General Education

Introduction

So why do we help you hide foods that contain seed oils in them?

Well seed oils, are novel items added to the food supply that are wildly high in a fatty acid called linoleic acid. The introduction of seed oils into food mean we’re eating too much and at too high a concentration.

Linoleic acid is a polyunsaturated Omega-6 fatty acid that plays a crucial role in human health.

It is considered an essential fatty acid because the human body cannot synthesize it; it must be obtained through diet.

Linoleic acid sources in the diet include nuts, seeds, and some meats, but primarily come from seed oils such as corn, soybean, sunflower, peanut, safflower, canola, rapeseed, grapeseed, cottonseed and rice bran oil.

While linoleic acid is vital for maintaining the structure of cell membranes and is involved in the production of signaling molecules, excessive consumption or an imbalanced consumption in relation to Omega-3 fats leads to negative health effects.

In a modern day context virtually every person living in the USA and other western nations is consuming linoleic acid at an imbalance to Omega-3 fats whilst also consuming excessive linoleic acid.

Metabolism of Linoleic Acid

Once ingested, linoleic acid undergoes metabolism in the body through a series of enzymatic reactions. Initially, linoleic acid is converted to gamma-linolenic acid (GLA) by the enzyme delta-6-desaturase.

GLA is then converted into dihomo-gamma-linolenic acid (DGLA), which can further be metabolized to form arachidonic acid (AA).

These metabolites, particularly arachidonic acid, are precursors to various eicosanoids, which are signaling molecules involved in inflammation and immune responses.

Peroxidation of Linoleic Acid

Lipid peroxidation, on the other hand, is a process that occurs under pathological conditions and involves the oxidative degradation of lipids.

Initiation: The reaction starts when a reactive oxygen species (ROS) or a free radical removes a hydrogen atom from a lipid, particularly from the unsaturated fatty acids in the lipid bilayer of cell membranes, creating a lipid radical.
Propagation: This lipid radical reacts with oxygen to form a lipid peroxyl radical, which can then react with another lipid molecule, creating a chain reaction of lipid radical formation and leading to widespread membrane damage.
Termination: The chain reaction ends when two radicals react together or are quenched by antioxidants.

The result of lipid peroxidation is the formation of a variety of breakdown products, including aldehydes like malondialdehyde (MDA) and 4-hydroxynonenal (4-HNE), which is toxic to cells and contributes to the pathology of various diseases, such as atherosclerosis, neurodegeneration, and cancer.

It is critical to understand that 4-HNE can create pathological oxidative stress such that the ingestion of linoleic acid creates a peroxidation cascade that is self fulfilling.

By many accounts the peroxidation of linoleic acid and its breakdown products in a western diet context, is the primary source of oxidative stress on the body.

Negative Effects of Consumption

1. Inflammation: A high intake of Omega-6 fatty acids, namely linoleic acid, relative to Omega-3 fatty acids, promotes inflammation in the body.

2. Oxidative Stress: Linoleic acid is more prone to oxidation than saturated or monounsaturated fats. The oxidation products of linoleic acid are the main driver of oxidative stress in the body, and cause cellular damage.

3. Unstable Cell Membranes: The incorporation of linoleic acid into human cell membranes creates inherently unstable cells. For example, the current level of consumption is such that linoleic acid levels in LDL cholesterol are artificially higher and as such these LDL particles are now more prone to oxidation than historically normal (LDL particles require oxidation to become atherosclerotic).

Sources of Excessive Consumption

As mentioned above, the main sources of excessive Linoleic Acid consumption are seed oils (also marketed as vegetable oils). Critically, if you are seeking to reduce your consumption the following should be avoided:

Soybean Oil
Corn Oil
Safflower Oil
Sunflower Oil
Canola Oil
Rapeseed Oil
Grapeseed Oil
Peanut Oil
Cottonseed Oil
Rice Bran Oil
Walnut Oil
Almond Oil

If you are then looking for fat/oil replacements in cooking, baking and eating the following are regarded as safe:

Coconut Oil
Avocado Oil
Olive Oil
Algae Oil
Cultured Oils (like Zero Acre)
Macadamia Nut Oil
Palm Oil
Palm Fruit Oil
Palm Olein Oil
Ghee (clarified butter)
Tallow (from ruminent fat)
Butter

Additionally the fat content in certain meats and their eggs, especially from mono-gastric grain-fed animals, can be a significant source of linoleic acid.

Unless you can ensure the source of the below and guarantee that it was raised on a species appropriate diet (no soy or grain feed) we generally recommend these are avoided or do not make up a significant proportion of your diet:

Pork & Bacon (including Lard)
Chicken (especially the skin)
Turkey
Duck
Oily Fish

A Statement On Understanding The Science Behind Linoleic Acid

Understanding the harmful effects of linoleic acid requires not just reviewing isolated studies, but a comprehensive synthesis of all available evidence across different animal models (including humans) and timelines.

Without this holistic approach, it’s easy to cherry-pick short-term studies to dismiss the long-term risks.

The ongoing debate over saturated fats (SFAs), polyunsaturated fats (PUFAs), and seed oils will never reach a conclusion unless there is a recognition of the need to integrate animal studies with both short-term and long-term human trials.

Critics often point to trials lasting no more than 12 weeks to argue against the findings from animal research, while ignoring pivotal long-term studies, such as the 8-year LA Veterans Administration Hospital Study.

They overlook mechanisms and instead treat the observed effects in short-term trials as standalone facts, missing the larger picture that understanding these mechanisms is essential to contextualizing the results.

To synthesize the evidence effectively, we must consider the following mechanisms:

1. Ethanol Metabolism and Fatty Liver: Ethanol’s metabolism via CYP2E1 generates reactive oxygen species (ROS), damaging ApoB and preventing the export of hepatic triglycerides.

2. Choline and ApoB Lipidation: In non-alcoholic models, choline deficiency impairs the lipidation of ApoB with phosphatidylcholine, a critical step in preventing fatty liver.

3. Nutrient Impact on Fatty Liver: Adequate protein, sulfur amino acids, and choline intake can eliminate fatty liver caused by alcohol, sugar, or fat.

4. Oxidation of PUFAs vs. SFAs: PUFAs oxidize more rapidly than SFAs, increasing the choline requirement for exporting SFAs from the liver.

5. Liver Fat and NASH Progression: In non-alcoholic models, SFAs worsen liver fat compared to PUFAs, but PUFAs accelerate progression to non-alcoholic steatohepatitis (NASH) due to oxidative damage, which is a more critical factor in NASH than the SFA/choline ratio.

6. Alcoholic Models: In contrast, SFAs protect against liver fat in alcoholic models because oxidative damage to ApoB outweighs the importance of the SFA/choline ratio.

7. Human Trials: Short-term human trials mimic non-alcoholic animal models, with SFAs increasing liver fat and PUFAs reducing it.

8. Long-Term Effects: Over extended periods, PUFAs are predicted to exacerbate NASH progression, the true threat to liver health and longevity.

9. The LA Veterans Administration Study: This study revealed that the detrimental effects of PUFAs in humans become apparent only after more than 8 years.

In sum, to truly understand the risks associated with linoleic acid, it’s essential to grasp the full scope of studies and the underlying mechanisms, rather than relying on selective, short-term evidence.

Bookmark this page for the next time a friend sends you an isolated study on how canola oil was more effective in lowering liver fat than ghee in patients with NAFLD or how safflower oil reduced insulin resistance when swapped with butter (in the short term).

Sources

Dietary Sources of Linoleic Acid (LA) Differ by Race/Ethnicity in Adults Participating in the National Health and Nutrition Examination Survey (NHANES) between 2017-2018

https://pubmed.ncbi.nlm.nih.gov/37375683

Effects of Native and Modified Low-Density Lipoproteins on Monocyte Recruitment in Atherosclerosis

https://www.ahajournals.org/doi/10.1161/hypertensionaha.107.089854

Importance of a balanced omega 6/omega 3 ratio for the maintenance of health: nutritional recommendations

https://pubmed.ncbi.nlm.nih.gov/21666970

Linoleic acid and the pathogenesis of obesity

https://pubmed.ncbi.nlm.nih.gov/27350414

Linoleic acid peroxidation–the dominant lipid peroxidation process in low density lipoprotein–and its relationship to chronic diseases

https://pubmed.ncbi.nlm.nih.gov/9853364

Lipids: Biochemistry, Biotechnology and Health

https://pure.southwales.ac.uk/en/publications/lipids-biochemistry-biotechnology-and-health

Lipid Peroxidation in Biological Systems