Topics » Nutrition Science » Why Saturated Fat Is Not the Villain and Plant Oils Are Not a Healthy Alternative
T. Colin Campbell Center for Nutrition Studies

The belief that saturated fat causes bad health outcomes is widespread and long held. This belief is especially prevalent regarding heart disease, and it has often been used to promote or defend vegan and vegetarian diets because saturated fat is found in greater proportions in animal-based foods. Unfortunately, it is a weak defense.

This view of saturated fat became prominent in the 1950s and 60s.[1][2][3][4][5] When researchers compared the health value of diets in the Mediterranean area with diets more commonly seen in the US, one of the most consistent findings was that diets higher in saturated fat were highly correlated with higher rates of heart disease and certain cancers. In contrast, polyunsaturated fats (PUFAs), found in higher proportions in plants, were inversely associated with those diseases. Consequently, PUFAs have been considered healthier than saturated fat.

So the narrative went: Down with the saturated fat-laden butter and lard, up with plant oils! I remember this phase in the marketplace very well. However, there was a practical problem with plant oils. People wanted fats that were solid at room temperature because they wanted to be able to spread it on their bread like butter. To solve that challenge, a chemical process was devised to bubble hydrogen through the unsaturated oil to make it solid at room temperature. Unfortunately, this process led to a mostly synthetic fat known as trans fat. You likely already know what happened next: Evidence emerged to show that this unnatural form of fat causes heart problems, and trans fats have been avoided by many health-conscious consumers since.[6][7]

Back to saturated fat, though, I believe that the high correlation between saturated fat-laden diets and heart disease is a classic case of correlation not necessarily equaling causation. It is, in my view, a misinterpretation of the research. Saturated fat as a cause of heart disease is not biologically plausible, and this relationship should have been questioned decades ago.

For one thing, saturated fat is relatively inert. I’ve written about this elsewhere: “If anything, unsaturated fat is far more likely to be the culprit in disease formation. Unsaturated fat is more biologically active, contributes to the formation of highly reactive oxygen species that promote diseases like cancer and heart disease, and promotes cancer more than saturated fat in experimental animal studies.”[8] That’s right—plant oils experimentally promote cancer much more than saturated fats do.[9] [10]This experimental observation is several decades old.

saturated fat

Does that mean we should consume saturated fats without concern? Not so fast. Excess saturated fat in the diet remains an excellent indicator of an unhealthy dietary pattern. Regardless of whether saturated fat is itself the cause of disease, the presence of foods high in saturated fat (mostly animal-based foods) remains a major concern.

Dietary saturated fat (and its companions, dietary cholesterol and total fat) is highly correlated with animal protein-based diets. And unlike saturated fat, animal protein is not biologically inert. For example, animal protein increases free radical oxidation, alters hormone activities, and creates metabolic acidosis.[11][12][13][14] For over a century, compelling evidence has shown that animal-based protein raises blood cholesterol and causes heart disease more than dietary cholesterol does.[15][16][17][18][19][20] (Later evidence in animal and human studies showed that this protein effect refers only to animal-based protein, not plant-based protein.[21][22][23]) But seriously, who would dare to question protein, the bastion of not only animal-based foods but also the Western diet?

I have been concerned with this topic since the 1970s. I can distill my experiences throughout that time and this article into three observations:

  1. The focus on saturated fat detracts from the health problems caused by animal-based foods, which primarily owe their unhealthy properties to their protein content. Animal-based protein not only stimulates mechanisms that lead to diseases like cancer and heart disease but also depresses mechanisms designed to protect us from those diseases.[24][25][26][27][28][29][30][31] Moreover, the increased consumption of animal-based foods results in the decreased consumption of whole plant-based foods proven to protect us from heart disease and cancer.
  2. Recommendations focused on saturated fat are much easier to discredit. They also provoke unnecessary confusion. For instance, individuals favoring an omnivorous diet would point out that despite decades of removing saturated fat from foods—as in skimmed milk and other low-fat products—we have achieved little or no health improvements. In a cohort of nearly 90,000 women in the Harvard Nurses’ Health Study, moderate reductions in fat did not result in substantial disease reduction.[32] A decrease in fat might even result in a slight increase in disease risk, perhaps as a result of a higher concentration of animal protein in the diet.
  3. The false saturated fat premise leads many to choose plant oils as a healthier alternative. But as I have already alluded to, plant oils and related synthetic products are not truly healthy alternatives. They are nutrient-deficient but calorically replete food fragments. Their excessive contribution to total calorie intake effectively displaces the consumption of whole plant-based foods. (Whole plants with fat, such as nuts, seeds, and avocados, provide far more nutrition than their corresponding oils; learn more about the nutritional value of oils versus whole foods.)

As the common misunderstanding about saturated fat (and cholesterol) became almost like a biblical verse, I predicted it might someday return to haunt us. And so it has.


  1. Keys A. The diet and the development of coronary heart disease. J Chronic Dis 4, 364–380 (1956).
  2. Keys A. Diet and the epidemiology of coronary heart disease. J. Am. Med. Assoc. 164, 1912–1919 (1957).
  3. Keys A., in Atherosclerosis and its origin (eds. M. Sandler & G. H. Bourne), 263–299 (Academic Press, 1963).
  4. Keys A. Coronary heart disease in seven countries. Circulation Suppl. 41, I1–I211 (1970).
  5. Keys A. Coronary heart disease—the global picture. Atherosclerosis 22, 149–192 (1975).
  6. Remig V, Franklin B, Margolis S, Kostas G, Nece T, Street JC. Trans fats in America: a review of their use, consumption, health implications, and regulation. J Am Diet Assoc. 2010;110(4):585-592. doi:10.1016/j.jada.2009.12.024
  7. Mozaffarian D, Katan MB, Ascherio A, Stampfer MJ, Willett WC. Trans fatty acids and cardiovascular disease. N Engl J Med. 2006;354(15):1601-1613. doi:10.1056/NEJMra054035
  8. Campbell TC. The Future of Nutrition (with Nelson Disla). BenBella Books, Inc., Dallas TX, 2020.
  9. Carroll KK & Khor HT. Effects of dietary fat and dose level of 7,12 dimethylbenz(a)anthracene on mammary tumor incidence in rats. Cancer Res. 30, 2260–2264 (1970).
  10. Hopkins GJ & Carroll KK. Relationship between amount and type of dietary fat in promotion of mammary carcinogenesis induced by 7, 12-dimethylbenzanthracene. J Natl Cancer Inst 62, 1009–1012 (1979).
  11. Youngman LD, Park JY, Ames BN. Protein oxidation associated with aging is reduced by dietary restriction of protein or calories. Proc. National Acad. Sci 89, 9112–9116 (1992).
  12. De AK, Chipalkatti S, Aiyar AS. Some biochemical parameters of ageing in relation to dietary protein. Mech Ageing Dev 21, 37–48 (1983).
  13. Sanz A, Caro P, Barja G. Protein restriction without strong caloric restriction decreases mitochondrial oxygen radical production and oxidative DNA damage in rat liver. J. Bioenergetics Biomembranes 36, 545–552 (2004).
  14. Huang HH, Hawrylewicz EJ, Kissane JQ, Drab EA. Effect of protein diet on release of prolactin and ovarian steroids in female rats. Nutrition Reports International 26, 807–820 (1982).
  15. Newburgh LH & Clarkson S. The production of arteriosclerosis in rabbits by feeding diets rich in meat. Arch. Intern. Med. 31, 653–676 (1923).
  16. Newburgh LH. The production of Bright’s disease by feeding high protein diets. Arch. Intern. Med. 24, 359–377 (1919).
  17. Newburgh LH & Clarkson S. Production of atherosclerosis in rabbits by diet rich in animal protein. JAMA 79, 1106–1108 (1922).
  18. Clarkson S & Newburgh LH. The relation between atherosclerosis and ingested cholesterol in the rabbit. J. Exp. Med. 43, 595–612 (1926).
  19. Campbell TC. Animal protein and ischemic heart disease. Am. J. Clin. Nutr. 71, 849–850 (2000).
  20. Campbell TC. A plant based diet and animal protein: questioning dietary fat and considering animal protein as the main cause of heart disease. J. Geriatric Cardiol. 14, 331–337 (2017).
  21. Meeker DR & Kesten HD. Experimental atherosclerosis and high protein diets. Proc. Soc. Exp. Biol. Med. 45, 543–545 (1940)..
  22. Meeker DR & Kesten HD. Effect of high protein diets on experimental atherosclerosis of rabbits. Arch. Pathology 31, 147–162 (1941).
  23. Kritchevsky D, Tepper SA, Williams DE, Story JA. Experimental atherosclerosis in rabbits fed cholesterol-free diets. Part 7. Interaction of animal or vegetable protein with fiber. Atherosclerosis 26, 397–403 (1977).
  24. Gurtoo HL & Campbell TC. A kinetic approach to a study of the induction of rat liver microsomal hydroxylase after pretreatment with 3,4-benzpyrene and aflatoxin B1. Biochem. Pharmacol. 19, 1729–1735 (1970).
  25. Nerurkar LS, Hayes JR, Campbell TC. The reconstitution of hepatic microsomal mixed function oxidase activity with fractions derived from weanling rats fed different levels of protein. Journal of Nutrition 108, 678–686 (1978).
  26. Preston RS, Hayes JR, Campbell TC. The effect of protein deficiency on the in vivo binding of aflatoxin B1 to rat liver macromolecules. Life Sci. 19, 1191–1198 (1976).
  27. Prince LO & Campbell TC. Effects of sex difference and dietary protein level on the binding of aflatoxin B1 to rat liver chromatin proteins in vivo. Cancer Res. 42, 5053–5059 (1982).
  28. Krieger E. Increased voluntary exercise by Fisher 344 rats fed low protein diets (undergraduate thesis, Cornell University, 1988).
  29. Krieger E, Youngman LD, Campbell TC. The modulation of aflatoxin (AFB1) induced preneoplastic lesions by dietary protein and voluntary exercise in Fischer 344 rats. FASEB J. 2, 3304 Abs. (1988).
  30. Horio F, Youngman LD, Bell RC, Campbell TC. Thermogenesis, low-protein diets, and decreased development of AFB1-induced preneoplastic foci in rat liver. Nutrition and Cancer 16, 31–41 (1991).
  31. Youngman LD, Park JY, Ames BN. Protein oxidation associated with aging is reduced by dietary restriction of protein or calories. Proc. National Acad. Sci 89, 9112–9116 (1992).
  32. Willett WC, Stampfer MJ, Colditz GA, Rosner BA, Hennekens CH, Speizer FE. Dietary fat and the risk of breast cancer. N Engl J Med. 1987;316(1):22-28. doi:10.1056/NEJM198701013160105

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