By 2050, it is estimated that the United States will have 260 million overweight and obese adults, 142.66 million people aged 50 or older with at least one chronic disease, and nearly 2.3 million cancer cases. Everyone involved in health care holds convictions about what drives these alarming numbers and what actions are necessary to address them.
More critical thinkers generally recognize that these are multifactorial diseases, and interventions must occur at multiple levels and across various fronts. These include medications, lifestyle changes, psychological support in some cases, and targeted political measures, such as increasing the availability of nutritionally dense, low-calorie foods (like fruits, vegetables, and legumes) and pushing for reformulations in the composition of ultra-processed foods.
However, some individuals propose more unifying, “simplistic” explanations. Secretary of HHS RFK Jr. and his MAHA followers claim that these diseases stem primarily from consuming certain foods, especially seed oils.
In a post on X, RFK Jr. stated:
“(...) We have — since 1990 — discovered that seed oils are one of the driving causes of the obesity epidemic. Interestingly enough, this began to drastically rise around the same time fast food restaurants switched from beef tallow to seed oils in their fryers. People who enjoy a burger with fries on a night out aren’t to blame, and Americans should have every right to eat out at a restaurant without being unknowingly poisoned by heavily subsidized seed oils. It’s time to Make Frying Oil Tallow Again”
If you think the term “poisoned” carries an excessively strong connotation and sounds more like a boast than a claim supported by evidence, congratulations, you're right.
The theoretical basis behind this hostility toward seed oils stems from several arguments:
- The high omega-6 content. Omega-6 is an essential polyunsaturated fat (meaning it has two or more double bonds in its structure and must be obtained through diet). After metabolism, it produces molecules with both pro- and anti-inflammatory effects, though the pro-inflammatory ones tend to appear in greater quantities.
The extraction process may involve using hexane, a petroleum-derived solvent considered toxic by critics. - The increasing imbalance in the omega-6/omega-3 ratio. This ratio was more balanced a few decades ago, but the current shift toward omega-6 dominance is thought to create a pro-inflammatory environment, potentially promoting chronic diseases.
- The widespread presence of seed oils in ultra-processed foods.
However, most of these claims are either based on in vitro or animal studies that, at best, identify a physiological mechanism not necessarily relevant clinically, or they are preliminary extrapolations that still require validation in human studies.
A recent study in Science identifies a potential mechanism between linoleic acid (a type of omega-6) and a specific form of breast cancer, triple-negative. Spoiler alert: It does not confirm that seed oils cause breast cancer. Since the study presents some compelling findings, it is worth examining in greater depth.
The new study
Published this year, the study describes a series of experiments designed to examine how linoleic acid influences specific cellular functions whose dysregulation is associated with cancer.
The researchers analyzed the effects of omega-6 linoleic acid and omega-3 linolenic acid on cellular functions. They found that omega-6 activated specific cancer-associated pathways, specifically the mTORC1 pathway [1], while omega-3 had no significant effect. This activation occurred exclusively in triple-negative breast cancer (TNBC) cells and led to increased cell proliferation, among other outcomes.
Researchers subjected the TNBC cells to a "fasting period" and then divided them into three groups supplemented with (1) amino acids, protein’s building blocks; (2) omega-3 linolenic acid; and (3) omega-6 linoleic acid. They found that omega-6 triggered the suspected activation, although less intensely than amino acids. Omega-3, by contrast, had no effect. Subsequent experiments confirmed these findings and raised the question of how omega-6 acted.
The researchers removed specific enzymes responsible for converting omega-6 into other molecules and observed the same increased cellular activity, suggesting that omega-6 had a direct stimulatory effect. Based on these results, they investigated genes involved in the metabolism and transport of essential fatty acids upregulated in triple-negative breast tumors.
This led to an unlikely key player: a small molecule called FABP5, part of the lipid-transport protein family that facilitates intracellular movement and signaling. FABP5 plays a central role in sensing the availability of omega-6 polyunsaturated fatty acids and linking these nutrients to the mTORC1 pathway. FABP5 is especially overactive in triple-negative breast cancer. Inhibiting FABP5, even in the presence of omega-6 exposure, blocks the MTORC1 pathway. Of all the lipids that activate MTORC1, only omega-6 LA required the molecule to exert its effects.
Leaving the lab and turning to humans, they analyzed levels of FABP5 and linoleic acid in clinical serum and tissue samples of different breast cancer subtypes. TNBC patients had significantly higher levels of FABP5 and omega-6 fats within tumors and in the bloodstream. In contrast, these elevated levels were not found in patients with other, more treatable forms of breast cancer. This suggests that FABP5 may be a key player in tumor progression and a potential biomarker for aggressive disease.
Having established a biological mechanism connecting omega-6 linoleic acid to triple-negative cancer models, the researchers assessed the role of dietary intake on this pathway. They fed the animals identical diets, differing only in fat composition: one high in omega-6 (with 80% of fat from safflower oil), the other high in omega-3 (from fish and flaxseed). The omega-6 group showed higher FABP5 levels in their blood, more active mTORC1 signaling in vital organs, and, most critically, faster and larger tumor growth when implanted with TNBC cells.
These findings suggest that increased omega-6 intake relative to omega-3 activates the FABP5–mTORC1 axis, promoting tumor growth in triple-negative breast cancer.
Context is important
The findings are compelling and shed light on a lesser-known aspect of fat intake and cellular function, but essential caveats remain. One key point concerns the diet used in the rodent experiments. The mice consumed high-fat diets (similar to ketogenic patterns, with 70% to 80% of total calories from fat) predominantly composed of omega-6. While Western diets are rich in omega-6, they rarely reach the extreme levels used in this study. The study must be replicated, and even if future animal studies support these results, they cannot be assumed to translate directly to humans.
While the study is relevant and underscores the need for more clinical trials, it cannot support definitive dietary recommendations. A large body of well-designed studies has shown omega-6 a generally healthy fat. However, moderating the intake of omega-6-rich oils, especially for patients with triple-negative breast cancer, may still be reasonable when properly contextualized as a recommendation based on an abundance of caution.
Despite the eye-catching headlines and RFK Jr.’s war on seed oils, this study doesn’t prove that omega-6 fats cause breast cancer — it reveals a potential molecular pathway worth further exploration, particularly in triple-negative cases. Until more robust human evidence emerges, calls to “Make Frying Oil Tallow Again” remain more sizzle than science.
[1] mTOR is a protein complex that regulates cell growth and metabolism by promoting protein and lipid synthesis, stimulating growth, and inhibiting autophagy.
Sources: Direct sensing of dietary ω-6 linoleic acid through FABP5-mTORC1 signaling. Science DOI:10.1126/science.adm9805
