Saturated Fat Was Never the Villain: Why Cholesterol Became the Wrong Target

We were told saturated fats were the bad guys, and that “heart-healthy” polyunsaturated fats would save us.

But that story was wrong.

New research (and the re-analysis of old research) continues to dismantle the saturated fat myth, and expose how cholesterol became the wrong target, while metabolic health has quietly deteriorated in the background. 

Yes, replacing saturated fat with seed oils can lower cholesterol numbers.

…but lowering cholesterol has not consistently translated into fewer heart attacks, fewer cardiovascular deaths, or longer life spans.

That gap between numbers and outcomes is where the story begins to unravel.

Because for decades, we weren’t actually testing whether these dietary changes improved health, we were assuming they did.

Note: This blog is not medical advice and is for educational purposes only.

Before Seed Oils: What Humans Actually Ate

For most of human history, the fats people consumed looked nothing like the modern diet.

Traditional diets across cultures included a mix of carbohydrates, fats, and protein, but the fats themselves came primarily from animals fats: butter, tallow, lard, ghee, milk, cheese, and the natural fats that accompanied meat and eggs. These fats were higher in saturated fat and relatively low in polyunsaturated fats (PUFAs). They were stable, minimally processed, and produced in close relationship with land, animals, and season.

By contrast, seed oils and vegetable oils that are high in PUFAs and low in saturated fats are a modern invention. They only became possible with the rise of industrial agriculture: monocropped corn and soy, chemical fertilizers and pesticides, and heavy machinery capable of extracting oil from seeds that humans historically did not consume in meaningful quantities.

To put the scale into perspective, producing vegetable oils requires enormous amounts of raw crops. For example, manufacturing just 2.5 gallons of corn oil (roughly 21 pounds) requires processing around 780 pounds of corn. Soybeans contain more oil than corn, but even then, many pounds of soybeans are needed to yield a single pound of edible oil.

These figures highlight an important reality: industrial seed oils are not traditional foods, but products of large-scale, mechanized systems designed to convert massive quantities of monocropped grain into concentrated fat.

This same industrial shift transformed animal agriculture as well. Livestock were moved into confinement systems and fed corn- and soy-based rations, dramatically increasing the PUFA content of meat, eggs, and dairy compared to what animals produced just a century ago.

In other words, both seed oils and today’s unusually high-PUFA animal fats are products of the same industrial system:one that separated food production from nature in the name of efficiency.

At the turn of the 20th century, these plant-based PUFAs made up only about 1–2% of daily calories. Today, they account for 15% or more (ref), a five- to six-fold increase in just over a century.

That shift didn’t happen by accident.

In 1911, the first industrial seed oil marketed as a household staple was introduced by Procter & Gamble: Crisco. From there, the use of vegetable and seed oils steadily expanded, made possible by industrial agriculture, chemical processing, and mass food manufacturing.

Crisco was originally made from partially hydrogenated cottonseed oil, a byproduct of the cotton industry that had previously been used for industrial purposes like soap and lamp oil. Hydrogenation, a novel chemical process at the time, allowed Procter & Gamble to turn this cheap, abundant waste product into a solid fat that looked and behaved like lard. 

It was marketed as a cleaner, more modern, and more “scientific” alternative to traditional animal fats, and Procter & Gamble supported this message with aggressive, highly effective advertising and branded cookbooks that reshaped American home cooking.

And people listened. Crisco introduced high levels of omega-6 PUFAs and trans fats into the human diet at a scale never before seen in history.

It is actually mind-blowing to think that people were convinced to use this stuff with the simple line “it’s digestible!” with zero studies on safety or health.

Within a few decades, Crisco had largely displaced butter, lard, and tallow in many households, not because of proven health benefits (there were zero tests), but because the messaging and marketing worked, extremely well.

Procter & Gamble was able to profit enormously from an industrial waste product, while Americans were encouraged to swap out traditional fats higher in saturated fats, and replace them with a seed oil high in polyunsaturated fats, quietly increasing PUFA intake in the process.

This matters historically because seed oils entered the diet before the diet–heart hypothesis emerged in the 1950s.

Prior to this point, no traditional food culture relied on large amounts of so-called “heart-healthy” seed oils because they simply did not exist in a usable form.

And yet, it was during this rapid dietary fat shift (less saturated fats and more PUFAs, not during centuries of ancestral saturated fat intake) that cholesterol and saturated fat suddenly became the primary suspects in heart disease.

How Cholesterol Became the Target

An important historical detail often gets overlooked: heart attacks were relatively rare in the 1800s and early 1900s.

Then, seemingly suddenly, heart disease rates began to climb. By the 1950s, cardiovascular disease had become a leading cause of death in the United States. The sharp rise in heart attacks and coronary events created intense urgency within the medical community to identify a cause, and fast.

Ironically, this surge occurred during the same period that industrial seed oils were becoming an increasingly dominant part of the food supply.

Faced with a growing public health crisis, researchers searched for a dietary explanation. Cholesterol offered a simple, measurable target, one that appeared to fit the emerging “data”.

The logic seemed straightforward at the time:

> High cholesterol was associated with heart disease
> Saturated fat raised cholesterol
> And thus, saturated fat must cause heart disease

From this, a hypothesis took hold in the 1950s: the diet–heart hypothesis, largely popularized by physiologist Ancel Keys. It proposed a clean chain of causation — eat saturated fat, cholesterol rises, arteries clog, and heart disease follows.

The problem was that this chain was built primarily on observational correlations, not on long-term randomized controlled trials demonstrating that changing dietary fat intake actually saved lives.

Despite that limitation, cholesterol was treated as a valid surrogate marker. If a diet lowered cholesterol, it was assumed to reduce heart disease risk, even in the absence of evidence showing fewer heart attacks or longer life. That assumption quietly shaped decades of research priorities, public health messaging, agriculture, and food policy that followed.

The Minnesota Coronary Experiment: The Trial That Was Supposed to Settle It

If replacing saturated fat with seed oils truly prevented heart disease, the Minnesota Coronary Experiment should have shown it.

Conducted between 1968 and 1973, the study was one of the largest and most rigorous dietary trials ever attempted at the time. Nearly 9,400 participants were enrolled in controlled feeding environments such as nursing homes and mental hospitals, where researchers could precisely control what people ate for years at a time (up to 4.5 years).

The premise was simple: replace saturated fat with corn oil rich in linoleic acid, lower cholesterol, and watch heart disease and mortality decline.

What they did show (and publish): replacing saturated fat with vegetable oil (corn oil) lowered serum cholesterol (this part was highlighted, shared and emphasized).

What they did NOT clearly report:

• Full mortality outcomes
• Complete coronary heart disease event data
• Subgroup analyses (especially in older adults)
• The relationship between degree of cholesterol lowering and death

Because cholesterol lowering was assumed to equal benefit, the trial was widely interpreted as supportive of saturated fat restriction, even though the outcomes that actually matter were never fully presented.

So the field assumed:

Lower cholesterol = fewer heart attacks = better outcomes

Policy Solidified Before the Evidence Did

By the late 1970s, the narrative had hardened into policy.

The 1977 Dietary Goals for the United States and the 1980 Dietary Guidelines for Americans formally advised reducing saturated fat and replacing it with vegetable oils. These recommendations were issued before long-term randomized controlled trials had demonstrated reductions in mortality.

Once those guidelines were in place, everything aligned around them: research funding, medical education, public health messaging (propaganda), and food production systems followed suit.

Saturated fat became dogma, seed oils became “heart healthy,” and cholesterol reduction became the goal (at all costs).

Reversing course would have required confronting decades of assumptions.

The Data That Was Never Fully Published

Decades later, that confrontation finally happened.

Turns out the original study results only reported half the story…

In 2016, researcher Christopher Ramsden and colleagues recovered and re-analyzed previously unpublished data from the Minnesota Coronary Experiment (ref). When the full dataset was examined, the conclusions looked very different from the narrative that had shaped policy.

Yes, cholesterol went down in the seed-oil group.

But there was no reduction in mortality or coronary events. In older adults, greater reductions in cholesterol were actually associated with higher mortality.

The core assumption that lowering cholesterol through replacing saturated fat with linoleic-acid-rich oils improves health failed in the very trial designed to test it.

Oops!

The authors concluded that incomplete publication of the original trial likely contributed to decades of overestimating the benefits of replacing saturated fat with seed oils.

And this wasn’t an isolated finding.

Ramsden’s team also re-analyzed the Sydney Diet Heart Study (ref) and conducted updated meta-analyses of randomized trials where saturated fat was replaced with seed oils.

Across these analyses, a consistent pattern emerged: cholesterol went down, but cardiovascular deaths and total mortality did not reliably follow.

And in another recent meta-analysis, higher linoleic acid intake was associated with increased cardiovascular events and all-cause mortality (ref).

Cochrane reviews (ref) and other meta-analyses (ref) have echoed this conclusion. While PUFA replacement may modestly reduce LDL cholesterol, it shows little to no consistent benefit for cardiovascular mortality or all-cause mortality.

Cholesterol is a Signal, Not the Root Cause

None of this means that cholesterol is irrelevant, that LDL never matters, or that statins never reduce risk. In certain contexts (particularly secondary prevention) statins do reduce cardiovascular events, and they do so through multiple mechanisms, not just LDL lowering.

What the data increasingly shows, however, is that targeting cholesterol alone as a dietary or therapeutic goal is an unreliable strategy for improving long-term heart health.

While statins do reduce risk, it’s important to remember that risk reduction ≠ no tradeoffs, and many of the downstream effects are well documented.

Many downstream effects of statin use are well documented, including

1.     Impaired glucose metabolism & diabetes risk (ref)

2.     Muscle pain, weakness and fatigue (ref)

3.     Mitochondrial dysfunction (ref)

4.     Reduce synthesis of essential compounds like CoQ10, dolichols, and cell-signaling proteins (ref)

As a result, statins may lower cardiovascular risk while simultaneously worsening aspects of metabolic health.

When you zoom out, this tradeoff makes sense.

Cholesterol is not a toxin, it is a necessary structural molecule involved in cell membranes, hormone production, bile acids, and brain function. Lowering it indiscriminately, without addressing underlying physiology, can come at a cost.

That doesn’t mean high cholesterol is “good.”

It isn’t.

But elevated cholesterol is best understood as a signal, not the root problem itself.

High cholesterol often reflects deeper metabolic stress. For example, in hypothyroid states (poor thyroid health from a down regulated metabolism), the conversion of cholesterol into downstream compounds slows, allowing cholesterol to accumulate in the blood. Adequate thyroid function and fat-soluble vitamins are required for this process to work properly.

Including carbohydrates that you personally tolerate well is also well established to lower serum cholesterol, in part because carbohydrates support thyroid function and overall metabolic rate. By carbohydrates, we mean whole-food sources (fruits, roots, tubers, and properly prepared grains), not ultra-processed foods like cookies, muffins, or pizza, which often contain more calories from industrial fats than from carbohydrates themselves!

Here’s the irony: diets high in polyunsaturated fats may lower cholesterol numbers, but over time they can worsen the underlying metabolic dysfunction that caused cholesterol to rise in the first place, since PUFAs interfere with efficient energy production.

Adding to the confusion is the persistent message that “lower is always better” when it comes to cholesterol.

Perhaps the most ironic finding from the reanalysis of the Minnesota Coronary Experiment (ref) is illustrated in this figure: greater reductions in serum cholesterol were associated with a progressively higher probability of death. In other words, participants who experienced the largest decreases in cholesterol had the highest mortality risk.

This directly challenges the long-standing assumption that “the lower the cholesterol, the better", a belief that was shaped using this very study, before its long-term outcomes were ever fully reported.

In reality, both excessively high and excessively low total cholesterol levels are associated with adverse outcomes. Large population studies have shown that total cholesterol below 200 mg/dL is not necessarily indicative of optimal health, and that deviations in either direction may correlate with increased risk.

"Our findings indicated that TC (total cholesterol) levels might be a critical risk factor in the general population, and TC levels < 200 mg/dL might not be indicative of good health... too low or too high serum total cholesterol levels might correlate with adverse outcomes."

How Industry Incentives Shaped the Narrative

It’s long past time to question whether industry-shaped dietary recommendations (so different from what humans consumed for centuries) are actually working.

We eat more “heart healthy” plant-based PUFAs today and metabolic health is on the decline, obesity rates and chronic diseases are climbing.

The mistake was never measuring cholesterol. The mistake was treating cholesterol as the primary cause of disease, rather than recognizing it as a downstream biomarker reflecting deeper metabolic conditions. That framing had consequences — not just scientifically, but economically.

A cholesterol-centered model proved extraordinarily profitable. Statins became the most financially successful drug class in history, driven by lifetime use and ever-expanding eligibility. At the same time, industrial agriculture scaled monocropping of corn and soy, producing vast quantities of seed oils promoted as “heart healthy” precisely because they lowered cholesterol.

This alignment of incentives matters. When lowering cholesterol became the primary goal, food quality, fat composition, and metabolic function faded into the background. The result was a system optimized to manipulate a number on a lab report, rather than restore physiological health.

If we stop assuming that PUFA-rich seed oils are heart healthy simply because they lower cholesterol, and instead return to traditionally consumed saturated fats, eaten in appropriate amounts within a whole-food diet (you don’t have to overdo fat consumption!!) much of their framework begins to unravel.

Ultimately, health cannot be reduced to a single biomarker. Food quality, fat stability, and metabolic resilience matter far more than chasing cholesterol numbers at all costs.

Re-Saturating the Food System

We’ve been PUFAd!

We’re living in a world that’s becoming increasingly unsaturated: not just because of seed oils, but because we’ve fundamentally changed how food is produced.

Higher PUFA intake doesn’t come only from vegetable oils. It also comes from the way modern livestock are raised and fed. The reality is simple: animals today are raised and fed very differently than they were 100 years ago.

Corn- and soy-heavy feeds have dramatically altered the fatty acid composition of animal foods. Today, chicken fat and pork fat can contain PUFA levels comparable to canola oil, something that would have been unrecognizable just a century ago.

And that shift has changed the fat composition of our food and the fat inside of us, with downstream effects on metabolism, gut health, and overall resilience.

While fear of saturated fat and enthusiasm for “heart-healthy” PUFAs continue to shape the modern food system, we’re choosing a different direction.

At Nourish Food Club, our mission is to do the reverse: to lower PUFA exposure and restore metabolism-supporting saturated fats, including stearic acid, by changing food production at the source.

We do this through custom-formulated livestock feed that is corn- and soy-free, carefully designed to reduce PUFA content while increasing more stable, traditional fats. Our food is lab tested, produced on small regenerative farms, and raised without pesticides: the way food was made before industrial shortcuts rewrote the system.

The result is farm-fresh food produced the old-fashioned way, with the transparency and convenience of modern delivery.

Because restoring metabolic health doesn’t start with drugs or in a lab.

It starts with what’s on your plate.

>> Shop the Nourish Food Club Difference today