon atoms that are connected to other carbon atoms by single chemical bonds and are otherwise connected to (saturated with) hydrogen atoms. In other words, SFA contain no double chemical bonds. This is very important.

Monounsaturated fatty acids (MUFA)

MUFA are found in natural foods such as olives, avocados, and macadamia nuts.

The use of the word “monounsaturated” means that MUFA contain at least one double bond between their carbon atoms.

Polyunsaturated fatty acids (PUFA)

PUFA occur naturally in very small amounts in things like meat, dairy, chia, flax seeds, and nuts. PUFA exist in two forms, namely omega-3 and omega-6, and they are considered as essential for life as SFA and MUFA, when present in naturally occurring small amounts.

As their name implies, PUFA contain more than one double bond between the carbon atoms in their chemical structure. This is very important as I’ll describe below.

Linoleic acid (LA) is a very common natural omega-6 PUFA which will feature heavily as I explore the potential harm caused by seed oils.

“...it is important to understand the difference between reactive and unreactive fatty acids.”

Natural occurrence and beneficial effects of fatty acids

SFA, MUFA and PUFA, including LA, all occur naturally and we evolved consuming all of them. Nature does not produce bad fats and each type plays its own role when we consume them in natural amounts. Each type of fatty acid provides structural integrity to our cell membranes, performs important functions within those membranes, and plays crucial roles in several human biological processes.

However, it is important to understand the difference between reactive and unreactive fatty acids. SFA are chemically unreactive and unlikely to be damaged under natural conditions [2]. MUFA and PUFA, on the other hand, because of the presence of double bonds in their chemical structure, can become damaged by a process called oxidation (more accurately lipid peroxidation) and may cause harm if left unchecked. Because PUFA contain more double bonds than MUFA, they are more prone to damage by oxidation.

Fortunately, real food also contains natural anti-oxidants (e.g., vitamin C) which can protect us from oxidative harm when we eat the small amounts of MUFA and PUFA we encounter in nature. We evolved to consume foods in which MUFA, PUFA, and anti-oxidants are well balanced.

Dietary requirement for LA versus current consumption

1% - 2% of daily calories from LA appears to be a safe upper limit [3, 5] in our diet. Today, because of seed oils, LA consumption is thought to comprise almost 33% of daily calories in America, nearly 25% in 12 westernised countries and approximately 14% in a basket of 64 countries [3].

Some of us, therefore, are consuming approximately 15 to 30 times more LA than is considered safe.

When do fatty acids become harmful?

The greatest risk we face today is an excess of PUFA in our diet because we cook with and consume seed oils which contain unnaturally high amounts of LA (Table 2) and no beneficial anti-oxidants.

Seed oils can contain up to 70% LA (Table 2) compared to the 1%-2% we are adapted to process naturally [3,4,5].

Table 2: Seed oils containing high amounts of LA (from reference 5)

This unnatural situation has arisen because we use an industrial process to transform the LA and anti-oxidants in seeds into an artificially manufactured oil.

The industrial manufacture of seed oils

Seed oils are created through a multi-step industrial manufacturing process [6]. The initial steps take place once the seed oil crop enters the factory where they undergoe sterilization, stripping, extraction, and purification creating crude seed oil. The crude oil then undergoes a chemical or physical refining process similar to that shown in Figure 1. The resulting refined oil with very high amounts of LA (Table 2) is used as an ingredient in processed food or sold directly to consumers for cooking.

The seed oil end-product of the industrial manufacturing process is chemically very different from the LA present naturally in real food. Consider the following:

The amount of LA can be as high as 70-fold greater than in real food (Table 2)
They contain none of the anti-oxidants produced in nature to protect us from LA oxidation
They contain no fat soluble vitamins (e.g., vitamins A, D3, E, and K2) we’d expect in nature

Seed oils, therefore, are biologically un-natural and act as a delivery vehicle exposing us to harmful levels of LA without any of the protection and nutrition we’d expect from real food.

Figure 1: Seed oil refining (from reference 6)

How are we exposed to seed oils and LA

Many of us will be exposed to seed oils every day through:

Cooking and other food preparation with seed oils
Processed food containing seed oils
Meats, dairy, and fish containing high amounts of LA
High LA-containing nuts and seeds

Cooking and other food preparation with seed oils

My lifestyle used to consist of regular international business travel with three days at home most weeks. I ate out in restaurants, cooked for myself using “heart healthy” seed oils when using a long-stay option and cooked with the same seed oils at home.

Every-day processed food containing seed oils

I ate all sorts of processed ingredients containing seed oils and simple sugars and starches. The protein bars I consumed after a run or a bike ride all contained seed oils.

Meats and dairy containing high amounts of LA

This is an interesting one. Many farm animals and farmed fish are now fed things like processed grains, corn, soy and artificial feeds containing seed oils. Even if the feeds have been produced organically, they can still contain high amounts of LA.

The extent to which farm animals absorb LA from their diet into their organs and meat depends on the types of stomachs they have. Animals like chickens and pigs have single stomachs (like us) and the LA content of their organs, meat, and eggs will (like us) reflect the LA content of their feed. Chicken and pigs raised in modern farms often contain 25% LA in their eggs and meat [3,5].

Ruminants such as sheep, cows, deer, and goats have multichambered stomachs. Those chambers contain extensive microbiota that are able to ferment LA and convert it into SFA and MUFA. The organs, flesh, and milk from ruminants, therefore, contain naturally low amounts of LA, irrespective of what they eat. Ruminant meat tends to contain only 2% LA [3,5].

Farmed fish are fed an artificial diet higher in PUFA than they would encounter in nature. Those PUFA have been shown to raise the level of PUFA in humans when farmed fish are consumed [7].

High LA-containing nuts and seeds

Nuts and seeds vary in their LA content but many tend to be quite high. For example poppy seeds (62%), walnuts (53%), and pine nuts (33%) are amongst my favourites. Only macadamia nuts are low in LA (2%) [5]. I previously paid no attention to these stats. If I was in the mood, I binged on mixed nuts, especially during long car rides to and from home.

As a general rule, I opted for organic but paid no attention to the likely seed oil content of what I ate. As far as I was concerned, I was the same weight in my late 50s as I was at 18, I ate what was recommended, I exercised regularly, I followed my doctor’s instructions, and I took the meds that he prescribed. Perfect, right? Wrong.

Table 3. Oils and fats containing medium and low amounts of LA (from reference 5)

Harms caused by seed oils

A recent summary [8] of the health effects of consuming seed oils provides the following:

Seed oils are the likely cause of increased death as revealed by long-term clinical trials measuring real clinical endpoints
- In one heart disease investigation, it was shown that LA was associated with reduced blood cholesterol concentrations and increased risk of death. This negative effect was especially noticeable in people older than 65
- In another heart disease study, dietary LA was associated with death from all causes and death from heart disease
People with the highest intake of LA were more at risk from certain types of heart disease
The chemical instability of seed oils and their tendency to produce harmful breakdown products supports their tendency to promote insulin resistance, obesity, heart disease, autoimmune diseases, cancer, and diabetes.

Another recent review of the literature [5] also reveals associations between high LA consumption and a number of so-called chronic diseases such as heart disease, Alzheimer’s, cancer, dementia, obesity, and type-2 diabetes.

A review of how fatty acid oxidation may affect heart disease concludes that all inflammatory diseases (e.g., heart disease, liver damage, psoriasis) involve exposure to too much LA [2].

“The literature is chock-full of theories about the harmful effects of seed oils containing unnaturally high amounts of LA”

Seed Oil Harm Mechanism of Action

The literature is chock-full of theories about the harmful effects of seed oils containing unnaturally high amounts of LA. I think it’s fair to say that the biochemical pathways causing harm are many and varied, that many are likely occurring simultaneously and that at a biochemical level, the effects are quite chaotic and harmful. That said, seed oils appear to cause harm for two main reasons [3,4], namely LA oxidation and the fact that LA stays in the human body for a long time.

Oxidation

The key to understanding why high amounts of LA cause us harm is its unstable chemical structure. Their double bonds make them easily altered through oxidation (lipid peroxidation). Oxidation occurs when we heat them during cooking and even when we simply metabolise them. This is because:

LA is easily converted to harmful metabolites by our bodies
Harmful metabolites cause cell and tissue damage
Harmful metabolites cause our fat storage cells to become resistant to insulin

LA stays in the human body for a long time

In addition to its inherent harm, once we have consumed LA it stays in our bodies for a long time. This is not a problem when we consume LA in small amounts from natural sources as we’ve seen. However, when we load unnaturally high amounts of LA into every structure in our body by consuming seed oils, we have a potential problem which requires sustained effort to reverse.

It takes 680 days, or almost two years, to replace 50% of harmful LA in our body with healthy, natural levels of fatty acids. This means that it takes roughly six years to eliminate 95% of the LA we’ve accumulated by consuming seed oils [3].

There are three very important implications of sustained excessive levels in our bodies. Prolonged exposure to LA can damage our cells, mitochondria and invoke a chronic inflammatory response by our immune system.

Cell and Tissue damage

When too much LA gets into the membranes and contents of our cells it can cause all sorts of damage. We have essentially introduced chemical instability into structures that evolved to be inherently stable and life-preserving. Chemically unstable LA built into our membranes are easily broken down into metabolites which can accelerate the natural processes of cell death.

Harmful LA metabolites have been shown to damage structures in our bodies including our DNA, cell membranes, proteins, and mitochondria [5].

Mitochondrial dysfunction

The existence of mitochondria has allowed life on earth to be multi-cellular, distinguishing us from bacteria. The human body contains approximately 100,000 trillion mitochondria and they are involved in the production of energy, neurotransmitters, and hormones. They also influence gene expression, cell growth and differentiation, cell maintenance, disposal of old and damaged cells, and regulate metabolism, the immune system, and stress response. Mitochondria can multiply, change shape and move around a cell depending on the needs of their host cell at any point in time [9].

When we consume too much LA, our mitochondria accumulate too much of it. This causes a change in membrane structure and the production of harmful metabolites. Both lead to mitochondria becoming less effective.

Chronic inflammation

Cellular damage by LA invokes an inflammatory response by our immune system. When we are repeatedly exposed to LA the inflammation does not subside and we enter a state of chronic inflammation which is associated with many chronic diseases [2,5].

Irrespective of how it happens, oxidized LA and its harmful metabolites are associated with accelerated aging and a number of so-called chronic diseases, including heart disease, cancer, mental health, obesity, and type-2 diabetes.

Specifically, how could seed oils have caused my heart disease?

Consuming too much LA likely damaged my artery lining, damaged the LDL particles transporting cholesterol in my blood, and altered the cholesterol contained within those LDL particles [2,3,4,5,10]. I conclude this because the damaging effects of oxidised LA are many and varied and likely to act simultaneously on the major elements of the heart and circulatory system [11].

The disease does appear to develop in a two-stage manner [2]. At first oxidized LA damages arterial walls, LDL particles and the cholesterol contained within the LDL, and the damaged entities enter the cells lining the artery [2,10]. At this stage, there is a possibility that our natural repair process can occur more quickly than the rate at which oxidized LA is causing harm. In that scenario, the injured arterial cells are replaced and no further harm is caused.

However, if the rate of oxidized LA damage is greater than the rate of natural cell repair, the second stage begins. At this stage the damaged artery cells plus the damaged LDL and cholesterol combine in an ever-increasing escalation which our natural repair process cannot catch up to.

Our immune system tries to help at the site of damage within the arterial wall. Immune cells (macrophages) gobble up the damaged LDL and cholesterol. With time, those immune cells become engorged with damaged LDL and cholesterol to form what are called foam cells. These foam cells get trapped inside our artery walls and contribute to what we call plaque. Eventually the foam cells die and their fatty contents become trapped inside our artery walls.

Note that the root cause of the entire process is oxidized LA, not cholesterol, not LDL and not foam cells.

“Complete elimination of seed oils is impossible with the level of effort that I’m prepared to undertake. Nevertheless, I’ve dramatically reduced my exposure to LA by adopting a healthier lifestyle”

How do I minimize my exposure to seed oils and LA?

Complete elimination of seed oils is impossible with the level of effort that I’m prepared to undertake. Nevertheless, I’ve dramatically reduced my exposure to LA by adopting a healthier lifestyle:

No cooking and food preparation with seed oils – use low LA SFA (e.g., butter, ghee, coconut oil, olive oil)
Very small amounts of processed food
Animal meats, dairy, and fish that are least likely to contain LA - ruminant meats and dairy, free-range chicken and pork, and wild-caught fish
Limited amounts of nuts and seeds

Evidence that avoiding seed oil is helping me

I don’t get sunburned now. I first noticed this in 2022 when I was fishing for mackerel in the Firth of Forth. It was warm and sunny, I was only wearing shorts and flip flops in the middle of the day and I lost track of time. I realised after a couple of hours that I had none of the burning sensation and reddening of my face, shoulders and top of my feet that I’d expected. Through the summers of 2022 and 2023 I didn’t use sunscreen or suffer any ill effects of prolonged sun exposure, and I now have the best sun tan ever.

Sunburn is caused by UVB light from the sun oxidizing (yes, that again) and damaging the skin [12]. When my skin was already loaded up with oxidised LA, I didn’t need much extra oxidation to cause sunburn.

By 2022, I’d been avoiding seed oils for about five years and had likely eliminated 90% to 95% of oxidized LA from my body. Hey presto, no sign of oxidized skin cell damage in the sun…!

“When we cook with seed oils and put them in our food, we expose ourselves to excessive LA and its harmful effects.”

Summary

We know that when we expose ourselves to small amounts of certain things they can be good for us but those same things can harm us if we’re exposed to too much. This effect is called hormesis and it applies to things like metals, chemicals, pharmaceuticals, radiation, exercise and food deprivation [13]. The same applies to PUFA and LA. Those fats, which are life-giving in naturally occurring small amounts, are very harmful in prolonged higher doses.

When we cook with seed oils and put them in our food, we expose ourselves to excessive LA and its harmful effects.

References

https://reallytanman.substack.com/p/what-oils-are-seed-oils
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Knobbe, C.A. and Alexander, S. (2023) The Ancestral Diet Revolution: How vegetable oils and processed foods destroy our health – and how to recover! Boulder, CO: Ancestral Health Foundation
Shanahan, C. and Shanahan, L. (2016) Deep Nutrition: Why your genes need traditional food. New York: Flatiron Books
Mercola J. and D'Adamo C.R. Linoleic Acid: A Narrative Review of the Effects of Increased Intake in the Standard American Diet and Associations with Chronic Disease. Nutrients. 2023 Jul 13;15(14):3129. doi: 10.3390/nu15143129. PMID: 37513547; PMCID: PMC10386285.
Piloto-Rodríguez, R. and Díaz-Domínguez, Y. (2022). Production process, methods of extraction, and refining technologies of unconventional seed oils. In Mariod, A. (Ed), Multiple Biological Activities of Unconventional Seed Oils (pp 413-430). London: Academic Press
https://chriskresser.com/9-steps-to-perfect-health-3-eat-real-food/
Noakes, T.D. et al (2023). Understanding human diet, disease, and insulin resistance: scientific and evolutionary perspectives. In T.D. Noakes et al (Eds.), Ketogenic: The science of therapeutic carbohydrate restriction in human health (1st ed, pp 3-700). Elsevier
Palmer, C.M (2022) Brain Energy: A revolutionary breakthrough in understanding mental health – and improving treatment for anxiety, depression, OCD, PTSD, and more. Dallas, TX: BenBella Books
Lawrence GD. Perspective: The Saturated Fat-Unsaturated Oil Dilemma: Relations of Dietary Fatty Acids and Serum Cholesterol, Atherosclerosis, Inflammation, Cancer, and All-Cause Mortality. Adv Nutr. 2021 Jun 1;12(3):647-656. doi: 10.1093/advances/nmab013. Erratum in: Adv Nutr. 2021 Oct 1;12(5):2040. PMID: 33693484; PMCID: PMC8166560.
Witztum JL, Steinberg D. Role of oxidized low density lipoprotein in atherogenesis. J Clin Invest. 1991 Dec;88(6):1785-92. doi: 10.1172/JCI115499. PMID: 1752940; PMCID: PMC295745.
https://drcate.com/seed-oil-makes-sunburn-worse-and-ages-your-skin/ and https://reallytanman.substack.com/p/seed-oils-the-real-cause-of-skin
Calabrese, E.J., Mattson, M.P. How does hormesis impact biology, toxicology, and medicine?. npj Aging Mech Dis 3, 13 (2017). https://doi.org/10.1038/s41514-017-0013-z