Authors: Jonny Bowden
A L
ITTLE
I
NTERNET
H
UMOR
1. The Japanese eat very little fat and suffer fewer heart attacks than the British or Americans.
2. The Mexicans eat a lot of fat and suffer fewer heart attacks than the British or Americans.
3. The Japanese drink very little red wine and suffer fewer heart attacks than the British or Americans.
4. The Italians drink excessive amounts of red wine and suffer fewer heart attacks than the British or Americans.
5. The Germans drink a lot of beers and eat lots of sausages and fats and suffer fewer heart attacks than the British or Americans.
Conclusion: Eat and drink what you like. Speaking English is apparently what kills you.
One scholar described this as the “yellow finger” phenomenon. Men with yellow fingertips are more likely to die of lung cancer. The reason: they are smokers. That’s why they
have
yellow fingers. The yellowed tips of their fingers are the result of holding twenty cigarettes a day for twenty years. Washing off the yellow will not reduce their risk for lung cancer.
This brings us to cholesterol, heart disease, and the low-carb diet.
The Birth of the Diet-Heart Hypothesis and the Demonization of Saturated Fat
When the diet-heart hypothesis—the idea that saturated fat causes heart disease—was first proposed in the 1950s by Ancel Keys (see
chapter 1
), very little was known about either fat or cholesterol. Cholesterol, which is actually not a fat at all but a waxy molecule classified as a sterol, is the parent molecule for all the sex hormones in the body. Without it, you would not have testosterone, the estrogens, progesterone, or DHEA, not to mention cortisol and aldosterone. Most of the cholesterol in your body is
produced
by your body.
Dietary
cholesterol has virtually
no effect
on the amount of cholesterol in your blood. Two major long-term studies, Framingham and Tecumseh, confirm this (see tables above);
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they show that those who ate the most cholesterol had exactly the same level of cholesterol in their blood as those who ate the least. Even Keys, the author of the diet-heart hypothesis, knew this and said, in 1991:
“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 at all unless you happen to be a chicken or a rabbit
.”
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What we do know is that dietary fat has an effect on serum cholesterol. What is a lot less clear is whether it matters much. (Michael and Mary Dan Eades call “Cholesterol Madness” the most important chapter in their book, “not because we believe cholesterol is such an important problem but because
everybody else does
.” I’m with the Eadeses, as I discussed in more detail in
chapter 3
.) Fully 50% of heart attacks happen to people with completely normal cholesterol numbers.
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The Tokelauan Islanders get 63% of their diet from the healthful saturated fat in coconuts, and, though their cholesterol levels are a bit high, they have virtually no heart disease.
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Fats: The Good, the Bad, and the Ugly
We know a lot more about fat than we did back in the ’50s and even in the ’80s, when the message was “All fat is bad.” Most people are now aware that there are “good” fats and “bad” fats, and most people believe that the bad fats are saturated. Not so fast. It’s turning out to be even more complicated than that. We now know that there is a type of fat far more dangerous and insidious than saturated fat:
trans-fat
; and virtually all of the data we have that “links” saturated fat with heart disease did not distinguish between
saturated
fats and
trans-fats
. Therefore, it is almost impossible to know whether or not saturated fats got the blame for something that was really being done by trans-fats.
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Saturated fats, for example,
lower
lipoprotein(a), a risk factor for heart disease, and
raise
protective HDL cholesterol; transfats not only do the exact opposite but also raise LDL cholesterol!
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Many of us now believe that saturated fats have gotten the blame for damage that is actually caused by trans-fats. Virtually every low-carbohydrate diet, by definition, contains incredibly low amounts of trans-fats.
Furthermore, we also know that “saturated fat” is not a homogenous entity. It consists of many different types of fatty acids, and some of them are downright beneficial for health. For example, lauric acid has antimicrobial and antiviral properties and is able to fight bacteria. Caprylic acid is used to fight yeast. Short- and medium-chain saturated fatty acids like those found in coconuts are actually much more likely to be burned for fuel than stored as fat, and can be a great adjunct to a weight-loss program.
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And others, like stearic acid, have no effect whatsoever on cholesterol, except to possibly
raise
protective HDL.
Consider this, as the brilliant investigative reporter and three-time National Association of Science Writers’ Science in Society Award-winner Gary Taubes did in a recent article in
Science.
A porterhouse steak cooks down to about half fat and half protein. Of that fat, 51% is monounsaturated, mostly all from oleic acid, the same monounsaturated fat found in heart-healthy olive oil. Forty-five percent is saturated, but a third of that is stearic acid, which at worst is harmless and at best raises HDL cholesterol. The remaining 4% is polyunsaturated. Thus, a porterhouse steak may actually be better for your heart—especially if eaten with a generous helping of vegetables—than a no-fat meal of high-glycemic, triglyceride-raising pasta.
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There’s More to Cholesterol than Just “Good” and “Bad”
Most people are aware that cholesterol comes in two “flavors,” good (HDL) and bad (LDL). But most people do not know that both HDL and LDL have different subclasses, and that these subclasses behave quite differently in the body. For example, LDL cholesterol has at least five sub-types, two of which are very important for the purposes of our discussion—pattern A, which are large, fluffy, cotton ball–like molecules, and pattern B, which are small, dense molecules that look like BB-gun pellets. It is these small, dense LDL molecules that cause plaque and contribute to heart disease; the fluffy LDL is fairly harmless. In recent years, studies have begun to look at the factors that affect these particle sizes.
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We are finding out that while the traditional high-carb, low-fat diet may in fact lower
overall
LDL, it
raises
the dangerous pattern B molecules and
lowers
protective HDL cholesterol. So while your overall cholesterol number may go down, your overall risk may go
up
. Not only that: high-carbohydrate diets significantly raise triglycerides—this is inarguable and has been shown in virtually every major study comparing high-carb to low-carb diets. The combination of high triglycerides and low HDL is far more predictive of heart disease (and far more dangerous) than an overall elevated cholesterol number.
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In the following story, you can see cholesterol madness in action: I have a dear friend who is in great shape and exercises every day. He came to me because he and his doctor were very concerned because his cholesterol was “too high.” I looked at his blood tests. He had normal lipoprotein(a), a fasting glucose under 100, a fasting insulin of 5, triglycerides under 100, an HDL of 60 (giving him a triglyceride/HDL ratio of less than 2!), a cholesterol ratio itself of 3, normal C-reactive protein (a measure of inflammation), and a homocysteine (a huge risk factor for heart disease) under 7—but his overall cholesterol was 240. I wish I had those numbers! This man had a better chance of winning the lottery than he did of ever getting heart disease. He will never have a heart attack. Yet his doctor was ready to put him on a lifetime of expensive medication with potentially damaging side effects to bring down a number that
did not matter!
You might reasonably ask at this point: if cholesterol is not as important an issue as we thought, how is it that the statin drugs (which reduce cholesterol) save lives?
Good question.
The statin drugs probably do save some lives (though the number is probably way less than you’ve been led to believe, and the cost remains to be seen). However, whether they do so by reducing cholesterol is an open question. What the statins do
in addition
to lowering cholesterol is reduce
inflammation,
which
is
a cause of heart disease. What they do to cholesterol, in my opinion, is the least important thing that they do in the body. You can reduce inflammation by consuming omega-3 fatty acids and reducing consumption of grains, without the possible statin drug side effects of liver toxicity and mitochondrial damage, and without the increased risk for death from other causes that is associated with cholesterol numbers that are too low.
Do Low-Fat Diets Prevent Heart Disease?
So, then, what about that famous Dean Ornish study that showed that lowfat diets reverse heart disease?
Actually, it showed no such thing. The Ornish study took forty-eight middle-aged white men with existing moderate to severe coronary heart disease. The researchers then did five—count ’em,
five
—simultaneous interventions with these men. They put them on a stress-reduction program. They got them to stop smoking. They gave them group therapy and support. They had them do daily aerobic exercise.
And
they put them on a very high-fiber diet, which also happened to be low in fat. Why anyone—including Ornish—would conclude that it was the low-fat part of this multiple intervention that caused their improvement is a mystery. If we put those same men on a program of exercise, stress reduction, smoking cessation, group support, and meditation and included a pack of M&M’s in their diet every day, would we conclude that M&M’s reduce heart disease? I would argue that Ornish would have gotten the identical results—perhaps even
better
ones—using all those good interventions plus a diet loaded with fiber, absent trans-fats, absent sugar, containing very low amounts of vegetable fats,
and
containing plenty of good-quality protein from grass-fed animals plus saturated, monounsaturated, and omega-3 fats. We’ll never know, because when five factors are involved, it is impossible to say which of them—or what combination of them—is responsible for the results.
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On a personal note: in researching this book, I read through literally hundreds of studies on cholesterol, fat, and heart disease. I could have rented a cot in the National Library of Medicine. I read the papers that appeared in the medical journals, I read the re-analysis of the data by scholars who questioned the cholesterol/saturated-fat hypothesis of heart disease, I studied their arguments, I read the rebuttals to their arguments, and I read the rebuttals to the
rebuttals
.
I have, I confess, come to believe—along with a growing number of health professionals—that saturated fat and cholesterol are, for the most part, innocent bystanders. They were in the wrong place at the wrong time, Your Honor, and they hung out with the wrong crowd. As I mentioned earlier, virtually every epidemiological study that linked saturated-fat consumption with increased risk of cardiovascular diseases failed to separate saturated fat from its extremely dangerous cohort, trans-fatty acids.
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Nor did the studies implicating saturated fat distinguish the
source
of the saturated fat consumed: saturated fat from natural foods like butter, eggs, and grain-fed cattle is
not
the same as saturated fat from fries and burgers; most people in industrial nations consume their saturated fat from hot dogs, fast-food hamburgers, and processed deli meats like salami and bologna. The people consuming the most saturated fat in those studies ate few fruits and vegetables and little fiber. But they ate something like 150 pounds of sugar per year (the latest figures from the USDA from 1997, projected to soon rise to 170 pounds). And for the most part, they did not exercise. Although it is extremely convenient to blame a single factor (like saturated fat) for heart disease, the fact is that a matrix of lifestyle and dietary characteristics such as the ones just mentioned are found
together
. In my opinion, saturated fat and cholesterol are not the bad guys here.