This article has been a long time coming. The nonsense surrounding saturated fat is one of the main reasons I got sucked into independent health research in the first place. And I’ve had an article ready to go on this topic in one revision or another for several months. But I decided that that article was a diatribe and it’d be better to try and keep this to the point. So I rewrote it.
There are two main theories to understand when discussing saturated fat and heart disease. The first is the lipid-hypothesis, and the second is the diet-heart-hypothesis. The lipid-hypothesis is based on the observation that heart disease usually correlates with elevated cholesterol levels and that arterial plaques contain a fair amount of cholesterol. The lipid-hypothesis puts forth the theory that the elevated cholesterol is a causal agent in the formation of arterial plaques.
The diet-heart-hypothesis is the theory that dietary saturated fat, via its ability to raise serum cholesterol, is causal to heart disease. It is important to note that the diet-heart-hypothesis must be tested separately and independently of the lipid hypothesis.
Now before we move on here, I just want to say a few things. First, all the evidence points to heart disease (and the other degenerative diseases) being problems of oxidation and inflammation. Note that this has nothing directly to do with cholesterol. Second, cholesterol is an extremely important lipid. It is a critical component of cell membranes, the precursor to all steroid hormones, a precursor to vitamin D, and the limiting factor that brain cells need to make connections with one another called synapses, making it essential to learning and memory. Third, there is no evidence that elevated cholesterol is causal to heart-disease. That is, the lipid-hypothesis has not been proven.
Now a little bit on atherosclerosis. How does all that cholesterol get in there? Generally via foam cells. A foam cell is a dead macrophage that was supposed to have helped clear up an infection. It could have been damaged by an oxidized LDL particle or infected by a germ it was unable to kill due to excess cortisol. Once a macrophage becomes a foam cell, it is itself highly inflammatory and furthers the process of inflammation. An atheroma is like a puss filled blister on the surface of your skin, except it’s inside your artery. The cholesterol is just a lot of left over junk from the inflammatory response.
The standard method of treating this problem is to try and reduce the amount of cholesterol in the blood to such a low level that only a few macrophages can turn into foam cells, rather than identifying and treating the source of the chronic inflammation. We’re getting away from the original topic of saturated fat, so I’d like to bring this around and tie it together.
We talked about cholesterol levels and correlation, and it is true, cholesterol levels are a marker for heart disease. What we should be concerned about here though is dyslipidemia and not elevated cholesterol per se. (Dyslipidemia simply means having an abnormal blood lipid profile.) This is because dyslipidemia is probably an indication that the inflammatory process that causes atherosclerosis is ongoing in your body. But there are better measures than total LDL, total HDL, and total cholesterol. You have to understand that these are somewhat arbitrary measures that happen to be easy to measure at most clinics, but which have a weak correlation with heart disease. There are better measures, such as the size of your LDL (pattern A or pattern B) and the total LDL particle count. I do not want to get into the physiology here but there are much better explanations as to why LDL particle size and count would affect heart disease as opposed to just total LDL cholesterol.
Getting back to saturated fat, it is well accepted that dietary saturated fat does increase total cholesterol levels, including LDL. In fact it increases both LDL and HDL. And this is where it becomes important to test the diet-heart-hypothesis directly. I would like to point out here that although saturated fat increases total LDL cholesterol, it does so by producing fewer and larger LDL molecules, an improvement in the overall lipid profile.
And what of the diet-heart-hypothesis itself? Here are a couple quotes:
“The diet-heart hypothesis has repeatedly been showing to be wrong, and yet, for complicated reasons of pride, profit and prejudice, the hypothesis continues to be exploited by scientists, fund-raising enterprises, food companies and even government agencies. The public is being deceived by the greatest health scam of the century.”
--George V. Mann, Coronary Heart Disease: The Dietary Sense and Nonsense
“The commonly held belief that the best diet for the prevention of coronary heart disease is a low saturated fat, low cholesterol diet is not supported by the available evidence from clinical trials. In the primary prevention, such diets do not reduce the risk of myocardial infarction or coronary or all cause mortaility…
“Similarly, diets focused exclusively on reduction of saturated fats and cholesterol are relatively ineffective for secondary prevention and should be abandoned. There may be other effective diets for secondary prevention of coronary heart disease but these are not yet sufficiently well defined or adequately tested…”
--Corr LA and Oliver MF. The low fat/low cholesterol diet is ineffective. European Heat Journal 1997; 18: 18-22
Primary prevention means preventing a first occurrence. Secondary prevention means preventing a second occurrence. Also, another term brought up here is “all cause mortality”, and it is a major point. Reducing our risk of heart disease only matters if it’s not increasing our risk of dying from other factors (i.e. by reducing endogenous production of cholesterol). That is to say, our life expectancy should be increasing. I’m not entirely sure the numbers on this, but anybody on a cholesterol-lowering diet or taking statins should be aware that although it prevents a few deaths from heart disease, it increases the number of deaths from other causes.
References and Further Reading:
The Cholesterol Wars: Steinberg Strikes Back
Chris Masterjohn reviews Daniel Steinberg’s book “The Cholesterol Wars: The Preponderance of Evidence”. I include this book because in it, Steinberg attempts to prove the diet-heart-hypothesis and I believe Masterjohn’s rebuttal is fairly solid.
Cholesterol and Health – Functions and Foods
Again from Masterjohn. This time an overview of the functional roles and importance of cholesterol.
The Potbelly Syndrome
An in depth look into the causes of modern degenerative diseases. I don’t agree entirely with what this book has to say, but I like its emphasis on cortisol as an important aspect. It contains a lot of information on the process of atherosclerosis. It is also where I got the two quotes I used in this post.
http://www.youtube.com/watch?v=dBnniua6-oM
Robert Lustig’s rant against sugar. This isn’t directly about saturated fat or lipid profiles, but there is a good rebuttal of Ancel Keys’ Seven Countries Study from 32:30 to 36:00.
http://freetheanimal.com/2009/09/saturated-fat-intake-vs-heart-disease-stroke.html
The interesting thing about the internet is the availability of information. Does lower cholesterol really correlate with lower mortality? A follower of the blog Free the Animal compiles some publicly available data from the British Heart Foundation into some easy to read graphs.
Dirty Little Secret of Heart Disease
Diet-Heart Controlled Trials: a New Literature Review
Saturated Fat Consumption Still Isn’t Associated with Cardiovascular Disease
Stephan Guyenet is a person I respect for well thought out, clear-minded opinions and he has written a lot on the issues of saturated fat and heart disease. So I’m throwing out a few links to his website.
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