This is a follow-up to the chart in "Inflammatory Effects Of Common Oils" where coconut oil showed up as pro-inflammatory (using NutritionData's methodology).
Here's a small study that found a meal rich in coconut oil, where the fat is primarily saturated (compared to a meal high in safflower oil where the fat is primarily unsaturated) impaired the anti-inflammatory action of HDL, and resulted in impaired blood vessel function for several hours after the meal:
Consumption of Saturated Fat Impairs the Anti-Inflammatory Properties of High-Density Lipoproteins and endothelial Function, Journal of the American College of Cardiology, 2006
The aim of the study was:
"... to define the effect of consuming a single high-fat meal, differing in fatty acid composition, on the ability of high-density lipoproteins (HDLs) to inhibit the expression of proinflammatory adhesion molecules by endothelial cells and on large and small vessel function."The meal:
"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. The first meal contained safflower oil. The second meal contained coconut oil."Findings: The coconut oil meal reduced the anti-inflammatory properties of HDL, while the polyunsaturated fat meal actually enhanced those properties. (HDL was found to inhibit release of adhesion molecules from endothelium - from the lining of blood vessels. That's good. The presence of adhesion molecules (ICAM-1 and VCAM-1) can promote atherosclerosis.)
"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."Also, forearm blood flow increased more after the polyunsaturated than saturated fat (coconut oil) meal.
"Post-hyperemic forearm blood [microvascular] flow significantly increased 3 h after consumption of the polyunsaturated fat by 45 +/-14% and by 21 +/- 11% after the saturated fat meal."The authors suspect it may be the result of fatty acid changes in the phospholipid layer (cell membrane) of the HDL after a meal.
Conclusion:
"The present study raises the possibility that the differential effects of dietary fats on the antiinflammatory potential of HDL and endothelial function may contribute to the apparent benefits of polyunsaturated over saturated diets observed in the epidemiologic literature."
11 comments:
Ew, glad I do NOT like coconut! So what about the people who have coconut rich diets but yet still are "okay" with their cholesterol? I think maybe because of their long history of this type of diet, they've built an immunity to the bad aspects of coconut oil? ;) peace
I'm with Leonard, I can't stand coconut, and I don't feel inclined to even try coconut oil.
Butter and avocados are my fatty foods of choice. I sometimes eat avocados and butter together.
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I see that coconut oil is being promoted as a health food. It's everywhere.
The researchers, for some odd reason, tested their hypothesis with carrot cake? The test subjects also experienced a low HDL with sat fat vice polyunsat fat.
In vitro experience are typically very limited in what they can "prove". Those who believe they can extrapolate the data to real life don't have a grasp on reality.
Um, did anybody notice that the error bars in the forearm blood flow statistic are overlapping? Notice also that in the total hyperemia measurement, the primary difference occurs in the _baseline_ group, not the actual 3-hour group (where numbers are practically identical). The p-value reported for this comparison is .26 - hardly a finding that should be emphasized on the front page.
In fact, almost ALL of the standard errors of mean listed in each direct comparison between the polyunsaturated and saturated fat consumption groups suggest that these two groups are indistinguishable. The only data here that appears compellingly different between the two groups is in Figure 1 (the ICAM-1 expression data), where there appears to be a significant difference between the meal types for cells incubated with HDL... outside of the body.
It looks to me as though these authors are trying to make a mountain out of a molehill. I can't say whether or not the conclusion might still be true, but I would be skeptical about drawing any conclusions from this study.
Oh my, that last study was funded by the National Dairy Council.
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Appreciate your comment y2fizzy. Just trying to figure out the saturated fat issue for myself.
I do see that flow-mediated dilation decreased after the saturated fat meal (P<0.05) but not after the polyunsaturated fat meal (P=NS). And that there was a 92% probability that the FMD difference between meals, not just compared to baseline, was not due to chance.
Total cholesterol and LDL increased significantly more after the saturated fat meal than the polyunsaturated fat meal (P=0.003 and 0.04 respectively, between meals, not just compared to baseline).
This was one meal. What occurs when a steady diet of saturated fat is consumed? Keogh investigated just that in 2005, feeding high-saturated fat for 3 weeks. Her saturated fat of choice was butter. She found that flow-mediated dilation was decreased by 50% in those eating high saturated fat, compared to those eating either a high monounsaturated fat diet, a high polyunsaturated fat diet, or a low-fat/high-carb diet.
I do see evidence in these studies, and others I've read, that supports the hypothesis that a diet high in saturated fat impairs endothelial function.
The meta-analysis from the AJCN, the one funded by the National Dairy Council, the one questioning the link between saturated fat and heart disease, is based on epidemiological studies.
Gary Taubes, in his book Good Calories, Bad Calories, takes a cynical view of epidemiological studies. He wrote:
"A common feature of epidemiological data is that they are almost certain to be biased, of doubtful quality, or incomplete (and sometimes all three)."
"Even when the data are generally accepted as accurate, there is much room for individual judgment, and the considered conclusions of the investigators on these matters determine what they will label 'cause.' "
I am so grateful to find this study. After 2 years of narrowing down my inflammation pain, it has recurred. While listing the very few changes in the last week, one change was coconut oil. I had been unable to find the unrefined oil in my stores for some period of time. And bought it last week and have used it. There are, of course, a couple of other possibilities. But I can test to see my own results.
How about the confounding variable of high carbohydrate, a proven inflammatory factor. This study would only be relevant if they controlled that very obvious variable
Well, then, this study, according to your criteria, would be "relevant" because the meals were identical and isocaloric. The carbohydrate content was controlled.
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