The Great Cholesterol Myth (12 page)

Well, the U.S. sugar industry, for one.

“Hoping to block the report . . . the Sugar Association threatened to lobby Congress to cut off the $406 million the United States gives annually to the WHO,” reported Juliet Eilperin in the
Washington Post
.
¹⁹
The
Post
quoted an April 14, 2003, letter from the Sugar Association’s president, Andrew Briscoe, to the general director of WHO in which he stated, “We will exercise every avenue available to expose the dubious nature of the
Diet, Nutrition and the Prevention of Chronic Diseases
report.”

Two senators wrote a letter to then Health and Human Services Secretary Tommy G. Thompson, urging him to squelch the report. Not soon afterward, the U.S. Department of Health and Human Services submitted comments on the report, stating that “evidence that soft drinks are associated with obesity is not compelling.”

Oh, really? Shades of the tobacco industry’s defense of cigarettes.

In a 2005 report by the Institute of Medicine,
the authors acknowledged that there was a ton of evidence suggesting that sugar consumption could increase the risk of heart disease and diabetes—and that it could even raise LDL (“bad”) cholesterol. The problem was they couldn’t say that the research was definitive. “There was enough ambiguity, they concluded, that they couldn’t even set an upper limit on how much sugar constitutes too much,” Taubes wrote.

This dovetailed nicely with the last assessment of sugar by the Food and Drug Administration (FDA) back in 1986 that basically said “no conclusive evidence on sugars demonstrates a hazard to the general public when sugars are consumed at the levels that are now current.”

“This is another way of saying that the evidence by no means refuted the [charges against sugar], just that it wasn’t definitive or unambiguous,” Taubes said. It’s also worth noting that at the time, we were consuming approximately 40 pounds per year of “added sugars,” meaning sugar beyond what we might naturally obtain from fruits and vegetables. (That comes to about two hundred extra sugar calories a day, about a can and a half of Coke.)

That doesn’t sound so bad, really, and if that were all the sugar we were consuming, most nutritionists in America would be pretty happy. The problem was it wasn’t 40 pounds a year. Even back then the Department of Agriculture said we were consuming 75 pounds a year, and by the early 2000s it was up to 90 pounds. As of late 2011, we’re up to 156 pounds a year. That’s the equivalent of thirty-one 5-pound bags for every man, woman, and child in America.
²⁰

The way in which sugar damages the heart can be directly related to insulin resistance.

Ordinary table sugar, known technically as
sucrose
, is actually composed of equal parts glucose and fructose, two simple sugars that are anything but metabolically equal. Glucose can be used by any cell in the body. Fructose, on the other hand, is metabolic poison. It’s the fructose in our sweetened foods that we should fear the most.

Before you point the finger of blame exclusively at high-fructose corn syrup (HFCS), an additive that’s made it into virtually every processed food on the market, consider the following:

• Regular sugar (sucrose) is 50 percent glucose and 50 percent fructose.

• High-fructose corn syrup is 55 percent fructose and 45 percent glucose, a difference that just doesn’t matter very much.

• So sugar and high-fructose corn syrup are
essentially
the same thing.

Because high-fructose corn syrup has gotten so much heat in the press, some food manufacturers now proudly advertise that their products contain none of it and are instead sweetened with “natural” sugar (meaning ordinary sucrose). Meanwhile, the Corn Refiners Association has claimed that high-fructose corn syrup is being unjustly targeted and is no worse than “regular” sugar.

Sadly, the association is technically right. Fructose is the damaging part of sugar, and whether you get that fructose from regular sugar or from
HFCS doesn’t make a whit of difference. That doesn’t absolve HFCS at all; it just means that “regular” sugar is
just as bad
as HFCS. It’s the fructose in each of them that’s causing the damage, and here’s why.

Fructose and glucose are metabolized in the body in completely different ways. They are
not
identical. Glucose goes right into the bloodstream and then into the cells, but fructose goes right to the liver. Research has shown that fructose is seven times more likely to form the previously mentioned artery-damaging AGEs (advanced glycation end products). Fructose is metabolized by the body like fat, and it turns into fat (triglycerides) almost immediately. “When you consume fructose, you’re not consuming carbs,” says Robert Lustig, M.D., professor of pediatrics at the University of California, San Francisco. “You’re consuming fat.”

Fructose is the major cause of fat accumulation in the liver, a condition known technically as
hepatic steatosis
but which most of us know as fatty liver. And there is a direct link between fatty liver and our old friend, insulin resistance.

A top researcher in the field of insulin resistance, Varman Samuel of the Yale School of Medicine, told the
New York Times
that the correlation between fat in the liver (fatty liver) and insulin resistance is remarkably strong. “When you deposit fat in the liver, that’s when you become insulin resistant,” he said.
²¹

And all together now, class: What causes fat to accumulate in the liver? Fructose.

If you want to watch a bunch of lab animals become insulin resistant, all you have to do is feed them fructose. Feed them enough fructose and, sure enough, the liver converts it to fat, which then accumulates in the liver—with insulin resistance right behind it. This can take place in as little as a week if the animals are fed enough fructose, whereas it might take a few months at the levels we humans normally consume. Studies conducted by Luc Tappy, M.D., in Switzerland revealed that feeding human subjects a daily dose of fructose equal to the amount found in eight to ten cans of soda produced insulin resistance and elevated triglycerides within a few days.
²²

Fructose found in whole foods such as fruits, however, is a different story. There’s not all that much fructose in, for example, an apple, and the apple comes with a hefty dose of fiber, which slows the rate of carbohydrate absorption and reduces insulin response. But fructose extracted from fruit, concentrated into a syrup, and then inserted into practically every food we buy at the supermarket—from bread and hamburger buns to pretzels and cereals—well, that’s a whole different animal.

High-fructose corn syrup was first invented in Japan in the 1960s and made it into the American food supply around the mid-1970s. It had two advantages over regular sugar, from the point of view of food manufacturers. Number one, it was sweeter, so theoretically you could use less of it. Number two, it was much cheaper than sugar. Low-fat products could be made “palatable” by the addition of HFCS, and before long, manufacturers were adding the stuff to everything. (Doubt us? Take a field trip to your local supermarket and start reading labels. See if you can find any processed foods that don’t contain it.)

The result is that our fructose consumption has skyrocketed. Twenty-five percent of adolescents today
consume 15 percent of their calories from fructose alone! As Lustig points out in a brilliant lecture, “Sugar: The Bitter Truth” (available on YouTube), the percentage of calories from fat in the American diet has gone down at the same time that fructose consumption has skyrocketed, along with heart disease, diabetes, obesity, and hypertension. Coincidence? Lustig doesn’t think so, and neither do we.

Remember our mention of metabolic syndrome? It’s a collection of symptoms—high triglycerides, abdominal fat, hypertension, and insulin resistance—that seriously increases the risk for heart disease. Well, rodents consuming large amounts of fructose rapidly develop it.
²³
In humans, a high-fructose diet raises triglycerides almost instantly; the rest of the symptoms associated with metabolic syndrome take a little longer to develop in humans than they do in rats, but develop they do.
²⁴
Fructose also raises uric acid levels in the bloodstream. Excess uric acid is well known as the defining feature of gout, but did you know that it also predicts future obesity and high blood pressure?

Fructose and glucose behave very differently in the brain as well, as research from Johns Hopkins has suggested. Glucose decreases food intake while fructose increases it. If your appetite increases, you eat more, thus making obesity, and an increased risk for heart disease, far more likely. “Take a kid to McDonald’s and give him a Coke,” Lustig said. “Does he eat less? Or does he eat more?”

M. Daniel Lane, Ph.D., of the Johns Hopkins University School of Medicine stated, “We feel that [the findings on fructose and appetite] may have particular relevance to the massive increase in the use of high-fructose sweeteners (both high-fructose corn syrup and table sugar) in virtually all sweetened foods, most notably soft drinks. The per capita consumption of these sweeteners in the USA is about 145 lbs/year and is probably much higher in teenagers/youth that have a high level of consumption of soft drinks.”
²⁵

All told, the case against fructose consumption as a key factor in the development of heart disease seems to us to be far more cogent than the case against fat. It’s also worth pointing out that every single bad thing that fructose does to increase our risk for heart disease—and it does a lot—has virtually nothing to do with elevated cholesterol.

The fact is that sugar is far more damaging to the heart than either fat or cholesterol are, but that has never stopped the diet establishment from continuing to stick to its story that fat and cholesterol are what we ought to be worried about.

As the old journalistic maxim goes, “Never let the facts get in the way of a good story.”

Unfortunately, this story is long past its expiration date. Sticking to it in the face of all evidence continues to make many people very sick indeed

CHAPTER 5

YOU CAN’T TALK ABOUT CHOLESTEROL WITHOUT ALSO TALKING ABOUT FAT,
which is convenient, because it’s exactly what we’re going to discuss in this chapter.

When you’re done reading it, you may have an entirely different perspective on fat and a much more accurate notion of what the terms “good fat” and “bad fat” mean. And no, we’re not just going to tell you the stuff you’ve heard a million times, such as “fat from fish is good” (completely true) and “saturated fat is bad” (very far from always true).

But let’s not get ahead of ourselves.

According to conventional wisdom, fat and cholesterol are the twin demons of heart disease, linked together in our minds as firmly as Hell and Damnation or Bonnie and Clyde. We’ve been admonished to lower our cholesterol and stop eating saturated fat. These two mandates are the basis of the diet–heart hypothesis, which has guided national health policy on healthy eating for decades and basically holds that fat and cholesterol in the diet are a direct and significant cause of heart disease.

Okay, so fat and cholesterol (whether they show up in your diet or in your bloodstream) are pretty much kissing cousins.

We’ve discussed cholesterol in the previous chapters, so let’s clear up some misconceptions about fat—what it is, what it does, what it doesn’t do—and why all this matters in the first place. Once we’ve done that, we’ll be able to look at the relationship among heart disease, fat in the diet, and cholesterol in the blood with completely new eyes.

Let’s get to work!

Fat is the collective shorthand name given to any big collection of smaller units called fatty acids. You can think of “fat” and “fatty acids” as analogous to paper money and a bunch of coins. The dollar bill is the “fat” and the coins are the “fatty acids.” Just as a dollar can comprise different combinations of coins—one hundred pennies, four quarters, ten dimes, twenty nickels, and so forth—a “fat” comprises different combinations of fatty acids.

There are more fatty acids in a big fat blob of butter than there are in a spoonful of butter, just as there are more coins in $5 than there are in $1, but whether you’re dealing with a spoonful of butter, a tub of lard, or a tablespoon of fish oil, all fat on earth is composed of fatty acids. The only difference between the fat in olive oil and the fat in lard is that if you looked at them under a microscope, you’d see that each is made up of a different mix of fatty acids (i.e., nickels, dimes, quarters, etc.).

There are three families of fatty acids: saturated fatty acids, monounsaturated fatty acids, and polyun-saturated fatty acids. (There’s actually a fourth class of fatty acids called trans fats, a kind of “Franken-fat,” but we’ll address that later.) In this section we’ll concentrate primarily on saturated fat, but keep a place on your dance card for two members of the polyunsaturated family called
omega-3 fatty acids
and
omega-6 fatty acids
. They’re of special importance, and we’ll be talking about them in depth later on.

Now a word of complete candor from your authors. We wrote this book for our families. We wanted the average intelligent person who didn’t have a background in science to be able to follow the basic arguments and have a clear sense of the takeaway messages. We wanted the discussions within the book to be simple enough that they could be easily grasped by nonmedical people. And, frankly, fat is complicated.

So this is the part of the book where we could easily slip into a short course on the biochemistry of fats. It’s interesting to write about, it fills a lot of pages—and it’s deadly dull for readers. Don’t worry, we’re not going to write about the chemical structure of fat, and here’s why. What makes one fatty acid “saturated” and another “unsaturated” has to do with fairly intricate details of fat architecture and composition that, frankly, most folks couldn’t care less about. (If you’re really dying to know, it has to do with the number of chemical double bonds that exist in the fatty acid’s molecular chain. Mono-unsaturated fats have one double bond. Polyunsaturated fats have more than one. There. Now you know.)