hibernators agree with this correlation; the evidence suggests that annual fluctuations in insulin secretion drive the yearly cycle of weight and eating behavior, although this has never been established with certainty.
This same mechanism might explain the annual patterns of weight fluctuation in humans as well—heavier in the fall and winter and lighter in the spring and summer—that are commonly attributed to increased physical activity supposedly accompanying the joys of spring or driven by the peer pressure and anxiety of the coming of bathing-suit season. When researchers have measured seasonal variations in insulin levels in humans, they have invariably reported that insulin is highest in late fall and early winter—twice as high, according to one 1984 study— and lowest in late spring and early summer. Moreover, as the University of Colorado’s Robert Eckel has reported, lipoprotein-lipase activity in fat tissue elevates in late fall and decreases in spring and summer; its activity in skeletal muscle follows an opposite pattern. This would stimulate weight loss in the spring and weight gain in the fall, whether we consciously desire either or not, and would certainly make it easier to lose weight in the spring and gain it in the fall.
One of the most radical implications of this hypothesis is that even such an intractable condition as anorexia nervosa—which, like obesity, is now universally considered a behavioral and psychological disorder—may be caused fundamentally 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 cells, for example, becoming prematurely or abnormally 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 smell of a cinnamon bun baking in the oven will be considerably more enticing when we’re hungry than after we’ve eaten. Our subjective interpretation of taste changes as well. 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 fulfills the animal’s nutritional requirements. Rats given the choice between caloric sugar solutions and zero-calorie but equally sweet saccharine solutions initially drink similar amounts of both, Le Magnen reported. They both taste good. But the rats will 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, metabolically, 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 will 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 will 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
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 well before the glucose actually 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. “All 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’appetit 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 well. 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 smell, sight, or even thought of food will induce a cascade of physiological reactions. These
