The one we have been waiting for...enjoy!
http://www.proteinpower.com/drmike/...ated_fat_s.html
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.
And again.
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.
Saturated fat study sucks
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