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.”