Things That Won't Kill You Volume 4: Saturated Fat Part II: Cholesterol Myths

Feb 5 2010

image In retrospect, this probably could have been an entirely separate article in the "things that won't kill you" series, as many people still believe that dietary cholesterol (i.e. cholesterol in food) is a bad thing. For example, the article that image was taken from claims:

If you get too much dietary cholesterol (over 300mg a day) the extra cholesterol will accumulate in the walls of the blood vessels, making your LDL (bad) blood cholesterol levels rise. Over time, your arteries will become narrower, which can cut off the blood supply to your heart (causing a heart attack), or your brain (causing a stroke).

However, that's pretty easily dismissed—even Ancel Keys, "Monsieur Cholesterol" himself, never argued that dietary cholesterol was related to serum cholesterol or heart disease. In a 1952 article in Circulation, the journal of the American Heart Association, Keys noted that although rabbits and chickens that eat high-cholesterol diets will develop high cholesterol and atherosclerosis, or hardening of the arteries:

No animal species close to man in metabolic habitus has been shown to be susceptible to the induction of atherosclerosis by cholesterol feeding…. Moreover, even in the favorite species for such  experimentation, the herbivorous rabbit, the necessary concentration of cholesterol in the diet is fantastically high in comparison with actual human diets. Moreover, there is reason to believe that man has a greater power of cholesterol regulation than does the rabbit or the chicken. From the animal experiments alone the most reasonable conclusion would be that the cholesterol content of human diets is unimportant in human atherosclerosis.

Two "moreovers" in one paragraph, people! “Most reasonable conclusion”! Moreover, five decades of subsequent research haven't given anyone any reason to think differently. In 1997, Keys was even more direct:

There’s no connection whatsoever between cholesterol in food and cholesterol in blood. And we’ve known that all along. Cholesterol in the diet doesn’t matter unless you happen to be a chicken or a rabbit.

Research done in the interim on the relationship between diet and heart disease in humans like the Framingham and Tecumseh studies showed no relationship between cholesterol consumption and blood cholesterol or heart disease. I'm not even going to modify this with "probably" or "as far as we know": There is no reason to believe that how much cholesterol you eat has any effect on your health.

But that doesn’t stop the AHA from recommending that “most people…limit cholesterol intake to less than 300 mg per day” and claiming that “an egg can fit within heart-healthy guidelines for those people only if cholesterol from other sources — such as meats, poultry and dairy products — is limited.” Despite repeated studies showing that egg consumption is not associated with higher serum cholesterol, myocardial infarction, cardiovascular disease, or all-cause mortality.

Backing up for a second: Ancel Keys, wherefore art thou Monsieur Cholesterol?

The reason Ancel Keys was called "Monsieur Cholesterol" wasn't because his theory had anything to do with cholesterol in food; it was because his theory depended on the idea that saturated fat consumption causes blood cholesterol levels to increase, presumably putting people at risk of heart disease.

If you read Part I of this article, you may remember that I said there were three things that convinced me that saturated fat wasn't a cause of heart disease. I explained the first two in that entry. (To recap, they were: 1) the fact that people in places like France and the Pacific Islands eat way more saturated fat than Americans but have much lower rates of heart disease and 2) the fact that the study that first led people to believe saturated fat was the cause of heart disease was bad science that has since been discredited--not that that's stopped people who think saturated fat is bad from citing it all the time anyway).

The third reason is that there's no evidence supporting the proposed mechanism—meaning the idea that saturated fat causes heart disease by raising serum cholesterol.

You'd never know that from the mainstream media reporting on the research. Take, for example, this 1998 US News and World Report cover story, which describes the Framingham Study and claims:

Thanks to Framingham, Americans have come to understand that how they live often determines when they'll die. After 50 years, 1,000 research papers, and $43 million, the Framingham Heart Study has shown that smoking is bad for the heart, that high blood pressure is not a normal consequence of aging, and that high cholesterol leads to heart disease. They know that women are at risk for cardiovascular disease, though later in life than men. They know that diabetes is a risk factor (a term coined by the study), that weight affects blood pressure, and that eating too much saturated fat affects cholesterol.

Compare that to what William Castelli, the director of the Framingham Study, wrote in a 1992 article in the Archives of Internal Medicine (quoted here):

In Framingham, Mass., the more saturated fat one ate, the more cholesterol one ate, the more calories one ate, the lower the person’s serum cholesterol.

The people who ate more saturated fat and calories were also more active, which might explain the results, but certainly doesn't explain the US News and World Report article claiming the opposite.

The Tecumseh Study, which compared dietary habits with serum cholesterol and triglyceride levels, found no significant difference between saturated fat consumption and cholesterol levels (see the chart on page 3, 1386 in the original).

And Just to Complicate Things Further...

The proposed mechanism relies on two causal relationships: 1) saturated fat consumption—> increased serum cholesterol and 2) increased serum cholesterol—> cardiovascular disease. I've just explained why the evidence for the former is, at best, conflicting, and that alone would undermine the lipid-heart hypothesis. But it turns out the evidence for the second part of the mechanism is also complicated.

Castelli, again:

Cholesterol levels by themselves reveal little about a patient's coronary artery disease risk. Most infarctions occur in patients who have normal total cholesterol levels." (From the American Journal of Cardiology)

from http://www.walgreens.com/marketing/library/careguides/careguide.jsp?docid=000225&doctype=28&subcontents=High%20CholesterolThe popular theory about cholesterol basically imagines that people’s arteries are like  pipes and cholesterol and fat are like grease that can gradually build up and narrow those pipes. Eventually, the arteries get clogged, and pieces of the plaque that break off or blood clots can get caught in those greased-up pipes and cause heart attacks and stroke.

It’s true that heart disease is generally caused by the buildup of a fatty plaque in the arteries, but cholesterol and fat don’t necessarily stick to and harden or clog arteries—not even so-called “bad cholesterol” or LDL. Oxidized LDL is what accumulates in white blood cells and become what are called “foam cells” which make up atherosclerotic plaque. Oxidized LDL also causes inflammation, which has been a major focus of recent research on cholesterol and heart disease. There is a much more complicated explanation, complete with citations from the relevant research here.

So the key to figuring out what causes heart disease is figuring out what causes (or prevents) the oxidation of LDL, not figuring out what causes increased levels of LDL qua LDL. Perhaps the most worrying finding is that one thing that seems to cause the oxidation of LDL is linoleic acid a poly-unsaturated fatty acid found primarily in vegetable oils. Saturated fat, on the other hand, actually seems to have a protective effect.

The literature is pretty complex, and I won’t pretend to have taken the time to parse out everything about atherosclerosis and cholesterol and essential fatty acids and endothelial cells. Nonetheless, I’ve been sufficiently moved by everything I’ve read to start using more butter and lard when I cook and seriously reconsider using vegetable oils anytime I’m preparing a meal that also includes substantial saturated fat. Because, again, there is no indication that the total volume of saturated fat or cholesterol one consumes increases the risk of heart disease or mortality, but a particular fatty acid found in vegetable oils oxidizes cholesterol, which does contribute to heart disease. Saturated fats and HDL or “good cholesterol” actually prevent oxidation and atherosclerosis.

That makes some sense with population studies too—populations that traditionally consumed large quantities of saturated fats and dietary cholesterol (Pacific Islanders, the Masai in Africa, the French) generally did not rely heavily on vegetable oils; populations that consumed large quantities of vegetable oils and fish oils (Mediterranean populations, the Japanese) generally consumed relatively little saturated fat and cholesterol.

That also means that eating lots of red meat, milk, and butter or other sources of saturated fat and cholesterol while also eating lots of olive oil, canola oil, and other sources of linoleic acid would be the worst combination possible. It would be a supreme irony if it turned out that one of the primary causes of atherosclerosis and the heart disease associated with it was the olive oil and vegetable oil that public health authorities have been urging a red-meat-eating people to substitute for animal fats for the last sixty years. 

Next up in this series…trans-fats and why they might actually kill you.

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Things That Won't Kill You Volume 4: Saturated Fat Part II:

Czym tak naprawdę istnieje cholesterol?

Cholesterol istnieje tak naprawdę niebezprzedmiotowym faktorem komórki
polskiego systemu. Jest niezastąpionym budulcem cel zaœ inkretów.

Cholesterol częściowo powstaje w polskim tworze — w wątrobie, natomiast częściowo
spada z pokarmu, jaki na co dzień zużywamy. Z natur onymi
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To co istnieje psotne, to jego zbytek. A dokładniej rzeczonymi ujmując
nadmiar "podstępnego cholesterolu" typu LDL. Przyjmuje się, iż jego stężenie we krwi onych
winieneœ naruszać 100 mg/dl. Z drugiej strony masz "utalentowany cholesterol" typu HDL, którego
stężenie nie powinniœcie naruszać 50 mg/dl
obok œwiniarki a 40 mg/dl obok mężczyzny. Całkowite stężenie cholesterolu w polskiej posoki powinniœmy mieścić się w przedziale 114-200
mg/dl.

Jednak jeżeli te reguł pozostają przeroœnięte i ten poziom twierdzi się poprzez dłuższy okres,
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Dlatego niego zezwalajże do takiego stanu — podtrzymuj cholesterol
na właściwym stanie.

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