Good Calories, Bad Calories (80 page)

One of the most radical implications of this hypothesis is that even such an intractable condition as anorexia nervosa—which, like obesity, is now universal y considered a behavioral and psychological disorder—may be caused fundamental y by a physiological defect of fat metabolism and insulin.

The behavior of undereating may be a compensatory response to a physiological condition, just as the behavior of overeating can. Any hormonal abnormality that makes it difficult to store calories as fat—the fat cel s, for example, becoming prematurely or abnormal y resistant to insulin—could conceivably induce a compensatory inhibition of eating behavior and/or an increase in energy expended. What appears to be purely a behavioral phenomenon, the anorexia itself (and perhaps even bulimia nervosa), would be the compensatory response to a physiological problem, the inability to store calories after a meal in the energy buffer of the fat tissue. Correctly identifying cause and effect in these conditions would be difficult, if not impossible, without the understanding that there is an alternative hypothesis to explain the observations.

One final point has to be made about this physiological hypothesis of hunger and weight regulation, and it’s almost as counterintuitive as it is important.

This is what the hypothesis says about our perception of taste. One seemingly obvious relationship between diet and obesity has always been that the more palatable the food, the more we’re likely to overindulge and so grow fat.

In the 1960s and 1970s, obesity researchers referred to this supposed effect of taste on food intake and weight as the palatability hypothesis. But these researchers defined palatability on the basis of how much their experimental animals ate. If their rats or mice ate more of one food than another, the researchers assumed that they did so because they liked it better. The problem is that this concept of palatability “arises mainly from human experience; its existence in animals is an inference,” as the physiological psychologist Mark Friedman explained in 1989. In other words, the animals’ preference for certain foods could have been explained by other factors.

In fact, our perception of what tastes good depends very much on circumstances. Le Magnen made this observation early in his career, and it’s one reason why the subject of his own research evolved from olfactory stimuli to food intake. Le Magnen first noted that our assessment of odor changes with food consumption. The smel of a cinnamon bun baking in the oven wil be considerably more enticing when we’re hungry than after we’ve eaten. Our subjective interpretation of taste changes as wel . With the possible exception of inordinately expensive meals at fashionable restaurants, the memorable meals of our lives are likely to be those we ate when we were particularly hungry—after a day of hard work or a particularly strenuous workout. “It is often said and not without reason,” as Pavlov wrote in the 1890s, “that ‘hunger is the best sauce.’”

Le Magnen established that an animal’s response to a particular food correlates with how depleted the animal happens to be at the time, with the caloric value of the food, and with how rapidly it fulfil s the animal’s nutritional requirements. Rats given the choice between caloric sugar solutions and zero-calorie but equal y sweet saccharine solutions initial y drink similar amounts of both, Le Magnen reported. They both taste good. But the rats wil drink more of the sugar solution with each passing day—drinking three times as much on day five as on day one—while rejecting the saccharine solution after three or four days, having apparently concluded, metabolical y, that it offers no nutritive value. If the rats drinking the saccharine solution, however, are simultaneously infused with calorie-bearing glucose directly into their stomachs, they wil continue to drink the saccharine solution as long as they get the calories along with it. The taste hasn’t changed, but their post-absorption metabolic responses have. Foods that supply calories and other nutritional requirements quickly and efficiently wil come to be perceived as tasting good, and so we learn to prefer them over others.

This offers up an alternative scenario to the common assumption that we are born with an innate preference for sugar because it would have been evolutionarily beneficial, prompting us to seek out those foods that are the densest source of calories in a world in which calories were supposedly hard to come by. “In evolution,” as the Yale psychologist Linda Bartoshuk told the New York Times in 1989, “we needed the energy of sweet-tasting, sugary foods, especial y during times of scarcity.” The research of Le Magnen and others suggests that these preferences have little to do with the presence of famine in our evolutionary history (as discussed on Chapter 14) and everything to do with the absence of these refined carbohydrate foods. We come to prefer these foods, according to the alternative hypothesis, because they induce an exaggerated version of the post-absorption responses to natural y occurring sources of glucose and fructose—either plant foods that are difficult to digest (the kinds of roots, tubers, or fruit eaten by Paleolithic populations) or the protein in meat and the relatively slow conversion of its amino acids into glucose.

Since insulin plays the critical role in our post-absorption responses to particular foods, it’s not surprising that insulin may play the critical role in our determination of palatability. A little-discussed observation in obesity research is that insulin is secreted in waves from the pancreas. The first wave begins within seconds of eating a “palatable” food, and wel before the glucose actual y enters the bloodstream. It lasts for perhaps twenty minutes. After this first wave ebbs, insulin secretion slowly builds back up in a more measured second wave, which lasts for several hours.*135 The apparent function of the first insulin wave is to prime the body for what’s coming. It takes insulin almost ten minutes to have a measurable effect on blood-glucose levels; it takes twice that long to have any significant effect. Meanwhile, glucose is entering the bloodstream from the meal and continuing to stimulate insulin secretion. When blood sugar is at a maximum, the signal to the pancreas to secrete insulin is also highest, but by this time enough insulin has already been secreted to do the necessary job of glucose disposal. “The pancreas has no idea what’s going on elsewhere in the body,” says University of California, San Francisco, biochemist Gerald Grodsky, who pioneered much of this work. “Al it sees is the glucose.” The way we apparently evolved to deal with this systems-engineering problem is the flooding of insulin into the circulation immediately upon beginning a meal; this prepares the body in advance to start taking up the glucose as soon as it appears.

Le Magnen described this first wave of insulin as increasing “the metabolic background of hunger.” In other words, this wave of insulin shuts down the mobilization of fat from the adipose tissue and stores away blood glucose in preparation for the imminent arrival of more. This leaves the circulation relatively depleted of nutrients. As a result, hunger increases. And this makes the food seem to taste even better. “In man,” suggested Le Magnen, “it is reflected by the increased feeling of hunger at the beginning of a meal expressed in the popular adage in French: L’appétit vient en mangeant”—i.e., “the appetite comes while eating.” As the meal continues and our appetite is satisfied, the metabolic background of hunger ebbs with the flood of nutrients into the circulation, and so the perceived palatability of the food wanes as wel . Palatability, by this logic, is a learned response, conditioned largely by hunger, which in turn is a response to the pattern of insulin secretion and the availability of fatty acids and/or glucose in the circulation.

A related observation that has been a part of scientific study since Pavlov’s famous research in the nineteenth century is that the smel , sight, or even thought of food wil induce a cascade of physiological reactions. These include the secretion of saliva, gastric juices, and, not surprisingly, insulin. By the 1970s, these cephalic*136 reflexes had been studied in humans, rats, monkeys, cats, sheep, and rabbits. Le Magnen’s student Stylianos Nicolaidis had demonstrated that rats wil secrete insulin in response to the mere taste of a sweet substance, and it doesn’t matter whether it is sugar or a no-calorie sugar substitute. The perceived taste of sweetness is sufficient to stimulate insulin secretion. Just as Pavlov demonstrated that dogs wil salivate at the sound of a bel they have learned to associate with feeding, Stephen Woods and his col eagues demonstrated that rats wil secrete insulin when confronted with similar eating-related stimuli. (These researchers arbitrarily chose the smel of mentholatum, a mixture of menthol and petroleum jel y, more commonly used as a topical rub for chest colds.) Humans wil do the same. This reflexive release of insulin, Nicolaidis suggested, is “pre-adaptive”: it anticipates the effects of a meal or a particular food, and so prepares the body. As Mark Friedman describes it, this cephalic release of insulin also serves to clear the circulation of “essential y anything an animal or a person can use for fuel. Not just blood sugar, but fatty acids, as wel . Al those nutrients just go away.” Hence, the thought of eating makes us hungry, because the insulin secreted in response depletes the bloodstream of the fuel that the peripheral tissues and organs need to survive.

This cephalic secretion of insulin in preparation for the act of eating provides yet another mechanism that may work to induce hunger, weight gain, and obesity in a world of palatable foods, which could mean, of course, simply those foods that induce excessive insulin secretion to handle the unnatural y easy digestibility of their carbohydrates. The idea was suggested in 1977 by the psychologist Terry Powley, who was then at Yale and is now at Purdue University. Powley was discussing the obesity-inducing effect of lesions in the hypothalamus and speculated that the lesions cause the animal to hypersecrete insulin when just thinking about, smel ing, or tasting food, and this amplifies its perception of hunger and palatability. The result would be what Powley cal ed a “self-perpetuating situation”—i.e., a vicious cycle. “Rather than secreting quantities of insulin and digestive enzymes appropriate for effective utilization of the ingested material,” Powley wrote, “the lesioned animal over-secretes and must then ingest enough calories to balance the hormonal and metabolic adjustments.”

Powley did not go so far as to suggest that this same phenomenon was at work in humans, but his then col eague Judith Rodin did. Rodin reported in 1980 that those individuals whose eating behavior is most responsive to the smel or sight of food—a gril ing steak, in her experiments—were those who also had the greatest cephalic-phase insulin response. Insulin had to be considered a “major candidate,” Rodin suggested, “for an intervening physiological mechanism that might be responsive to environmental stimuli.” By 1985, Rodin was speculating that the chronic hyperinsulinemia of the obese would also exacerbate this phenomenon. “A feedback loop is suggested by these findings in which hyperinsulinemia in turn leads to increased consumption, which, unless compensated for, could lead to further weight gain,” she wrote. “Because acute hyperinsulinemia can also be produced in some individuals by simply looking at or thinking about food, it, too, can in turn lead to increased consumption and possible weight gain.”

The possibility that insulin determines what Le Magnen cal ed 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 stil 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 typical y 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 fil s 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 cel s 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 cel s 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 Cahil 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 cel s 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 wil work to store these nutrients rather than al ow 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 al diets fail eventual y because the subjects inevitably fal of the diet, just as they do calorie-restricted diets. But this argument is based on the assumption that al 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 initial y 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.