Consumption of Saturated Fat Impairs the Anti-Inflammatory Properties of High-Density Lipoproteins and Endothelial Function – A response
|Step Away from the Burger and No One Will Get Hurt
by Regina Wilshire
|Saturated fat study sucks
by Michael R. Eades, M.D.
|Myth: One High-Saturated Fat Meal Can Be Bad
by Chris Masterjohn
|One High-Saturated Fat Meal Harms Your Arteries? Rubbish!
by Anthony Colpo
Step Away from the Burger and No One Will Get Hurt
Of all the headlines generated by the recent study, Consumption of Saturated Fat Impairs the Anti-Inflammatory Properties of High-Density Lipoproteins and Endothelial Function, from the August 15th issue of the Journal of the American College of Cardiology, one stands above all the others:
The first sentence is equally ominous, “Scientists at The Heart Research Institute in Sydney, Australia warned that a single bite of a burger or one meal high in saturated fat is enough to cause a heart attack.”
The use of argumentum ad metam (an appeal to fear) begs our attention; created in this instance, as a logical fallacy, to support the dogma that dietary saturated fat is deadly – if we eat it, even just one bite of it in a foof that has saturated fat, like a burger, we risk an immediate death by heart attack.
Really, who wants to risk taking a single bite of a burger if it might cause them immediate death?
This is exactly the fear cojured up in the headline and first sentence – eat that bite and you’ll die of a heart attack.
Makes you wonder how many people died eating just one bite of a burger in the study? Oh, that would be none.
So, then, how many people died eating a high fat meal that included eating a whole burger? Oh, that too would be none.
Why then the histrionics about taking a bite of a burger?
Surely someone had to keel over eating just a bite of something laden with saturated fat, no?
But, we must convince the population that the evil, unnessasary, artery clogging, heart damaging saturated fat must be banished from their diet…NOW!
The American Heart Association, American Diabetes Association, American Dietetics Association, and well, every leading medical/disease oriented organization and even the US government all repeatedly insist saturated fat is deadly; recommendations over the past few decades have dropped steadily as more and more “proof” is presented that consuming saturated fat will give you a heart attack.
This particular study is being promoted in the media as evidence that the cause-and-effect of saturated fat is immediate in the body and therefore it is deadly to eat in even small or moderate amounts.
You may be wondering, what exactly did the study find?
The short answer – they found that when you give a small number of subjects a slice of carrot cake and a milkshake rich with poly-unsaturated fat (75% of the total fat was PUFA; safflower oil) it had a less damaging effect in the hours following the “meal” than when the slice of carrot cake and milkshake was rich with saturated fat (89.6% of the total fat was SFA; coconut oil).
Pay no mind to the fact that:
- both types of fat had acute effects that could be called “damaging” but with no real statistically significant differences. As the researchers put it, “a non-significant trend toward impairment…” Not only was it a “trend” – it was a NON-SIGNIFICANT trend, basically nothing to get your panties in a wad about;
- the high-polyunsaturated fat “meal” resulted in a statistically significant rise in LDL (remember that pesky “bad” cholesterol) compared to the saturated fat “meal”;
- there were NO STATISTICALLY SIGNIFICANT DIFFERENCES in HDL, triglycerides, insulin, non-esterfied fatty acids (NEFA), forearm bloodflow, peak flow, total hyperenemia, flow-mediated dialation, or blood vessel size;
- the researchers failed consider or measure the effect of a major confounding variable – the effect of sugar on blood glucose levels and thus insulin levels when combined with either type of fat;
- the researchers failed to completely isolate the effects of either fat type because they fed a high-fat, high-sugar mixed meal concoction that would not be replicated in a real world experience!
Add to this:
- oleic acid, found in safflower oil, has previously been shown to inhibit endothelial activation in the short-term;
- saturated fatty acids do not activate endothelial expression, they simply do not inhibit it;
- variation in serum insulin and sympathetic tone are physiological determinants of endothelial function;
- hyperglycemia (and thus higher insulin) is implicated in the activation of endothelial expression;
- hyperglycemia interferes with the activity and function of endothelial cells;
- insulin’s normal stimulatory action on human endothelial cell vasodilator pathways may be impaired under conditions of …hyperglycaemia;
But, hey, it’s the saturated fats….they’re deadly. Just step away from the burger and no one will get hurt.
Facts, data or findings that go against the preconceived notions are going to be ignored. People who have made up their minds and don’t want to be confused by the lack of hard data are no longer an exception these days, but accepted as “expert” as long as they continue to perpetuate the dogma that saturated fat is deadly in any and every dietary context.
These days, it is apparent that scholars, as well as journalists, have made their minds up and don’t want to be confused by the facts and instead will make a massive effort to muddy the waters even more; sow confusion; and instill a fear that saturated fats are lethal – even with just one bite – in the diet of humans.
Thus, we’re expected to be good little soldiers in the war against obesity and heart disease and ignore any potential defects in studies such as this.
By establishment standards, I’m not being a good little soldier here pointing out the glaring flaws with this data. I simply cannot, in good consciousness, ignore the methods used to scare the begeebers out of those reading the various headlines this week, nor the flaws in the very short study with too few subjects (that alone render it meaningless) that had confounding variables (fatty acid composition, fatty acid chain length, sugar, blood glucose, insulin) the researchers did not control for and completely failed to even mention in the findings and discussion!
The lead researcher, Dr. Stephen Nicolls was quoted in the media, “The take-home, public-health message is this: It’s further evidence to support the need to aggressively reduce the amount of saturated fat consumed in the diet.”
Even though the full-text of the paper was specific, “In summary, the present study raises the possibility that the differential effects of dietary fats on the anti-inflammatory potential of HDL and endothelial function may contribute to the apparent benefits of polyunsaturated over saturated diets observed in the epidemiologic literature.”
Pray tell, which population can we find that observation in the literature?
It’s certainly not obeserved in the French, where “[c]onsumption studies…show a high dietary fat contribution (37-38% even 40% of total energy) with over-consumption of saturated fatty acids, under-consumption of monounsaturated fat and, to a lesser extent of polyunsaturated fatty acids.” That is, of course “over consumption” defined by our dogma that any level above 7-10% of calories is excessive and harmful. Ignore the fact the French live longer than we, in better health, with significantly less cardiovascular disease.
Let’s just call them a “paradox.”
Oh no, we better call Spain a paradox too since “[t]rends in food consumption show increases in intakes of meat, dairy products, fish, and fruit, but decreases in consumption of olive oil, sugar, and all foods rich in carbohydrates. Although fat and saturated fat intakes increased, these changes were not accompanied by an increase in CHD mortality rates.” Ignore the fact they live longer than we, in better health, with significantly less cardiovascular disease and declining rates of cardiovascular disease despite increases in their consumption of saturated fat!
Gosh, even the epidemiologists concede “Between-population ecologic studies have demonstrated an association between intake of fat, specifically saturated fat and total cholesterol and coronary heart disease (CHD) mortality. However, results are inconsistent from within-population cohort studies.”
So, again, where is that proof in the literature? Where’s the data? Where’s the evidence?
Rather than present hard data, the tactic now is to scare the daylights out of people with headlines that warn of immediate death by heart attack if they take just one bite of a burger.
Repeat the lie often enough and people hold it as truth.
Except of course by those who take the time to actually read the studies, investigate the referenced citations of support of the findings, review the design and methods in various studies, check to see if statistically significant findings synch with the abstract, figure out if the study had any statistical power, and examine if all confounding variables were controlled for.
Or those who take the time to read the analysis of those of us who do!
A critical look at nutritional science and anything else that strikes my fancy.
August 14, 2006
Saturated fat study sucks
The latest saturated fat study to come down the pike has been picked up by all the newspapers it seems, reinforcing one of my favorite Mark Twain quotes:
If you don’t read the newspaper, you are uninformed. If you do read the newspaper, you are misinformed.
This latest piece of whatever has followed the typical trajectory of such things. Study done, pre-publication press release, dissemination by gullible press that doesn’t have sense enough to ask the right questions, publication in scientific journal. In this case it goes to show that the gullible press is really gullible where saturated fat is concerned. No study is too moronic as long as it implicates saturated fat as a bad nutritional actor.
Let’s look at a sampling of what a number of “health and science’ outlets have to say. Medical News Today warns that meals high In saturated fat Impair “good” cholesterol’s ability to protect against clogged arteries and cautions us that
Before you bite into that burger or devour that doughnut, first chew on this: New research shows that just one meal high in saturated fat can affect the body’s ability to protect itself against some of the underlying causes of heart disease and stroke.
HealthDay asks us if we ‘need more proof that a diet high in saturated fats is bad for [our] heart[s]?’ Then informs us that ‘just a little high-saturated fat can be hard on the arteries.’
Good ol’ reliable WebMD (reliable, that is, if what you want to know is the low-fat take on things) comes through with the caveat that ‘even one fatty meal affects arteries’ and tells us that
a new study that shows eating a meal high in saturated fats, like a cheeseburger and fries, can reduce the ability of the body’s “good” HDL cholesterol to protect against clogged arteries.
And enlists the aid of an expert to help make the case
“It’s further evidence to support the need to aggressively reduce the amount of saturated fat consumed in the diet,” says researcher Stephen J. Nicholls, MBBS, PhD, PRACP, FACC, a cardiologist at The Cleveland Clinic in Ohio.
And you thought that all those letters behind someone’s name make him smart?
Reuters chimes in with ‘saturated fat impedes “good” cholesterol activity.’
What I’ve laid out is just the short list. I found this study mentioned in practically every newspaper I read from throughout the world. They were all the same. Not an ounce of questioning, but a ton of implication instead. Notice how in the above examples the reporters are so certain. There is no equivocation. In their minds saturated fat is, by God, bad for you, and that’s how they’re going to report it.
Let’s take a look at the actual study to see if it lives up to all it’s hype, let’s see if it’s worthy of all the knee jerk substantiation by the finest minds in the medical reporting world.
The study, published in the current issue of the Journal of the American College of Cardiology, looks at what happens to the arteries of subjects who consume a high-saturated-fat meal as compared to those who eat a high-polyunsaturated-fat meal.
Fourteen thin (BMI 23.6), healthy subjects (average age 29.5), after an overnight fast consumed a single meal containing primarily saturated fat or primarily polyunsaturated fat. A month later the process was repeated with the opposite diet.
The first meal contained safflower oil (fatty acid composition: 75% polyunsaturated, 13.6% monounsaturated, and 8.8% saturated fat). The second meal contained coconut oil (fatty acid composition: 89.6% saturated fat, 5.8% monounsaturated, and 1.9% polyunsaturated fat). The order of meals ingested was determined by random allocation and was blinded to the investigators.
How did they provide the saturated and polyunsaturated meals? I mean it’s hard to down a bunch of safflower oil and coconut oil all by themselves, so how did they get the subjects to eat all this fat?
Well, according to the paper
Subjects consumed 1 of 2 isocaloric meals comprising a slice of carrot cake and a milkshake containing 1 g of fat/kg of body weight.
Say what? Carrot cake and a milkshake?
Is there anything else in carrot cake and milkshakes besides fat? How about sugar and flour? Let’s see what the article says about the nutritional breakdown of the carrot cake and milkshake meal. Would you believe that it doesn’t say anything at all? Nada. Zip. Zero. Other than the fact that there is about 70 gms of fat per meal and that one meal contains 89.6% saturated fat and the other 75% polyunsaturated fat, we are provided with no nutritional information.
Never one to let researcher lack of openness stand in my way, I looked up a milkshake and carrot cake in my handy nutritional analysis program and worked backwards to calculate what else we would find in these foods along with the 70 grams of fat. Turns out that a piece of carrot cake contains about 55 grams of fat and 24 ounces of milkshake contains the other 15 grams. What else is in there along with the fat? How about 173 grams of carbohydrate, 143 grams of which is sugar. Remember, 100 grams of sugar is about a half cup, so 143 grams is almost 3/4 cup. Of sugar.
So, what we have are two meals: one high in refined carbohydrates and saturated fat, the other high in refined carbohydrates and polyunsaturated fats. In fact, both diets are higher in carbohydrates (in terms of calories) than they are in fat. Each diet contains 692 kcal of carb and 630 kcal of fat. If you add it all up, including the protein, you get a single meal containing 1426 kcal, most of which is carb.
We all know that the standard American diet, which is the high everything diet, causes problems. So, what these researchers have done is studied the standard American diet with two different types of fat. Assuming they found a difference, all they can really say is that saturated fat in combination with a ton of carbohydrates (mainly sugar) causes more problems than the same diet using polyunsaturated fat. What of value can we take away from any of these findings, assuming there are some? The researchers have used two foods that allow this kind of fat substitution and maintain their taste and mouthfeel. Any more–thanks to the food police–most foods containing saturated fat do so only because saturated fat has some cooking property that is necessary in the preparation of that particular food. Anything else is made with unsaturated fat. So, we have a study that may tell us that there is a difference between the actions of saturated fat and unsaturated fat in a giant, calorically dense meal that contains more carbohydrate than anything else. Who cares? The great unwashed masses who flock to the fast food places and chow down on ‘indulgent’ items certainly don’t care. And the study isn’t applicable to those following either low-fat or low-carb diets.
Let me get off my soap box and let’s move on. The researchers did a number of evaluations on the subjects while they were fasting, gave them the 1426 kcal cake and milkshake diet, then repeated the evaluations at 3 hours and 6 hours after the meal.
What did they look at?
The researchers looked at four different parameters. They wanted to see if the difference in fat type made a difference in blood lipid and insulin levels, if it made a difference in the way the subjects arteries reacted in a couple of different ways, and they wanted to see if the different fats made the HDL particles less anti-inflammatory.
First, looking at the difference between serum total cholesterol, LDL, HDL, triglycerides, Insulin, and non-esterified fatty acid levels after the two diets, we find that only two–total cholesterol levels and LDL levels–are different to a statistically significant degree. Both were lower after the saturated fat meal. Now most low-fat advocates believe that LDL is the single most important lipid parameter in existence, but for some reason these guys chose to not even mention the fact that in this study LDL was lower on the saturated fat diet than on the polyunsaturated fat diet. I wonder why?
Next, the researchers performed two different tests for evaluating arterial function on the subjects. One of these tests was a measurement of forearm blood flow; the other was a measurement of brachial artery (a large artery in the arm) diameter change. Both of these methods of evaluation are difficult to explain using non-technical language, but basically both work in similar ways. When blood vessels are compressed with a tourniquet for a period of time, the arteries downstream from the area of restriction receive little to no blood. When the tourniquet is released, blow flows into the artery and the artery dilates. You can press your thumb hard into the inside of your forearm and hold it for 10 seconds. When you remove your thumb, the area underneath will be white. As you watch, the area under your thumb print will become pinkish red as blood flows back into it. The more quickly blood flows back in, the better your arterial and capillary function. The two tests used in this study look at this same thing only using much more sophisticated techniques.
In one of the two tests there was a slight difference in the negative direction at the 3 hour mark with the saturated fat diet, but overall there was no statistically significant difference between the two diets in either test.
Finally, the researchers performed a complicated evaluation of HDL samples incubated with human umbilical vein endothelial cells. I’ll let them explain it.
Human umbilical vein endothelial cells were isolated and incubated with HDL samples at a concentration of 2, 4, or 8 μmol/l apoA-I in media containing 10% heat-inactivated serum for 16 h at 37°C in 5% CO2. Cells were incubated for a further 5 h in the basal or stimulated state following the addition of tumor necrosis factor-alpha (0.2 ng/ml). The cell surface expression of adhesion molecules was assessed with an enzyme-linked immunosorbent assay technique. Cellular viability was determined to be greater than 95% by trypan blue exclusion.
After incubation with the HDL collected after both the meals, there was a higher level of expression of ICAM-1 and VCAM-1 in the ‘activated’ cells incubated with the HDL from the saturated fat diet than from that from the polyunsaturated fat diet. This difference would seem to indicate that there may be a decrease in inhibition of these inflammatory molecules by the HDL from the saturated fat diet. And, although the data was difficult to determine from the paper, this difference apparently reached statistical significance. What we can’t tell from the paper is if the difference really makes any difference in the real world of arterial function. In other words, I may get a statistically greater amount of ethanol in gasoline I purchase from Mobil than I do in gas I purchase from Chevron, but does it make a difference in how my car runs? Given all this, I will readily stipulate that HDL from the subjects who ate the high-carb, high-saturated fat diet has a reduced anti-inflammatory potential as measured in incubated human umbilical vein endothelial cells compared to the other HDL. But no one can tell me what it means–if anything–in real life.
I suspect that it doesn’t mean a lot since the authors of the paper went to great lengths to play up the non-significant differences in the more direct tests. As mentioned before, there was not a single word about the differences in total cholesterol and LDL levels, which were significant.
The authors reported
A nonsignificant trend toward impairment of endothelium-dependent vascular reactivity in conduit arteries was also demonstrated after the saturated fat meal.
Hey, guys, there ain’t no such animal. Just like a woman can’t be trending toward pregnancy, there is no nonsignificant trend toward anything. It’s either significant or it isn’t. Period. Unless, of course, you’re trying to pull the wool over someone’s eyes.
There was a trend toward a greater post-prandial impairment seen after the consumption of the saturated compared with the polyunsaturated fat.
There they go again.
Although the meals had different effects on hyperemia in conduit and resistance vessels, the direction of the meal-related changes was similar in large and small vessel studies, with a trend toward a greater increase in flow after consumption of polyunsaturated fats.
Let’s see what the conclusions of this study are. First, let’s look at the conclusion in the abstract, which is the only part of this study that the vast majority of people will ever see.
Consumption of a saturated fat reduces the anti-inflammatory potential of HDL and impairs arterial endothelial function. In contrast, the anti-inflammatory activity of HDL improves after consumption of polyunsaturated fat. These findings highlight novel mechanisms by which different dietary fatty acids may influence key atherogenic processes.
Pretty darn unequivocal, I would say. These guys aren’t shy. No pussyfooting around here.
Now let’s look at the conclusions at the end of the paper, the ones someone would see who actually took the trouble to read the paper and see all the references to nonsignificant trending.
In summary, the present study raises the possibility that the differential effects of dietary fats on the anti-inflammatory potential of HDL and endothelial function may contribute to the apparent benefits of polyunsaturated over saturated diets observed in the epidemiologic literature.
Quite a difference I would say.
Now, go back and read the press reports now that you know the real story behind this study.
Once again, I’ve got to say, the anti-saturated fat bias is so pronounced that this mealy mouthed study was picked up by news services and newspapers all over the world and reported as gospel. All because the press report spun it the way they did. Well, I have to say it. The spin stops here.
Why you don’t need vegetable oil in your carrot cake and milk shake to protect your arteries.
By Chris Masterjohn
Published August 20, 2006
Newspapers the world over have recently declared that a single meal rich in saturated fats will disrupt the functioning of your arteries and contribute to the inflammation of your blood vessels, following an Associated Press story by Joe Milicia.1 Milicia reported on a recent study2 published by a team of researchers led by Dr. Stephen J. Nicholls of the Australian Heart Research Institute in theJournal of the American College of Cardiology entitled, “Consumption of Saturated Fat Impairs the Anti-Inflammatory Properties of High-Density Lipoproteins and Endothelial Function.”
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.” Of course, the study showed no such thing.
Dr. Nicholls, the lead author of the study, was quoted in the article as saying the study showed the “need to aggressively reduce the amount of saturated fat consumed in the diet.” The AP article then clarified for us 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. Wow! This study had the power to make sweeping conclusions about over 15 different foods! But in reality, of course, the study showed no such thing.
The study has already been widely criticized on the internet. Some of the criticism has been good; some has been rather poor. My own view is that this was a well-designed and interesting study; the authors of the report, however, unfortunately made unjustified conclusions from their data in the report itself, and the press articles further sensationalized the story and distorted the study’s findings, making rather hysterical claims, unfortunately with the support of the study’s lead author.
You may be surprised to find out that arterial function was actually better after the coconut oil meal than the safflower oil meal! Or that, contrary to the claims of the Associated Press article, the authors never measured inflammatory components in the subjects’ blood. Or further, that they provided absolutely no evidence that different types of fatty acids, such as saturated or unsaturated, had anything to do with their findings!
In fact, they completely overlooked an alternative explanation that has substantial evidence in the scientific literature to support it: the differences they observed between the anti-inflammatory effects of the different diets may have been due largely or entirely to the difference in vitamin E content of the diets rather than the type of fatty acids present in the oils.
So, let’s take a look at what the researchers actually found, and what it might actually mean.
One High-Saturated Fat Meal: The Real Story
The researchers fed fourteen adults a meal of carrot cake and a milk shake on two separate occasions. In half of the meals, the food was made with coconut oil, which is about 90% saturated fat, while in the other half, the food was made with safflower oil, which is about 75% polyunsaturated fat.
Both oils were non-hydrogenated, organic, unrefined and virgin (David Celermajer and Jason Harmer, personal communication).
Each subject received each of the two types of meals on separate occasions after an overnight fast. Half of them received the safflower oil meal first and the coconut oil meal second, while the other half received the coconut oil meal first and the safflower oil meal second, to ensure that the order in which they received the meals did not affect the result. The two meals were separated by a month, to ensure that the first meal had as little an effect as possible on the second meal. Finally, the researchers were blinded to which meals the subjects were receiving, to minimize the effect of bias on the collection of the data.
The researchers took three types of measurements before the meals were fed and at 3 hours and 6 hours after the meals were fed. 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. For example, they tested the amount of blood flowing through the subjects’ forearms at each point, and they tested the subjects’ “vascular reactivity.” That is, they used pressure to stop blood flow through an artery in the arm and then tested how quickly and to what extent the artery reacted once the pressure was 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’s believed to be in.
Finally, the researchers extracted HDL from the subjects’ blood at each time point. Then, they incubated endothelial cells from human umbilical veins with the HDL at various concentrations. After the incubation period, they added an inflammatory chemical called TNF-alpha to the cells, which stimulates the production of adhesion molecules such as ICAM-1 and VCAM-1, which are believed to play a role in the adhesion of plaque to arteries. HDL has been shown to inhibit the expression of these inflammatory molecules, and the researchers conducted this part of the study to see if how you eat can affect how much potential HDL has to inhibit the expression of presumably harmful adhesion molecules. (See note 1 for brief comments on the sample size and study design.)
The researchers claimed to generate two findings:
- Flow-mediated dilation, or the ability of blood vessels to dilate and return blood flow after being occluded with pressure, 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 ICAM-1 and VCAM-1 in response to TNF-alpha 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-alpha 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 are justified by the study.
Let’s take a closer look at each.
Coconut Oil and Flow-Mediated Dilation: Harmful or Helpful?
The researchers claim that consumption of the saturated fat meal impaired flow-mediated dilation — that is, it hurt the ability of blood vessels to dilate and return blood flow to an area from which blood flow had been stopped with pressure. The researchers did indeed show that at the 3-hour mark the decline in flow-mediated dilation was almost twice as great in the coconut oil group as it was in the safflower oil group. (See note 2 for a brief comment on statistical significance.)
Yet as Anthony Colpo, author of The Great Cholesterol Con has already pointed out,4 the flow-mediated dilation 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% better flow-mediated dilation than those who were about to eat the safflower oil meal. Even at the 3-hour point, when flow-mediated dilation had declined the most, it was still 9% higher in the coconut oil group than the safflower oil group!
There are two ways we could look at this. Figure 1 shows the changes that took place in flow-mediated dilation three and six hours after the meals, relative to the flow-mediated dilation before the meals (called “baseline”). (See note 3 for why I’m presenting it this way.) You can see for both the coconut oil meal and the safflower oil meal, flow-mediated dilation declined substantially at the 3-hour mark.
Figure 1. Percent change in the degree of flow-mediated dilation compared to baseline values.
|Group||Baseline||3 hours||6 hours|
|Safflower Oil||No change.||17% lower.||8% lower.|
|Coconut Oil||No change.||32% lower.||10% lower.|
Now let’s look at it another way. Figure 2 compares the relative degree of flow-mediated dilation between the coconut oil group and the safflower oil group. Surprise, surprise — the flow-mediated dilation 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 in the coconut oil group to that in the safflower oil group at three time points.
|Baseline||3 hours||6 hours|
|33% higher in coconut oil group.||9% higher in coconut oil group.||29% 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 flow-mediated dilation in the coconut oil group? Or is the reason for this decline the simple fact that the people who ate the coconut oil started out with a higher value of flow-mediated dilation in the first place, and therefore, so to speak, had more to lose?
There are two reasons that the latter might be true: first, the decline in flow-mediated dilation after a meal might not be a function of the flow-mediated dilation before the meal; second, a randomly high sampling error for the flow-mediated dilation before the meal could result in what’s called “regression to the mean,” which is explained below.
In the first case, it could be that eating carrot cake and drinking a milkshake, regardless of whether it is made with safflower oil or coconut oil, depresses flow-mediated dilation to a certain point regardless of fasting levels of flow-mediated dilation. For example, eating the meal might depress flow-mediated dilation to about 5%, regardless of whether the person’s fasting level of flow-mediated dilation was 6% or 9%, in which case a person with a higher fasting level would experience a greater decline simply by virtue of the higher fasting level.
Thus, the coconut oil group, who by random chance had a 33% higher fasting rate of flow-mediated dilation, would exhibit a greater relative decline than the safflower oil group for no other reason than that they started off with substantially better flow-mediated dilation in the first place!
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 [flow-mediated dilation] 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.
And of course that’s exactly what we saw here. 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 flow-mediated dilation, “damage to the vessels happens immediately” 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 statistical arterial dysfunction with one, single meal.
Does Coconut Oil Cause Inflammation?
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 people consuming the meals. 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-alpha to the cells, and measured whether the HDL isolated after the different meals had a different ability to lower the amount of adhesion molecules released after stimulation with the TNF-alpha.
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-alpha than 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 cells incubated with HDL isolated from fasting subjects.
There are a number of problems with the large leap of logic it takes to conclude from this that a meal rich in saturated fat causes inflammation. First, others4, 5 have already questioned how relevant this finding with isolated cells is to how our arteries actually function within us. After all, 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 specifically of HDL. The researchers 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 (David Celermajer, personal communication). Virgin coconut oil is rich in very powerful polyphenols,6 some types of which have been shown to decrease expression of TNF-alpha and adhesion molecules,7, 8 and which are carried by water-soluble proteins in the blood and not by HDL.9 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 plasma. 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. 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 between safflower oil and coconut oil does not stop at the relative saturation of their fatty acids. Figure 3 shows the difference in vitamin E content between the two oils. Safflower oil is 77 times higher in alpha-tocopherol and 47 times higher in total tocopherols.10
Figure 3. Typical tocopherol (vitamin E) content of coconut oil and safflower oil. Source: (Enig, 2000).
|Tocopherol||Coconut Oil||Safflower Oil|
|Alpha-tocopherol||5 mg/kg||387 mg/kg|
|Delta-tocopherol||6 mg/kg||240 mg/kg|
|Total tocopherols||11 mg/kg||801 mg/kg|
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.11 In fact, Chinese researchers performed a very similar experiment to the one we’ve been discussing, where 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.12 Another group found vitamin E to reduce both ICAM-1 and VCAM-1 in the heart cells of rats.13
Vitamin E suppressed ICAM-1 and VCAM-1 levels in vivo in rabbits, although the effect on VCAM-1 was not statistically significant.14 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.15
Vitamin E travels in the blood associated with lipoproteins, including HDL.16 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.17 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? From what I can find, data is very limited on the effects of eating a meal on the distribution of vitamin E in the blood. The one study I’ve found so far16 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. (See note 4.) 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, while the safflower oil added enough vitamin E to the meal 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’ve 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.
This 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 this is a plausible explanation. Further research would be needed to confirm or refute my hypothesis (see note 5.)
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. (My emphasis.)
So Which Oils Should We Eat?
If it turns out to be true that the difference in 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 doesn’t even mean we should eat safflower oil!
It simply means that coconut oil is not a good source of vitamin E. Coconut oil is still the best source of medium-chain fatty acids that 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.18Safflower 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 a high 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. Palm oil is an excellent example of such a source.
Palm oil is only 9% polyunsaturated, compared to safflower, which is 75% polyunsaturated. In terms of absolute amount of vitamin E, 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% higher in palm oil than safflower oil.
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 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.”
Drawing Conclusions: One Meal High In Saturated Fat is Not So Bad
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.
This is all on the basis of a study that couldn’t differentiate the effect of coconut oil from the effect of random sampling error on flow-mediated dilation and showed people consuming coconut oil to havebetter flow-mediated dilation at all time points than people consuming safflower oil.
It is on the basis of a study that could not differentiate between the effects of saturated fats and the effects of low-vitamin E meals on the capacity of HDL to prevent inflammation in a Petri dish.
It is on the basis of a study that told us nothing about the amount of inflammation going on within the people consuming the meals, who are much more complex than globs of cells in a Petri dish.
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 mean time, I’m going to continue cooking with CLA-rich clarified butter, and continue eating vitamin E-rich red palm oil and polyphenol-rich virgin coconut oil and extra virgin olive oil. I will continue to get my essential fatty acids from animal sources including butterfat, egg yolks from pasture-raised chickens, organ meats, cod liver oil, and fatty fish, so I can obtain the most benefit from the hormone precursors and structurally useful essential fatty acids while not overdosing on peroxide-promoting, free radical-generating, vitamin E-depleting polyunsaturates from vegetable oils like safflower oil.
Whoever’s going to convince me to do otherwise has a bit more work to do.
1. One internet blogger has claimed that the small sample size (14 people) and the short duration of the study “alone render it meaningless,” and further criticized the researchers for “fail[ing] to completely isolate the effects of either fat type because they fed a high-fat, high-sugar mixed meal concoction that would not be replicated in a real world experience.”3
I would certainly like to see the study repeated in the context of a more nutritious and less refined meal, but the researchers effectively controlled for the sugar, flour, milk and other parts of the meal by keeping them the same and varying only the oil with which the food was made. While a larger sample size would be better and a longer study would be easier to understand the implications of, neither a small sample size nor a short duration make the study “meaningless.”
Researchers conduct statistical analyses that determine whether their study has the statistical power to conclude that a correlation they’ve observed is real. Since these researchers did observe some findings that were statistically significant, this shows ipso facto that their sample size was sufficiently large to generate the conclusion that those particular correlations were real.
This is, of course, different than drawing an inference about what the correlation means from the data. This is more of an art, and subject to error. The blogger cited above misses the more important point that the researchers, doctors who were interviewed in the press, and journalists were careless in interpreting the meaning of the results. [Back]
2. This finding has been brushed aside by several authors because the difference between the two meals did not reach statistical significance.4, 5 In the context of this study, “statistically significant” means that the authors performed statistical tests showing that the likelihood their finding was due to chance was 5% or less.
Actually, the decline in flow-mediated dilation after the coconut oil meal did indeed reach statistical significance. The difference between the coconut oil and safflower meals were close to significance: an 8% likelihood the finding was due to chance. This is good reason to be less sure of the data and to be more cautious in interpreting it, but it doesn’t somehow make the finding disappear into thin air or become irrelevant. Setting the significance level at 5% is simply an arbitrary convention. [Back]
3. If you’ve read Anthony Colpo’s article, my numbers might confuse you at first because Colpo presented the data as absolute change in percentage points, reporting changes of 0.9% and 2.2%, whereas I’m reporting the relative change in dilation. Thus, my numbers are much larger.
Here’s the difference: The researchers tested the change in the diameter of the blood vessel after the pressure they applied to restrict blood flow was released. When the pressure is released, the diameter increases to rush blood to the area that has been deprived of blood. Among the various groups, the change in diameter ranged from a 4.3% increase in diameter to a 6.9% increase in diameter. Before the coconut oil group ate their meal, the average increase in blood vessel diameter after restriction was 6.9%. At three hours following the coconut oil meal, the average increase in blood vessel diameter after restriction was 4.7%. Colpo reported this as a 2.2% decline by subtracting 4.7% from 6.9%. I reported it as a 32% decline by dividing 4.7% by 6.9%, then subtracting this figure from 100%, showing the relative decline as a percentage of the baseline value.
This strikes me as a much more valuable figure, because the absolute percentage of increase in blood vessel diameter is small. Reporting absolute percentage change, by contrast, does not give us any sense of the importance of the change. If we expected a blood vessel to double in diameter, which would be an increase of 100%, then it might be relatively unimportant if the diameter increases by 97.8% instead of 100%. Why? Because the additional volume of blood that can be transferred in a given section of the blood vessel to compensate the tissues for previous oxygen deprivation would only be about 4.4% lower. By contrast, if we expect the blood vessel diameter to increase to a maximum of, say, 10%, then an absolute reduction of 2.2% to 7.8% dilation is suddenly much more profound. In this case, the additional volume of blood that can be transferred in a given section of the blood vessel would be 39.2% lower. Cells that are starving for oxygen to whom compensatory additional oxygenated blood is supplied at an almost 40% lower rate probably don’t care that the absolute change is only 2.2%! [Back]
4. The only study I could find on the effects of a meal on the distribution of vitamin E between the various lipoproteins in the blood16 seems to show, but does not show conclusively, that eating a meal, in and of itself, either reduces the total amount of vitamin E in the blood or causes it to shift from HDL and LDL to other lipoproteins, while the vitamin E content of the meal compensates for this effect, such that a low-vitamin E meal would reduce the amount of vitamin E carried in these lipoproteins and a high-vitamin E meal would raise it.
After a meal containing 18 mg of alpha-tocopherol, the alpha-tocopherol content of HDL declined at three hours, and bottomed out after six hours, after which it rose. After a meal containing 27 mg of alpha-tocopherol, the alpha-tocopherol content of HDL bottomed out at three hours instead of at six hours, after which it rose, although it did not reach baseline values until at about 9 hours. After a meal containing 25 mg of gamma-tocopherol, the gamma-tocopherol level of HDL decreased slightly at three hours, but was raised beyond baseline levels at six hours. After a meal containing 51 mg of gamma-tocopherol, the gamma-tocopherol of HDL began increasing immediately or at least before the first postprandial measurement at three hours, with no initial decrease.
These results suggest two things:
- First, although gamma-tocopherol is present in HDL in smaller amounts than alpha-tocopherol (in the fasting state, there was roughly five times as much alpha-tocopherol than gamma-tocopherol in the HDL), it accumulates specifically in HDL more readily after a meal than does alpha-tocopherol. This is suggested because 25 mg of gamma-tocopherol accumulated in HDL more quickly and to a greater degree than 27 mg of alpha-tocopherol.
- Second, there is a general trend for a low-vitamin E meal to reduce the amount of vitamin E in HDL and a high-vitamin E meal to raise the amount of vitamin E in HDL. This is suggested because raising the amount of alpha-tocopherol from 18 mg to 27 mg reduced the amount of time for which the alpha-tocopherol level of HDL was reduced, and raising the gamma-tocopherol from 25 mg to 51 mg changed the trend from a reduction of the gamma-tocopherol level of HDL at three hours to an increase of this level at three hours.
It should be kept in mind that the reduction is occurring specifically in HDL, IDL and LDL. Vitamin E is initially transported by chylomicrons when it is absorbed, and all of the meals substantially increased the amount of vitamin E being carried by chylomicrons in the blood.
Unfortunately, we can’t draw any conclusive implications from this study for the following reasons:
- First, the researchers reported some of the measurements as a combination of HDL, IDL and LDL measured together, and other measurements for HDL and LDL measured separately. Since the trends for HDL and LDL matched each other closely when measured separately, it is probably valid to assume that the trends showed for HDL, IDL and LDL measured together reflect the trends for HDL alone, but it is also possible that this is invalid.
- Second, the researchers combined the high dose of gamma-tocopherol with the low-dose of alpha-tocopherol, and vice versa. We can’t discern from the study whether the amount of alpha-tocopherol affects how much gamma-tocopherol accumulates in the HDL and vice versa.
- Third, the researchers only looked at alpha-tocopherol and gamma-tocopherol. Safflower oil contains roughly 30% of its vitamin E as delta-tocopherol (see Figure 3), which was not measured in the study.
Nevertheless, as far as the data go, it is plausible that the low-vitamin E coconut oil meal reduced the total tocopherol content of the HDL fraction by virtue not of any specific attributes of coconut oil but by virtue of the effect of eating a meal per se, and that the high-vitamin E safflower oil meal increased the total tocopherol content of the HDL fraction by virtue of its high tocopherol content.[Back]
5. My hypothesis makes several testable predictions, allowing researchers to confirm or refute the hypothesis:
- The experiment should be repeated, and the total tocopherol levels of the HDL fractions should be analyzed after they are extracted. If the HDL extracted after the safflower oil meal is not higher in vitamin E than the HDL extracted after the coconut oil meal, this would completely refute my hypothesis. If the HDL taken after the coconut oil meal is not lower than that taken from the same subjects in the fasting state but nevertheless fails to inhibit adhesion molecule expression as well as HDL taken from the same subjects in the fasting state, this would partially but not completely refute my hypothesis.
- The total tocopherol and individual tocopherols of the HDL particles should be analyzed, and it should be determined whether the difference in any of the individual tocopherols or in the total tocopherols can account for the difference in adhesion molecule expression. If the difference in vitamin E cannot account for any of the difference in adhesion molecule expression, this would completely refute my hypothesis. If the tocopherol concentration of the HDL could account for some or all of the difference in adhesion molecule expression, this would be consistent with my hypothesis, but would not confirm it, because the tocopherol could simply be a marker for dietary intake of unsaturated fatty acids.
- In order to dissociate the effect of dietary vitamin E from that of dietary unsaturated fatty acids, the experiment could be modified in several ways. First, purified fatty acids that are devoid of vitamin E could be fed. Vitamin E could also be supplemented at various doses in various subgroups. This has the benefit of completely eliminating the confounding effect of vitamin E. It has the drawback of potentially failing to replicate the effect of natural fatty acids within their natural content as they are found in unrefined oils for any number of unforeseen reasons.
- Another way to dissociate the effect of dietary vitamin E from that of dietary unsaturated fatty acids would be to use different mixes of unrefined oils to achieve either a standardized fatty acid composition and differing vitamin E contents or a standardized vitamin E content with differing fatty acid compositions. This has the benefit of eliminating any unforeseen confounding factors introduced by refining oils and purifying fatty acids, and the drawback of being unable to completely eliminate vitamin E and other constituents and thereby perfectly isolate the effect of fatty acids. Here is one example of how this type of standardization could be achieved:
- 100 grams of palm oil yields an almost identical fatty acid composition to a combination of 50 grams of olive oil and 50 grams of coconut oil if we consider saturation only and disregard chain length. The two mixtures are identical in proportion of monounsaturated fat (39 grams), while the former yields 52 grams of saturated fat and 9 grams of polyunsaturated fat and the latter yields 54 grams of saturated fat and 7 grams of polyunsaturated fat. By contrast, the total vitamin E content of the former would be 117 mg, while the total vitamin E content of the latter would be only 8 mg. 100 grams of olive oil would provide only 16 grams of saturated fat and only 13 mg of vitamin E.
- If HDL isolated from subjects consuming unrefined palm oil was no more or less effective than HDL isolated from subjects consuming the mixture of unrefined coconut oil and unrefined olive oil, but was less effective than HDL taken from subjects consuming unrefined olive oil alone, it would strongly refute my hypothesis that dietary vitamin E is more important than the saturation of dietary fat. If, on the other hand, the HDL isolated from subjects consuming unrefined palm oil was much more effective than both the HDL isolated from subjects consuming the mixture of coconut oil and olive oil and the HDL isolated from subjects consuming olive oil alone, it would strongly refute the hypothesis that the saturation of dietary fat is most important and strongly support my hypothesis that the dietary vitamin E is most important.
- In order to completely dissociate the direct effect of vitamin E content of HDL particles from its potential role as a marker for other effects on HDL composition mediated by the degree of unsaturation of dietary fats, HDL particles could be artificially enriched with tocopherols or a combination of tocopherols and tocotrienols. If the variation in adhesion molecule expression by cells incubated in different sources of HDL particles can be completely accounted for by the degree of artificial enrichment of the HDL particles with vitamin E, this would support my hypothesis. If the variation in vitamin E content of the HDL particles could not account for the variation in adhesion molecule expression, it would refute my hypothesis.
We need to maintain perspective, though, and realize that this question is merely of academic interest, and has no practical relevance for which oils we should consume in our diet. Just because one oil increases the anti-inflammatory capacity of HDL more than another oil does not mean that it increases the total anti-inflammatory capacity of all of the constituents of the blood more than the other oil. Furthermore, adding an inflammatory cell signaling compound such as TNF-alpha to a Petri dish does not approximate the much more complex conditions that the cells lining our blood vessels experience.
Nevertheless I would like to see the answers to the questions I have raised in this article. To my knowledge, these are original research suggestions, but it is possible that others have already raised them elsewhere. [Back]
1. Milicia, Joe, “One High-Saturated Fat Meal Can Be Bad,” Associated Press. Carried by theWashington Post. August 7, 2006.
2. 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.
3. Wilshire, Regina, “Step Away From the Burger and No one Will Get Hurt,” Weight of the Evidence http://weightoftheevidence.blogspot.com. Published August 10, 2006. Accessed August 19, 2006.
4. Colpo, Anthony, “One High-Saturated Fat Meal Harms Your Arteries? Rubbish!” http://www.theomnivore.com/One_High-Saturated_Fat_Meal%20.html. Published August 12, 2006. Accessed August 19, 2006.
5. Eades, Michael R., MD, “Saturated fat study sucks,” http://www.proteinpower.com/drmike/archives/2006/08/saturated_fat_s.html. Published August 14, 2006. Accessed August 19, 2006.
6. 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.
7. 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].
8. 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.
9. 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.
10. 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; 122.
11. 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.
12. 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.
13. 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.
14. 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.
15. 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.
16. 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.
17. 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.
18. Harvey and Champe, eds., Biochemistry: 3rd Edition, Baltimore: Lippincott Williams and Wilkins (2005) 389.
by Anthony Colpo,
August 12, 2006.
For over five decades, the health and medical establishment has been telling us that saturated fat and cholesterol cause heart disease. My recently published book, The Great Cholesterol Con (Lulu 2006), explains clearly and concisely why this theory is utter rubbish. For most laymen, that sounds like an outrageous claim, but I readily challenge ANYONE to refute the arguments I have presented in my book.
The medical orthodoxy has successfully perpetuated the highly lucrative lipid hypothesis simply by ignoring contradictory evidence whilst aggressively publicizing ‘supportive’ evidence (health authorities also have no qualms about taking unsupportive evidence and ‘reinterpreting” it so that it appears supportive–my book gives numerous examples of this very phenomenon).
A textbook example of the establishment practice of ignoring contradictory evidence but relentlessly hyping ‘supportive’ evidence occurred this last week, with the publication of a study comparing the effects of a single high-saturated fat meal with a single high-polyunsaturated fat meal. According to the study, the saturated fat-enriched meal produced harmful increases in inflammatory factors and negative changes in arterial function. Headlines in the ever-compliant mainstream media immediately trumpeted the study as further proof that saturated fat was public health enemy number one. In robot-like fashion, media outlets all around the world mindlessly parroted the Associated Press headline “One High-Saturated Fat Meal Can Be Bad”.
One Over-Hyped Study Confirms Modern Health Research is Intellectually Bankrupt.
The study that caused all the kerfuffle was performed in Sydney, Australia (Nicholls SJ, et al). On two occasions one month apart, fourteen healthy subjects consumed a high-fat meal comprising a slice of carrot cake and a milkshake. The fat source in one of these meals was safflower oil, while the other contained highly saturated coconut oil. The researchers collected blood samples from the subjects before the meals, and 3 and 6 hours after. They extracted HDL from these samples, placed it into a solution containing human umbilical vein endothelial cells, and then observed the effect of the HDL on the endothelial cells expression of intercellular adhesion molecule-1 (ICAM-1) and vascular cell adhesion molecule-1 (VCAM-1). For those of you not familiar with scientific gobbledegook, adhesion molecules play vital roles in numerous cellular processes. They are believed to play an important role in the atherosclerotic process by facilitating the components of atherosclerotic plaque to proliferate at the site/s of arterial damage.
So let’s be clear: The researchers were not observing actual plaque formation in human arteries; this objective would be impossible in such a study. They were instead observing the effects of HDL extracted from humans after eating the test meals on the amount of ICAM-1 and VCAM-1 expressed by umbilical vein endothelial cells in a petri dish.
The other reported outcome was forearm blood flow. To listen to the mainstream media reports, one gets the impression that the subjects’ arteries were struggling to cope with blood flow after eating the saturate-enriched meal. A look at the data helps put the results into better perspective. Both meals caused decreases in arterial flow mediated dilation by a “whopping”—wait for it—0.9 and 2.2% in the polyunsaturated and saturated groups respectively. With these piddling changes, we’re not exactly talking life-threatening arterial spasm! Furthermore, looking at the data, one sees that the baseline flow mediated dilation was higher when the subjects ate the highly saturated test meal; was the greater reduction in FMD due to saturated fat, or simply a reversion-to-the-mean effect? Who knows, and who cares, because the difference was not even statistically significant! To quote the researchers themselves:
“Flow-mediated dilation (FMD) decreased at 3 h following consumption of the saturated meal (p _0.05 compared with pre-meal) but not 3 h after the polyunsaturated meal (p _ NS compared with the fasting state), although the difference in post-prandial change in FMD between the meals just failed to meet the conventional criteria for statistical significance. The FMD at 6 h after both meals did not significantly differ compared with the fasted state…, There was no significant change in the vessel size, estimated flow within the brachial artery, and glyceryl trinitrate response following both meals.”
Please note the section I have highlighted: “the difference in post-prandial change in FMD between the meals just failed to meet the conventional criteria for statistical significance.”
Translation: “As much as we really want to dump on saturated fat, the differences were not statistically significant, damn it!”
And what about the changes in ICAM-1 and V-CAM-1? Both ICAM-1 and V-CAM-1 were higher at six hours after consumption of the saturate-rich meal, but lower after consumption of the polyunsaturated-rich meal. It’s anyone’s guess as to the long-term relevance of acute reactions observed in a petri dish to plaque formation in human arteries. To claim that these reactions demonstrate that saturated fat is indeed atherosclerotic is to make a massive leap of faith. But that’s just what the researchers and many of their peers did.
Stephen Nicholls, the head researcher, had no qualms about making the great leap when he stated: “the take-home, public-health message is this: It’s further evidence to support the need to aggressively reduce the amount of saturated fat consumed in the diet.”
According to Dr. James O’Keefe, a cardiologist at the Mid America Heart Institute in Kansas City, the study showed “a really important concept – when you eat the wrong types of food, inflammation and damage to the vessels happens immediately afterward.”
Also jumping with unbridled anti-saturate abandon was Dr. Richard Milani, head of preventive cardiology at Ochsner Clinic Foundation in New Orleans, who advised: “…given a choice between something with polyunsaturated fat and saturated fat, please avoid the saturated fat”.
Let’s now find out why you should avoid Milani’s advice like a putrid smell.
The Importance of Long-Term Studies
When I ride my bike up a steep hill, or perform a weight training session, my blood pressure temporarily rises to very high levels. In fact, when high-intensity exercises like squats or deadlifts are performed with heavy weights, blood pressure often rises to astronomical levels. Does that mean I should stop lifting weights or riding my bike? If we applied the mentality of the researchers conducting the single-meal study, the answer would be yes. But if we use common-sense and reason, the answer is a resounding “NO!”.
Because the increases in blood pressure evident during physical exertion are not permanent, but transient. When I’m out of the gym or off my bike, my blood pressure is a perfectly healthy 110/70, which is actually lower than average. All that riding and pumping iron is actually stimulating my heart and arteries to become more efficient! The short-term blood pressure elevations I experience whilst exercising in no way reflect the long-term decrease in blood pressure that I have enjoyed.
The take home message is that it is the long term effects of diet and exercise that matter. Atherosclerotic heart disease is a process that takes many years to develop, which is why the majority of heart attacks occur in those over 65 years of age. Heart disease is not caused or prevented by a single meal.
So if it’s the long-term effects of diet or exercise that matter, then that is exactly what should be tested. This may sound like commonsense to many of you, but commonsense is a quality sadly lacking among a large proportion of those conducting research and dispensing health advice today.
Long-Term Studies are Non-Supportive, So They Are Ignored
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 (these trials are all discussed at length in The Great Cholesterol Con, with accompanying references).
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. 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 (Dayton S, et al).
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.
Conflict of Interest Information
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”. As the following list shows, polyunsaturated vegetable oils and margarines contribute a significant portion of certified products: Heart Foundation Tick.
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.
Anthony Colpo is the author of The Great Cholesterol Con, a no-holds-barred expose 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.
Milicia J. One High-Saturated Fat Meal Can Be Bad. Associated Press, Monday, August 7, 2006.
Nicholls SJ, et al. 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: 715–720.
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.