Why We Get Fat: And What to Do About It (12 page)

Of all the dangerous ideas that health officials could have embraced while trying to understand why we get fat, they would have been hard-pressed to find one ultimately more damaging than calories-in/calories-out. That it reinforces what appears to be so obvious—obesity as the penalty for gluttony and sloth—is what makes it so alluring. But it’s misleading and misconceived on so many levels that it’s hard to imagine how it survived unscathed and virtually unchallenged for the last fifty years.

It has done incalculable harm. Not only is this thinking at least partly responsible for the ever-growing numbers of obese and overweight in the world—while directing attention away from the real reasons we get fat—but it has served to reinforce the perception that those who are fat have no one to blame but themselves. That eating less invariably fails as a cure for obesity is rarely perceived as the single most important reason to make us question our assumptions, as Hilde Bruch suggested half a century ago. Rather, it is taken as still more evidence that the overweight and obese are incapable of following a diet and eating in moderation. And it puts the blame for their physical condition squarely on their behavior, which couldn’t be further from the truth.

There has to be a reason, of course, why anyone would eat more calories than he or she expends, particularly since the penalty for doing so is to suffer the physical and emotional cruelties of obesity.
There must be a defect involved somewhere; the question is where.

The logic of calories-in/calories-out allows only one acceptable answer to this question. The defect cannot lie in the body—perhaps, as the endocrinologist Edwin Astwood suggested half a century ago, in the “dozens of enzymes” and the “variety of hormones” that control how our bodies “turn what is eaten into fat”—because this would imply that something other than overeating was fundamentally responsible for making us fat. And that’s not allowed. So the problem must lie in the brain. And, more precisely, in behavior, which makes it an issue of character. Both eating too much and exercising too little, after all, are behaviors, not physiological states, a fact that’s even more obvious if we use the biblical terminology—gluttony and sloth.

The entire science of obesity, in effect, got caught up in the circular logic of the calories-in/calories-out hypothesis, and it’s never been able to escape. Establishing the cause of obesity as something that has to happen when people get fat—take in more calories than they expend—prevents any legitimate answer to the question of why anyone would ever do such a thing. Or, at least, why they would do it if they weren’t driven to it by forces outside their control.

We have the same problem if we ask why diets fail. Why is it that obesity is so rarely, if ever, cured by what should be the simple act of eating less? If we suggest as an answer that fat people respond to food restriction just as fat animals do—they reduce their energy expenditure, while experiencing increased hunger (as Jeff Flier and Terry Maratos-Flier explained in
Scientific American
)—then we’ve opened up the possibility that the same physiologic mechanism that drives obese individuals to hold on to their fat in the face of semi-starvation might have been the cause of their obesity in the first place. Again, that’s not allowed. So instead we blame the failure of the diet on the failure of the fat person to stay on it. It’s a failure of will, a lack of the necessary strength of character to do what lean people do and eat in moderation.

Once overeating is established as the fundamental cause of obesity, blaming behavior—and thus a lack of character and willpower—is the only acceptable explanation. It’s the only one that doesn’t lend itself to further meaningful research and so, perhaps, the identification of a defect more fundamental still that would explain why people would willingly overeat if they had any choice—that is, why they really got fat.

This insidious logic began to pervade the scientific discussions of obesity in the late 1920s, courtesy of Louis Newburgh, a University of Michigan professor of medicine who would eventually become the most prominent American authority on obesity. Until Newburgh came along, most physicians who thought about obesity assumed that anything so intractable must be a physical disorder, not the end product of a mental state. Newburgh argued the opposite, insisting that those who got fat had a “perverted appetite,” which was (for the era) a technical way of saying that these individuals had an urge to consume more calories than they expended, and lean people didn’t. Newburgh based this conclusion on the fact that all obese people have literally to overeat to get fatter—which is true, of course, but irrelevant.

This left unanswered, as I said, the obvious questions: Why do people who get fat overeat? Why don’t these people control their urges? Why don’t they eat in moderation and exercise as lean people do? Well, the choices were no different in Newburgh’s era from those we’re left with today: fat people are unwilling to make the effort, they lack the willpower, or they’re simply unaware of what they should be doing. In short, as Newburgh put it, fat people suffer from “various human weaknesses such as over-indulgence and ignorance.” (Newburgh himself was lean.)

Had Newburgh’s pronouncements been taken with even the slightest bit of skepticism—all medical pronouncements should be, until they are supported by rigorous scientific data—obesity might be far less common today than it is (and this book might
not be necessary). But Newburgh was preaching to a medical establishment that had been taught to revere authority figures, not question their pronouncements.

In the United States at least, in the years immediately following the Second World War, Newburgh’s word was treated as gospel by a generation of doctors, who should have known better. What they chose to believe is what Newburgh insisted was true, that the obese and overweight belong in one of two categories: those trained since childhood by their parents to take in more food than needed (which was Newburgh’s explanation for the observation, clear then as it is now, that a predisposition to obesity runs in families), and those in whom “the combination of weak will and a pleasure seeking outlook upon life” is to blame. And this has been the prevailing attitude ever since, though it is inexcusably simplistic and wrong.

The only thing that’s changed over the years is that the experts now couch the concept in ways that don’t immediately appear to have such demeaning implications. If we refer to obesity as an eating disorder, for example, as has been common since the 1960s, we’re not actually saying that the obese can’t eat like the lean because they lack the willpower—we’re only saying that they
don’t
eat like the lean.

Maybe those who get fat are just too susceptible to external food cues, which was one common explanation in the 1970s, and not susceptible enough to internal cues, which tell them when they’ve eaten enough but not too much. This doesn’t say explicitly that they lack willpower; it suggests instead that something about the brains of obese people makes it harder for them than for lean people to resist the smell of a cinnamon bun or the sight of a McDonald’s. Or they’re more likely to order a larger portion or keep eating it, whereas a lean person either wouldn’t order it to begin with or wouldn’t feel compelled to finish it.
^*

By the 1970s, an entire field of what’s technically (and tellingly) called “behavioral medicine” had emerged to treat obese individuals with behavioral therapies, all subtle or not so subtle ways of inducing the obese to behave like the lean, that is, to eat in moderation.
^†
None of these therapies has ever been shown to work; many are still us with us today even so. Slowing down the pace of eating is a typical behavioral treatment. Not eating anywhere other than in the kitchen or at the dining-room table is another one.

Today it’s still the case that many, if not most, of the leading authorities on obesity are psychologists and psychiatrists, people whose expertise is meant to be in the ways of the mind, not of the body. Imagine how many more dead diabetics we’d have if victims of that disease were treated by psychologists instead of physicians. And yet diabetes and obesity are so closely linked—most type 2 diabetics are obese, and many obese people become diabetic—that some authorities have taken to calling the two disorders “diabesity,” as though they’re two sides of the same pathological coin, which they assuredly are.

Much of the last half-century of professional discourse on obesity can be perceived as attempts to circumvent what we could call the “head case” implications of calories-in/calories-out: how to blame obesity on eating too much without actually blaming the fat person for the human weaknesses of self-indulgence and/or
ignorance. If the obesity epidemic is blamed on “prosperity,” as I discussed earlier, or a “toxic food environment,” we can shift the responsibility for obesity away from the character of the obese while still recognizing that they only got that way by failing to eat in moderation. If the food industry is blamed for making too much tasty and tempting food available, this further shifts the blame. It’s the environment we live in that makes us fat, we’re being told, not just our weakness of will. Then why don’t lean people get fat in this toxic environment? Is the answer only willpower?

In the 1930s, Russell Wilder of the Mayo Clinic asked the pertinent question of Newburgh’s perverted-appetite idea, and that question is still the one we should be asking today when anyone tries to blame society or the food industry for why we get fat: “There must be some device other than appetite to regulate weight because we continue to be protected against obesity, most of us,” Wilder said, “even though we hoodwink our appetite by various tricks, such as cocktails and wines with our meals. The whole artistry of cookery, in fact, is developed with the prime object of inducing us to eat more than we ought. Why, then, do we not all grow fat?” If some of us don’t, why not? Why are some of us protected from obesity despite the “whole artistry of cookery” and some not?

In 1978, Susan Sontag published an essay called
Illness as Metaphor
, in which she discussed cancer and tuberculosis and the “blame the victim” mentality that often accompanied these diseases in different eras. “Theories that diseases are caused by mental states and can be cured by will power,” Sontag wrote, “are always an index of how much is not understood about the physical terrain of a disease.”

So long as we believe that people get fat because they overeat, because they take in more calories than they expend, we’re putting the ultimate blame on a mental state, a weakness of character, and we’re leaving human biology out of the equation entirely. Sontag had it right: it’s a mistake to think this way about
any disease. And it’s been disastrous when it comes to the question of why we get fat. How
should
we be approaching the problem? How do we have to think about it to make progress? Those are the questions I’ll begin to answer in the next chapter.

The fate of the laboratory rat is rarely enviable. The story I’m about to tell offers no exception. Still, we can learn from the rat’s experience, as scientists do.

In the early 1970s, a young researcher at the University of Massachusetts named George Wade set out to study the relationship between sex hormones, weight, and appetite by removing the ovaries from rats (females, obviously) and then monitoring their subsequent weight and behavior.
^*
The effects of the surgery were suitably dramatic: the rats would begin to eat voraciously and quickly become obese. If we didn’t know any better, we might assume from this that the removal of a rat’s ovaries makes it a glutton. The rat eats too much, the excess calories find their way to the fat tissue, and the animal becomes obese. This would confirm our preconception that overeating is responsible for obesity in humans as well.

But Wade did a revealing second experiment, removing the ovaries from the rats and putting them on a strict postsurgical diet. Even if these rats were ravenously hungry after the surgery, even if they desperately wanted to be gluttons, they couldn’t satisfy their urge. In the lingo of experimental science, this second experiment
controlled
for overeating. The rats, postsurgery, were only allowed the same amount of food they would have eaten had they never had the surgery.

What happened is not what you’d probably think. The rats got just as fat, just as quickly. But these rats were now completely sedentary. They moved only when movement was required to get food.

If we knew only about the second experiment, this, too, might confirm our preconceptions. Now we would assume that removing a rat’s ovaries makes it lazy; it expends too little energy, and this is why it gets fat. In this interpretation, once again we have support for our belief in the primacy of calories-in/calories-out as the determining factor in obesity.

Pay attention to both experiments, though, and the conclusion is radically different. Removing the ovaries from a rat literally makes its fat tissue absorb calories from the circulation and expand with fat. If the animal can eat more to compensate for the calories that are now being stashed away as fat (the first experiment), it will. If it can’t (the second), then it expends less energy, because it now has fewer calories available to expend.