A recent study published in Science found that linoleic acid, the main omega-6 fat found in vegetable oils, can directly promote tumor growth in triple-negative breast cancer (TNBC).
Researchers found that linoleic acid specifically activates a growth pathway in TNBC cells by binding to a protein called FABP5 (fatty acid–binding protein 5). This activation turns on mTORC1, a pathway that increases cancer growth.
In animal studies, a diet high in safflower oil (a rich source of linoleic acid) caused TNBC tumors to grow faster. This suggests that dietary linoleic acid may worsen TNBC by overstimulating this growth pathway.
They also found that even before any treatment, patients with newly diagnosed triple-negative breast cancer already had high levels of linoleic acid and the fat-shuttling protein FABP5 in both their blood and tumor tissue. Because of this, researchers concluded that linoleic acid may not simply feed cancer once it’s established, but actually drives its development from the very beginning.
This is one of the first studies to identify a clear molecular mechanism linking dietary linoleic acid to cancer growth.
Research is confirming what we’ve known for decades: what we eat influences how cancer develops and grows at the molecular level.
Today linoleic acid is the most common fatty acid in the Western diet. It’s found in:
- Seed oils such as soybean, corn, sunflower, safflower, canola, and cottonseed oil
- Most processed and packaged foods
- Nuts and seeds, especially sunflower seeds and walnuts
- Conventional meat, poultry, and eggs, particularly from animals fed high-PUFA grain-based diets
However, this high intake of linoleic acid is not evolutionarily consistent. TheFor most of human history, the main fats in the human diet were oleic acid, found in olive oil, lard, and tallow, and palmitic and stearic acid, found in butter, beef fat, pork, and full-fat dairy. These fats are more stable and less inflammatory than LA, which is prone to oxidation and capable of disrupting cellular signaling.
The shift to seed oils such as soybean, corn, and safflower has increased linoleic acid intake by an estimated 200 to 300 percent over the last century. Many researchers believe the surge in LA intake plays a role in the rise of obesity, heart disease, and cancer.
Linoleic acid can disrupt cellular signaling, fuel oxidative stress, and alter metabolic pathways in ways the body was never designed to handle.
- To decrease dietary intake of linoleic acid:
- Cook meals at home.
- Avoid industrial seed oils (soybean, corn, safflower, sunflower, cottonseed, grapeseed, and canola).
- Choose traditional fats (butter, ghee, coconut oil, beef tallow, and olive oil).
- Read ingredient labels. Processed snacks, dressings, sauces, and baked goods often contain seed oils, even in “healthy” products.
- Limit fast food and fried foods.
Buy animal products from pasture-raised sources. Conventional meat, eggs, and dairy from grain-fed animals can have higher LA content due to their feed. Grass-fed or pasture-raised options are naturally lower in omega-6 fats.
Before the rise of industrial seed oils, the most common fatty acids in the Western diet came from saturated and monounsaturated fats, not PUFAs like linoleic acid. The primary fatty acids were oleic acid, found in olive oil, lard, and tallow, and palmitic and stearic acid, found in butter, beef fat, pork, and dairy. These fats are more stable and less inflammatory than LA, which is prone to oxidation and capable of disrupting cellular signaling.
The shift to seed oils such as soybean, corn, and safflower has increased linoleic acid intake by an estimated 200 to 300 percent over the last century. This change is evolutionarily inconsistent with our biology and it’s one reason many researchers believe LA plays a role in the rise of obesity, heart disease, and cancer. I believe that removing industrial seed oils from the diet is one of the most important steps we can take in both cancer treatment and prevention. This study gives us one more reason to reconsider what’s on our plate and how it might be influencing cancer at the cellular level.