What Just One High-Saturated-Fat Meal Can Do
Fourteen healthy Australian volunteers between the ages of 18 and 40 were fed two special meals one month apart. Each meal comprised a slice of carrot cake and a milkshake. But one of the meals was high in saturated fat (made with coconut oil) while the other was high in polyunsaturated fat (using safflower oil). Neither the researchers nor the participants knew which meal was eaten during which visit. The meals were prepared so that each volunteer ate 1 gram of fat per kilogram (2.2 pounds) of body weight—roughly the equivalent of a double cheeseburger, large fries and a large milkshake for a 150-pound person.
Three hours after eating the saturated-fat cake and shake meal, the artery linings were unable to expand sufficiently to increase blood flow to the body’s tissues and organs. The arteries showed some reduced ability after the polyunsaturated meal, but these results were deemed not statistically significant.
After six hours, researchers noted that the anti-inflammatory qualities of HDL cholesterol were reduced after eating the saturated-fat meal, whereas they improved after eating the polyunsaturated meal.
It’s long been thought that diets high in saturated fat tend to clog our arteries with plaque, putting us at increased risk of heart attack and stroke. If this is what one meal can do in a few hours, imagine what a lifelong diet of high-saturated-fat food will do. This study seems to show not only that the negative effects of eating certain fats is more immediate than we thought, but also that the positive effects of HDL cholesterol in our bodies is dependent on other factors. And for those who promote coconut oil as a healthier kind saturated fat, since it’s a plant-based saturated fat, this study may be a setback.
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This is interesting stuff, which I had also seen on another site. What isn’t clear to me is this — how long do the negative effects of “one high-saturated-fat meal” last? E.g., if one had one such meal every month, would there be cumulative effects? Thanks! — Kevin
Yes, we need to know whether everything reverts after, say, 24 hours. But even if that does turn out to be the case, we can’t say with any certainty that no harm was done.
The fact that eating one meal can temporarily impede anti-inflammatory agents from preventing a build-up of plaque in the arteries in such a short time is a surprise.
More research is clearly needed.
Every day it’s something new to make us paranoid, and fearful to “live”. One day something is good for you- next day-oops- we made a istake- it’s no longer good for you. I say, eat in moderation- eat from all of the foodgrups when possible- exercise regularly and try to be happy instead of fretting about the adverse effects of everything you do, eat, etc etc
I think fat that causes symptom like the ones mentioned in the article are enough to convince me. I can’t see much that goes on inside my body, but with research that highlights some facts can go a long way in helping me make better eating habits and decisions. I liked the artical and found it very informative.
Keep us informed more on health issues
we wish every one a good christmas this year and we love to get the word out this way
Very good article, really interesting. Be interesting to find out how long the effect lasts indeed. This information will make my eating decisions easier and will lead me to a
fretted, harder, unhealthierhealthier, more fulfilled lifeYou are missing the real point. You are trying to take a single variable experiement and ignoring a glaring variable that is probably the true cause of this result which is the sugar. Refined sugars and fats are a very very bad mix. I think this is way overzealous reporting on the issue–especially the end of the article, “imagine what a lifelong diet of high-saturated-fat food will do.”. Lets not imagine lets study it–except by in large it has been studies. Tribes in Africa and Inuit peoples have long lived on almost purely saturated fat diets and have been studied as having normal cholesterol. “Low Fat” is not the answer–”Low Refined Sugars” is. It is only a matter of time before doctors (and apparently you too since you are in lock step with some of teh bunk science they are pushing like low fat) will have to open up their minds to the multivariate nature of nutrition and accept that it isn’t the saturated fat but the potatoes that are being eaten with it (and hence the insulin response in combination with that fat). I mean–are we to beleive that our paleologic ancestors were not eating large quantities of nuts, meat, eggs, ets?
Ryan,
In this particular study, the only stated difference in the meals was the type of fat: one was high in saturated fat, the other was high in polyunsaturated fat. So this isn’t about high fat vs. low fat at all. That wasn’t my point in reporting this story.
This was about so-called bad fats vs. so-called good fats. And although the effects of sugar weren’t part of this study, both meals likely contained the same amount of sugar, so it’s not unreasonable for the researchers to conclude that the type of fat was the key to their findings. Now perhaps it was the combination of saturated fat with refined sugar that caused problems, whereas the combination of polyunsaturated fat and refined sugar is less of an immediate problem. So which is the variable element here?
In real life, a steady diet of carrot cake and milkshake obviously can’t be considered nutritious. But nor can a diet of double cheeseburgers and fries, bun or not.
You’re right: nutrition is much more complex than simply cutting out whole food groups, which makes replacing fat with refined sugar as nonsensical as replacing refined sugar with high-saturated-fat foods.
But I concede that we absolutely need fat in our diet, and that we don’t need refined sugar in our diet. No argument from me there.
Thanks for engaging.
I am a nutrition science analyst. After nearly three decades of studying nutrition in general and fat metabolism in particular, I’m forced to conclude that there appears to be no evidence that there is evidence that saturated fat is “bad”. Even the research discussed above supports this assertion. Under the heading “BACKGROUND” the researchers stated, “The effect of dietary fatty acids on atherogenesis remains uncertain.” Apparently, those who wrote the press release and subsequent articles don’t share the researchers’ reluctance to demonize saturated fat.
Another important consideration is the fact that saturated fat did not stimulate as much production of the sort of HDL that fights inflammation as did the polyunsaturated fat. In the conclusion, researchers said, “Consumption of saturated fats reduces the anti-inflammatory potential of HDL… In contrast, the anti-inflammatory activity of HDL improves after consumption of polyunsaturated fat.”
Actually, the opposite of reduces is increases, not improves. So read that, “… the anti-inflammatory activity of HDL increases after consumption of polyunsaturated fat.” Why the increase? Because polyunsaturated fat tends to produce inflammation and the body responds by producing more HDL with anti-inflammatory properties. Seems to me the researchers have interpreted this portion of their findings backwards.
David Brown
Nutrition Education Project
A few days ago, I sent the following book excerpt to Dr. David Celermajor, one of the scientists involved in the research being discussed here.
David Brown
Nutrition Education Project
Book excerpt: (my thanks to Dr. Donald R. Davis, Jr. Ph.D. University of Texas at Austin, for permission to use this material in my Nutrition Education Project).
The following paragraphs are from pages 81-83 of Nutrition Against Disease (1972) by Roger J. Williams, PhD. More information about Dr. Williams and his work is available at http://www.doctoryourself.com. I encourage you to read the references and notes. They are every bit as interesting as the associated text. Dave Brown
No discussion of heart disease would be complete without mention of the question of saturated fats. It has come to be almost an orthodox position that if one wishes to protect oneself against heart disease, one should avoid eating saturated (animal) fats. While this idea may not be entirely in error, it is misleading in its emphasis. The evidence shows that high fat consumption, when accompanied by plenty of the essential nutrients which all the cells need, does not cause atherosclerosis or heart disease.
Rats have been used extensively to study the effects of diet on atherosclerosis. Under ordinary dietary conditions the inclusion of saturated fats in their diet will consistently promote the deposition of cholesterol in their arteries.(50) For 285 days rats were fed a diet containing 61.6 percent animal fat, but highly superior with respect to protein, mineral, and vitamin content, without producing any pathological changes in the aorta or in the heart.(51) The animals did, to be sure, become obese, as much as three to four times their normal weight. Animals fed vegetable fats at the same level fared essentially no better and no worse. These findings were based upon extensive long-term experiments at Yale, using a total of 600 rats, which were observed for as long as two years. There were no findings suggestive that either high animal fat diets or high vegetable fat diets were conducive under these conditions to atherosclerosis.
These animals represented an extreme condition, since 81 percent of their energy came from fats. Their diets otherwise were extremely good. The protein was of high quality (casin) and was kept at a high level (20 percent); the vitamin levels were double those ordinarily used in this laboratory. The Yale findings were corroborated almost a decade later (1965) at Tufts University School of Medicine.(52)
That cardiovascular disease is not associated with high fat diets is also shown by comparison study of matched groups of twenty-eight railwaymen from North India and twenty-eight from Southern India.(53) The consumption of fats, mostly of animal origin, was ten times higher among the North Indians than the South Indians, but there were no significant differences between their lipid and cholesterol levels. Among the South Indian population, the incidence of heart disease is said to be fifteen times as high as among the North Indians where the fat content of the diet is ten times higher. Dietary factors are doubtless very important in connection with the incidence of heart disease, but fat is only one factor, and other dietary factors are considerably more important.
This is also corroborated by a study of 400 Masai men in Tanganyika.(54) In spite of the fact that the diet of these men is almost exclusively milk and meat (consumption of whole blood is relatively rare), both of which contain much fat and plenty of cholesterol, the cholesterol levels in the blood of the Masai are extraordinarily low, and there was “no evidence of arteriosclerotic heart disease.” It should be noted that a diet containing large quantities of meat is free from “naked calories,” and is certain to supply an assortment of amino acids, minerals, and vitamins in liberal amounts. Though the Masai have other health disorders – many of infective origin – they probably escape heart disease because their body cells are furnished with an environment that is adequate enough to protect their hearts and blood vessels.
A corollary of the notion that saturated fats are archvillains is the idea that one should eat substantial amounts of polyunsaturated fats. (The phrase “polyunsaturated fatty acids” has become virtually synonymous with “heart protection” in both popular and orthodox medical thinking.) While everyone should have unsaturated fats in his diet, their presence does not by any means afford adequate protection against atherosclerosis and heart disease. The current consumption of polyunsaturated fatty acids in the USA is higher than it has ever been, yet this does not curb heart disease.(55) There are many reasons on which to base our conclusion that other factors are far more important.(56) When other deficiencies are eliminated, the amount of unsaturated fat is of secondary importance. If there is plenty of vitamin B6 in the diet, fat metabolism tends to take care of itself.
I have said a good deal about vitamin B6, but I do not mean to imply that it is, by itself, the answer to heart disease. All the nutrients contribute to the prevention of heart trouble.
References and notes:
50. Thomas, W.A., and Hartroft, W.S. “Myocardial infarction in rats fed diets containing high fat, cholesterol, thiouracil, and sodium cholate.” Circulation, 19:65, 1959; Taylor, C. B., et al. “Fatal myocardial infarction in rhesus monkeys with diet-induced hyper-cholesterolemia.” Circulation, 20;975, 1959.
In the above experiments, the investigators found that prolonged feeding of butter or lard to rats resulted in hyperlipemia and finally coronary thrombosis and myocardial infarction with lesions similar to those found in human beings. The diets of these animals were regarded as otherwise “normal” in respect to their intake of supplementary vitamins, minerals, and amino acids. Other data, however (see reference note 52 below) demonstrate that when fat and cholesterol (or animal protein) are increased in the diet, certain nutrients (particularly pyridoxine) must be increased above “average” or “normal” requirements.
51. Barboriak, J.J., et al. “Influence of high-fat diets on growth and development of obesity in the albino rat.” J. Nutr., 64: 241, 1958.
52. Naimi, S., et al. “Cardiovascular lesions, blood lipids, coagulation and fibrinolysis in butter-induced obesity in the rat.” J. Nutr., 86:325, 1965.
In this more recent study, Naimi and his colleagues were directly interested in the effects of a high fat butter-induced obesity on the cardiovascular system of seventeen male Wistar albino rats. Butter constituted 65 percent of the total calories, with 20 percent protein (casin) and generous vitamin and mineral supplements equal to if not superior to those used in the above-mentioned Yale study.
Under the conditions of their experiment, these investigators found that a high fat butter diet causing obesity in rats did not produce changes in blood cholesterol nor result in cardiovascular lesions, as other data had led them to expect. The authors note, “The absence of such adverse changes, despite, the development of gross obesity in these animals may be significant, since both obesity and animal fats have been considered to be associated with lipemia and vascular lesions. It may be suggested that other dietary factors might have protected the experimental group against such changes. Yet, even if this happens to be the case, it should not detract from the significance of the fact that large amounts of saturated fat and obesity are not necessarily associated with lipemia and vascular lesions.”
We are confident that other dietary factors did protect these rats, and that only in the absence of sufficient supportive nutrients are obesity and high fat and high cholesterol diets associated with atherosclerosis and heart disease in the human population.
53. Malhotra, S.L., “Serum Lipids, dietary factors and ischemic heart disease,” Am. J. Clin. Nutr., 20:462, 1967.
See also Malhotra, S.L., “Geographical aspects of acute myocardial infarction in India, with special reference to the pattern of diet and eating.” Brit. Heart J., 29:777, 1967.
54. Mann, G.V., et al. “Cardiovascular disease in the Masai.” J. Atheroscler. Res., 4:289, 1964.
In an extensive review of the various peoples of the earth who have little or no atherosclerosis and are virtually free of heart disease, Lowenstein found that the fat intake ranged from 21 grams per day to as much as 355 grams per day (Lowenstein, F.W. Am. J. Clin. Nutr., 15:175, 1964). In both the Somalis and the Samburus of East Africa, the diet is from 60 to 65 percent fat (animal), and yet they are nearly free from atherosclerosis and heart attacks. While it might be argued that ethnic differences are involved here, population groups of wide ethnic variation have been reported who subsist on high fat, high cholesterol, high caloric diets while remaining virtually free of coronary heart disease.
In the text we have mentioned the report of Mann and his colleagues of the Masai tribe who subsist on a diet excessively high in butter fat (and cholesterol), the fat constituting as much as 60 percent of the total calories consumed, yet are virtually free of cardiovascular disease. Gsell and Mayer report that the semiisolated peoples of the Loetschental valley in the Valaisian Alps of Switzerland habitually eat a diet high in saturated fat and cholesterol, high in calories, but evidence low serum cholesterol values and little cardiovascular disorders (Gsell, D., and Mayer, J. “Low blood cholesterol associated with high calorie, high saturated fat intake in a Swiss Alpine village population.” Am. J. Clin. Nutr., 10:471, 1962).
Stout and his coworkers report that an Italian immigrant colony in Roseta, Pennsylvania, consumes diets much richer than other Americans, yet have less than half the incidence of coronary heart disease (J. A. M. A., 188:845, 1964).
In a survey study of 27,000 Kenya East Indians, A. D. Charters and B. P. Arya report (Lancet, 1:288, 1960) that the animal fat consumption was relatively high among the Punjabi nonvegetarians and relatively low among the vegetarian Gujeratis, but the percentage of heart disease morbidity “is closely proportional to that of the population.” The statistics of their survey, conclude these investigators, suggest that in the case of the East Indian population in Kenya, “the ingestion of animal fats is not an important etiological factor” in heart disease morbidity. Interestingly, besides their low animal fat diet, the Gujerati vegetarians consume foods rich in polyunsaturated oils, as groundnut, cottonseed, and simsim oils, yet were not “protected from coronary occlusion by a high intake of unsaturated fatty acids.”
In an epidemiological study of coronary heart disease in a general population of 106,000 Americans conducted over a one year period, W.J. Zukel and his coworkers found the highly provocative fact that farmers showed a much lower incidence of coronary heart disease than males of other groups, in spite of the fact that there were no substantial differences in their mean caloric intake or fat and cholesterol consumption (Zukel, W. J., et al. Am. J. Pub. Health, 49:1630. 1959).
In an epidemiological study of two Polynesian island groups, Hunter compared the diet, body build, blood pressure, and serum cholesterol levels of the tradition-following Atiu and Mitiaro with the more Europeanized Raroyongan Neighbors (Hunter, J.D. Fed. Proc., 21, Supp. 11:36, 1962). The Atiu-Mitiaro people live on a diet low in calories and protein but rich in highly saturated coconut fat. Hunter found that 25 percent of Rarotongans (males) suffered from hypertension as compared to only 10 percent of the Atiu-Mitiaro males. While the serum cholesterol levels of the saturated coconut fat-eating Atiu-Mitiaro males were higher (as high as European males), Hunter was unable to discover by electrocardiographic readings any tendency to coronary heart disease.
Finally we turn to the early primitive Eskimo who subsisted almost totally on an excessively high animal fat diet. In an early 1927 issue of the Journal of the American Medical Association (May), in an article titled “Health of a Carnivorous Race,” Dr. William Thomas reports that of 142 adults between the ages of forty and sixty who were completely examined, he found no unusual signs of vascular or renal morbidity, and all indications were that diseases of the cardiovascular system were not prevalent among these people. This is in agreement with other reports of scientists of the primitive Eskimo (e.g. C. Lieb. J. A. M. A., July, 1926; V. Stefannsson, in his book Cancer: Disease of Civilization, p. 76; I. M. Rabinowitch, Canad. Med. Assoc. J., 31:487, 1936; W. Price, Nutrition and Physical Degeneration. New York: Hoeber, 1939).
It is clear, therefore, that adult males of a widely differing ethnic stock can subsist on a high fat, high cholesterol, high caloric diet, and yet remain relatively free of cardiovascular disorders. Even if prevailing views are to the contrary, I think that the evidence points strongly toward the conclusion that the nutritional environment of the body cells – involving minerals, amino acids, and vitamins – is crucial, and that the amount of fat or cholesterol consumed is relatively inconsequential.
55. Antar, M.A., et al. “Changes in retail market food supplies in the United States . . . .” Am. J. Clin. Nutr., 14:169, 1964
I have also encountered on another site this type of experiments and discussions. It occured to me that majority of cardiac and health experts agree on one thing, HDL on high doses is not good for the health. Reduction of this type of fats will greatly reduce the chances of having heart failures.
I’ve written an article on my web site criticizing the recent study on saturated fat by Nicholls et al., showing how they overlooked an alternative hypothesis that can explain their data and is substantiated by the scientific literature, and critically reviewing the coverage it has received in the press:
Myth: One High-Saturated Fat Meal Can Be Bad: Why You Don’t Need Vegetable Oil In Your Carrot Cake
Chris Masterjohn
Glad to see people who actually know what they are talking about commenting on this nonsense. I am sick to death of seeing all this rubbish about fats everywhere, from self-proclaimed experts, or worse, from abstracts that bear no resemblance to the actual data. Here’s the best bit of health advice you’ll ever get, fatties: Exercise.
This is b.s. – arteries are clogged by polyunsaturated fats, not saturated ones, and these people were eating CAKE – not a steak or piece of pure animal fat. Modern health declined as soon as people started eating grain and sugar – our ancestors ate 10X or more animal fat than we do now with little/no heart disease. Your body is made up of saturated fat and animal protein, not bread and vegetable oil.