How Seed Oils Break Insulin

An essay on what programs the body into storage mode

At 8% dietary linoleic acid, ground squirrels enter hibernation successfully. Their metabolism shifts into storage mode, body temperature drops, and they survive winter on accumulated fat.

At 1.5% dietary linoleic acid, they cannot enter torpor at all. They burn through their entire fat reserves in nine days of fasting and die.

The hibernation literature reveals that torpor performance is highly sensitive to pre-hibernation linoleic acid content, with performance degrading when LA deviates from the animal’s natural dietary composition—too low or too high. What the research demonstrates is that linoleic acid acts as a powerful metabolic lever, programming whether an organism stores fat efficiently or burns it.

Americans now eat 8–12% of their calories as linoleic acid. In 1865, the figure was roughly 2%. We have pushed ourselves far beyond any evolutionary band for this fat—not into deficiency, but into chronic excess.

The metabolic pathways that control this fat storage program—PPAR-gamma, SCD1, the desaturase enzymes—are conserved across mammals. They operate in ground squirrels preparing for winter. They operate in humans. The question is what activates them.

We have, without understanding what we were doing, triggered an ancient metabolic program designed to prepare mammals for seasonal scarcity. The problem is that the scarcity never comes. The fat storage program runs continuously. And the consequences extend far beyond weight gain.

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The Upstream Question

A previous essay in this series established that insulin—not calories—is the master regulator of fat storage. Eight physicians using different methodologies arrived at the same conclusion: chronic insulin elevation keeps the body locked in storage mode, and any intervention that doesn’t lower insulin addresses symptoms while ignoring the cause.

It’s the Insulin

Readers raised questions that essay couldn’t answer. Why was there no obesity epidemic 60–70 years ago, when people also ate sugar and processed foods? What changed? One commenter noted that none of the eight physicians mentioned seed oils. Another pointed out that something beyond insulin must explain why populations eating high-carbohydrate diets remained lean for millennia while modern humans on similar macronutrient ratios become diabetic.

That essay answered what controls fat storage. This one answers a different question: what programs the body into storage mode in the first place?

The insulin model is correct but incomplete. Seed oils are upstream of insulin. They reconfigure the metabolic machinery that determines what happens after insulin acts. When linoleic acid accumulates in cell membranes, it triggers a cascade of changes that shift the body from burning mode to storage mode. Carbohydrates become problematic—shunted toward fat synthesis rather than oxidation—because the system that should burn them has been disabled.

This isn’t a competing theory. It’s the missing piece that explains why populations eating high-carbohydrate diets remained lean for millennia, and why carbohydrate restriction works for metabolically damaged modern humans but wasn’t necessary for our ancestors.

Five investigators, working independently with different methodologies, converged on this answer.

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Different Methods, Same Destination

Brad Marshall is an independent researcher focused on evolutionary biology and metabolic regulation. He studies hibernation physiology and the mechanisms that control whether an organism stores fat or burns it. His evidence base: animal studies, desaturase enzyme activity, and the metabolic signatures that distinguish lean from obese humans.

Tucker Goodrich is a molecular biologist who came to seed oil research through his own health crisis. His focus: mitochondrial function, specifically the role of linoleic acid in damaging the energy-producing structures within cells. His evidence base: biochemistry of cardiolipin, lipid peroxidation, and the toxic metabolites generated when polyunsaturated fats oxidize.

Chris Knobbe is an ophthalmologist and researcher who founded the Ancestral Health Foundation. He came to seed oils through macular degeneration research and expanded to chronic disease broadly. His evidence base: population-level epidemiology spanning 150 years, comparative analysis of traditional versus modernized societies, and the mathematical relationship between dietary linoleic acid and disease rates.

Cate Shanahan is a family physician who served as the nutritionist for the Los Angeles Lakers. She came to seed oils through clinical practice—watching patients improve or deteriorate based on dietary changes. Her evidence base: thousands of patient outcomes, biochemistry of lipid oxidation, and the epigenetic damage that accumulates across generations.

Paul Saladino is a physician trained in mainstream medicine who became skeptical of conventional dietary advice. His focus: evaluating the clinical trial evidence directly. His evidence base: systematic analysis of all eleven randomized controlled trials conducted on seed oils in humans, plus documentation of how harmful findings were suppressed.

An evolutionary biologist studying hibernation. A molecular biologist studying mitochondria. An epidemiologist tracking population health across centuries. A family physician tracking patient outcomes. A clinician analyzing randomized controlled trials.

The same variable keeps emerging: linoleic acid.

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The Simple Version

Before examining what each investigator found, here’s what their work adds up to:

Linoleic acid is an essential fatty acid—the body cannot make it and requires it from diet. But “essential” refers to a minimum requirement, roughly 0.5–1% of calories. Humans consumed approximately this amount for all of evolutionary history. Modern Americans consume 8–12%—six to twelve times the physiological requirement. The question is not whether linoleic acid is necessary. It’s what happens when intake exceeds evolutionary norms by an order of magnitude.

Your body has two metabolic modes. One burns calories as heat—you stay warm, energetic, lean. The other stores calories as fat—you conserve energy, accumulate reserves, slow down.

These modes exist because our ancestors needed to survive winters, famines, and seasonal food scarcity. The ability to switch into storage mode and pack on fat was a survival advantage. The signal that triggered this switch was dietary: when animals ate foods high in certain fats, their bodies interpreted this as “winter is coming” and shifted into storage mode.

Seed oils contain linoleic acid, the specific fat that triggers this switch. Modern humans consuming seed oils are sending their bodies a constant “prepare for winter” signal. The storage program activates. But unlike a squirrel that hibernates for a season, we never enter the winter phase where we’d burn those reserves. We’re stuck in perpetual fat-accumulation mode.

Meanwhile, the linoleic acid accumulates in cell membranes throughout the body. There, it oxidizes—essentially rusts—creating toxic byproducts that damage mitochondria, the structures that generate cellular energy. As mitochondria become impaired, the body loses its ability to burn glucose efficiently. Carbohydrates increasingly get shunted toward fat production rather than energy production.

This is why carbohydrate restriction works for metabolically damaged people—their glucose-burning machinery is compromised, so reducing glucose intake reduces the burden on a broken system. But it’s also why traditional populations eating 80–90% carbohydrate diets stayed lean: their mitochondria were intact, their membranes weren’t loaded with linoleic acid, and they could burn carbohydrates efficiently.

Seed oils came first. Insulin dysfunction followed. The standard model has the causation backwards.

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The Hibernation Trigger

Brad Marshall’s contribution is the torpor hypothesis—the recognition that linoleic acid is the dietary signal that triggers hibernation physiology in mammals.

The ground squirrel study is the clearest demonstration. Researchers fed squirrels different diets before winter. Those given 8% linoleic acid hibernated normally. Those restricted to 1.5% could not enter torpor. When forced to fast, the low-linoleic-acid squirrels burned through their fat reserves in nine days rather than months.

The difference: linoleic acid upregulates an enzyme called SCD1 (stearoyl-CoA desaturase-1), which converts saturated fat to monounsaturated fat—specifically, oleic acid. Oleic acid then activates a transcription factor called PPAR-gamma, which shifts the body into storage mode. This creates a self-reinforcing loop: more oleic acid leads to more SCD1 activity, which produces more oleic acid.

The fat-tailed dwarf lemur, a tropical primate that hibernates despite warm temperatures, reaches 70% oleic acid in its body fat when preparing for dormancy. The signal isn’t cold weather. It’s the fat composition of the diet and the body.

Marshall’s key insight: “Olive oil is the trigger, PUFA is the fuel.” Monounsaturated fat locks in the hibernation state. Polyunsaturated fat (linoleic acid) initiates the process and provides the substrate for extended fat storage.

What does this look like in humans?

The desaturase index—the ratio of monounsaturated to saturated fat in the body—correlates strongly with obesity. Obese people have higher SCD1 activity. When researchers took muscle tissue from obese individuals and cultured it in a lab, the cells stored fat and wouldn’t burn it. When they overexpressed SCD1 in lean people’s muscle tissue, it began behaving like obese tissue—storing fat instead of burning it.

Marshall’s framework predicts specific observations that hold up against the data: American metabolic rates dropped approximately 15% as vegetable oil consumption increased, according to analyses of basal metabolic rate trends over the twentieth century. China, as of 2016 still eating primarily starch-based diets with minimal vegetable oil, showed metabolic rates 15% higher than predicted by standard models in comparative population studies. The Tsimane, a forager-horticulturalist population in Bolivia eating traditional diets, have resting metabolic rates 30% higher than Americans in the same body-composition analyses that predicted lower rates for Americans.

The implications are uncomfortable. If this model is correct, then metabolically damaged individuals aren’t simply eating too much or exercising too little. They’re running different physiological software—a fat-storage program appropriate for surviving winter, activated by a dietary signal that never stops.

This PPAR-gamma pathway has been independently confirmed through mitochondrial biochemistry research. When linoleic acid oxidizes, it generates metabolites (including 4-HNE and oxidized linoleic acid metabolites) that function as PPAR-gamma agonists—they activate the same fat-storage transcription factor through a completely different mechanism. The torpor signal isn’t just initiated by linoleic acid. It’s reinforced by linoleic acid’s breakdown products.

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The Mitochondrial Damage

Tucker Goodrich’s contribution focuses on what happens after linoleic acid accumulates in cells—specifically, in mitochondria.

Mitochondria are the structures that produce cellular energy. They convert food into ATP, the molecule that powers everything the body does. Their inner membranes contain a specialized fat called cardiolipin, which is essential for energy production.

When dietary linoleic acid is high, it gets incorporated into cardiolipin. This creates a problem: linoleic acid is highly susceptible to oxidation. Inside the mitochondrial membrane, in close proximity to iron-containing enzymes, it begins to break down. The oxidation of linoleic acid in cardiolipin produces a cascade of toxic metabolites.

The main ones:

4-HNE (4-hydroxynonenal) — a reactive aldehyde that damages proteins and DNA. It’s a major component of oxidized LDL, the form of cholesterol actually associated with heart disease.

MDA (malondialdehyde) — another aldehyde, widely used as a marker of oxidative stress. It directly damages DNA.

OxLAMs (oxidized linoleic acid metabolites) — a class of compounds that drive inflammation and are essential for atherosclerosis progression.

As cardiolipin becomes damaged, the cristae—the folded inner structures of mitochondria—begin to collapse. This specifically impairs Complex I of the electron transport chain, which handles inputs from glucose metabolism. The result: mitochondria lose their ability to burn glucose efficiently.

Goodrich cites studies where mice fed high-linoleic-acid diets plus excess glucose developed collapsed mitochondria and metabolic dysfunction within days. Even lean mice on high-linoleic-acid diets developed liver failure.

Goodrich’s claims about aldehyde toxicity find confirmation in mainstream biochemistry. Hermann Esterbauer, an Austrian biochemist who discovered aldehydes as peroxidation products in 1964, published a landmark review in 1991. His assessment is sobering: aldehydes are extremely chemically reactive, causing “rapid cell death,” interfering with DNA and RNA, and disturbing basic cell functioning. He documented “a great diversity of deleterious effects” to health, all of which were “rather likely” to occur at levels normally consumed by humans.

A. Saari Csallany, the main researcher of these compounds in the United States, refined the ability to detect HNE and showed that it was produced by a range of vegetable oils at temperatures well below those used for frying—long before the oils start to smoke or smell. When she bought fries at six fast-food restaurants near her office at the University of Minnesota, she found people could easily consume substantial amounts of these toxic compounds. Giuseppe Poli, a biochemist at the University of Turin who co-founded the International 4-HNE Club, confirms that the strongest evidence now points to HNE’s role in atherosclerosis and neurodegenerative diseases like Alzheimer’s.

This mechanism explains a paradox Tucker notes: linoleic acid can actually improve insulin sensitivity in the short term. Cells remain responsive to insulin’s signal to take up glucose. But inside the cell, the glucose can’t be burned properly because the mitochondrial machinery is damaged. It gets shunted toward fat synthesis instead.

The cell is insulin-sensitive for uptake but metabolically configured for storage rather than oxidation. This is worse than simple insulin resistance—it’s a deeper dysfunction that insulin metrics won’t fully capture.

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The Oxidation Framework

Chris Knobbe approaches seed oils through population-level epidemiology and the concept of oxidative damage.

His core argument: oxidation, not inflammation, is the root cause of chronic disease. Inflammation is secondary—the body’s response to oxidized tissues. And nothing in the modern diet promotes oxidation more than seed oils.

The evidence is historical and mathematical.

In 1865, Americans consumed approximately 2–3 grams of linoleic acid daily—about 1% of calories. Seed oils didn’t exist as food. Cottonseed oil entered the food supply in 1866, initially sold as lamp oil and machine oil. By 1880, French authorities were complaining that “olive oil” imported from America was adulterated cottonseed. Crisco, hydrogenated cottonseed oil marketed for cooking, launched in 1911.

By 2008, Americans consumed 29 grams of linoleic acid daily—about 12% of calories. A 13-fold increase.

This change is reflected in body composition. A study analyzing 37 datasets from 1959 to 2008 found that linoleic acid in American body fat rose from 9.1% to 21.5%. The correlation between dietary linoleic acid and adipose tissue linoleic acid is 0.81—nearly linear.

Why does this matter? Because the body incorporates dietary polyunsaturated fats directly into cell membranes. Unlike saturated and monounsaturated fats, which the body can synthesize, linoleic acid can only come from diet. Whatever you eat becomes what you’re made of, and highly oxidizable fats become highly oxidizable membranes.

Knobbe quantifies oxidation potential with what’s called a peroxidation index. Coconut oil scores 2. Beef tallow scores 5. Olive oil scores 13. Corn oil scores 57. Soybean oil scores 65.

The higher the score, the more readily the fat oxidizes—rusts—inside the body.

Traditional populations eating high-fat diets remained free of chronic disease because their fats were low on this scale. The Maasai, Inuit, Tokelauans, and 19th-century Americans all consumed substantial fat, but their linoleic acid intake stayed below 2% of calories. It wasn’t the quantity of fat that mattered. It was the type.

Knobbe’s most striking evidence comes from Japan. Between 1954 and 2007:

• Diabetes prevalence increased 345-fold

• Obesity in men doubled

• Breast cancer increased 5-fold

• Age-related macular degeneration increased 57-fold

During this period, caloric intake declined. Carbohydrate consumption declined. Sugar consumption declined steadily after 1989—yet diabetes and obesity continued climbing. The divergence is critical: if sugar were the primary driver, disease rates should have followed sugar downward after 1989. They didn’t. The only dietary factor that continued increasing in lockstep with disease rates throughout this period: vegetable oil consumption.

The same pattern appears in the Maori. Obesity rose from 10% in 1977 to 50% in 2017. Linoleic acid in Maori body fat increased from 2.6% in 1969 to 10.5% in 1981. Vegetable oil consumption rose from 2.5 grams daily in 1966 to 28 grams in 2008.

The carbohydrate theory of chronic disease cannot explain Japan. Populations that industrialized while maintaining low seed oil consumption did not experience the same disease explosion. Seed oils are the variable that tracks with the outcomes.

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The Clinical Evidence

Cate Shanahan brings the perspective of a physician watching these mechanisms play out in patients.

Her clinical observation: removing vegetable oils and reducing sugar produces rapid improvement in conditions that shouldn’t respond to dietary intervention—high triglycerides, hypertension, eczema, recurring infections, migraines. She documents case after case of reversal.

Her framework emphasizes that the damage from seed oils is mutagenic—it causes DNA damage that accumulates over time and across generations.

The aldehydes produced when linoleic acid oxidizes (4-HNE, MDA) are not merely irritants. They directly modify DNA bases, creating lesions that can lead to mutations. MDA is an established mutagen. 4-HNE inhibits the DNA repair mechanisms that would normally fix such damage.

Shanahan connects this to rising rates of birth defects, autism, and childhood illness. The damage isn’t limited to the person eating the seed oils. It’s written into their germ cells and passed to offspring. Traditional cultures that maintained dietary practices across generations were protecting not just their own health but their genetic legacy.

Her practical contribution is directness: seed oils are toxic, not merely suboptimal. She lists the common denominator in junk food—Doritos, Oreos, McDonald’s fries, Twinkies, Krispy Kreme donuts—and it’s not sugar. They all contain vegetable oils. The most reliable predictor of whether a processed food is harmful is whether it contains seed oils.

She also emphasizes that the problem isn’t omega-6 per se. It’s the processing. Industrial extraction using hexane, heating to 400–500°F, deodorization to mask rancidity—these processes create oxidized, toxic oils before they even reach the consumer. Then the oils are used repeatedly in fryers, oxidizing further with each use. Restaurant fryer oil typically gets changed once a week. By then, the lipid peroxide content is astronomical.

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The Suppressed Trials

Paul Saladino analyzed all eleven randomized controlled trials conducted on seed oils in humans. His conclusion: the trials that showed harm were suppressed; the trials that showed benefit were methodologically flawed; and the meta-analyses that currently inform dietary guidelines cherry-pick the evidence.

The Rose Corn Oil Trial, conducted in the late 1950s, was the first clear signal. It compared seed oils to saturated fat and found significantly more heart attacks in the seed oil group. The P-value was between 0.05 and 0.1. Rather than prompting urgent follow-up, the finding was set aside because it didn’t reach the conventional 0.05 threshold.

The Sydney Diet Heart Study and the Minnesota Coronary Experiment confirmed what Rose had suggested. Both found that replacing saturated fat with seed oils increased mortality. The Minnesota data was collected in the 1960s and 1970s but not fully analyzed and published until 2016—after the principal investigator had died. When researchers finally examined the complete dataset, they found that participants who lowered their cholesterol the most by eating seed oils had the highest mortality rates.

Taken together—Rose, Sydney, Minnesota, and Ramsden’s modern re-analyses—this body of RCT evidence should have forced a re-evaluation decades ago. Instead, meta-analyses continue to exclude the unfavorable trials.

Meanwhile, trials with design flaws that obscure seed oil harm get cited as evidence of safety. Saladino’s thread on X details how researchers like Dariush Mozaffarian at Tufts construct meta-analyses by selectively including favorable studies and excluding unfavorable ones, then write abstracts claiming seed oils are “benign or trend toward cardiovascular benefit.”

The corruption extends beyond individual researchers. Nina Teicholz, author of The Big Fat Surprise and a contributor to Saladino’s documentary Fed a Lie, documented that 19 of 20 members of the USDA Dietary Guidelines Committee (2020–2025) had ties to pharmaceutical or processed food companies.

The result: official dietary advice continues recommending seed oils as “heart healthy.” The American Heart Association’s stamp of approval appears on bottles of corn oil. Hospitals serve patients recovering from heart attacks meals cooked in soybean oil.

Saladino’s framing is blunt: “I would see this as you go to McDonald’s, that is a metabolic toxin. You are actively poisoning yourself.”

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The Convergence

Five investigators. Different training—molecular biology, evolutionary biology, epidemiology, family medicine, clinical trial analysis. Different evidence bases—animal studies, biochemistry, population data, patient outcomes, RCTs.

They agree on the following:

Seed oils are evolutionarily novel. Humans consumed 1–2% of calories as linoleic acid for all of human history until the late 19th century. Current consumption of 8–12% is unprecedented. The body is not adapted to handle this load.

The threshold effect is demonstrated cleanly in diabetic-prone (db/db) mice: they only become obese when linoleic acid exceeds approximately 5% of calories. When stearic acid (a saturated fat) is substituted, obesity is completely prevented—even in animals genetically predisposed to metabolic dysfunction. The genetic susceptibility requires the dietary trigger.

Linoleic acid accumulates in tissues. Unlike saturated fat, which the body can synthesize, linoleic acid comes only from diet. It incorporates directly into cell membranes and adipose tissue. Body fat linoleic acid content in Americans has more than doubled since 1960. The half-life of linoleic acid in adipose tissue is approximately two years—meaning the damage accumulates faster than the body can clear it.

The accumulation triggers metabolic reprogramming. Dietary linoleic acid activates PPAR-gamma and upregulates SCD1, shifting the body toward a storage-oriented metabolic state. This is the torpor signal—the body preparing for a winter that never comes.

The reprogramming is compounded by oxidative damage. As linoleic acid accumulates in mitochondrial membranes, it oxidizes, producing toxic aldehydes that damage cardiolipin and impair Complex I. This progressively degrades the body’s capacity to burn glucose oxidatively, reinforcing the storage state.

The result is a self-reinforcing loop: seed oil consumption → torpor activation → impaired glucose oxidation → substrate shunted to fat synthesis → mitochondrial damage → further impaired oxidation. Carbohydrates become problematic because the system that should burn them has been disabled.

The endpoint is chronic disease. Not just obesity, but cardiovascular disease, diabetes, cancer, neurodegeneration, macular degeneration. Across these conditions, the pattern indicates a common denominator: chronic oxidative damage to cellular machinery driven by excess linoleic acid.

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Explaining It to a Six-Year-Old

Your body is like a house with a furnace. The furnace burns food to keep you warm and give you energy to run and play.

Some foods help the furnace burn cleanly. Other foods gum up the furnace so it doesn’t work well.

Seed oils are like putting the wrong fuel in the furnace. They make sticky gunk that clogs everything up. The furnace can’t burn properly anymore. Instead of making heat and energy, your body just stores the food as fat.

Also, seed oils are like a metal that rusts really easily. When you eat them, they go into every part of your body—your muscles, your brain, your heart. And then they start to rust, which hurts those parts and makes them not work right.

Now here’s where insulin comes in. Insulin is like a delivery truck driver. Its job is to bring food to your cells and say “here, take this and use it for energy.” When everything works right, the cells take what they need, and the delivery truck drives away.

But seed oils break this system in a sneaky way. They make your cells open their doors too wide. The delivery truck keeps bringing more and more food, and the cells keep taking it even when they’re already stuffed full. The cells get so packed they start to burst and break.

When the cells are damaged and overstuffed, they eventually stop opening their doors at all—even when they actually need food. The delivery truck keeps honking but nobody answers. That’s called insulin resistance. The body makes more and more insulin trying to get the cells to listen, but they can’t because they’re broken.

So seed oils break insulin in two steps: first they make cells listen too much (so they overstuff), then the overstuffed cells stop listening at all (so you get diabetes).

People used to eat butter and animal fat, which don’t cause this problem. Their furnaces worked great and their delivery system worked great. Now people eat seed oils, and both systems are broken.

That’s why so many people are tired and sick and overweight even when they try really hard to be healthy. Their furnaces are gummed up, rusty, and the delivery trucks can’t do their jobs.

To fix it, you stop eating the rusty oils and start eating the good fats. It takes a long time—years—because you have to wait for your body to slowly replace all the rusty parts with good parts. But it does work.

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The Practical Synthesis

If the mechanisms described above are correct, what follows?

First, eliminate seed oils. This is the primary intervention. Soybean oil, corn oil, canola oil, sunflower oil, safflower oil, cottonseed oil, grapeseed oil, rice bran oil—all must go. Check labels; they’re in nearly every processed food, every restaurant fryer, every commercial salad dressing.

Second, understand the timeline. Linoleic acid stored in adipose tissue and cell membranes doesn’t disappear overnight. Paul Saladino cites research suggesting full membrane turnover takes four or more years. Improvement will be gradual. The damage accumulated over decades; repair takes years.

Third, replace with traditional fats. Butter, tallow, ghee, lard from pasture-raised animals, coconut oil. These are the fats humans consumed for the entirety of our evolutionary history. They are low on the peroxidation index. They do not oxidize readily in cell membranes.

Fourth, consider the role of olive oil. This is where the investigators diverge somewhat. Knobbe and Shanahan consider high-quality olive oil acceptable. Marshall’s torpor model suggests that monounsaturated fat (oleic acid) may perpetuate the hibernation state via PPAR-gamma activation. Those with severe metabolic damage who want to optimize recovery may need to avoid even olive oil temporarily, focusing on saturated fats to re-saturate membrane composition.

Fifth, recognize that carbohydrate tolerance will improve. As mitochondrial function recovers, the body regains its ability to burn glucose. Populations eating 80–90% carbohydrate with minimal linoleic acid did not develop diabetes or obesity. Carbohydrate restriction is a workaround for broken mitochondria, not a permanent biological requirement. Some individuals may be able to reintroduce carbohydrates as they heal; others may have accumulated damage that makes lifelong restriction necessary.

Sixth, understand the relationship to insulin. The insulin model remains valid. Lowering insulin remains important. But seed oil elimination is upstream—it addresses why the metabolic machinery became dysfunctional in the first place. The most powerful intervention combines both: eliminate seed oils to allow cellular repair while managing insulin to prevent ongoing fat storage during the recovery period.

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Why This Isn’t Common Knowledge

The evidence presented here is not fringe. Tucker Goodrich’s work on cardiolipin draws on mainstream biochemistry. Knobbe’s epidemiological data comes from peer-reviewed sources. The suppressed clinical trials—Sydney Diet Heart, Minnesota Coronary Experiment—are real studies that really showed harm.

So why does official dietary advice still recommend seed oils?

The short answer: institutional capture. The edible oil industry is enormous. Soybean oil alone is a multi-billion-dollar market. The companies that produce these oils fund nutrition research, sponsor professional associations, and employ lobbyists—five for every member of Congress, according to one estimate.

The longer answer involves well-meaning institutions that drove the shift to seed oils while believing they were protecting public health. In 1984, the Center for Science in the Public Interest—the most powerful food-focused consumer group in the country—launched an enormous campaign called “Saturated Fat Attack.” CSPI pressured fast-food chains including McDonald’s and Burger King to abandon beef tallow for partially hydrogenated soybean oil in their fryers. Saturated fats should be replaced by “healthy” hydrogenated oils, CSPI argued. Due to their persistent public urgings throughout the 1980s, all major fast-food chains converted their operations to partially hydrogenated soybean oil.

A Nebraska millionaire named Philip Sokolof ran full-page newspaper ads with the headline “THE POISONING OF AMERICA!” targeting companies that used coconut and palm oil. Food manufacturers responded by switching to trans fats. When trans fats were later identified as harmful, companies switched again—to liquid vegetable oils that produce toxic aldehydes when heated.

As investigative journalist Nina Teicholz documented in The Big Fat Surprise, Americans have moved from saturated fats at the beginning of the twentieth century to partially hydrogenated oils to polyunsaturated oils. “We have therefore unwittingly been subject to a chain of events starting with the elimination of animal fats and eventually winding up with aldehydes in our food.” Each correction created a new problem. Lars Wiedermann, a longtime oil chemist who worked for Kraft and other food companies, told Teicholz: “Someone will surely discover how deadly used frying oils are.”

Over the past century, vegetable oils grew from zero to almost 8 percent of all calories consumed by Americans—by far the biggest change in eating patterns during that time. This didn’t happen because the evidence supported it. It happened because institutions committed to a hypothesis before testing it, then couldn’t reverse course without admitting error.

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References

Brad Marshall

• “How We Get Fat with Brad Marshall” (The Natural State podcast)

• “The Science Behind Fat Storage” (The Natural State podcast, Episode 138)

• Fire in a Bottle blog (fireinabottle.net)

Tucker Goodrich

• “How Seed Oils Destroy Your Mitochondria and Lead to Chronic Disease” (podcast interview)

• Yelling Stop blog (yelling-stop.blogspot.com)

Chris Knobbe

• The Ancestral Diet Revolution (book)

• Ancestral Health Foundation presentations

• “Diseases of Civilization: Are Seed Oil Excesses the Unifying Mechanism?” (peer-reviewed paper)

Cate Shanahan

• Deep Nutrition: Why Your Genes Need Traditional Food (Flatiron Books, 2017 revised edition)

• DrCate.com

Paul Saladino

• “Why ‘Heart-Healthy’ Seed Oils Are Actually Poison” (The Ultimate Human podcast, Episode 129)

• Fed a Lie (documentary, Heart & Soil, 2024)

• The Carnivore Code (Houghton Mifflin Harcourt, 2020)

Nina Teicholz

• The Big Fat Surprise: Why Butter, Meat and Cheese Belong in a Healthy Diet (Simon & Schuster, 2014)

• Nine years of research, thousands of scientific papers reviewed

• Documents the institutional forces that drove adoption of vegetable oils

• Hermann Esterbauer’s 1991 aldehyde review cited within

Additional Sources

• Ramsden CE, et al. “Re-evaluation of the traditional diet-heart hypothesis: analysis of recovered data from Minnesota Coronary Experiment (1968-73).” BMJ, 2016.

• Ramsden CE, et al. “Use of dietary linoleic acid for secondary prevention of coronary heart disease and death: evaluation of recovered data from the Sydney Diet Heart Study.” BMJ, 2013.

• Guyenet SJ, Carlson SE. “Increase in adipose tissue linoleic acid of US adults in the last half century.” Advances in Nutrition, 2015.

• Teicholz N. The Big Fat Surprise: Why Butter, Meat and Cheese Belong in a Healthy Diet (Simon & Schuster, 2014).

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