Fred Kummerow, Trans Fats, and Heart Disease

by Jeffrey Dach MD

For fifty-eight years, America was told to eat margarine instead of butter. In 1957, a University of Illinois biochemist named Fred Kummerow examined the arteries of people who died of coronary artery disease and found something else. Trans-fats were present in the plaque. Kummerow asked the FDA to ban trans-fats and he was ignored. The government finally acted in 2015 when he was one hundred years old. This is not a mystery novel. It is a story about a 50 year public-health delay.

Above Header image: Book Cover courtesy of: Cholesterol Won’t Kill You, but Trans Fat Could: Separating Scientific Fact from Nutritional Fiction  by Fred A. Kummerow (Author), Jean M. Kummerow (Author) 

Why Not Examine the Wall of the Artery?

In 1957 Dr. Fred Kummerow published his paper in Science after examining autopsy and biopsy tissue from people who had died of heart disease. The diseased vessels contained trans fatty acids, fats that barely exist in nature and came mainly from hydrogenated vegetable shortening and margarine. The authors asked a simple question: what do these industrially made fats do to normal metabolism? [1]

Dr. Fred August Kummerow was a lipid chemist at University of Illinois Champaign-Urbana campus who studied tissue from about two dozen subjects and found trans fats in every sample examined. What are trans-fats? Trans fats are made by Hydrogenation, the process of bubbling hydrogen through the vegetable oil. This hydrogenation process made margarine spreadable and gave processed foods a long shelf life. It also created a new synthetic fat not fit for human consumption. [2]

In 2013, Melanie Warner wrote in the New York Times about Dr. Kummerow’s discovery of trans fats. At the time, Dr. Kummorow was a young nutrition scientist who persuaded the local hospital pathology department to give him samples of arteries from patients who had died of heart attacks. The fat packed into those arteries was not the butter-and-egg fat the population was told to fear. It was the artificial trans fat from hydrogenated oils. [3]

A Lonely Voice, Then a Lawsuit

In 2017, Katie Hafner (2017) wrote again in the New York Times Dr. Kummerow’s story. When he published his report in 1957, he was dismissed and ignored. The cooking oil, margarine, trans-fat industry had friends in high places, on legislative committees and they had firm control of the narrative which blamed saturated fat and cholesterol for causing heart disease, not trans-fats. Although Kummerow’s research funding had dried up, he kept his laboratory open into his nineties. [4]

In 2015, Fred Kummerow was 100 years old, and he was still spunky and outspoken. His campaign to get trans fats out of the food supply began in earnest in 1968. He sat on an American Heart Association subcommittee, measured the trans fat in grocery-store margarine and shortening, and pressed manufacturers to reduce the content. His pleas were partially successful. Trans-fat content fell from roughly forty-three percent to about twenty-seven percent. Heart-disease death rates also began to decline after 1968. This was no coincidence. [5]

Above left image: Courtesy of Fred Kummerow and The Chronicle. Article is entitled: Even at 100, Professor Keeps Up Fight Against Trans Fats. Dated: February 16, 2015

In 2014, Geoffrey Cannon reviewed Dr. Fred Kummerow’s efforts to ban trans-fats. Taking the first step, the American Heart Association drafted a warning label for partial hydrogenation and trans-fats. However, the shortening and margarine trade group voiced their opposition to the drafted AHA trans-fat warning, which was then discarded. Even so, a deal was made secretly behind closed doors. Margarine/Trans-fat Industry agreed to reduced trans fats quietly on their own, making a public statement avoiding naming a problem with trans fats. [6]

Eggs in Butter, Not Margarine

This heading is not a breakfast slogan. It is the point of Kummerow’s whole career, stated in food language. In 2013, Melanie Warner visited Fred Kummerow when he was ninety-nine and still directing a small laboratory at the University of Illinois. She watched how he actually ate. Breakfast was an egg scrambled in butter. He drank whole milk every day. He ate red meat several times a week. He did not use margarine. He could not remember the last time he ate anything deep-fried. [3]

Kummerow’s diet was the opposite of official advice for half a century. From the 1960s onward, the public was told that cholesterol and saturated fat, eggs, butter, whole milk, red meat, clogged arteries. Margarine and hydrogenated vegetable shortening were sold as the “heart-healthy” replacement. Kummerow rejected this narrative because he had already looked at the tissue samples of arterial walls showing the trans-fats in the plaque.

In 1957, when Dr. Kummerow examined arteries from people who died of heart disease. What did he find? He found the fat packed into those vessels included trans fatty acids made by partial hydrogenation of vegetable oil. Those are the same industrial fats that made margarine spreadable and gave cookies, crackers, and shortening a long shelf life. The 1957 paper did not find Kummerow’s “breakfast” in the plaque. Instead they reported factory made trans-fat inside the arterial plaque. Saturated fat from butter, cheese, and meat, eaten in moderate amounts with fruit, vegetables, and whole grains, was not the arterial villain the guidelines claimed. Fed Kummerow called eggs one of nature’s most complete foods: all the essential amino acids needed to build cells, plus vitamins and minerals. Eating only egg whites, he said, was a mistake. Dr. Kummerow argued for decades that oxidized and industrially altered fats were the problem, not the cholesterol the body makes and uses for cell membranes and hormones. [1-4]

How to Make a Healthy Breakfast

In 2014, Dr. Kummerow described his own plate to Richard Passwater: one egg scrambled in butter each morning, three glasses of whole milk, meat or another protein at meals, and a large amount of fruit and vegetables. No processed or fried food. No margarine. That was not a publicity stunt. It was the diet that matched what he had measured in tissue and in animals. When Kummerow analyzed diseased human arteries, he did not find the fat from an egg cooked in butter. He found trans fats from hydrogenated margarine and shortening. He therefore ate the foods the committees had condemned and avoided the foods the committees had blessed. He lived to one hundred two. What does that tell you? (11)

In 2017, Katie Hafner made the same point after Kummerow’s death at one hundred two: Kummerow argued that moderate amounts of saturated fat from butter, cheese, and meat were not the arterial culprit the guidelines claimed. The industrial trans fat was. [4]

The Petition the FDA Ignored

In August 2009, at age ninety-four, Kummerow filed a citizen petition with the Food and Drug Administration asking for a ban on artificial trans fats and partially hydrogenated oils. Kummerow ‘s petition stated that “Artificial trans fat is a poisonous and deleterious substance, and the FDA has acknowledged the danger.”

Federal rules give the FDA agency one hundred eighty days to respond. Four years later, there was still no answer from the FDA. Kummerow wrote that anything under half a gram trans-fat per serving could still be labeled zero trans fat, so people were eating the stuff without knowing it. [7-9]

How to Sue the FDA

On 9 August 2013, at age ninety-eight, Fred Kummerow sued the FDA and HHS to force a decision. Court records list the case as filed in the Central District of Illinois. [8]

Three months later the FDA issued a tentative determination that partially hydrogenated oils were not generally recognized as safe. In June 2015 the final determination followed. Manufacturers received three years to remove the fats. The gap from the 1957 paper in Science to the 2015 rule was fifty-eight years. [4]

Conclusion:  The official industry funded narrative was that the dietary villains causing heart disease are eggs and butter, and meat. Everyone was told a healthier substitute was the hydrogenated oils and margarine, and that would be better for your health. Nothing was further from the truth. This was just another of the many errors in modern medicine.

Heart Book: How to Keep Your Heart Healthy by Jeffrey Dach MD

My book is available on Amazon:
Link to Kindle Version
Link to Paperback Version

Heart Book is a journey through the confusing maze of literature on coronary artery disease, the number-one killer in America. With his years of practice in vascular radiology, Dr. Dach has the background, credentials, and experience to transform your understanding of heart disease. The old medical paradigms have been upended, yet mainstream cardiology clings to these tired dogmas as if nothing has changed. Be prepared to be shocked, amazed, provoked, and gratified as this book empowers you to take control of your own heart health.

Jeffrey Dach MD
7450 Griffin Road, Suite 190
Davie, Florida 33314
954-792-4663
www.jeffreydachmd.com

Articles with related Interest:

Challenging the Cholesterol Hypothesis Part four

Atherosclerotic Plaque and Infection Part Two

The Failure of Cholesterol Lowering Drugs

Coronary Artery Disease: Questions and Answers

Does Cholesterol Cause Coronary Artery Disease ?

Calcium Score Determines Who to Treat with Statin Drug

Calcium Score Diabetes and Statin Drugs

Plant Based Diet, Health Benefits for Coronary Artery Disease

LDL-Cholesterol Does Not Cause Coronary Artery Disease

Low Level Endotoxemia, Depression, Endocrinopathy and Coronary Artery Disease

Fibrinolytic Enzymes, Nattokinase, Lumbrokinase Prevent and Reverse Atherosckerosis

Reverse Heart Disease with Coronary Calcium Score

Low Level Endotoxemia LPS Theory of Coronary Artery Disease

Calcium Score Paradigm Shift in Cardiology

Coronary Calcium Score Benefits of Aged Garlic

The Art of the Curb Side Cholesterol Consult

Evolocumab Are You Joking Me?

Cholesterol and Atherosclerosis:Autopsy Studies Show No Correlation

Statin Denialism Internet Cult with Deadly Consequences

Defending the Cholesterol Hypothesis in the Elderly

Does High Cholesterol Cause Heart Disease ?

Familial Hypercholesterolemia and Statin Drugs

Donating Blood Prevents Heart Disease

Does Cholesterol Cause Heart Disease ?  Part two

Atherosclerotic Plaque as Infected Biofilm on Electron Microscopy

Coronary Calcium Score Paradigm Shift Podcast

References

1. Johnston, Patricia V., Ogden C. Johnson, and Fred A. Kummerow. “Occurrence of Trans Fatty Acids in Human Tissue.” *Science*, vol. 126, no. 3276, 11 Oct. 1957, pp. 698–699. https://www.science.org/doi/10.1126/science.126.3276.698.b

2. University of Illinois Archives. “Kummerow, Fred A.” https://archives.library.illinois.edu/archon/index.php?p=creators/creator&id=3018

3. Warner, Melanie. “A Lifelong Fight Against Trans Fats.” *The New York Times*, 16 Dec. 2013. https://www.nytimes.com/2013/12/17/health/a-lifelong-fight-against-trans-fat.html

4. Hafner, Katie. “Fred A. Kummerow, an Early Opponent of Trans Fats, Dies at 102.” *The New York Times*, 1 June 2017. https://www.nytimes.com/2017/06/01/science/fred-kummerow-dead-biochemist-ban-trans-fatty-acids.html

5. “At Long Last, a Ban on Transfat.” *Illinois Times*, 11 June 2015. Interview with Fred Kummerow. https://www.illinoistimes.com/news-opinion/at-long-last-a-ban-on-transfat-11444816/

6. Cannon, Geoffrey. “Fred Kummerow. The Biochemist Who Walked Alone.” *World Nutrition*, 2014. https://worldnutritionjournal.org/index.php/wn/article/download/282/231/

7. Kummerow, Fred A. Citizen Petition to the U.S. Food and Drug Administration. Docket FDA-2009-P-0382, filed 7 Aug. 2009. https://www.regulations.gov/document/FDA-2009-P-0382-0001

8. *Kummerow v. U.S. Food and Drug Administration*, No. 2:13-cv-02180 (C.D. Ill. filed 9 Aug. 2013). https://www.courtlistener.com/docket/4248631/kummerow-v-us-food-and-drug-administration/

9. “Nonagenarian Researcher Petitions FDA to Ban Trans Fats.” University of Illinois / MedicalXpress, 3 Sept. 2009. https://medicalxpress.com/news/2009-09-nonagenarian-petitions-fda-trans-fats.html

10. U.S. Food and Drug Administration. Final Determination Regarding Partially Hydrogenated Oils, 16 June 2015. Coverage and contemporaneous reporting: Hafner (2017), above; also FDA Federal Register notice of the 2015 determination.

11. Passwater, Richard A. Interview with Fred Kummerow. *WholeFoods Magazine*, Sept.–Oct. 2014. https://www.wholefoodsmagazine.com/articles/8604-from-pellagra-to-trans-fats-and-beyond-how-a-legendary-nutritional-scientist-is-still-saving-countless-thousands-from-premature-deaths

12. Cholesterol Won’t Kill You, but Trans Fat Could: Separating Scientific Fact from Nutritional Fiction  by Fred A. Kummerow (Author), Jean M. Kummerow (Author) Format: Paperback

13. Johnston, Patricia V., Fred A. Kummerow, and C. H. Walton. “Origin of the Trans Fatty Acids in Human Tissue.” *Proceedings of the Society for Experimental Biology and Medicine*, vol. 99, no. 3, Dec. 1958, pp. 735–736. https://doi.org/10.3181/00379727-99-24483 (or summary at https://eurekamag.com/research/014/133/014133385.php). Confirmed dietary origin; no *trans* in fetal tissues.

14. Heckers, H., F. W. Melcher, and K. Dittmar. “Occurrence of Individual Trans-Isomeric Fatty Acids in Human Myocardium, Jejunum and Aorta in Relation to Different Degrees of Atherosclerosis.” *Atherosclerosis*, vol. 28, no. 4, Dec. 1977, pp. 389–398. https://doi.org/10.1016/0021-9150(77)90065-X. Capillary GC found individual *trans* isomers in all samples; mean total *trans* <1% of fatty acids and unrelated to atherosclerosis grade.

15. Ohlrogge, J. B., E. A. Emken, and R. M. Gulley. “Human Tissue Lipids: Occurrence of Fatty Acid Isomers from Dietary Hydrogenated Oils.” *Journal of Lipid Research*, vol. 22, no. 6, Aug. 1981, pp. 955–960. https://www.jlr.org/article/S0022-2275(20)37333-8/fulltext (PubMed: https://pubmed.ncbi.nlm.nih.gov/7276754/). *Trans*-octadecenoate 0.4–5.0% (average 2.7%) in heart, brain, liver, aorta, and adipose; positional isomers matched dietary hydrogenated fat.

16. Thomas, L. H., J. A. Winter, and R. G. Scott. “Concentration of 18:1 and 16:1 Transunsaturated Fatty Acids in the Adipose Body Tissue of Decedents Dying of Ischaemic Heart Disease Compared with Controls: Analysis by Gas Liquid Chromatography.” *Journal of Epidemiology and Community Health*, vol. 37, no. 1, Mar. 1983, pp. 16–21. https://pmc.ncbi.nlm.nih.gov/articles/PMC1052248/. Higher “lower” (16:1 and 18:1) *trans* acids—more characteristic of commercial hydrogenation—in adipose of 136 IHD deaths versus controls who died of other causes.

17. Thomas, L. H., J. A. Winter, and R. G. Scott. “Concentration of Transunsaturated Fatty Acids in the Adipose Body Tissue of Decedents Dying of Ischaemic Heart Disease Compared with Controls.” *Journal of Epidemiology and Community Health*, vol. 37, no. 1, Mar. 1983, pp. 22–24. https://pmc.ncbi.nlm.nih.gov/articles/PMC1052249/. Companion paper; higher total *trans*/ruminant-fat ratio in IHD cases.

18. Stachowska, Ewa, et al. “Trans Unsaturated Fatty Acids Are Components of Atheromatous Plaque.” *Acta Angiologica*, vol. 8, no. 3, 2002, pp. 99–104. https://journals.viamedica.pl/acta_angiologica/article/view/9952. Elaidic acid and other *trans* isomers present in plaques from 21 surgical patients.

19. Stachowska, Ewa, et al. “Dietary Trans Fatty Acids and Composition of Human Atheromatous Plaques.” *European Journal of Nutrition*, vol. 43, no. 5, Oct. 2004, pp. 313–318. https://doi.org/10.1007/s00394-004-0479-x (PubMed: https://pubmed.ncbi.nlm.nih.gov/15309454/). All 31 plaques contained *trans* isomers (elaidic acid most abundant); linolelaidic acid (exclusively industrial) also present. Adipose *trans* pool correlated poorly with plaque *trans*.

20. Dlouhý, Pavel, et al. “Higher Content of 18:1 Trans-Fatty Acids in Subcutaneous Fat of Persons with Coronarographically Documented Atherosclerosis of the Coronary Arteries.” *Annals of Nutrition and Metabolism*, vol. 47, no. 6, 2003, pp. 302–305. Cited in later reviews as supporting higher industrial *trans* in people with documented coronary atherosclerosis.

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Part 1 — Three most-cited human cohort studies:

These are observational. They cannot prove “X grams of trans fat caused this person’s death” the way a randomized trial would. They show that people who ate more industrial trans fat later had more heart attacks and CHD deaths, after researchers tried to account for smoking, age, other fats, and calories. Combined with feeding trials that raise LDL and lower HDL, they formed the case that industrial trans fats increase CHD mortality.

1. Willett, Walter C., et al. “Intake of Trans Fatty Acids and Risk of Coronary Heart Disease among Women.” *The Lancet*, vol. 341, no. 8845, 6 Mar. 1993, pp. 581–585.**
https://www.thelancet.com/journals/lancet/article/PII0140-6736(93)90350-P/fulltext
DOI: 10.1016/0140-6736(93)90350-P

Followed 85,095 U.S. nurses who had no diagnosed heart disease in 1980. Diet was measured with a food-frequency questionnaire. Over 8 years they counted 431 new cases of CHD (non-fatal heart attack or death from CHD).

Women in the highest fifth of trans-fat intake had about 50% higher risk of CHD than women in the lowest fifth (RR 1.50). Margarine, cookies, cake, and white bread—the main sources of partially hydrogenated oil—were each linked to higher risk.

Trans fats raise LDL (“bad”) cholesterol, lower HDL (“good”) cholesterol, promote inflammation, and impair the vessel lining. Over years that combination speeds plaque growth and makes clots more likely. A first heart attack or sudden coronary death is the clinical result. The study mixed fatal and non-fatal events; later updates of the same cohort and meta-analyses that isolated CHD death kept the same direction of risk.

2. Pietinen, Pirjo, et al. “Intake of Fatty Acids and Risk of Coronary Heart Disease in a Cohort of Finnish Men. The Alpha-Tocopherol, Beta-Carotene Cancer Prevention Study.” *American Journal of Epidemiology*, vol. 145, no. 10, 15 May 1997, pp. 876–887.**
https://doi.org/10.1093/oxfordjournals.aje.a009047
PubMed: https://pubmed.ncbi.nlm.nih.gov/9149659/

Followed 21,930 Finnish male smokers, age 50–69, free of CVD at the start. Diet was measured at baseline. After 6.1 years they counted 635 deaths from coronary disease.

Men in the top fifth of trans-fat intake (median 6.2 g/day) had a 39% higher risk of dying of coronary disease than men in the bottom fifth (median 1.3 g/day): multivariate RR 1.39, *p*-trend = 0.004.

This paper isolates death, not just heart attacks. The same lipid and inflammatory mechanisms apply. Finnish men in the 1980s still ate appreciable industrial trans fat from margarines and baked goods. The dose–response (higher intake, higher death rate) is the pattern expected if the fats themselves contribute to fatal plaque rupture or thrombosis.

3. Oomen, Claudia M., et al. “Association between Trans Fatty Acid Intake and 10-Year Risk of Coronary Heart Disease in the Zutphen Elderly Study: A Prospective Population-Based Study.” *The Lancet*, vol. 357, no. 9258, 10 Mar. 2001, pp. 746–751.**
https://www.thelancet.com/journals/lancet/article/PIIS0140-6736(00)04166-0/fulltext
DOI: 10.1016/S0140-6736(00)04166-0

Followed 667 Dutch men aged 64–84 who were free of CHD in 1985. Diet was assessed repeatedly. After 10 years there were 98 fatal or non-fatal CHD events. Average trans-fat intake in the population fell from 4.3% to 1.9% of energy as manufacturers lowered trans content of fats.

A 2-percentage-point higher share of energy from trans fat at baseline was associated with 28% higher 10-year CHD risk (RR 1.28). The authors estimated that the observed drop in intake could have cut coronary deaths substantially.

Elderly men already have more plaque; extra trans fat can tip unstable plaques toward rupture or clotting. The study also captured a natural experiment: when the food supply’s trans content fell, the risk association still tracked the remaining intake. That is consistent with a causal contribution to fatal and non-fatal events.

Part 2 — Six widely cited animal feeding studies

Animal work tests whether feeding trans fat actually produces arterial lesions, not just worse blood lipids. Results are mixed in older large-animal studies (some showed little extra plaque beyond cholesterol feeding). The clearer modern mouse studies and several swine/rabbit papers are the ones most often cited as showing atherogenic effects.

1. Bassett, C. M. C., et al. “Trans-Fatty Acids in the Diet Stimulate Atherosclerosis.” *Metabolism*, vol. 58, no. 12, Dec. 2009, pp. 1802–1808.**
https://www.metabolismjournal.com/article/S0026-0495(09)00254-6/abstract
DOI: 10.1016/j.metabol.2009.06.010

LDL-receptor-deficient mice were fed diets with or without industrial trans fat, with or without extra cholesterol, for 14 weeks. Trans fat alone (no added cholesterol) produced significantly more aortic atherosclerotic lesions than the matching low-trans or high-fat control diets. Adding cholesterol made lesions worse still, but trans fat did not add much extra damage on top of a high-cholesterol diet.

In a mouse that already handles cholesterol poorly, industrial trans fat is enough by itself to grow plaques. That supports the idea that the fats are not merely “innocent bystanders” that happen to travel with other bad diet habits.

2. Chen, C. L., et al. “A Mechanism by Which Dietary Trans Fats Cause Atherosclerosis.” *Journal of Nutritional Biochemistry*, vol. 22, no. 7, July 2011, pp. 649–655.**
https://pmc.ncbi.nlm.nih.gov/articles/PMC3125015/
DOI: 10.1016/j.jnutbio.2010.05.004

Ordinary C57BL/6 mice (not genetically engineered for extreme hyperlipidemia) ate a Western-style diet high in partially hydrogenated vegetable oil (~30% of the fat as trans) for 24 weeks. They developed early atherosclerotic lesions in the aorta and heart valves. The same animals showed suppressed TGF-β signaling in the aortic lining (fewer TGF-β receptors, less phosphorylated Smad2) and more cholesterol packed into cell membranes.

Trans fat can start plaque even in “normal” mice. One proposed pathway: the fats change membrane cholesterol packing, which dampens a protective growth-factor signal that normally keeps the vessel lining healthy.

3. Machado, Roberta M., et al. “Omega-6 Polyunsaturated Fatty Acids Prevent Atherosclerosis Development in LDLr-KO Mice, in Spite of Displaying a Pro-inflammatory Profile Similar to Trans Fatty Acids.” *Atherosclerosis*, vol. 224, no. 1, Sept. 2012, pp. 66–74.**
https://doi.org/10.1016/j.atherosclerosis.2012.06.059
(Related PDF commonly cited from the same group’s work.)

LDL-receptor knockout mice ate high-fat diets (40% of energy from fat) based on trans fat, saturated fat, or omega-6 PUFA for 16 weeks. The trans-fat and saturated-fat groups developed larger aortic-root lesions, more macrophage infiltration, and more unstable-looking plaques (thin cap, necrotic core) than the PUFA group, even though inflammatory blood markers were not always lower on PUFA.

When calories and total fat are matched, swapping industrial trans fat for omega-6 oil reduces plaque size in a standard genetic mouse model of human-like atherosclerosis.

4. Toda, Takayoshi, et al. “Composition of Swine Arterial Tissue.” *Acta Pathologica Japonica*, vol. 34, no. 5, Sept. 1984, pp. 1031–1040.**
https://doi.org/10.1111/j.1440-1827.1984.tb07625.x

Two-month-old swine were fed a basal diet or the same diet plus 8.3% margarine or butter for 4 months. Both the margarine (high industrial trans) and butter groups developed significantly more intimal thickening in the coronary arteries than the basal-diet group. Arterial fatty-acid composition shifted and omega-6 metabolites fell.

In an animal whose coronary arteries resemble humans more than a mouse’s do, adding hydrogenated fat or butter to an otherwise ordinary diet thickened the inner lining of the coronaries—the first structural step toward obstructive plaque. (A companion 1985 paper by the same Kummerow group comparing hydrogenated soybean oil, lard, and safflower oil found more mixed lesion severity; the 1984 paper is the clearer “added fat vs basal” contrast.)

5. Roy, A., et al. “Butters Rich either in Trans-10-C18:1 or in Trans-11-C18:1 plus Cis-9, Trans-11 CLA Differentially Affect Plasma Lipids and Aortic Fatty Streak in Experimental Atherosclerosis in Rabbits.” *Animal*, vol. 1, no. 3, Mar. 2007, pp. 467–476.**
https://doi.org/10.1017/S175173110770530X
PubMed: https://pubmed.ncbi.nlm.nih.gov/22444345/

Rabbits received 12% butter plus a little cholesterol for 6 or 12 weeks. One butter was enriched in industrial-style *trans*-10-18:1; another was enriched in the natural ruminant pair *trans*-11-18:1 + CLA. The *trans*-10 butter raised the non-HDL/HDL ratio and produced more aortic lipid deposition than the *trans*-11 + CLA butter.

Not all 18-carbon *trans* isomers behave the same. The industrial-type *trans*-10 isomer worsened lipids and early aortic streaks in a classic rabbit atherosclerosis model; the main natural ruminant isomer did not.

6. Bassett’s finding is reinforced by later mechanism papers; a sixth highly referenced feeding study is:
**Chen, C. L., et al.** (already listed as #2) is often paired with
**Machado et al.** (#3). For a sixth distinct citation that is frequently referenced in reviews of trans-fat atherogenicity:

Kritchevsky, David, et al. “Effect of Trans-Unsaturated Fats on Experimental Atherosclerosis in Vervet Monkeys.” *Atherosclerosis*, vol. 51, no. 1, Apr. 1984, pp. 123–133.**
https://doi.org/10.1016/0021-9150(84)90148-5
PubMed: https://pubmed.ncbi.nlm.nih.gov/6426484/

Honest summary (this one did *not* show extra plaque). Vervet monkeys ate semi-purified diets with 3.2% or 6% trans fat for up to a year. Serum and liver trans-fat levels rose and fell with the diet, and hepatic cholesterol synthesis changed, but aortic atherosclerosis and arteriosclerosis scores were *not* significantly higher than in controls.

It is one of the most-cited primate feeding papers. It shows that simply putting trans fat into a monkey does not automatically produce more Sudan-stained aortic surface.

Later mouse work (Bassett, Chen, Machado) used more sensitive genetic models and lesion quantification and did find extra plaque.

The contrast is useful: trans fats reliably worsen human-type lipoproteins; whether they add extra anatomic plaque beyond cholesterol load depends on species, dose, duration, and how lesions are measured.

Bottom line.  In people, higher industrial trans-fat intake tracked with more CHD events and CHD deaths in the three largest early prospective cohorts. In animals, industrial trans fat can grow aortic and coronary lesions on its own in genetically susceptible mice and can thicken swine coronary intima; older monkey and some rabbit work was less dramatic. The shared “how” is worse LDL/HDL balance, inflammation, impaired endothelial signaling (prostacyclin, TGF-β), and incorporation of *trans* isomers into membranes and plaques. That package makes fatal coronary thrombosis and plaque rupture more likely.

————————- –

Industrial trans fats promote atherosclerosis through well-documented systemic and cellular mechanisms that do not require large quantities of the fats themselves to be stored inside plaques. The 2025 Salk/Cell Metabolism mouse study, human OCT imaging data, population policy studies, and earlier plaque-composition work all support the core claims. A few phrasings (“consistently,” “independent of how much…stored”) are interpretive but rest on real findings.

Lipid-profile effects (raise LDL-C and triglycerides, lower HDL-C)

Multiple controlled trials and meta-analyses show industrial trans fats raise LDL-C and triglycerides while lowering HDL-C.

Mensink, Ronald P., and Martijn B. Katan. “Effect of Dietary Trans Fatty Acids on High-Density and Low-Density Lipoprotein Cholesterol Levels in Healthy Subjects.” *New England Journal of Medicine*, vol. 323, no. 7, 1990, pp. 439–445. https://www.nejm.org/doi/full/10.1056/NEJM199008163230703

Mozaffarian, Dariush, et al. “Trans Fatty Acids and Cardiovascular Disease.” *New England Journal of Medicine*, vol. 354, no. 15, 2006, pp. 1601–1613. https://www.nejm.org/doi/full/10.1056/NEJMra054035

Inflammation, oxidative stress, and endothelial dysfunction

Human feeding studies and animal models show rises in CRP, IL-6, TNF-α, adhesion molecules, and markers of endothelial dysfunction.

Mozaffarian, Dariush, et al. “Trans Fatty Acids and Cardiovascular Disease.” *New England Journal of Medicine*, vol. 354, no. 15, 2006, pp. 1601–1613. https://www.nejm.org/doi/full/10.1056/NEJMra054035

Oteng, Antwi-Boasiako, and Sander Kersten. “Mechanisms of Action of trans Fatty Acids.” *Advances in Nutrition*, vol. 11, no. 3, 2020, pp. 697–708. https://pmc.ncbi.nlm.nih.gov/articles/PMC7231579/

Membrane properties and eicosanoid metabolism

Trans isomers alter membrane fluidity and reduce availability of precursors for certain prostaglandins. The 2004 plaque-composition paper explicitly links elaidic and linolelaidic acids to eicosanoid pathways.

Stachowska, Ewa, et al. “Dietary Trans Fatty Acids and Composition of Human Atheromatous Plaques.” *European Journal of Nutrition*, vol. 43, no. 6, 2004, pp. 313–318. https://link.springer.com/article/10.1007/s00394-004-0479-x

Preferential incorporation into sphingolipids by SPT, increased hepatic VLDL secretion

The 2025 Salk Institute paper demonstrates that serine palmitoyltransferase prefers trans fats, producing sphingomyelin that is secreted in VLDL and drives atherogenesis even on diets without added cholesterol. Inhibiting SPT reduced lesions.

Gengatharan, Jivani M., et al. “Altered Sphingolipid Biosynthetic Flux and Lipoprotein Trafficking Contribute to Trans-Fat-Induced Atherosclerosis.” *Cell Metabolism*, vol. 37, no. 1, 2025, pp. 274–290.e9. https://www.cell.com/cell-metabolism/fulltext/S1550-4131(24)00412-1

Animal studies show greater aortic lesion area, more macrophages, and more vulnerable features versus cis controls

True for multiple Ldlr-/- and other models. The 2025 paper and earlier work (e.g., Bassett et al.) report larger lesions and more inflammatory cells with industrial trans-fat feeding.

Gengatharan, Jivani M., et al. “Altered Sphingolipid Biosynthetic Flux…” *Cell Metabolism*, 2025 (citation above).

Bassett, Chantal M. C., et al. “Trans-Fatty Acids in the Diet Stimulate Atherosclerosis.” *Metabolism*, vol. 58, no. 11, 2009, pp. 1632–1639. https://www.metabolismjournal.com/article/S0026-0495(09)00254-6/abstract

Human circulating/adipose trans fats (especially elaidic acid) linked to thin-cap fibroatheroma on OCT, lesion severity, and events

True. Serum elaidic acid independently associated with TCFA on OCT in patients already on guideline therapy.
Nagasawa, Yoshinori, et al. “The Impact of Serum Trans Fatty Acids Concentration on Plaque Vulnerability in Patients with Coronary Artery Disease: Assessment via Optical Coherence Tomography.” *Atherosclerosis*, vol. 265, 2017, pp. 312–317. https://www.atherosclerosis-journal.com/article/S0021-9150(17)31171-1/fulltext

Population-level restrictions (New York) followed by extra declines in MI and stroke

True. After ≥3 years, counties with restaurant trans-fat restrictions had an additional 6.2 % decline in combined MI + stroke admissions beyond background trends.

Brandt, Eric J., et al. “Hospital Admissions for Myocardial Infarction and Stroke Before and After the Trans-Fatty Acid Restrictions in New York.” *JAMA Cardiology*, vol. 2, no. 6, 2017, pp. 627–634. https://jamanetwork.com/journals/jamacardiology/fullarticle/2618359

Researchers who measured plaque composition concluded elaidic and linolelaidic acids “seem to be of relevance to plaque formation” via eicosanoid pathways

True. The exact wording is close to the 2004 paper: “The presence of trans isomers of fatty acids in the atheromatous plaque seems to be of relevance to plaque formation. Of much concern is the detection of elaidic and linolelaidic acids which adversely affect the physiologically important metabolism of eicosanoids.”

Stachowska, Ewa, et al. “Dietary Trans Fatty Acids…” *European Journal of Nutrition*, 2004 (citation above).

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