EPILOGUE
The community of science thus provides for the social validation of scientific work. In this respect, it amplifies that famous opening line of Aristotle's Metaphysics: "All men by nature desire to know." Perhaps, but men of science by culture desire to know that what they know is really so. ROBERT MERTON, Behavior Patterns of Scientists, 1968
The first principle is that you must not fool yourself—and you are the easiest person to fool. RICHARD FEYNMAN, in his Commencement Address at Caltech, 1974
ON FEBRUARY 7, 2003, THE EDITORS OF
Science published a special issue dedicated to the critical concerns of obesity research. It included four essays written by prominent authorities, all communicating the message of the toxic-environment hypothesis of the obesity epidemic and
the belief that obesity is caused by "consuming more food energy than is expended in activity." The one article that offered a potential solution to the national and global problem of burgeoning waistlines—other than the promise of future obesity-fighting drugs—was written by James Hill of the University of Colorado, John Peters of Procter & Gamble, and two colleagues.
Hill and Peters introduced the concept of an "energy gap" that could purportedly explain the existence of the obesity epidemic and illuminate a path of action by which it might be halted or reversed. By their calculation, the obesity epidemic represented an energy gap of a hundred calories per person among the American public per day that had been consumed but not expended. To undo the epidemic, Hill and Peters suggested, Americans would have to make either comparable increases in daily energy expenditure—walking one extra mile, perhaps—or decreases in energy consumption, such as "eating 15% less (about three bites) of a typical premium fast-food hamburger." Two years later, when the U.S. Department of Agriculture released the sixth edition of its Dietary Guidelines for Americans, it offered similar advice based on the identical logic: "For most adults a reduction of 50 to 100 calories per day may prevent gradual weight gain."
This proposition should evoke a distinct sensation of deja vu, because it is the precise argument that Carl von Noorden made over a century ago.
Hill, Peters, and the USDA authorities, like von Noorden, were treating the regulation of body weight as though it were a purely arithmetical process, in which a small excess of calories consumed, day in and day out, accumulates into pounds of flesh and then tens of pounds, and a small deficit, day in and day out, does the opposite. That
this argument is now the cornerstone of the official U.S. government recommendations for obesity prevention made the single caveat in Hill and Peters's Science article all that much more remarkable. Speaking of the hundred-calorie energy gap, they said that their "estimate is theoretical and involves several assumptions"—in particular, "Whether increasing energy expenditure or reducing energy intake by 100 kcal/day would prevent weight gain
remains to be empirically tested."
The more important point, though, which Hill and Peters did not discuss, was
why a century of research had not produced such an empirical test. Two immediate possibilities suggest themselves: Either the accumulated research and observations on weight regulation in humans or animals had never provided sufficient reason to believe that such a proposition should be true, which is a necessary condition for anyone to expend the effort to test it; or, perhaps, nobody cared to test it. In either case,
we have to wonder whether the individuals involved in the pursuit of the cure and prevention of human obesity, as Robert Merton would have put it, have the desire to know that what they know is really so.
In the 1890s, Francis Benedict and Wilbur Atwater, pioneers of the science of nutrition in the United States, spent a year in the laboratory testing the assumption that the law of energy conservation applied to humans as well as animals. They did so not because they doubted that it did, but precisely because it seemed so obvious. "No one would question" it, they wrote. "The quantitative demonstration is, however, desirable, and an attested method for such demonstration is of fundamental importance for the study of the general laws of metabolism of both matter and energy."
This is how functioning science works. Outstanding questions are identified or hypotheses proposed; experimental tests are than established either to answer the questions or to refute the hypotheses, regardless of how obviously true they might appear to be. If assertions are made without the empirical evidence to defend them, they are vigorously rebuked. In science, as Merton noted, progress is made only by first establishing whether one's predecessors have erred or "have stopped before tracking down the implications of their results or have passed over in their work what is there to be seen by the fresh eye of another." Each new claim to knowledge, therefore, has to be picked apart and appraised. Its shortcomings have to be established unequivocally before we can know what questions remain to be asked, and so what answers to seek—what we know is really so and what we don't. "This unending exchange of critical judgment," Merton wrote, "of praise and punishment, is developed in science to a degree that makes the monitoring of children's behavior by their parents seem little more than child's play."
The institutionalized
vigilance, "this unending exchange of critical judgment," is nowhere to be found in the study of nutrition, chronic disease, and obesity, and it hasn't been for decades. For this reason,
it is difficult to use the term "scientist" to describe those individuals who work in these disciplines, and, indeed, I have actively avoided doing so in this book.
It's simply debatable, at best, whether what these individuals have practiced for the past fifty years, and whether the culture they have created, as a result, can reasonably be described as science, as most working scientists or philosophers of science would typically characterize it.
Individuals in these disciplines think of themselves as scientists; they use the terminology of science in their work, and they certainly borrow the authority of science to communicate their beliefs to the general public, but "the results of their enterprise," as Thomas Kuhn, author of The Structure of Scientific Revolutions, might have put it, "do not add up to science as we know it."
Though the reasons for this situation are understandable, they offer scant grounds for optimism. Individuals who pursue research in this confluence of nutrition, obesity, and chronic disease are typically motivated by the desire to conserve our health and prevent disease. This is an admirable goal, and it undeniably requires reliable knowledge to achieve, but it cannot be accomplished by allowing the goal to compromise the means, and this is what has happened. Practical considerations of what is too loosely defined as the "public health" have consistently been allowed to take precedence over the dispassionate, critical evaluation of evidence and the rigorous and meticulous experimentation that are required to establish reliable knowledge. The urge to simplify a complex scientific situation so that physicians can apply it and their patients and the public embrace it has taken precedence over the scientific obligation of presenting the evidence with relentless honesty.
The result is an enormous enterprise dedicated in theory to determining the relationship between diet, obesity, and disease, while dedicated in practice to convincing everyone involved, and the lay public, most of all, that the answers are already known and always have been—an enterprise, in other words, that purports to be a science and yet functions like a religion.
The essence of the conflict between science and nutrition is time. Once we decide that science is a better guide to a healthy diet than whatever our parents might have taught us (or our grandparents might have taught our parents), then the sooner we get reliable guidance the better off we are. The existence of uncertainty and competing hypotheses, however, does not change the fact that we all have to eat and we have to feed our children. So what do we do?
There are two common responses to this question, as there will be to the arguments made in this book. One response is to take into account the uncertainties about the health effects of fats and carbohydrates and then suggest that we simply eat in moderation. This in turn implies eating a balanced diet in moderation. "Perhaps our most sensible public health recommendation should be moderation in all things, and moderation in that," as the University of Michigan professor of public health Marshall Becker suggested back in 1987.
But some of us do eat with admirable restraint of the four major food groups and yet are obese or overweight anyway, and presumably have an increased risk of other chronic diseases because of it; some of us are suitably lean, eat balanced diets in moderation, and exercise regularly and yet are insulin- resistant and maybe even diabetic.
The more optimistic response is a compromise position: to
take virtually every reasonable hypothesis from the past fifty years that can coexist with the saturated-fat/cholesterol hypothesis of heart disease and fold them all into one seemingly reasonable diet that might do us good and probably won't do harm. Thus, the current conception of a healthy diet is one that minimizes salt content and maximizes fiber; has plenty of good fats (monounsaturated and omega-three polyunsaturated fats) and minimal bad fats (saturated fats and trans fats); has plenty of olive oil and fish, and little red meat, butter, lard, and dairy products. When meat is consumed, it's lean, which keeps saturated-fat content down and reduces energy density and thus, supposedly, calories. 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 really so. The diet has the advantage of being politically 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 still 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 virtually 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 follow 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 challenge 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 well-being.
3. Sugars—sucrose and high-fructose corn syrup specifically—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 taller. 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 chronically or after a meal—we accumulate fat in our fat tissue. When insulin levels fall, 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 will 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 called 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 all 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 genetically 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, will 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 millennia, 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 million years, unequivocally, 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 specifically 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 still 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 will 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 will 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, will, by definition, include considerable fat and protein, there will 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 allowance" at 130 grams to allow margin for error. But the IOM report also acknowledges that the brain will be fine without these carbohydrates, because it runs perfectly well 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 all 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 called 5 percent vegetables) but only starchy vegetables (e.g., potatoes), refined grains and sugars, and thus only those foods that are virtually 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 all calories by a third, as John Yudkin noted, will also cut essential nutrients by a third. A diet that prohibits sugar, flour, potatoes, and beer, but allows eating to satiety meat, cheese, eggs, and green vegetables will still include the essential nutrients, whether or not it leads to a decrease in calories consumed.
My hope is that this book will 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 will begin with the quantity and quality of the carbohydrates contained, rather than the fat. As a challenge 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 all 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 finally 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 allows us to do so with more or less facility than semi-starvation diets that reduce calories directly or reduce fat calories specifically.
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 ideally 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 calorically 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 well as the carbohydrate hypothesis.
Such a trial would not be ideal, because many dietary variables would differ between the two groups—calories and fats among them. The subjects would also know what diet they're consuming, and so the study would not be done blindly (although, ideally, the physicians who treated the subjects and the investigators themselves would be unaware). Nonetheless, it would be a good starting point.
Would those eating the carbohydrate-rich diet be more likely to become glucose-intolerant, hyperinsulinemic, and insulin-resistant? Would they be fatter and have a greater incidence of obesity, metabolic syndrome, and Type 2 diabetes? Would they have more heart disease and cancer? Would they die prematurely or live longer? These are the questions we need to answer.
Another question that needs to be addressed urgently regards the health effects of sugar and high-fructose corn syrup alone. Since the 1980s, as we discussed (see Chapter 12), sugar and high-fructose corn syrup have been exonerated as causes of chronic disease on the basis that the evidence was ambiguous. Since then, virtually no studies have been funded; there have been no attempts to clarify the picture. Today I can imagine no research more important to the public health than rigorous, controlled trials of the long-term health effects of sugar and high-fructose corn syrup.
For the past decade, the National Institutes of Health has been funding trials that test whether "lifestyle modification" will prevent diabetes and metabolic syndrome. But these trials are done only in the context of the conventional wisdom on diet, obesity, and disease. In the largest of these trials to date,
the $150 million Diabetes Prevention Program, the lifestyle modification included 150 minutes of exercise each week and a low-fat, low-calorie diet. The results confirmed that such a program of diet and exercise will indeed prevent or delay the appearance of diabetes and metabolic syndrome, but they said nothing about what aspect of this lifestyle modification was responsible. Was it the reduction in fat calories or total calories? Was it the exercise? Or was it a change in the type of carbohydrates consumed or a reduction in the total amount of carbohydrates? As we discussed (see Chapter 19),
even if the goal of a diet is to reduce calories by preferentially reducing fat, it will inevitably cut back on carbohydrates as well, and usually sugars in particular.*138
The
NIH is currently spending $200 million on a decade-long trial called Look AHEAD to test the hypothesis that if obese diabetics lose weight they'll be healthier for the effort. This is "the largest, most expensive trial ever funded by NIH for obesity outcome research," says the Baylor University psychologist John Foreyt, who is one of the trial's principal investigators. But o
nce again, the trial tests only the conventional wisdom. The goal of Look AHEAD is to induce five thousand obese diabetics to lose weight by the same lifestyle modification used in the Diabetes Prevention Program: cutting calories and fat calories, and exercising. If these obese diabetics do lose weight, and if they do end up healthier for it, we still won't know whether it was the calories, the fat calories, the exercise, some combination of all three, or maybe just the carbohydrates or the sugar that made the difference. And we won't know whether, if they restricted carbohydrates alone and ate protein and fat to their hearts' content, they would have been healthier still.
Because
these trials are planned as a test of only one hypothesis—and a poorly defined hypothesis at that—the research ensures that we won't have the kind of reliable answers that we so desperately need. If the Diabetes Prevention Program had included a test of the carbohydrate hypothesis, the investigators could have compared the effect of a low-fat, low-calorie diet and exercise to the effect of carbohydrate restriction alone, and that would have told us whether it's the carbohydrates or the calories and the sedentary behavior that cause these chronic diseases.
If Look AHEAD were to include a test of the carbohydrate hypothesis, we might at least know the answer in another decade. It doesn't, and we won't.
The scientific obligation, as I said in the prologue, is to establish the cause of obesity, diabetes, and the chronic diseases of civilization beyond reasonable doubt. By doing so, we can take the necessary steps to prevent these disorders, rather than trying to cure them or ameliorate them after the fact. If there are competing hypotheses, it does us little good to test one alone. It does little good to continue basing public-health recommendations and dietary advice on association studies (the Framingham Heart Study and the Nurses Health Study are prominent examples) that are incapable of reliably establishing cause and effect. What's needed now are randomized trials that test the carbohydrate hypothesis as well as the conventional wisdom. Such trials would be expensive. Like the Diabetes Prevention Program and Look AHEAD, they'll cost tens or hundreds of millions of dollars. And even if such trials are funded, it might be another decade or two before we have reliable answers. But it's hard to imagine that this controversy will go away if we don't do them, that we won't be arguing about the detrimental role of fats and carbohydrates in the diet twenty years from now. The public will certainly not be served by attempts of interest groups and industry to make this controversy go away.
If the tide of obesity and diabetes continues to rise around the world, it's hard to imagine that the cost of such trials, even a dozen or a hundred of them, won't ultimately be trivial compared with the societal cost.