Good Calories, Bad Calories

The possibility that insulin determines what Le Magnen called the metabolic background of hunger also explains two observations we discussed in the sections on fattening and reducing diets.

The first is the observation by Ethan Sims that he could stuff his convict subjects with as much as ten thousand calories a day of mostly carbohydrate and they would still feel “hunger late in the day,” and yet subjects fed eight hundred superfluous calories of fat “developed marked anorexia.” On a more familiar level: why is it that most of us can imagine eating a large bag (twenty ounces) of movie popcorn—more than eleven hundred calories if popped in oil,^*137 as it typically is—but not so the equivalent caloric amount of cheese: say, fifteen slices of American cheese, or a cup and a half of melted Brie?

The simple explanation is that the insulin induced by the carbohydrates serves to deposit both fats and carbohydrates (fatty acids and glucose) as fat in the adipose tissue, and it keeps those calories fixed in the adipose tissue once they get there. As long as we respond to the carbohydrates by secreting more insulin, we continue to remove nutrients from our bloodstream in expectation of the arrival of more, so we remain hungry, or at least absent any feeling of satiation. It’s not so much that fat fills us up as that carbohydrates prevent satiety, and so we remain hungry.

The second observation is the carbohydrate craving associated with obesity. Here the metabolic background of hunger is established by chronic hyperinsulinemia rather than the immediate insulin secretion during a carbohydrate-rich meal. In both cases the insulin induces hunger or prevents satiety. In the case of hyperinsulinemia and obesity, however, this happens even between meals, when the cells should be living off a fuel mixture of predominantly fatty acids. Instead, the insulin traps the fat in the fat tissue, and it signals the cells to burn glucose. As far as the body is concerned, the elevated insulin is the indication that we’ve just eaten—“high levels of insulin herald the ‘fed’ state,” as George Cahill put it—and the signal that carbohydrates are available to be burned. But in this case, they’re not. Now the homeostatic system that evolved to maintain blood sugar in a healthy range establishes an internal environment in which the cells are primed to burn glucose for fuel, and only glucose can satisfy that demand, yet there’s no expendable glucose in the system. High insulin levels even prevent the liver from releasing the glucose that’s stored there as glycogen. As a result, it’s glucose that we crave. Even if we eat fat and protein—our cheese slices, for instance—the hyperinsulinemia will work to store these nutrients rather than allow them to be used for fuel.

The practical implication of this situation is critical to how we perceive the dietary treatment of obesity, or simply the maintenance of a healthy weight, in a world of inexpensive, easily digestible carbohydrate-rich foods. Among the more pessimistic arguments wielded against carbohydrate-restricted diets is that all diets fail eventually because the subjects inevitably fall of the diet, just as they do calorie-restricted diets. But this argument is based on the assumption that all diets work by limiting the calories consumed. It also ignores any physiological difference between a craving for carbohydrates and the hunger that results from semi-starvation. The latter is caused by the absence of sufficient calories to satisfy physiological demands. The craving for carbohydrates is more closely akin to an addiction, which is how it was described by the British clinician Robert Kemp in 1963. It is the consequence of hyperinsulinemia, which in turn is caused initially by the presence of carbohydrates in the diet, just as an addiction to nicotine or cocaine or any other addictive substance is caused by the use of these substances. There is nothing inherently natural about such addictions. The hunger that accompanies calorie restriction is an unavoidable physiological condition; the craving for carbohydrates is not.

Sugar (sucrose) is a special case. Just like cocaine, alcohol, nicotine, and other addictive drugs, sugar appears to induce an exaggerated response in that region of the brain known as the reward center—the nucleus accumbens. This suggests that the relatively intense cravings for sugar—a sweet tooth—may be explained by the intensity of the dopamine secretion in the brain when we consume sugar. When the nucleus accumbens “is excessively activated by sweet food or powerful drugs,” says Bartley Hoebel of Princeton, “it can lead to abuse and even addiction. When this system is under-active, signs of depression ensue.” Rats can be easily addicted to sugar, according to Hoebel, and will demonstrate the physical symptoms of opiate withdrawal when forced to abstain.