Do Seed Oils Cause Heart Attacks?

By Tucker Goodrich

As someone who has pioneered the political discourse around industrial seed oils and their ill-effects on daily broadcast radio, I have counted Tucker Goodrich as an invaluable research ally and good friend along the way. With the rise of RFK Jr to HHS and Steak n Shake tallow fries, we have come quite far from the days when people looked at us befuddled when we mentioned the word “seed oils,” but there is much work to be done.

I have asked Tucker to provide the science for how seed oils are driving cardiovascular disease. As a main driver of poor health and medical costs in this nation, we must address this disease head on regardless of our preconceived notions and food and pharma industry-supported groupthink.

As St. Augustine said, “Truth is like a Lion. You do not have to defend it. Set it free and it will defend itself.”
- David Gornoski

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Do Seed Oils Cause Heart Attacks?

By Tucker Goodrich

Heart disease is the leading cause of death in the United States and industrial countries around the world. This is hardly news, but what is not widely understood is that this has not always been the case.

Even as recently as the early 20^th Century in the United States and United Kingdom, what we now call atherosclerotic cardiovascular disease (ASCVD) was unusual. If you find this hard to believe, consider that while a comprehensive list of causes of death was first commenced in 1836 in the U.K., and an International Causes of Death list (building upon the previous work from several nations) was created in 1893, it wasn’t until 1930 that coronary disease was included as a cause (Strong, 1936), 18 years after it was first described (Herrick, 1912). Heart disease previously had been ‘rheumatic’, or caused by damage from infection.

And lest you think that this was a result of incompetence, lack of attention, or increasing lifespan, the foremost cardiologist of the 20^th Century, Dr. Paul Dudley White, goes through all these possibilities in his 1971 “Perspectives” (60 years after graduating from medical school) and dismissed them all; ultimately noting that it must be some change in the lifestyle, as children dying before their parents of this novel disease became common.

“The automobile, richer food, more tobacco, a faster life, and more pollution of everything have become available to all of us in the United States.” (White, 1971)

“What has been most disturbing is the fact that the children appear to be afflicted with coronary disease at a much earlier age than were their parents.” (Levine, 1963)

No doubt smoking had a major impact on heart disease: no factor correlates more closely. However, the massive decline in smoking after it was recognized to contribute to heart disease in the 1960s did not reduce the prevalence to its levels in the early 1900s.

At the same time, a theory of how to reduce heart disease emerged. It was commonly observed upon autopsy that the plaques which could clog arteries and lead to heart attacks were composed of fats and cholesterol. Fats and cholesterol enter the circulation through two pathways: they are eaten, or are exported by the liver. It was quickly recognized that eating cholesterol had little effect on the levels in circulation.

"From the animal experiments alone the most reasonable conclusion would be that the cholesterol content of human diets is unimportant in human atherosclerosis." (Keys, 1952)

Cholesterol levels in the blood were regulated by the liver, if you ate more cholesterol the liver would produce less, and levels would stay the about the same—yes, physicians have always been wrong about eggs and cholesterol.

So that leaves the fat. It’s unquestionable that if you eat fat it raises the level of fat and of cholesterol in the blood, both as part of digestion and chronically (Keys, 1952). What had not been demonstrated was that altering fat intake would reduce the level of heart disease in the population.

It was also observed that not all types of fat had identical effects. While certain types of saturated (solid) fats tend to raise blood fat and cholesterol levels, polyunsaturated (liquid) fats, like those in fish or seed oils, lower them.

Based on these observations, but without experimental confirmation that these changes would be effective, the ‘authorities’ recommended that all Americans consume increased amounts of polyunsaturated fats, mainly from seed oils, and avoid saturated fats (Page, 1961).

“It must be emphasized that there is as yet no final proof that heart attacks or strokes will be prevented by such measures” (Page, 1961).

That paper was published in January of 1961. The following was already scheduled for publication, and was published in April:

“This result would support the view that linoleic acid is essential for the production of atherosclerotic plaques.” (Gresham, 1961)

These papers were published amid a national epidemic of heart disease, which had already taken a toll on President Eisenhower, Dr. White’s most famous patient.

Linoleic acid is the primary fat in seed oils, that subset of vegetable oils produced from the seeds of various plants.

And atherosclerotic plaques are of course the harbinger of death from heart attack.

Gresham and Howard further noted that:

“Our results are in accord with the recent work of Bottcher [et al.] (1960) who showed conclusively that human atherosclerotic plaques have a high content of linoleic acid which increases with the severity of the disease.”

So while the presence of cholesterol and ‘fat’ generally led to admonitions that they should be reduced to prevent heart disease, the evidence that linoleic acid was “essential” for the promotion of heart disease was ignored. The largest problem with the idea that seed oils could prevent heart disease was that the rise of heart disease was accompanied by a massive increase in the consumption of seed oils, and a corresponding decline in the consumption of saturated animal fats (Lee 2022). Many of the researchers involved were aware of this (Enig, 1998). In fact, Dr. White in 1956 explained:

“See here, I began my practice as a cardiologist in 1921 and I never saw an [heart attack] patent until 1928. Back in the MI-free days before 1920, the fats were butter and lard and I think that we would all benefit from the kind of diet that we had at a time when no one had ever heard the word corn oil.” Enig, 1998)

In a pattern that continues to the modern day, such evidence was ignored.

The obvious next step to confirm the Diet-Heart Hypothesis would be to do a human randomly-controlled trial, to test if Page et al.’s recommendations would be safe, and effective in reducing heart disease.

“It is concluded that under the circumstances of this trial corn oil cannot be recommended in the treatment of ischaemic heart disease.” (Rose, 1965)

That didn’t go well. Notably more patients died in the corn oil intervention. (Corn oil was what had been prescribed to Pres. Eisenhower.) Corn oil is high in linoleic acid, so was an effective test of the hypothesis. A barrage of other, similar experiments followed, all with similar results (Ramsden, 2016).

One test inadvertently compared seed oil consumption to smoking. The group with approximately double the levels of smokers did better than the group prescribed seed oils, both in terms of deaths from CVD and from all causes (Christakis, 1966; Singman, 1980). This was the only human trial mentioned in (Page, 1961), as it was already underway, and had been organized in cooperation with some of the authors.

Page and his colleagues were planning their own trial, however; they had started planning it prior to publication. This became a massive undertaking, the National Diet-Heart Study. They involved insurance companies, the Federal Government including the Census Bureau, and many food companies—to make the synthetic foods deemed necessary. Since natural foods don’t have high levels of linoleic and low levels of saturated fat, what was required was a menu of ultra-processed foods, where the levels and types of fat were altered to match the prescription. The trial version of the study was a bit of a failure, but I’ll save you why, as it’s not really relevant (Newport, 2024). But the two researchers who were to conduct the most-rigorous part of the trial study continued their part. It became known as the Minnesota Coronary Experiment (MCE) (Ramsden, 2016).

Ending in 1973, the outcome of the MCE was consistent with the earlier experiments: the group that received the treatment did worse. What’s worse, is that they did worse in proportion to how effective the treatment was at lowering their cholesterol. What’s even worse, is that instead of being forthcoming about the results, the authors initially claimed that there was no effect (Ahrens, 1976), and then didn’t publish the results for 16 years, until 1989 (Frantz, 1989); and even then didn’t fully disclose the results, which had to await the forensic efforts of (Ramsden, 2016), 46 years later.

“When I asked Frantz [the principal investigator of the MCE] in late 2003 why the study went unpublished for sixteen years, he said, ‘We were just disappointed in the way it came out.’” (Taubes, 2008)

So Page & Co. never produced their “final proof”, instead, they disproved their hypothesis. By the time these results finally were unearthed, the debate was considered to have long been settled, and the cardiology profession was so committed to this harmful prescription that it has been unable to admit error. By the time (Ramsden, 2016) came along, the Diet-Heart Hypothesis was firmly established in law via its inclusion in the U.S. Dietary Guidelines (Newport, 2024).

“The widespread consumption of diets with more than 2% energy as LA should be recognized for what it is—a massive uncontrolled human experiment without adequate rationales or proven mechanisms.” (Ramsden, 2009)

When a study finally came along that offered a massive 70% reduction in heart disease (de Lorgeril, 1994), the ‘authorities’ could only ignore that a key element of the study was a rejection of the idea that linoleic acid could improve heart disease (Kris-Etherton, 2001):

“This could be due to … a lower intake of linoleic acid, easily oxidized in low density lipoproteins.” (de Lorgeril, 1994)

“Easily oxidized” refers to a new body of evidence that arose in the 1970s and -80s. Cardiologists had moved along from cruder measures of ‘cholesterol’ to more specific ones, alighting on a variety of cholesterol-containing particles, low-density lipoproteins (LDL).

Most of the cholesterol in blood is contained in LDL, but LDL doesn’t contain just cholesterol. LDL particles are produced in either the liver or the gut, and the original payload of these particles is fat, either ingested or released from the liver (Campos, 2005). Cholesterol is a secondary payload, and is mostly bound to fat in these particles—which are in a protein wrapper called apolipoprotein B (ApoB).

The plaques in atherosclerosis are composed of these particles, some of which have been consumed by a special type of white blood cell called a macrophage. Macrophages are cells that dispose of debris from injury, or pathogens. Macrophages that have gorged on LDL particles (known as foam cells, for their appearance) sufficiently to start forming a plaque in the artery (atherosclerosis) are thought to start the process that ultimately leads to a heart attack (Goldstein, 1977).

All well and good: two scientist-cardiologists (Brown and Goldstein) even won a Nobel Prize in Medicine for discovering how LDL enters the cell.

But then they ran into a couple of problems. LDL doesn’t cause macrophages to become foam cells, unless it is modified. “Native” LDL, as the unmodified LDL was called, is harmless. First it must become “modified”, and ironically, when it is sufficiently modified it no longer uses the LDL receptor that Brown and Goldstein discovered (Goldstein, 1979).

It didn’t take long for another pair of scientist-cardiologists to discover what got modified in the LDL. In 1961, as quoted above, Gresham and Howard had written: “This result would support the view that linoleic acid is essential for the production of atherosclerotic plaques.”

And sure enough, in 1990 Brown and Goldstein acknowledged that it was linoleic acid that became modified, specifically, oxidized, and this change altered the LDL to become atherogenic (Brown, 1990). Linoleic acid is the most common fat in the LDL molecule (Goldstein, 1977), and as it can only come from the diet, this finally explained the connection between seed oils and heart disease. The paper from which they took this information was titled “Beyond Cholesterol”, as it finally (one would think) allowed Cardiology to move beyond the failed Diet-Heart Hypothesis (Steinberg, 1989).

“We need only find drugs or dietary treatments that slow the conversion of native LDL to the relevant modified form” (Steinberg, 1989)

Amazingly, neither (Brown, 1990) nor (Steinberg, 1989) mention seed oils, linoleic acid, or that this finding flies in the face of the recommendations that Cardiology had made since 1961.

Steinberg and Witztum continued their exploration, and in a 1991 paper finally made the connection between linoleic acid and heart disease explicit:

The importance of the fatty acid composition was impressively demonstrated by our recent studies of rabbits fed a diet high in linoleic acid… or in oleic acid… for a period of 10 wk. LDL isolated from the animals on oleic acid-rich diet were greatly enriched in oleate and low in linoleate. This LDL was remarkably resistant to oxidative modification, measured either by direct parameters of lipid peroxidation… or by the indirect criterion of uptake by macrophages” (Witztum, 1991).

They found a similar result in humans, and other researchers confirmed what could have been known in the 1960s:

“Correlations were found between plaque [linoleic acid] content and serum and adipose tissue [linoleic acid]… demonstrating that the dietary intake of this essential fatty acid directly influences the plaque composition” (Felton, 1994).

This modified LDL is called oxidized LDL, hence de Lorgeril’s aforementioned comment about the oxidization of linoleic acid in 1994.

It would seem that the mystery of what causes heart disease has been solved.

And indeed, modern cardiology papers reviewing causation of CVD, cite the “Beyond Cholesterol” paper (Steinberg, 1989), and, while superficially blaming LDL, in fact only cite evidence that it is the modified LDL which is to blame (Borén, 2020). (Navigating through the logical contortions of (Borén, 2020) is a spelunking expedition worthy of its own long article.)

So we are left with a situation where all the evidence we have is for the causal role of seed oils in ASCVD, where there is essentially no other theory presented for causation, and yet the ‘authorities’ continue to recommend a hypothesis they themselves debunked decades ago.

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References

Ahrens, E. H. (1976). The Management of Hyperlipidemia: Whether, Rather Than How. Annals of Internal Medicine, 85(1), 87–93. https://doi.org/10.7326/0003-4819-85-1-87

Borén, J., Chapman, M. J., Krauss, R. M., Packard, C. J., Bentzon, J. F., Binder, C. J., Daemen, M. J., Demer, L. L., Hegele, R. A., Nicholls, S. J., Nordestgaard, B. G., Watts, G. F., Bruckert, E., Fazio, S., Ference, B. A., Graham, I., Horton, J. D., Landmesser, U., Laufs, U., … Ginsberg, H. N. (2020). Low-Density Lipoproteins Cause Atherosclerotic Cardiovascular Disease: Pathophysiological, Genetic, and Therapeutic Insights: A Consensus Statement from the European Atherosclerosis Society Consensus Panel. European Heart Journal, 41(24), 2313–2330. https://doi.org/10.1093/eurheartj/ehz962

Brown, M. S., & Goldstein, J. L. (1990). Scavenging for Receptors. Nature, 343(6258), 508–509. https://doi.org/10.1038/343508a0

Campos, H., Khoo, C., & Sacks, F. M. (2005). Diurnal and acute patterns of postprandial apolipoprotein B-48 in VLDL, IDL, and LDL from normolipidemic humans. Atherosclerosis, 181(2), 345–351. https://doi.org/10.1016/j.atherosclerosis.2004.12.045

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For more articles on building a healthy diet and lifestyle visit Tucker Goodrich at tuckergoodrich.substack.com

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