Why We Get Fat: And What to Do About It (14 page)

The photo on the right was taken three years later, after he had gained nine inches in height and weighed fifty-one pounds.

He gained seventeen pounds in three years, so he certainly consumed more calories than he expended. He overate. Those excess calories were used to create all the necessary tissues and structures that a larger body needed, including, yes, even more fat. But he didn’t grow because he consumed excess calories. He consumed those excess calories—he overate—because he was growing.

My son’s growth, like every child’s, is caused fundamentally by the action of growth hormones. As he gets older, he’ll occasionally go through growth spurts that will be accompanied by a voracious appetite and probably a fair share of sloth, but the appetite and the sloth will be driven by the growth, not vice versa. His body will require excess calories to satisfy the demands of the growth—to build a bigger body—and it will figure out a way to get them, by increasing his appetite or decreasing his energy expenditure or both. When he goes through puberty, he’ll lose fat and gain muscle; he’ll still be taking in more calories than he expends, and this, too, will be driven by hormonal changes.

August 2007—thirty-four pounds
(photo credit 9.2)

August 2010—fifty-one pounds
(photo credit 9.2)

That growth is the cause and overeating the effect is almost assuredly true for our fat tissue as well. To paraphrase what the German internist Gustav von Bergmann said about this idea more than eighty years ago, we would never even consider the possibility that children grow taller because they eat too much and exercise too little (or that they stunt their growth by exercising too much). So why assume that these are valid explanations for growing fat (or remaining lean)? “That which the body needs to grow it always finds,” von Bergmann wrote, “and that which it needs to become fat, even if it’s ten times as much, the body will save for itself from the annual balance.”

The only reason to think that this isn’t true, that the cause and effect go in one direction when we get taller (growth causes overeating) and the other when we grow fatter (overeating causes growth), is that this is what we grew up believing and we never stopped to consider if it actually makes sense. The far more reasonable assumption is that growth in both cases determines appetite and even energy expenditure—not the other way around. We don’t get fat because we overeat; we overeat because we’re getting fat.

Since this is so counterintuitive but so critical to understand, I want to return to the examples of animals. African elephants are the world’s largest land animals. The males typically weigh more than ten thousand pounds, although surprisingly little of this is
fat. Blue whales are the largest animals, on or off land. They can weigh three hundred thousand pounds, and much of that is fat. African elephants will eat hundreds of pounds of food a day, and blue whales, thousands,
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prodigious amounts, but neither species grow to be enormous because they eat so much. They eat prodigious amounts because they’re enormous animals. With or without large quantities of body fat, body size determines how much they eat.

The infants of these species also eat relatively enormous quantities. They do so because they’re born exceedingly large to begin with and because their genes predispose them to grow many thousands of pounds (elephants) or hundreds of thousands of pounds (blue whales) larger still. Now both growth
and
body size are driving appetite. This is true whether these animals are using the calories to store fat, or to enlarge muscle and other tissues and organs. Whether or not they have enormous quantities of fat, the same cause and effect holds true.

Now consider what researchers call animal models of obesity—animals, like Wade’s rats, that are made obese in the laboratory but wouldn’t be naturally. Over the past eighty years, researchers have learned that they can make rats and mice obese by breeding, by surgery (removing the ovaries, for instance), by the manipulation of their diets, and by any number of genetic manipulations. The animals on which these indignities are inflicted do indeed become obese, not just functionally fat (like blue whales or hibernating ground squirrels). They tend to suffer from the same metabolic disturbances, including diabetes, that we do when we become obese.

It doesn’t matter, though, what technique is used to make the animals obese; they’ll still get that way, or at least significantly fatter (just as Wade’s rats did), whether or not they can eat any more calories than otherwise identical animals that remain lean. They
get obese not because they overeat but because the surgery or breeding or genetic manipulation or even the change in diet has disturbed the regulation of their fat tissue. They begin stockpiling calories as fat, and then their bodies have to compensate: they eat more, if possible; they expend less energy if not. Often they do both.
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Take, for example, the preferred method of making laboratory rodents obese from the 1930s through the 1960s. This was a surgical technique that required inserting a needle into a part of the brain known as the hypothalamus, which controls (not coincidentally) hormone secretion throughout the body. After the surgery, some of these rodents would eat voraciously and get obese; some would become sedentary and get obese; some would do both and get obese. The obvious conclusion, suggested first by the neuroanatomist Stephen Ranson, whose Northwestern University laboratory pioneered these experiments in the 1930s, is that the surgery has the direct effect of increasing body fat on these rodents. After the surgery, their fat tissue sucks up calories to make more fat; this leaves insufficient fuel for the rest of the body—what Ranson called “hidden semi-cellular starvation”—and “force[s] the body either to increase its general food intake or to cut down its expenditure, or both.”

The only way to prevent these animals from getting obese is to starve them—to inflict what a Johns Hopkins University physiologist in the 1940s called “severe and permanent” food restriction. If these animals are allowed to eat even moderate amounts of food, they end up obese. In other words, they get fat not by
over
eating but by eating at all. Even though the surgery is in the brain, it has
the effect of fundamentally altering the regulation of body fat, not appetite.

The same thing holds true for animals that are bred to be obese, for which obesity is in their genes. In the 1950s, Jean Mayer studied one such strain of obese mice in his Harvard laboratory. As he reported it, he could get their
weight
below that of lean mice if he starved them sufficiently, but they’d “still contain more fat than the normal ones, while their muscles have melted away.” Once again, eating too much wasn’t the problem; these mice, as Mayer wrote, “will make fat out of their food under the most unlikely circumstances, even when half starved.”

Then there are Zucker rats. Researchers began studying these rats in the 1960s, and they are still a favorite obesity model today. Here’s a picture of a Zucker rat looking suitably corpulent.

(photo credit 9.3)

These rats, like Mayer’s mice, are genetically predisposed to get fat. When Zucker rats are put on a calorie-restricted diet from the moment they’re weaned from their mothers’ milk, they don’t end up leaner than their littermates who are allowed to eat as much as they want. They end up fatter. They may weigh a little less, but they have just as much or even more body fat. Even if they want to be gluttons, which they assuredly do, they can’t, and they still get even fatter than they would have had they never been put on a diet. On the other hand, their muscles and organs, including their brains and kidneys, are smaller than they’d otherwise be. Just as the muscles in Mayer’s mice “melted away” when starved, the muscles and organs in these semi-starved Zucker rats are “significantly reduced” in size compared with those fat littermates who get to eat freely. “In order to develop this obese body composition in the face of calorie restriction,” wrote the researcher who reported this observation in 1981, “several developing organ systems in the obese rats [are] compromised.”

Let’s think about this for a second. If a baby rat that is genetically programmed to become obese is put on a diet from the moment it’s weaned, so it can eat no more than a lean rat would eat, if that, and can
never
eat as much as it would like, it responds by
compromising
its organs and muscles to satisfy its genetic drive to grow fat. It’s not just using the energy it would normally expend in day-to-day activity to grow fat; it’s taking the materials and the energy it would normally dedicate to building its muscles, organs, and even its brain and using that.

When these obese rodents are starved to death—an experiment that fortunately not too many researchers have done—a common result reported in the literature is that the animals die with much of their fat tissue intact. In fact, they’ll often die with more body fat than lean animals have when the lean ones are eating as much as they like. As animals starve, and the same is true of humans, they consume their muscles for fuel, and that includes, eventually, the heart muscle. As adults, these obese animals are willing to compromise their organs, even their hearts and their lives, to preserve their fat.

The message of eighty years of research on obese animals is simple and unconditional and worth restating: obesity does not come about because gluttony and sloth make it so; only a change in the regulation of the fat tissue makes a lean animal obese.

The amount of body fat on obese animals is determined by a balance of all the various forces that work on the fat tissue—on the fat cells, as we’ll see—either to put fat in or to get fat out. Whatever has been done to these animals to make them fat (surgery, genetic manipulation), the effect is literally to change this balance of forces so that the animals increase their fat stores. Now “eating too much” is a meaningless concept, because otherwise normal amounts of food are now “too much.” The fat tissue is not reacting to how much these animals are eating but only to the forces making them accumulate fat. And because increasing body fat requires energy and nutrients that are needed elsewhere in their bodies, they will eat more if they can. If they can’t—if
they are on a strict diet—they will expend less energy, because they have less to expend. They may even compromise their brains, muscles, and other organs. Half-starve these animals and they’ll still find a way to stockpile calories as fat, because that’s what their fat tissue is now programmed to do.

If this is true of humans, and there’s little reason to think it’s not, it is the explanation for the paradigm-challenging observation I mentioned earlier, regarding extremely poor but overweight mothers with thin, stunted children. Both mother and children are, indeed, half-starved. The emaciated children, their growth stunted, respond as we’d expect. The mothers, however, have fat tissue that has developed its own agenda (we’ll see shortly how this can happen). It will accumulate excess fat, and does so, even though the mothers themselves, like their children, are barely getting enough food to survive. They must be expending less energy to compensate.