Why We Get Fat: And What to Do About It (25 page)

The first thing to question is the very idea that a diet that makes us lean by removing the fattening carbohydrates is also a diet that gives us heart disease. Recall Mayer’s mass-murder argument: if we eat fewer carbohydrates, we’ll replace those calories with fat. We will. Protein tends to stay in a narrow range in modern diets—15 to 25 percent of calories—whereas fat is traded off against carbohydrates: eating less of one means eating more of the other. If the one causes heart disease, then the other, almost by definition, has to prevent it. This is why carbohydrates became “heart-healthy” (even bread, pasta, potatoes, and sugar), and we were told to eat more of them when the authorities decided that eating fat clogged our arteries.

This would have little to do with the alleged evils of saturated fats except that there’s a well-documented relationship between obesity and heart disease. Remember Blake Donaldson’s “fat cardiacs”? Middle-aged men with a gut have always been obvious candidates for a heart attack. Fat, at least above the waist, and heart disease go hand in hand. (The fatter we are, or at least the more obese we are, the more likely we are to get virtually every major chronic disease.) That’s why doctors are always urging their overweight patients to lose weight—even a little. The risk of having a heart attack should decrease significantly as a result.

So, if carbohydrates make us fat, which they do, and fat or saturated fat causes heart disease, which the authorities tell us they do, then we have a paradox: now the diet that naturally makes us leaner is also the diet that gives us heart disease. Getting leaner now increases our risk of heart disease, whereas it should do the opposite.

This paradox suggests that only one of these two things can be true: either carbohydrates make us fat
or
dietary fat gives us heart disease but not both. And, indeed, the fact that carbohydrates
do
make us fat—particularly, to repeat myself, easily digestible carbohydrates
and sugars—suggests that these same carbohydrates are the likely nutritional causes of heart disease as well. This suggests that our obsession with the fat and saturated fat in our diets is simply misconceived.

Health authorities who insist that saturated fat causes heart disease have tried to escape this paradox—the diet that naturally makes us lean gives us heart disease—by blaming dietary fat for weight problems as well. They’ll argue that fat is the most energy-dense nutrient in the diet, and this makes it fattening. It has nine calories per gram, compared with four for either protein or carbohydrates. Because of this high energy density, you are supposedly fooled more easily into overeating by fat than you are by the less dense calories of carbohydrates and protein. If you eat ten grams of fat for a midday snack, for instance, you’ll be consuming fifty calories more than if you eat ten grams of protein or carbohydrates. Your body will care only about the ten grams, by this argument, not about the nutrients or the actual fuel available in those grams.

This idea is simplistic almost beyond belief. Imagine: hundreds of millions of years of evolution leading to organisms that determine how much fuel and essential nutrients they consume based only on the weight or energy density of the food, or the volume of the stomach cavity in which that food is digested. Not only is it hard to believe, but the experimental evidence has always refuted it. Even by the 1960s, high-fat, carbohydrate-restricted diets had been repeatedly shown to make people lose weight, not gain it. Still, by the 1970s, dietary fat had become the official dietary villain, and health authorities could now argue that saturated fat clogs our arteries and dietary fat in general makes us fat.

In 1984, this low-fat doctrine was officially set in stone when the National Heart, Lung, and Blood Institute (NHLBI) launched a “massive health campaign” to convince Americans that low-fat diets “will afford significant protection against coronary
heart disease.” The curious fact is that the NHLBI officials were actually less confident about the connection between dietary fat and heart disease than they were about the dietary fat/obesity idea. Here’s how two of the leading experts in the science of cholesterol and heart disease—Nancy Ernst at the NHLBI, and Robert Levy, a former NHLBI director—described this logic at the time:

As a nation, we were told to eat less fat and less saturated fat, which we did, or at least tried to do—saturated-fat consumption steadily declined over the years that followed, according to U.S. Department of Agriculture statistics—and yet, rather than getting leaner, we got fatter.

What’s more, the incidence of heart disease has not even diminished, which goes against expectations, if eating less fat or saturated fat makes a difference. This has been documented in numerous studies, the latest of which appeared in
The Journal of the American Medical Association
in November 2009 by Elena Kuklina and her colleagues at the Centers for Disease Control and Prevention. The authors made much of the fact that the number of Americans with high levels of LDL cholesterol has recently been decreasing, as would be expected in a nation avoiding saturated fat (and spending billions of dollars yearly on cholesterol-lowering drugs), but the number of heart attacks was not decreasing with it.

That the official embrace of low-fat, high-carbohydrate diets coincided not with a national decline in weight and heart disease but with epidemics of both obesity and diabetes (both of which increase heart disease risk), should make any reasonable person question the underlying assumptions of the advice. But that’s not how people tend to think when confronted with evidence that one of their long-held beliefs is wrong. It’s not how we typically deal with cognitive dissonance. It’s certainly not how institutions and governments do it.

For the moment, I’ll just say that the obesity/heart-disease link, combined with the obesity and diabetes epidemics that began more or less coincidentally with the advice to eat less fat, less saturated fat, and more carbohydrates, is a good reason to doubt that it’s the fat and the saturated fat that we have to worry about.

Another reason to question the belief that saturated fat is bad for our health is that experimental evidence in support of the idea has always been surprisingly hard to come by. I know this seems difficult to believe, considering how forcefully we’ve been told that saturated fat is a killer. But what we’ve been told and what the evidence actually supports parted ways in 1984, when the National Heart, Lung, and Blood Institute launched its massive health campaign. At the time, the NHLBI experts lacked confidence in the fat/heart-disease connection, for good reason: the institute had spent $115 million on a huge, decade-long clinical trial to test the idea that eating less saturated fat would curb heart disease, but not a single heart attack had been prevented.
^*

This could have been taken as reason to abandon the idea entirely, but the institute had also spent $150 million testing the benefits of a cholesterol-lowering drug, and this second trial had succeeded. So the institute’s administrators took a leap of faith, as
one of them, Basil Rifkind, later described it: They had spent twenty years and an inordinate amount of money trying to demonstrate that cholesterol-lowering, low-fat diets would prevent heart disease, Rifkind explained, and they had, up until then, failed. Trying again would be too expensive and would take at least another decade, even if the institute could afford it. But once they had compelling evidence that lowering cholesterol with a drug would save lives, it seemed like a good bet that a low-fat, cholesterol-lowering diet would as well. “It’s an imperfect world,” Rifkind had said. “The data that would be definitive are ungettable, so you do your best with what is available.”

The ambition was admirable, but the results have been, as I said, disappointing. Researchers have continued to demonstrate that cholesterol-lowering drugs can prevent heart attacks and apparently allow some people to live longer (at least those who are at particularly high risk of a heart attack). But it has still not been demonstrated that either low-fat or low-saturated-fat diets will do the same.

One problem here is that when people, experts or not, decide to review the evidence on an issue dear to their hearts (me included), they tend to see what they want to see. This is human nature, but it doesn’t lead to trustworthy conclusions. To get around this problem, at least in medicine, an international organization was formed in the mid-1990s specifically to do
unbiased
reviews of the literature. This organization, known as the Cochrane Collaboration, is now widely considered to be among the most reliable sources for judgments about whether some intervention—a diet, a surgical procedure, a diagnostic technique—will actually do what doctors hope it does.

The Cochrane Collaboration assessed the benefits of eating less fat or less saturated fat in 2001. All told, the authors could find only twenty-seven clinical trials in the entire medical literature, dating back to the 1950s, that were conducted well enough so that a reliable judgment could be made about whether changing the fat content of our diet would prevent heart attacks and premature
death. Many of the trials were actually designed to study whether these diets had effects on other conditions (such as breast cancer, hypertension, polyps, or gallstones), but the researchers who did the trials had also reported whether their subjects had heart attacks or died from them, and so the studies could be used to assess those issues as well. The evidence was anything but compelling.

“Despite decades of effort and many thousands of people randomized,” the Cochrane Collaboration authors concluded, “there is still only limited and inconclusive evidence of the effects of modification of total, saturated, monounsaturated, or polyunsaturated fats on cardiovascular morbidity [i.e., sickness] and mortality [death].”

Since that Cochrane Collaboration analysis, the results of the largest, most expensive diet trial ever done have been published. That trial tested the benefits and risks of eating less fat and less saturated fat for women, who were rarely included in any of the earlier trials. This was the Women’s Health Initiative that I mentioned back in
chapter two
. Forty-nine thousand middle-aged women were enrolled in the diet study, and twenty thousand of them were chosen at random to eat low-fat, low-saturated-fat diets, with less meat, more vegetables, more fresh fruits, and more whole grains. (This trial was funded not because the authorities were willing to doubt publicly that eating less fat would prevent heart disease but because previous trials had not included women, and the authorities were being pressured to take women’s health as seriously as they did men’s.)

After six years on the diet, these women had cut both their total fat consumption and their saturated-fat consumption by a quarter, lowering their total cholesterol and their LDL cholesterol below (albeit only very slightly below) that of the other twenty-nine thousand women, who were eating whatever they wanted and yet their low-fat diet, as the final reports stated, had
no
beneficial effect on heart disease, stroke, breast cancer, colon cancer, or, for that matter, fat accumulation. Eating less total fat and
saturated fat, and replacing the fatty foods with fruits and vegetables and whole grains, had no observable beneficial effect at all.
^*

There are many problems with the kind of leap-of-faith, do-your-best, it’s-a-good-bet logic that health authorities put into action in 1984, admirable and reasonable as it may have seemed at the time. The obvious one is that they will have our best interests in mind as they advise us to do something, but this something will end up doing more harm than good. The law of unintended consequences will take effect. In this case, we are told to eat less fat and more carbohydrates, and rather than avoid heart disease and get thinner, as the authorities had hoped we would, we’ve had as much heart disease as ever, and dramatic increases in obesity and diabetes.

A more insidious problem is that all involved—the researchers, the physicians, the public-health authorities, the health associations—commit themselves to a belief early in the evolution of the science, arguably at the stage at which they know the least about it, and then they become so invested in their belief that no amount of evidence to the contrary can convince them that they’re wrong. As a result, when trials like the Women’s Health Initiative find that eating less fat and less saturated fat has no beneficial effect (at least not for women), the authorities don’t respond by acknowledging that they have made an error all along. Doing so might make them (and us) question their credibility, as it should. Instead, they tell us that the study must have been flawed, and thus the results can be ignored.

This is what happened with saturated fat. The belief that saturated
fat clogs arteries by raising cholesterol levels is a hangover from the state of the science thirty to forty years ago. Back then, the evidence was poor, and it is still poor. But the belief was locked into the conventional wisdom, and still is, for a simple reason: LDL and total cholesterol are the two risk factors most obviously modified by cholesterol-lowering drugs, particularly statins (which are now worth billions of dollars yearly to the pharmaceutical industry). These drugs prevent heart attacks, and they may save lives. So the leap of faith is the same today as it was in 1984: if a drug that lowers cholesterol (and particularly LDL cholesterol) can prevent heart disease, then surely a diet that lowers cholesterol (and particularly LDL cholesterol) will prevent heart disease, whereas a diet that raises it must be a cause of heart disease. Saturated fat raises total cholesterol and LDL cholesterol. Ergo, saturated fat must cause heart disease, and diets that restrict saturated fat must prevent it.