Can One Meal Containing Saturated Fat Really Be that Bad?
Or Why You Don’t Need Vegetable Oil in Your Carrot Cake and Milk Shake to Protect Your Arteries
Newspapers around the world have recently published the results of a study indicating that a single meal rich in saturated fats will disrupt the functioning of your arteries and contribute to the inflammation of your blood vessels. The Associated Press story by Joe Milicia1 was heard round the internet, and reported in papers throughout the world.
The news article quoted the Kansas City cardiologist Dr. James O’Keefe as claiming the study showed that “when you eat [saturated fat], inflammation and damage to the vessels happens immediately afterward.”
Dr. Nicholls, the lead author of the study that generated such an amazing amount of attention in the press, was quoted as saying that his research showed the “need to aggressively reduce the amount of saturated fat consumed in the diet.” The article then clarified that this meant reducing our intake of beef, pork, lard, poultry fat, butter, milk, cheeses, coconut oil, palm oil and cocoa butter, and replacing them with safflower oil, sesame oil, sunflower seeds, corn and soybeans. Amazingly, this study had the power to make sweeping conclusions about over 15 different foods!
The study in question was published by a team of researchers led by Dr. Stephen J. Nicholls of the Australian Heart Research Institute in the Journal of the American College of Cardiology entitled, “Consumption of Saturated Fat Impairs the Anti-Inflammatory Properties of High-Density Lipoproteins and Endothelial Function.”2
In reality, none of the dire conclusions reported in the press is justified by the study. There was no clearly discernable effect of any type of fat on arterial function, and those consuming saturated fat had the best arterial function at all time points measured.
In fact, the researchers did not even study the inflammation occurring in the blood vessels of the people eating the meals. Instead, they performed an interesting experiment on isolated cells in which they found high-density lipoprotein (HDL) isolated from people eating safflower oil to have greater anti-inflammatory power than HDL isolated from people eating coconut oil. They attributed this observation to the saturation of fat that the study subjects consumed without a shred of evidence, and overlooked the more plausible explanation that these effects were due to the large difference in vitamin E contents of the two diets.
The researchers fed fourteen adults a meal of carrot cake and a milk shake on two separate occasions one month apart, once made with highly saturated coconut oil and once made with highly polyunsaturated safflower oil. Both oils were non-hydrogenated, organic, unrefined and virgin.3
The researchers, who were blinded to which meals the subjects were receiving, took each of three types of measurements at three different time points: first, after an overnight fast and before the meal was administered; second, three hours after the meal was administered; third, six hours after the meal was administered.
The first type of measurement they took was the levels of various constituents in the subjects’ blood: total cholesterol, LDL, HDL, triglycerides, insulin and free fatty acids.
The second type of measurement they took was of various parameters of blood flow, including the total amount of blood flow through the subjects’ forearms and the degree of “flow-mediated dilation” in their brachial arteries. Flow-mediated dilation is the ability of a blood vessel to dilate to rush blood to an area that has been deprived of oxygen. To measure it, researchers use pressure to stop blood flow through an artery and then test to what extent the artery reacts once the pressure is released by dilating to increase the return of blood to the blood-deprived area. With this type of test, the more the blood vessel dilates when pressure is released, the better shape it is believed to be in.
Finally, the researchers extracted HDL from the subjects’ blood at each time point. They incubated isolated endothelial cells from human umbilical veins with the HDL at various concentrations. After the incubation period, they added an inflammatory chemical called tumor necrosis factor-alpha (TNF-a) to the cells, which stimulates the production of adhesion molecules with long-winded names like intercellular adhesion molecule 1 (ICAM-1) and vascular cell adhesion molecule 1 (VCAM-1), which are believed to play a role in the adhesion of immune cells to arterial plaque. HDL has been shown to inhibit the expression of these inflammatory molecules, and the researchers conducted this part of the study to see whether how you eat can affect how much potential HDL has to inhibit the expression of these presumably harmful adhesion molecules.
The researchers claimed to generate two findings:
- Flow-mediated dilation decreased more strongly after the coconut oil meal than after the safflower oil meal. From this, they concluded that “consumption of saturated fat impairs . . . endothelial function.”
- When cells were incubated with HDL taken from subjects after they ate the coconut oil meal, the expression of the inflammatory adhesion molecules in response to TNF-a stimulation was increased compared to cells incubated with HDL taken from fasting subjects. By contrast, when cells were incubated with HDL taken from subjects after they ate the safflower oil meal, the expression of inflammatory molecules in response to TNF-a stimulation was decreased compared to cells incubated with HDL taken from fasting subjects. From this, the authors concluded that “consumption of saturated fat impairs the anti-inflammatory properties of high-density lipoproteins.”
Although both of these conclusions are more conservative than the statements written in the Associated Press article, neither of them is justified by the study.
Let’s take a closer look at each.
Flow Mediated Dilation
The researchers claim that consumption of the saturated fat meal impaired flow-mediated dilation (FMD). They did indeed show that at the three-hour mark the decline in FMD was almost twice as great in the coconut oil group as it was in the safflower oil group. Yet the FMD was actually higher in the coconut oil group than in the safflower oil group at every point along the way! The reason? When the subjects were fasting, those who were about to eat the coconut oil meal had 33 percent better FMD than those who were about to eat the safflower oil meal. Even at the three-hour point, when FMD had declined the most, it was still 9 percent higher in the coconut oil group than in the safflower oil group.
There are two ways we could look at this paradoxical situation. Figure 1 shows the changes that took place in FMD three and six hours after the meals, relative to the FMD before the meals (called “baseline”). You can see that for both the coconut oil meal and the safflower oil meal, FMD declined substantially at the three-hour mark, although the rate at which it declined was nearly double after the coconut oil meal.
Figure 1. Percent change in the degree of flow-mediated dilation (FMD) compared to baseline values.
|17 percent lower
|8 percent lower
|32 percent lower
|10 percent lower
Now let’s look at these findings another way. Figure 2 compares the relative degree of FMD of the coconut oil group with that of the safflower oil group. Here you can see that the FMD is higher (a good thing) in the coconut oil group at every single time point during the study.
Figure 2. Comparison of the degree of flow-mediated dilation (FMD) in the coconut oil group to that in the safflower oil group at three time points.
|33 percent higher in coconut oil group
|9 percent higher in coconut oil group
|29 percent higher in coconut oil group
Thus, we have to ask: is consumption of coconut oil rather than safflower oil the reason for the greater decline of FMD in the coconut oil group? Or, is the reason for this decline the simple fact that the people who ate the coconut oil meal started out with a higher value of FMD in the first place, and therefore, so to speak, had more to lose?
There are two reasons that the latter scenario might be true: first, the decline in FMD after a meal might not even be a function of the FMD; second, a randomly high sampling error for the FMD before the meal could result in what is called “regression to the mean.”
In the first case, it could be that eating carrot cake and drinking a milkshake, whether made with safflower oil or coconut oil, depresses FMD to a certain point regardless of fasting levels. For example, eating the meal might depress FMD to about 5 percent, regardless of whether the person’s fasting level was 6 percent or 9 percent.
In such a scenario, a person whose fasting level is 9 percent would experience a 44 percent decline in FMD, while a person whose fasting level is 6 percent would experience only a 17 percent decline in FMD.
Thus, if the effect of a meal on FMD is not a function of fasting FMD, the coconut oil group, which by random chance had a 33 percent higher fasting FMD, would exhibit a greater relative decline than the safflower oil group for no other reason than that they started off with substantially better FMD in the first place!
Regression to the Mean
The authors themselves admitted a very similar explanation in the journal article, writing that “it is possible that ‘regression to the mean’ may have contributed to some of the FMD reduction observed after consumption of the saturated fat.” The concept of “regression to the mean” is essentially this: if by random sampling error an initial value tends to be higher than the mean, a second value will tend to be closer to the mean. Thus, a decline in values could result simply from the first value being randomly high.
Yet was this caveat noted in the press? Of course not. Instead, we were told that when we eat saturated fat, “damage to the vessels happens immediately afterward,” and thus we must “aggressively reduce the amount of saturated fat consumed in the diet.”
No one warned us that if when fasting, by random sampling error we happen to have a higher-than-average value of FMD, rapid but unmeaningful FMD reduction will occur after we eat due to “regression to the mean.” No one warned us that we must “aggressively reduce the amount of random sampling error” lest we suffer statistically indicated arterial dysfunction with one, single meal.
Inflammation in the Test Tube
Contrary to the Associated Press report’s claim that “fewer inflammatory agents were found in the arteries” after the safflower oil meal than before it, the researchers did not measure any type of inflammation in the arteries of the test subjects. Instead, they incubated isolated umbilical vein endothelial cells with HDL taken from these subjects at various time points before and after the meals, and then stimulated these isolated cells to produce inflammatory adhesion molecules by adding a compound called TNF-a to them. Finally, they measured whether HDL isolated after the different meals had a different ability to lower the amount of adhesion molecules released after stimulation with TNF-a.
The researchers found that cells incubated with the HDL isolated from subjects after they had eaten the coconut oil meal produced more adhesion molecules (ICAM-1 and VCAM-1) after stimulation with TNF-a than did cells incubated with HDL isolated from fasting subjects, and that cells incubated with HDL isolated from subjects after they had eaten the safflower oil meal produced fewer adhesion molecules after stimulation than did cells incubated with HDL isolated from fasting subjects. In other words, eating safflower oil seemed to make the HDL a more powerful anti-inflammatory agent, while eating coconut oil seemed to make the HDL a less powerful anti-inflammatory agent.
There are a number of problems with the large leap of logic it takes to conclude from this finding that a meal rich in saturated fat causes inflammation. First, we are neither test tubes nor petri dishes, but complex organisms with many different chemical and electrical feedback systems that do not exist in laboratory dishes. The researchers could have directly measured the levels of ICAM-1 and VCAM-1 in the subjects’ blood, but that is not what they chose to study.
Second, the researchers only studied the anti-inflammatory potential of HDL. They could have incubated the cells with whole plasma to measure the total anti-inflammatory capacity of the blood, but they chose not to, for the simple reason that they were only trying to answer one small question about HDL and not look at the bigger picture.4
Virgin coconut oil is rich in very powerful polyphenols,5 some types of which have been shown to decrease expression of TNF-a and adhesion molecules,6, 7 and which are carried by water-soluble proteins in the blood and not by HDL.8 Thus, virgin coconut oil’s contribution to the anti-inflammatory capacity of the blood could be primarily in the non-HDL fraction, whereas safflower oil’s contribution to the anti-inflammatory capacity of the blood might be primarily in the HDL fraction. We simply do not have enough knowledge at this point to say for sure.
The only way to determine the effect of safflower oil and coconut oil on the total anti-inflammatory capacity of the blood is to perform the experiment by incubating the cells with whole blood. The only way to determine the effect of safflower oil and coconut oil on the actual level of inflammation in the people consuming the oils is to measure the inflammatory compounds being directly produced in their blood. This study did neither.
Finally, and most importantly, the researchers provided no evidence whatsoever that the effects they observed were due to the type of fat in the two meals. They simply assumed that the difference they observed between safflower oil and coconut oil was due to the fact that coconut oil is high in saturated fat and safflower oil is high in unsaturated fat. In doing so, they overlooked a very interesting hypothesis that could explain their results and that has substantial support in the scientific literature.
An Alternative Hypothesis: Vitamin E
The difference between safflower oil and coconut oil does not stop at the relative degree of fatty acid saturation. Figure 3 shows the difference in vitamin E content between the two oils. Safflower oil is 77 times higher in alpha-tocopherol and 74 times higher in total tocopherols.9
Figure 3. Typical tocopherol (vitamin E) content of coconut oil and safflower oil.
Source: (Enig, 2000).
Is it plausible that the difference in vitamin E content of the oils could account for the difference in the expression of adhesion molecules in the isolated cells? Absolutely.
A recent review of alpha-tocopherol’s role in regulating gene expression listed the suppression of the gene that codes for ICAM-1 as one of its functions.10 In fact, Chinese researchers performed a very similar experiment to the one we have been discussing, wherein they incubated endothelial cells taken from human umbilical veins with vitamin E instead of HDL. They found that incubating the cells with alpha-tocopherol, gamma-tocopherol and mixed tocopherols all inhibited the ability of oxidized LDL to induce ICAM-1 expression in the cells in a dose-dependent manner.10 Another group found vitamin E to reduce both ICAM-1 and VCAM-1 in the heart cells of rats.11
Vitamin E suppressed ICAM-1 and VCAM-1 levels in vivo in rabbits, although the effect on VCAM-1 was not statistically significant.13 In humans, the combination of vitamins E and C, but not vitamin C alone, decreased blood levels of ICAM-1 after six months. When the supplementation was stopped, blood levels of ICAM-1 returned to their initial levels. A similar effect was seen on VCAM-1, but it was not statistically significant. Unfortunately the researchers did not study the effect of vitamin E alone.14
Vitamin E travels in the blood associated with lipoproteins, including HDL.15 When endothelial cells are incubated with vitamin E-enriched HDL, they selectively take up vitamin E from the HDL at ten times the rate at which they take up the HDL particles themselves.16
It is therefore reasonable to suggest that the high vitamin E content of safflower oil led to an enrichment of the subjects’ HDL particles with vitamin E, which was then taken up by the endothelial cells where it suppressed the expression of adhesion molecules.
Yet one question remains: why would the HDL taken from subjects after they ate the coconut oil meal be less effective at suppressing the expression of adhesion molecules than HDL taken from subjects when they were fasting? The one study I’ve found on the effect of a meal on the distribution of vitamin E in the blood15 suggests that the fraction of vitamin E in HDL actually declines temporarily after a meal when the meal is relatively low in vitamin E, but rises if the meal is high in vitamin E. It may be, then, that the vitamin E content of HDL declined after the coconut oil meal not because of the coconut oil itself but because any low-vitamin E meal reduces the amount of vitamin E in circulating HDL. On the other hand, the safflower oil meal may have been high enough in vitamin E to make the vitamin E content of HDL rise.
The only way to actually know would be to directly measure the vitamin E content of the HDL particles after the meal. Although the researchers who conducted the study we have been discussing measured the amount of protein, phospholipid, triglyceride and cholesterol in the HDL particles that they extracted, they unfortunately did not measure the amount of vitamin E in these particles.
The foregoing is, of course, a hypothesis. I have not shown conclusively that the effects observed in the study must have been due to vitamin E; I have simply shown that this is a plausible explanation. Further research would be needed to confirm or refute the hypothesis.
Likewise, it is an unconfirmed hypothesis that the effect observed was a result of the consumption of saturated fat. This unfortunately did not stop the researchers from titling their paper “Consumption of Saturated Fat Impairs the Anti-Inflammatory Properties of High-Density Lipoproteins and Endothelial Function” as if they had actually shown this to be the case.
So Which Oils Should We Eat?
If it turns out to be true that the difference in the protective effect of HDL in the test tube was in fact due to the high vitamin E content of safflower oil and the low vitamin E content of coconut oil, that does not mean we should avoid coconut oil. It does not even mean we should eat safflower oil.
These findings simply reflect the fact that coconut oil is not a good source of vitamin E. Coconut oil is still the best source of medium-chain fatty acids, which boost metabolism and support the immune system, and virgin coconut oil is rich in powerful antioxidant polyphenols.
Polyunsaturated fatty acids such as those found in safflower oil actually deplete the body of vitamin E and thereby increase the body’s need for vitamin E–this is basic textbook biochemistry.17 Safflower oil may raise the amount of vitamin E in lipoproteins immediately after a vitamin E-rich meal, but what is the long-term effect on vitamin E status of an excessive intake of polyunsaturated fats?
It makes sense then that the best way to obtain vitamin E would be from sources that are high in vitamin E but low in polyunsaturated fat. Unrefined palm oil is an excellent example of such a source.
Palm oil is only 9 percent polyunsaturated, compared to safflower, which is 75 percent polyunsaturated. In terms of the absolute amount of vitamin E, compared to safflower oil, palm oil has a somewhat lower level of alpha-tocopherol, more than double the gamma-tocopherol, and large amounts of tocotrienols, which are another important part of the vitamin E complex that are completely absent in safflower oil. The combined absolute value of tocopherol and tocotrienol forms of vitamin E is 46 percent higher in palm oil than safflower oil.9
When one takes into account the high polyunsaturated fat content of safflower oil, which increases the need for vitamin E, the advantage of more saturated palm oil becomes obvious: the ratio of vitamin E to polyunsaturated fatty acids in palm oil is 12 times greater than the same ratio in safflower oil!
Yet newspapers the world over carrying the Associated Press article told us to reduce our intake of palm oil and other saturated fats “aggressively.”
We’ve been told that this study shows that when “you eat [saturated fat], inflammation and damage to the vessels happens immediately afterward.” We’ve been told that it shows we must “aggressively reduce the amount of saturated fat consumed in the diet.” We’ve been further told to throw out the beef, pork, lard, poultry fat, butter, milk, cheeses, coconut oil, palm oil and cocoa butter, replacing all these fats with safflower oil, sesame oil, sunflower seeds, corn and soybeans.
These dire warnings are based on a study that couldn’t differentiate the effect of coconut oil from the effect of random sampling error on flow-mediated dilation and that showed people consuming coconut oil to have better flow-mediated dilation at all time points than people consuming safflower oil; they are based on a study that could not differentiate between the effect of saturated fat and the effect of vitamin E on the capacity of HDL to prevent inflammation in isolated, laboratory-cultured cells; and they are based on a study that tells us nothing about the amount of inflammation going on within the people consuming the meals, who are much more complex than globs of isolated laboratory-cultured cells.
Further research should uncover whether the effects seen in the test tube are due to vitamin E, to saturated or unsaturated fats, or to other causes entirely, and what relevance these observations in the test tube have for real, living people.
In the meantime, traditional animal fats, tropical oils and olive oil remain our best bet for avoiding the modern diseases that suspiciously ascended to prominence soon after researchers began heralding seed oils like safflower oil as a healthy alternative to traditional, saturated fats.
We can, however, draw two conclusions from the present study to make life safer for all of us and to advance the public health. First, always avoid random sampling error before you eat; otherwise, it would take only a single meal for “regression to the mean” to result in statistically induced markers of arterial dysfunction immediately afterward. Second, if you do eat a meal high in saturated fats, resist the urge to extract your HDL and throw it into the nearest petri dish. Chances are there’s a researcher just waiting for your defenseless lipoproteins with a pipette full of inflammatory chemicals, and at that point, all hope of preventing cell-to-cell adhesion is lost.
A Better Experiment
A major drawback of the current study is that it could not distinguish between the effect of the saturation of the fats that the study subjects consumed and the amount of vitamin E in their diets. One way to conduct an experiment while avoiding this pitfall would be to use palm oil, which is very rich in vitamin E despite being a highly saturated fat.
A better experiment would use three groups: one fed palm oil alone, a second fed a mixture of coconut oil and olive oil, and a third fed olive oil alone. This experiment would be able to differentiate between the effects of saturated fat and those of vitamin E because the dietary fat of the first and second groups would be similarly and highly saturated but the first group would receive 15 times as much vitamin E as the second group. Conversely, the second and third groups would receive similar amounts of vitamin E, but the dietary fat of the third group would be much lower in saturated fat.18
If HDL isolated from the first group was much more effective at inhibiting the expression of adhesion molecules by stimulated endothelial cells than HDL isolated from the second and third groups, this would support the hypothesis that it is the vitamin E content of the diet rather than the saturation of the dietary fat that is operative. If, on the other hand, HDL isolated from the first group was no more or less effective than HDL isolated from the second group but considerably less effective than HDL isolated from the third group, this would support the hypothesis that the saturation of the dietary fat rather than the amount of vitamin E is operative.
But even these findings would be tenuous. HDL is only one constituent of many in the blood, and the functioning of an artery within a living human is much more complex than the functioning of a mass of cells in a petri dish upon which a researcher has dropped solutions of isolated chemicals with a pipette. The ultimate test to teach us which oils to eat is which oils are consumed by the people who live the longest, are the healthiest, and have the best quality of life.
Anthony Colpo Comments on the Carrot Cake & Milkshake Study
The study discussed in this article was supported by a Pfizer Cardiovascular Lipid award. Pfizer makes over ten billion dollars per year from sales of Lipitor, the world’s best-selling cholesterol-lowering drug.
Dr. Nicholls is supported by a postgraduate research scholarship from the National Heart Foundation of Australia. Co-author Dr. Rye is a National Heart Foundation of Australia Principal Research Fellow. The National Heart Foundation of Australia operates a program in which it charges a fee so that food manufacturers can display the “Heart Foundation Tick.” Polyunsaturated vegetable oils and margarines contribute a significant portion of ingredients in these certified products.
Another co-author of the study, Dr. Lundman, is supported by postdoctoral scholarships from the Swedish Heart and Lung Foundation, which counts among its sponsors Unilever, the food giant that manufactures numerous vegetable oil and margarine products.
There have been numerous randomized controlled CHD prevention trials conducted since the 1960s, in which people have been given either high-polyunsaturate diets or high-saturate diets as the sole intervention. In these trials, extending up to eight years, no cardiovascular or overall mortality advantage has ever been observed that can be attributed to saturated fat restriction. In fact, a number of these trials observed poorer mortality outcomes in the high-polyunsaturate group.
Healthy subjects placed on high polyunsaturated diets for four-week periods have exhibited higher levels of free radical activity and blood clotting markers than those on high-saturated diets. In animal studies, polyunsaturated vegetable oils consistently promote cancer growth; an eight-year trial with real live humans that observed significantly higher cancer incidence in the polyunsaturated group suggests this phenomenon is not merely confined to lab rats.a This same study, by the way, showed little difference in extent of atherosclerosis among autopsied subjects from the high-saturate and high-polyunsaturate diets. If anything, the aortas of those eating the polyunsaturated-enhanced diet tended to show more plaque build-up.
So when clueless health “experts” tell you to opt for polyunsaturated fat instead of saturated fat, ignore the living daylights out of them. Doing so could well save your life.
Anthony Colpo is the author of The Great Cholesterol Con, a no-holds-barred exposé of the farcical cholesterol theory of heart disease. Unlike the authors of the above study, Colpo has absolutely no ties to any food, drug, medical, or supplement industry groups, nor health organizations that receive money from these groups.
a. Dayton S, et al. A controlled clinical trial of a diet high in unsaturated fat in preventing complications of atherosclerosis. Circulation, 1969; XL: II-1-63.
References and Notes
- Milicia, Joe, “One High-Saturated Fat Meal Can Be Bad,” Associated Press. Carried by the Washington Post. http://www.washingtonpost.com/wp-dyn/content/article/2006/08/07/AR2006080700905.html. Published August 7, 2006. Accessed August 19, 2006.
- Nicholls SJ, Lundman P, Harmer JA, Cutri B, Griffiths KA, Rye KA, Barter PJ, Celermajer, DS. Consumption of Saturated Fat Impairs the Anti-Inflammatory Properties of High-Density Lipoproteins and Endothelial Function. Journal of the American College of Cardiology, 2006; 48(4): 715-720.
- David Celermajer and Jason Harmer, personal communication.
- David Celermajer, personal communication.
- Nevin KJ, Rajamohan T. Beneficial effects of virgin coconut oil on lipid parameters and in vitro LDL oxidation. Clin Biochem. 2004 Sep; 37(9): 830-5.
- Ukil A, Maity S, Das PK. Protection from experimental colitis by theaflavin-3,3′-digallate correlates with inhibition of IKK and NF-kappaB activation. Br J Pharmacol. 2006 Jul 31; [Epub ahead of print].
- Mazzon E, Muia C, Paola RD, Genovese T, Menegazzi M, De Sarro A, Suzuki H, Cuzzocrea S. Green tea polyphenol extract attenuates colon injury induced by experimental colitis. Free Radic Res., 2005 Sep; 39(9): 1017-25.
- Manach C, Scalbert A, Morand C, Remesy C, Jimenez L. Polyphenols: food sources and bioavailability. Am J Clin Nutr. 2004 May; 79(5): 727-47.
- Enig, Mary G, PhD, Know Your Fats: The Complete Primer for Understanding the Nutrition of Fats, Oils, and Cholesterol, Silver Spring, MD: Bethseda Press (2000) 115; 118; 122.
- Azzi A, Gysin R, Kempna P, Munteanu A, Negis Y, Villacorta L, Visarius T, Zingg JM. Vitamin E mediates cell signaling and regulation of gene expression. Ann NY Acad Sci, 2004 Dec; 1031:86-95.
- Fan Y, Liu ML, Qi YY, Ren ZW. [Effect of different isofoms of tocopherols on expression of intercellular adhesion molecule-1 in human umbilical vein endothelial cells]. Beijing Da Xue Xue Bao, 2004 Feb; 36(1):70-4.
- Schulte I, Bektas H, Klempnauer J, Borlak J. Vitamin E in heart transplantation: effects on cardiac gene expression. Transplantation, 2006 Mar 15; 81(5):736-45.
- Koga T, Kwan P, Zubik L, Ameho C, Smith D, and Meydani M. Vitamin E supplementation suppresses macrophage accumulation and endothelial cell expression of adhesion molecules in the aorta of hypercholesterolemic rabbits. Atherosclerosis, 2004 Oct; 176(2): 265-272.
- Tahir M, Foley B, Pate G, Crean P, Moore D, McCarroll N, Walsh M. Impact of vitamin E and C supplementation on serum adhesion molecules in chronic degenerative aortic stenosis: a randomized controlled trial. Am Heart J, 2005 Aug; 150(2): 302-6.
- Meydani M, Cohn JS, Macauley JB, McNamara JR, Blumberg JB, Schaefer, EJ. Postprandial Changes in the Plasma Concentration of [alpha]- and [gamma]-Tocopherol in Human Subjects Fed a Fat-Rich Meal Supplemented with Fat-Soluble Vitamins. Journal of Nutrition, 1989; 119:1252-1258.
- Balazs Z, Panzenboeck U, Hammer A, Sovic A, Quehenberger O, Malle E, Sattler W. Uptake and transport of high-density lipoprotein (HDL) and HDL-associated alpha-tocopherol by an in vitro blood-brain barrier model. J Neurochem, 2004 May; 89(4): 939-50.
- Harvey and Champe, eds., Biochemistry: 3rd Edition, Baltimore: Lippincott Williams and Wilkins (2005) 389.
- If each meal contained 100 grams of fat, the first and second groups would receive identical amounts of monounsaturated fat (39 g), similar amounts of saturated fat (54 g and 52 g), and similar amounts of polyunsaturated fat (7 g and 9 g), while the third group would receive more monounsaturated fat (72 g), much less saturated fat (16 g), and more polyunsaturated fat (12 g). The first group would receive 117 mg of vitamin E, while the second would receive 8 mg and the third would receive 13 mg. If the second group received a supplement of 5 mg of natural vitamin E, the second and third groups would receive equivalent amounts of this vitamin. See reference 9.
This article appeared in Wise Traditions in Food, Farming and the Healing Arts, the quarterly magazine of the Weston A. Price Foundation, Fall 2006.🖨️ Print post