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,
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
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
In the past decade, the National Institutes of Health finally began funding randomized-control trials of
