I thought it worthwhile to post some of this vehemently opposing view on coconut oil sent to me by a public health nutritionist. This story is contained within a widely available publication called the Healthy Food Guide.
The story is pretty typical of the factual and evidential inaccuracies that we are routinely subjected to on a daily basis re saturated fats.
In response, I wrote to Professor Murray Skeaff and asked for the studies he was using to substantiate his statements. He cited two main meta studies – ie studies that summarise other studies.
We thought it worthwhile sending these two articles off to Chris Masterjohn an expert in molecular nutrition for his review.
Chris’s response is posted in full here
Both of these papers are meta-analyses, which pool large numbers of studies together. The weakness is that the individual studies may differ in method and quality, but the strength is that they see the “big picture” and look at the totality of the evidence, and that they are statistically much more powerful. These particular meta-analyses seem very solid, using good criteria for study inclusion.
The Prospective Study Collaboration paper showed that total cholesterol was the least valuable predictor of heart disease risk and that the total-to-HDL cholesterol was the most valuable predictor (the higher, the worse; the lower, the better).
It would be a mistake to assume that this ratio is causal in and of itself and that anything that modifies this ratio would modify heart disease risk accordingly, but let’s assume that to be the case just for a moment.
The Mensink paper showed that replacing carbohydrates with saturated fats had no effect on this ratio. However, animal fats and tropical oils contain unsaturated fats, which reduce it. The authors stated the following: “As a result, even the replacement of dairy fat and tropical fats with carbohydrates will increase the ratio of total to HDL cholesterol.”
In other words, even the most saturated fats on the market improve this ratio relative to carbohydrate. Do the people you are communicating with recommend a low-carbohydrate diet? Do they oppose the inclusion of carbohydrates in the diet as much as they oppose the inclusion of saturated fats?
The paper also looked at individual fatty acids. It found that palmitic acid lead to a slight non-significant increase and myristic acid led to a slight non-significant decrease, but that stearic acid decreased the ratio substantially and that lauric acid decreased the ratio enormously. The authors stated the following: “As a result, lauric acid had a more favorable effect on total:HDL than any other fatty acid, either saturated or unsaturated.”
Thus, tropical oils like coconut oil not only decrease the ratio compared to carbohydrates because of their small content of unsaturated fat, but their high content of lauric acid makes them favorable even compared to unsaturated fats! Do the people you are communicating with recommend the inclusion of coconut oil in the diet?
The authors also found that carbohydrates increase triglyceride levels and cited a study showing they shift LDL to a small, dense pattern, which is considered much more dangerous than large, buoyant LDL.
Despite all this, the authors noted that the *correlation* of the total-to-HDL ratio with heart disease risk does not prove *causation.* And they correctly noted that we cannot assume that just because the dietary changes noted above change the ratio that they will correspondingly change heart disease risk. So they concluded that we should rely on randomized trials, which have shown that replacing saturated fats with unsaturated fats is beneficial.
However, these trials were not part of the meta-analysis and simply mentioned in the discussion. They are of poor quality, and the authors ignore trials that showed the exact opposite. Anthony Colpo has a chapter on these trials in his book, _The Great Cholesterol Con_. I have discussed them here: http://www.cholesterol-and-health.com/Daniel-Steinberg-Cholesterol-Wars.html#diet
I suggest reviewing my article on the cause of heart disease:
The main issue in terms of atherosclerosis, which is a specific type of arteriosclerosis and the most common kind, is the oxidation of LDL. The ratio of oxidative liabilities (mainly PUFAs) to antioxidants (especially coenzyme Q10) in the LDL particle is an important determinant of its capacity to oxidize, but the most important factor appears to be the amount of time LDL spends in the blood. This is most importantly determined by LDL receptor activity, which is a result of a number of genetic and homeostatic factors as well as thyroid hormone levels. People who have a genetic defect with increased LDL receptor expression have an 88% reduced risk of heart disease, which is near abolition of the disease:
So where does the total-to-HDL cholesterol ratio come in to play?
HDL does play a protective causal role. The mainstream thinks this is because of “reverse cholesterol transport,” but I don’t buy it. When LDL sits around in the blood, it is exposed to enzymes produced by the endothelial lining that will oxidize it. HDL prevents this oxidation. I suspect this is at least in part because HDL is responsible for delivering the antioxidant vitamin E to endothelial cells.
But there is something else, and it is not causal. The longer LDL spends in the blood, the longer it is exposed to cholesterol ester transfer protein (CETP), which transfers cholesterol from HDL to LDL in exchange for triglycerides. Thus, the slower the uptake of LDL, the more cholesterol will migrate from HDL to LDL, and the higher the total-to-HDL cholesterol ratio will become.
The HDL-boosting-specific intervention trials have ranged from unimpressive to disastrous. So, the protective causal role of HDL is probably a smaller part of the correlation than what I just wrote in the above paragraph. It is a marker for the amount of time the LDL spends in the blood.
Therefore, it does not make sense to assume that the impact foods have on the total-to-LDL cholesterol ratio shows what impact they will have on heart disease risk. It makes more sense to believe that their effects on oxidation and thyroid hormone signaling will impact heart disease risk. What we really need to find out is what type of foods maximize LDL receptor activity, but little research has been done to my knowledge in this area.
I hope that helps,
Well it certainly does when it seems that our quoted expert in the Healthy Food Guide had trouble interpreting the results and findings of studies he cited in support of his own statements.
Chris’s observations that “As a result, lauric acid had a more favorable effect on total:HDL than any other fatty acid, either saturated or unsaturated.” is of particular interest given it makes up 50% of coconut oil.
The Healthy Food Guide article is really typical of the mindless bagging of coconut oil and saturated in mainstream media and by those we are informed, experts in this area.
Antony Colpos “The Great Choleserol Con – Why everything you’ve been told about cholesterol, diet and heart disease is wrong, ” is a very complete expose of the lies, deceit, complete misuse of vast sums of public money and travesty that has come about in Western societies since the early 1950’s over the issue of saturated fact and cholesterol.
To understand this issue, is to understand just how the political economy of the food and drug industries combined have worked together to seriously undermine the health status of millions of people.
We’ll have some more in a following post.
– See more at: http://dev.titechnologies.in/zenianlive/?p=162#sthash.fkdRzKJR.dpuf