Good Calories, Bad Calories (82 page)

Dairy is low-fat or no-fat. The diet has plenty of nuts and legumes and good carbohydrates, which are those with copious vitamins, minerals, antioxidants, and fiber (vegetables, fruits, and unrefined grains), but few bad carbohydrates, which are energy-dense and thus contribute to obesity (highly refined carbohydrates and sugars).

It may be true that such a diet is uniquely healthy—but we have no idea if that’s real y so. The diet has the advantage of being political y correct; it can be recommended without fear of ostracism from the medical community. Whether it is healthier, however, than, say, a meat diet of 70–80 percent fat calories and absent carbohydrates almost entirely, as Stefansson suggested in the 1920s, or any diet of animal products (meat, fish, fowl, eggs, and cheese) and green vegetables but absent entirely starches, sugar, and flour or even sugar alone, is stil anybody’s guess. And whether such a diet would prevent us from fattening or reverse obesity, or do it better than a mostly meat diet, has also never been tested. If it doesn’t, then it’s probably not the healthiest diet, because excessive fat accumulation is certainly associated with increased risk of chronic disease.

I have spent much of the last fifteen years reporting and writing about issues of public health, nutrition, and diet. I have spent five years on the research for and writing of this book alone. To a great extent, the conclusions I’ve reached are as much a product of the age we live in as they are my own skeptical inquiry. Just ten years ago, the research for this book would have taken the better part of a lifetime. It was only with the development of the Internet, of search engines and the comprehensive databases of the Library of Medicine, the Institute for Scientific Information, research libraries, and secondhand-book stores worldwide now accessible online that I was able, with reasonable facility, to locate and procure virtual y any written source, whether published a century ago or last week, and to track down and contact clinical investigators and public-health officials, even those long retired.

Throughout this research, I tried to fol ow the facts wherever they led. In writing the book, I have tried to let the science and the evidence speak for themselves. When I began my research, I had no idea that I would come to believe that obesity is not caused by eating too much, or that exercise is not a means of prevention. Nor did I believe that diseases such as cancer and Alzheimer’s could possibly be caused by the consumption of refined carbohydrates and sugars. I had no idea that I would find the quality of the research on nutrition, obesity, and chronic disease to be so inadequate; that so much of the conventional wisdom would be founded on so little substantial evidence; and that, once it was, the researchers and the public-health authorities who funded the research would no longer see any reason to chal enge this conventional wisdom and so to test its validity.

As I emerge from this research, though, certain conclusions seem inescapable to me, based on the existing knowledge: 1. Dietary fat, whether saturated or not, is not a cause of obesity, heart disease, or any other chronic disease of civilization.

2. The problem is the carbohydrates in the diet, their effect on insulin secretion, and thus the hormonal regulation of homeostasis—the entire harmonic ensemble of the human body. The more easily digestible and refined the carbohydrates, the greater the effect on our health, weight, and wel -being.

3. Sugars—sucrose and high-fructose corn syrup specifical y—are particularly harmful, probably because the combination of fructose and glucose simultaneously elevates insulin levels while overloading the liver with carbohydrates.

4. Through their direct effect on insulin and blood sugar, refined carbohydrates, starches, and sugars are the dietary cause of coronary heart disease and diabetes. They are the most likely dietary causes of cancer, Alzheimer’s disease, and the other chronic diseases of civilization.

5. Obesity is a disorder of excess fat accumulation, not overeating, and not sedentary behavior.

6. Consuming excess calories does not cause us to grow fatter, any more than it causes a child to grow tal er. Expending more energy than we consume does not lead to long-term weight loss; it leads to hunger.

7. Fattening and obesity are caused by an imbalance—a disequilibrium—in the hormonal regulation of adipose tissue and fat metabolism. Fat synthesis and storage exceed the mobilization of fat from the adipose tissue and its subsequent oxidation. We become leaner when the hormonal regulation of the fat tissue reverses this balance.

8. Insulin is the primary regulator of fat storage. When insulin levels are elevated—either chronical y or after a meal—we accumulate fat in our fat tissue.

When insulin levels fal , we release fat from our fat tissue and use it for fuel.

9. By stimulating insulin secretion, carbohydrates make us fat and ultimately cause obesity. The fewer carbohydrates we consume, the leaner we wil be.

10. By driving fat accumulation, carbohydrates also increase hunger and decrease the amount of energy we expend in metabolism and physical activity.

In considering these conclusions, one must address the obvious question: can a diet mostly or entirely lacking in carbohydrates possibly be a healthy pattern of eating? For the past half century, our conceptions of the interaction between diet and chronic disease have inevitably focused on the fat content.

Any deviation from some ideal low-fat or low-saturated-fat diet has been considered dangerous until long-term, randomized control trials might demonstrate otherwise. Because a diet restricted in carbohydrates is by definition relatively fat-rich, it has therefore been presumed to be unhealthy until proved otherwise. This is why the American Diabetes Association even recommends against the use of carbohydrate-restricted diets for the management of Type 2 diabetes. How do we know they’re safe for long-term consumption?

The argument in their defense is the same one that Peter Cleave made forty years ago, when he proposed what he cal ed the saccharine-disease hypothesis. Evolution should be our best guide for what constitutes a healthy diet. It takes time for a population or a species to adapt to any new factor in its environment; the longer we’ve been eating a particular food as a species, and the closer that food is to its natural state, the less harm it is likely to do.

This is an underlying assumption of al public-health recommendations about the nature of a healthy diet. It’s what the British epidemiologist Geoffrey Rose meant when he wrote his seminal 1985 essay, “Sick Individuals and Sick Populations,” and described the acceptable measures of prevention that could be recommended to the public as those that remove “unnatural factors” and restore “‘biological normality’—that is…the conditions to which presumably we are genetical y adapted.” “Such normalizing measures,” Rose said, “may be presumed to be safe, and therefore we should be prepared to advocate them on the basis of a reasonable presumption of benefit.”

The fat content of the diets to which we presumably evolved, however, wil always remain questionable. If nothing else, whatever constituted the typical Paleolithic hunter-gatherer diet, the type and quantity of fat consumed assuredly changed with season, latitude, and the coming and going of ice ages.

This is the problem with recommending that we consume oils in any quantity. Did we evolve to eat olive oil, for example, or linseed oil? And maybe a few thousand years is sufficient time to adapt to a new food but a few hundred is not. If so, then olive oil could conceivably be harmless or even beneficial when consumed in comparatively large quantities by the descendants of Mediterranean populations, who have been consuming it for mil ennia, but not to Scandinavians or Asians, for whom such an oil is new to the diet. This makes the science even more complicated than it already is, but these are serious considerations that should be taken into account when discussing a healthy diet.

There is no such ambiguity, however, on the subject of carbohydrates. The most dramatic alterations in human diets in the past two mil ion years, unequivocal y, are (1) the transition from carbohydrate-poor to carbohydrate-rich diets that came with the invention of agriculture—the addition of grains and easily digestible starches to the diets of hunter-gatherers; (2) the increasing refinement of those carbohydrates over the past few hundred years; and (3) the dramatic increases in fructose consumption that came as the per-capita consumption of sugars—sucrose and now high-fructose corn syrup

—increased from less than ten or twenty pounds a year in the mid-eighteenth century to the nearly 150 pounds it is today. Why would a diet that excludes these foods specifical y be expected to do anything other than return us to “biological normality”?

It is not the case, despite public-health recommendations to the contrary, that carbohydrates are required in a healthy human diet. Most nutritionists stil insist that a diet requires 120 to 130 grams of carbohydrates, because this is the amount of glucose that the brain and central nervous system wil metabolize when the diet is carbohydrate-rich. But what the brain uses and what it requires are two different things. Without carbohydrates in the diet, as we discussed earlier (see Chapter 19), the brain and central nervous system wil run on ketone bodies, converted from dietary fat and from the fatty acids released by the adipose tissue; on glycerol, also released from the fat tissue with the breakdown of triglycerides into free fatty acids; and on glucose, converted from the protein in the diet. Since a carbohydrate-restricted diet, unrestricted in calories, wil , by definition, include considerable fat and protein, there wil be no shortage of fuel for the brain. Indeed, this is likely to be the fuel mixture that our brains evolved to use, and our brains seem to run more efficiently on this fuel mixture than they do on glucose alone. (A good discussion of the rationale for a minimal amount of carbohydrates in the diet can be found in the 2002 Institute of Medicine [IOM] report, Dietary Reference Intakes. The IOM sets an “estimated average requirement” of a hundred grams of carbohydrates a day for adults, so that the brain can run exclusively on glucose, “without having to rely on a partial replacement of glucose by [ketone bodies].” It then sets the “recommended dietary al owance” at 130 grams to al ow margin for error. But the IOM report also acknowledges that the brain wil be fine without these carbohydrates, because it runs perfectly wel on ketone bodies, glycerol, and the protein-derived glucose.) Whether a carbohydrate-restricted diet is deficient in essential vitamins and minerals is another issue. As we also discussed (see Chapter 19), animal products contain al the amino acids, minerals, and vitamins essential for health, with the only point of controversy being vitamin C. And the evidence suggests that the vitamin C content of meat products is more than sufficient for health, as long as the diet is indeed carbohydrate-restricted, with none of the refined and easily digestible carbohydrates and sugars that would raise blood sugar and insulin levels and so increase our need to obtain vitamin C

from the diet. Moreover, though it may indeed be uniquely beneficial to live on meat and only meat, as Vilhjalmur Stefannson argued in the 1920s, carbohydrate-restricted diets, as they have been prescribed ever since, do not restrict leafy green vegetables (what nutritionists in the first half of the twentieth century cal ed 5 percent vegetables) but only starchy vegetables (e.g., potatoes), refined grains and sugars, and thus only those foods that are virtual y without any essential nutrients unless they’re added back in the processing and so fortified, as is the case with white bread. A calorie-restricted diet that cuts al calories by a third, as John Yudkin noted, wil also cut essential nutrients by a third. A diet that prohibits sugar, flour, potatoes, and beer, but al ows eating to satiety meat, cheese, eggs, and green vegetables wil stil include the essential nutrients, whether or not it leads to a decrease in calories consumed.

My hope is that this book wil change our views of the nature of a healthy diet, as the research for it changed my own; that future discussions of the nature of a healthy diet wil begin with the quantity and quality of the carbohydrates contained, rather than the fat. As a chal enge to the conventional wisdom on diet, obesity, and chronic disease, however, it presents a dilemma to public-health authorities; to nutritionists and physicians who believe that the advice they have been giving for the past few decades has been correct and based in sound science; and to al of us who simply want to eat healthy but have trouble accepting that everything we have come to believe could be as misguided as I have portrayed it. The resolution to this dilemma is to test the carbohydrate hypothesis rigorously, just as the fat-cholesterol hypothesis of heart disease should have been tested forty years ago.

In the past decade, the National Institutes of Health final y began funding randomized-control trials of carbohydrate-restricted diets, as has the Dr.Robert C. Atkins Foundation, but these trials have been designed to test only the hypothesis that such diets can be used safely and effectively as a means to lose weight. The subjects are overweight and obese, and the studies compare weight loss and heart-disease risk factors with the results of low-fat or calorie-restricted diets. These trials are neither planned nor interpreted as tests of the hypothesis that it is the carbohydrates in the diet—“the sugar and starchy elements of food,” as The Lancet phrased it 140 years ago—that cause fattening and obesity to begin with. Rather, the underlying assumption here, too, is that weight loss is caused inevitably by negative caloric balance—consuming fewer calories then we expend—and the investigators perceive these trials as testing whether carbohydrate restriction al ows us to do so with more or less facility than semi-starvation diets that reduce calories directly or reduce fat calories specifical y.

A direct test of the carbohydrate hypothesis asks the opposite question: not whether the absence of refined and easily digestible carbohydrates and sugars causes weight loss and is safe, but whether the presence of these carbohydrates causes weight gain and chronic disease. Such a trial would ideal y be done with lean, healthy individuals, or with a spectrum of subjects from lean through obese, including those with metabolic syndrome and Type 2 diabetes. They would be randomized into two groups, one of which would consume the sugary and starchy elements of food and one of which would not, and then we would see what happens. We might randomly assign a few thousand individuals to eat the typical American diet of today—including its 140–50 pounds of sugar and high-fructose corn syrup a year, nearly 200 pounds of flour and grain, 130-plus pounds of potatoes, and 27 pounds of corn—and we could assign an equal number to eat a diet of mostly animal products (meat, fish, fowl, eggs, cheese) and leafy green vegetables. Since the latter diet would be relatively high in fat and saturated fat and calorical y dense, the conventional wisdom is that it would cause heart disease and, perhaps, obesity and diabetes. So this would test the dietary-fat/cholesterol hypothesis of heart disease, as wel as the carbohydrate hypothesis.