Few driving factors have had such a profound influence on the transition from traditional to modern industrial diets as the campaign against animal fats and tropical oils. We have responded to this campaign not only by depriving ourselves of the nutrient-dense animal foods so important to human health, but also by replacing these traditional fats with processed foods laden with refined vegetable oil, flour, and sugar.
Since its inception, this campaign has been based on a series of myths. These include the myths that saturated fat is the “bad fat” while polyunsaturated fat is the “good fat,” that arachidonic acid is the “bad fat,” and that so-called “solid fats” are empty calories with no nutritional value. We will consider each of these myths in the pages that follow.
MYTH 1: SATURATED FAT IS BAD, POLYUNSATURATED FAT IS GOOD
The myth that saturated fatty acids are “bad fat” while polyunsaturated fatty acids (PUFA) are “good fat” emerged in the 1950s as the diet-heart hypothesis. This hypothesis stated that the saturated fat found in animal fats and tropical oils would contribute to heart disease by raising blood cholesterol levels while the PUFA found in vegetable oils would do just the opposite.
If the nutritional and medical establishments had taken the approach of Weston Price and endeavored to begin unraveling the causes of heart disease by studying the diets and lifestyles of populations that were immune to the disease, it is unlikely the diet-heart hypothesis would ever have emerged. The traditional diets of Pacific islanders free of heart disease, for example, vary widely in their proportions of fat and carbohydrate, but as can be seen in Figure 1, they are all rich in saturated fat and low in PUFA when compared to the standard American diet.1,2,3 Each of these traditional diets is based primarily on starches, fruits, coconut and fish, so the PUFA comes mostly from fish rather than from vegetable oils.
The foundation of the establishment’s approach to the riddle of heart disease featured no such investigation of traditional diets, and the result of this negligence was the diet-heart hypothesis. Advocates of this hypothesis supported it in the early 1950s with two key pieces of evidence. The first was that blood cholesterol levels were statistically associated with heart disease risk.4 The second was that, in highly controlled laboratory experiments, replacing saturated fats like butter, lard or coconut oil with polyunsaturated oils like corn or safflower oil would lower blood cholesterol levels.5,6 Playing a game of connect the dots, they argued that substituting vegetable oils for traditional animal fats and tropical oils would lower the risk of heart disease.
In 1957, the American Heart Association called the hypothesis “highly speculative,” and concluded that “the evidence at present does not convey any specific implications for drastic dietary changes, specifically in the quantity or type of fat in the diet of the general population, on the premise that such changes will definitely lessen the incidence of coronary or cerebral artery disease.”7 Four years later, the state of the evidence remained the same but three members of the committee were dropped and replaced by four new members, including Ancel Keys, a leading proponent of the hypothesis. The updated report recommended that men who are overweight, have high blood pressure or high cholesterol, lead “sedentary lives of relentless frustration,” or have a strong family history of heart disease should replace part of the saturated fat in their diets with PUFA.8
The hypothesis nevertheless remained controversial in the scientific community for decades. The tide turned in 1984 when the Coronary Primary Prevention Trial showed that cholestyramine could prevent heart attacks.9 Cholestyramine is a drug that binds bile acids in the intestine and causes their excretion in the feces. As a result, the liver takes cholesterol in from the blood in order to make more bile acids and the concentration of cholesterol in the blood falls. Time magazine hailed the trial as a vindication of the American Heart Association’s twenty-three-year-old stance against animal fats. Butter, eggs, and bacon were all conspicuously absent from the treatment protocol of this trial, but Time nevertheless ran a cover story entitled “Hold the Eggs and Butter,” which artfully featured a frowning face with eyes of sunnyside up eggs and a downturned mouth of a slice of fried bacon. The article declared, “cholesterol is proved deadly, and our diet may never be the same.”10
In our own day, the American Heart Association continues to promote the hypothesis with vigor. In 2009, it updated its official stance, recommending at least 5 to 10 percent of calories as omega-6 PUFA with additional PUFA coming from omega-3 sources, and concluded that intakes even higher than this “appear to be safe and may be even more beneficial (as part of a low-saturated fat, low-cholesterol diet).”11 It was one thing to promote this hypothesis in 1961 when it had never been tested, but to throw a PUFA party in 2009 and suggest we all wash away our cardiovascular concerns with swigs of soybean oil is to ignore with callow abandon all the lessons we have learned from clinical trials published in the intervening decades.
Six randomized, controlled trials specifically testing the effect of the substitution of polyunsaturated vegetable oils for animal fats on heart disease have been published.12-17 These trials were all published between 1965 and 1989. Two of them found that vegetable oils increased the risk of heart disease,12, 14 although one of these creatively concluded from this that “men who have had myocardial infarction are not a good choice for testing the lipid hypothesis.”14 Two of them reported no effect of vegetable oil.13, 15 The authors of one of these two trials, however, only reported the results half-way through the study.15 In the final report, they pooled the two groups together and compared them to a new control group that had not received any dietary advice at all.18 As a result, we have no way of knowing the true effect of vegetable oil in that study. Two of the six trials were double-blind, and deserve special attention.16, 17 These are the Minnesota Coronary Survey and the Los Angeles Veterans Administration Hospital Study.
The Minnesota Coronary Survey tested the effect of substituting vegetable oils for animal fats in hospital patients who were on the diets for an average duration of only one year.16 As shown in Figure 2, vegetable oil had no effect on cardiovascular disease. While its effect on total mortality was not statistically significant, however, total survival was nevertheless better in the group eating saturated fat. We naturally must wonder what would have happened to total mortality had the subjects been on the diets for longer than one year.
The Los Angeles Veterans Administration Hospital Study lasted over eight years, and most of the subjects were enrolled for at least six years.17 It is the only one of these six studies where the mean age of the subjects was greater than sixty, so it allows us to better see the effect of vegetable oils on the risk of cancer, if such an effect exists.
Subjects eating the diet rich in vegetable oils had a lower risk of cardiovascular mortality, but a higher risk of mortality from other causes. As a result, diet had no effect on total mortality. This is clearly shown in Figure 3. As shown in Figure 4, deaths from cancer began to increase in the vegetable oil group after two years, and the increase became much larger after five years.19 As shown in Figure 5, the difference in the incidence of all deaths from non-cardiovascular causes began to increase in the vegetable oil group only after four years and remained extremely small until seven years.17 After seven years, non-cardiovascular mortality began to increase rapidly. The disturbing possibility that the true harms of vegetable oils take years to emerge did not escape the authors, and they concluded that “future clinical trials of diets rich in unsaturated fat must be planned for periods well in excess of eight years, rather than for the five-year periods that have been the usual goal.” Such longer trials have never been conducted.
Although a superficial analysis of this study would suggest that vegetable oils decrease the risk of heart disease while increasing the risk of cancer and other diseases, this may not be the case. Even though the investigators randomly allocated the subjects to each group, the randomization failed to equally balance rates of smoking between the two groups. There were twice as many heavy smokers and 60 percent more moderate smokers in the group consuming traditional animal fats, while there were more light smokers and non-smokers in the group consuming vegetable oils.17 The diet rich in animal fats, moreover, was deficient in vitamin E. Animal experiments suggest that we should obtain 0.6 milligrams of vitamin E for every gram of PUFA we consume. The vegetable oil diet came close to this requirement, supplying a ratio of over 0.5, but the animal fat diet fell miserably short of it, supplying a ratio of less than 0.2.20
Animal fats are not intrinsically deficient in vitamin E, however. The average store-bought butter, for example, easily meets the vitamin E requirement, and a high-quality pastured butter can provide more than double this requirement. 21,22 It is thus unclear why the animal fat diet was so deficient in the vitamin, but this deficiency in combination with the higher rate of smoking may have contributed to the greater risk of cardiovascular disease in the animal fat group.
It appears from these studies, then, that vegetable oils promote cancer while animal fats protect against it even in the presence of smoking and vitamin E deficiency. Vegetable oils may promote heart disease as occurred in two studies,12, 14 but the results of the LA Veterans Administration Hospital Study make this unclear. The authors of this study themselves concluded as follows: “. . . we consider our own trial, with or without the support of other published data, to have fallen short of providing a definitive and final answer concerning dietary prevention of heart disease.”
The solid line represents the survival in
the group fed vegetable oils while the dotted
line represents the survival in the group fed
traditional animal fats. There is no difference
in total mortality between the two groups.
As shown in Figures 4 and 5, however, non-cardiovascular
deaths began to increase in the
vegetable oil group rapidly only towards the
end of the study, raising the question of what
would have happened to total mortality had
the study lasted longer.
These studies leave many questions to be answered. Are the effects of vegetable oils with different proportions of omega-6 and omega-3 fatty acids different from one another? What is the effect of vegetable oils over a lifetime, beginning in youth? Are there certain dietary contexts that make vegetable oils harmful, and others that make them safe? The larger question, however, is whether, given all this uncertainty, we should make ourselves guinea pigs for these newfangled foods. No one has yet offered a better summary of the issue than that offered by the late endocrinologist Broda Barnes in his 1976 book, Solved: The Riddle of Heart Attacks:
Everyone should have the privilege of playing Russian Roulette if it is desired, but it is only fair to have the warning that with the use of polyunsaturated fats the gun probably contains live ammunition.23
MYTH 2: ARACHIDONIC ACID IS A “BAD FAT”
The second myth is that animal fats promote inflammation because they contain a small amount of the omega-6 PUFA arachidonic acid, found primarily in liver and egg yolks with smaller amounts in butter and meat fats. This hypothesis emerged in the scientific literature in the 1980s and 1990s as researchers began attributing the low rate of heart disease among traditional Inuit to their consumption of large amounts of omega-3 fatty acids from marine oils.24 Researchers argued that these omega-3 fatty acids were protective precisely because they counteracted the inflammatory effects of arachidonic acid. Barry Sears popularized this idea in his best-selling 1995 book The Zone Diet.25 Therein, he proclaimed excess arachidonic acid “your worst biological nightmare.” Not only is it inflammatory, he wrote, but it “is so potent and so dangerous that when you inject it into the bloodstream of rabbits the animals die within three minutes.”
Despite these sensational claims, arachidonic acid is not inherently inflammatory. Its deficiency, in fact, produces a number of inflammatory symptoms, including dandruff, hair loss, infertility and irritated, red, sore, swollen, and scaly skin.26,27 Inhibiting supposedly “inflammatory” products made from arachidonic acid such as prostaglandin E2 using over-the-counter nonsteroidal anti-inflammatory drugs (NSAIDs) can produce a number of inflammatory outcomes. These drugs induce intestinal pathologies that closely resemble celiac disease in laboratory animals in response to gluten or even egg white,28,29 and they interfere with the resolution of autoimmune conditions.30
Although it is true that our bodies use arachidonic acid to initiate inflammation—a vital process if we want to survive to adulthood without being wiped out by pathogenic microbes —our bodies also use this fatty acid to suppress inflammation or to resolve inflammation once it has run its course. We use arachidonic acid to make cell-to-cell junctions that form physical barriers against toxins and pathogens,31-33 to create a unique environment in the gut that causes our immune system to react to food proteins with tolerance instead of intolerance,34 and to make important molecules called lipoxins that help resolve existing inflammation.30,35 We even use arachidonic acid to signal the conversion of omega-3 fatty acids to resolvins, another class of molecules that help resolve inflammation.30 It makes little sense to characterize this fatty acid as singularly inflammatory in nature when it has so many anti-inflammatory functions, and when it is present in so many traditional foods consumed by populations free of inflammatory diseases.
MYTH 3: SOLID FATS = EMPTY CALORIES
The third myth, that “solid fats” are empty calories with no nutritional value, has emerged more recently with the latest revision of the USDA’s Dietary Guidelines for Americans. This document defines a “nutrient-dense” food as one whose “nutrients and other beneficial substances . . . have not been ‘diluted’ by the addition of calories from added solid fats, added sugars, or added refined starches, or by the solid fats naturally present in the food.”36 This peculiar definition of “nutrient-dense” allows the addition of liquid oils but requires the removal of natural solid fats. “Solid fats” are defined as “fats with a high content of saturated and/or trans fatty acids, which are usually solid at room temperature.” Using this definition, one could ostensibly make milk more “nutrient-dense” by replacing its natural butterfat with corn oil.
The natural fats present in foods carry all of their fat-soluble vitamins, and added fats further increase their bioavailability. Human trials, for example, have clearly shown that butterfat increases the absorption of vitamin E,37 and that canola oil increases the absorption of carotenoids from salad.38 The more fat one adds, according to these studies, the greater the absorption of fat-soluble nutrients. This can hardly be considered a decrease in nutrient density!
Animal experiments, moreover, suggest that fats and oils low in PUFA provide the best absorption of fat-soluble nutrients. When compared to corn oil, for example, olive oil roughly doubles the absorption of lycopene and astaxanthin in rats.39 If the lower absorption seen with corn oil is a result of its higher PUFA content, then so-called “solid fats” might prove superior even to olive oil, and certainly to canola oil.
THE TRUTH SHALL SET US FREE
Clinical trials have failed miserably to support the hypothesis that replacing saturated animal fats with polyunsaturated vegetable oils would prevent heart disease. They have shown instead that vegetable oils likely promote cancer and perhaps even heart disease. Arachidonic acid in animal fat is not “deadly,” but is necessary for our bodies to initiate, suppress, or resolve inflammation as needed. These are all vital processes that allow us to respond appropriately to our environment. “Solid fats” do not “dilute” the nutrient density of our food. On the contrary, they carry fat-soluble nutrients and provide for their absorption.
When we observe the ease with which these myths arise and the vigor with which they are promulgated to the public, it is important for us not to create our own equal and opposite myths. We should keep in mind that traditional diets varied widely in their fat and carbohydrate contents. Nutritional needs vary from person to person, and from one stage of life to another. Any health-promoting component of the diet, including animal fat, can become harmful if it displaces other health-promoting components. It is thus entirely plausible that some people under some circumstances may benefit by reducing their intakes of animal fat and increasing their intakes of other traditional foods. We should thus beware of promoting any “correct” amount of animal fat to consume. We should instead look upon the earth’s menu of natural, traditional foods without fear, and choose those foods we need and enjoy in freedom.
1. Lindeberg S, et al. Age relations of cardiovascular risk factors in a traditional Melanesian society: the Kitava study. Am J Clin Nutr. 1997;66(4):845-52.
2. Prior IA, et al. Cholesterol, coconuts, and diet on Polynesian atolls: a natural experiment: the Pukapuka and Tokelau island studies. Am J Clin Nutr. 1981;34(8):1552-61.
3. USDA Agricultural Research Service.What We Eat in America, NHANES 2007-2008. Table 5. Energy Intakes: Percentages of Energy from Protein, Carbohydrate, Fat, and Alcohol, by Gender and Age, in the United States, 2007- 2008 http://www.ars.usda.gov/SP2UserFiles/Place/12355000/pdf/0708/Table_5_EIN_GEN_07.pdf Accessed December 29, 2011.
4. Keys A. Atherosclerosis: a problem in newer public health. J Mt Sinai Hosp NY. 1953;20(2):118-39.
5. Kinsell LW, et al. Dietary modification of serum cholesterol and phospholipid levels. J Clin Endocrinol. Metab. 1952;12(7):909-13.
6. Ahrens EH Jr., et al..Effect on human serum lipids of substituting plant for animal fat in diet. Proc Soc Exp Biol Med. 1954;86(4):872-8.
7. Page IH, et al. Atherosclerosis and the Fat Content of the Diet. Circulation. 1957;16:163-178.
8. Dietary fat and its relation to heart attacks and strokes: report by the Central Committee for Medical and Community Program of the AHA. 1961;23:133-6.
9. The Lipid Research Clinics Coronary Primary Prevention Trial results. II. The relationship of coronary heart disease to cholesterol lowering. JAMA. 1984;251(3):365-74.
10. Wallis C, Crook C, Delaney P, Gribben S. Hold the Eggs and Butter. Time magazine. March 26, 1984.
11. Harris WS, et al. Omega-6 fatty acids and risk for cardiovascular disease: a science advisory from the AHA Nutrition Subcommittee of the Council on Nutrition, Physical Activity, and Metabolism; Council on Cardiovascular Nursing; and Council on Epidemiology and Prevention. Circulation. 2009;119(6):902- 7.
12. Rose GA, et al. Corn oil in treatment of ischaemic heart disease. Br Med J. Jun 12 1965;1(5449):1531- 1533.
13. Controlled trial of soya-bean oil in myocardial infarction. Lancet. Sep 28 1968;2(7570):693-699.
14. Woodhill JM, et al. Low fat, low cholesterol diet in secondary prevention of CHD. Adv Exp Med Biol. 1978;109:317-330.
15. Bierenbaum ML, et al. Modified-fat dietary management of the young male with CD. A five-year report. JAMA. Dec 25 1967;202(13):1119-1123.
16. Frantz ID, Jr., et al. Test of effect of lipid lowering by diet on cardiovascular risk. Minnesota Coronary Survey. Arteriosclerosis. Jan-Feb 1989;9(1):129-135.
17. Dayton S, et al. A Controlled Clinical Trial of a Diet High in Unsaturated Fat in Preventing Complications of Atherosclerosis. Circulation. 1969;150(1 Suppl 2):II-1-II-2.
18. Bierenbaum ML, et al. Ten-year experience of modified-fat diets on younger men with coronary heartdisease. Lancet. 1973;1(7817):1404-7.
19. Pearce ML and Dayton S.Incidence of Cancer in Men on a Diet High in Polyunsaturated Fat. Lancet. 1971;297(7697):464-467.
20. Dayton S, et al. Vitamin E Status of Humans During Prolonged Feeding of Unsaturated Fats. J Lab Clin Med. 1965;65:739-47.
21. NutritionData: know what you eat. Butter, without salt. http://www.nutritiondata.com/facts/dairy-andegg- products/133/2 Accessed April 21, 2009.
22. Searles SK, et al. Vitamin E, Vitamin A, and Carotene Contents of Alberta Butter. J Dairy Sci. 1970;53(2):150-5.
23. Barnes BO, Solved: The Riddle of Heart Attacks. Fries Communications, 1976.
24. Mann NJ, et al. Arachidonic Acid Content of the Australian Diet Is Lower than Previously Estimated. J Nutr. 1995;125:2528-35.
25. Sears B. The Zone Diet. HarperCollins, 1995.
26. Burr GO, Burr MM. A New Deficiency Disease Produced by the Rigid Exclusion of Fat From the Diet. J Biol Chem. 1929;LXXXII(2):345-67.
27. Turpeinen O. Further Studies on the Unsaturated Fatty Acids Essential in Nutrition. J Nutr. 1938;15(4):351-66.
28. Newberry RD, Stenson WF, Lorenz RG. Cyclooxygenase-2-dependent arachidonic acid metabolites are essential modulators of the intestinal immune response to dietary antigen. Nat Med. 1999;5(8):900-6
29. D’Arienzo R, Stefanile R, Maurano F, Luongo D, Bergamo P, Mazzarella G, Troncone R, Auricchio S, David C, Rossi M. A deregulated immune response to gliadin causes a decreased villus height in DQ8 transgenic mice. Eur J Immunol. 2009;39(12):3552-61.
30. Chan MM, Moore AR. Resolution of Inflammation in Murine Autoimmune Arthritis Is Disrupted by Cyclooxygenase-2 Inhibition and Restored by Prostaglandin E2-Mediated Lipoxin A4 Production. J Immunol. 2010;184(11):6418-6426.
31. Agrawal R, Daniel EE. Control of gap junction formation in canine trachea by arachidonic acid metabolites. Am J Physiol. Mar 1986;250(3 Pt 1):C495-505.
32. Civitelli R, Ziambaras K, Warlow PM, et al. Regulation of connexin43 expression and function by prostaglandin E2 (PGE2) and parathyroid hormone (PTH) in osteoblastic cells. J Cell Biochem. Jan 1 1998;68(1):8-21.
33. Blikslager AT, Roberts MC, Rhoads JM, Argenzio RA. Prostaglandins I2 and E2 have a synergistic role in rescuing epithelial barrier function in porcine ileum. J Clin Invest. Oct 15 1997;100(8):1928-1933
34. du Pre MF, Samson JN. Adaptive T-cell responses regulating oral tolerance to protein antigen. Allergy. 2011;66(4):478-90.
35. Banneberg G, Serhan CN. Specialized pro-resolving lipid mediators in the inflammatory response: An update. Biochim Biopys Acta. 2010; 1801(12):1260-73.
36. U.S. Department of Agriculture, U.S. Department of Health and Human Services. Dietary Guidelines for Americans 2010. www.dietaryguidelines.gov. Accessed December 30, 2012.
37. Bruno RS, Leonard SW, Park SI, Zhao Y, Traber MG. Human vitamin E requirements assessed with the use of apples fortified with deuterium-labeled alpha-tocopheryl acetate. Am J Clin Nutr. 2006;83(2):299- 304.
38. Brown MJ, Ferruzzi MG, Nguyen ML, Cooper DA, Eldridge AL, Schwartz SJ, White WS. Carotenoid bioavailability is higher from salads ingested with full-fat than with fat-reduced salad dressings as measured with electrochemical detection. Am J Clin Nutr. 2004;80(2):396-403.
39. Clark RM, Yao L, She L, Furr HC. A comparison of lycopene and astaxanthin absorption from corn oil and olive oil emulsions. Lipids. 2000;35(7):803-6.
This article appeared in Wise Traditions in Food, Farming and the Healing Arts, the quarterly magazine of the Weston A. Price Foundation, Spring 2012.🖨️ Print post