Why We Get Fat: And What to Do About It (15 page)
Read Why We Get Fat: And What to Do About It Online
Authors: Gary Taubes
Before I leave the laws of adiposity and this animal research behind, I want to ask one more question: What do these laws and this research have to say about people who are habitually lean? Over the years, researchers have also created what we might call animal models of leanness—animals whose genes have been manipulated so they are leaner than they’d otherwise be. These animals will remain lean even when the researchers force them to consume more calories than they prefer—by infusing nutrients through a tube into their guts, for instance, pumping in calories directly. In such cases, the animals will surely have to increase their expenditure to burn off the calories.
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The implication is as counterintuitive as anything we’ve discussed so far. Just as the animal research tells us that gluttony and sloth are side effects of a drive to accumulate body fat, it also says that eating in moderation and being physically active (literally, having the energy to exercise) are not evidence of moral rectitude.
Rather, they’re the metabolic benefits of a body that’s programmed to remain lean. If our fat tissue is regulated so that it will
not
store significant calories as fat, or our muscle tissue is regulated to take up more than its fair share of calories to use for fuel, then we’ll either eat less than those of us predisposed to be fat (the first case), or we’ll be more physically active (the second), or both, because of it.
This implies that our emaciated marathoners are not lean because they train religiously and burn off thousands of calories doing so; rather, they’re driven to expend those calories—and so perhaps to work out for hours a day and become obsessive long-distance runners—because they’re wired to burn off calories and be lean. Similarly, a greyhound will be more physically active than a basset hound, not because of any conscious desire to exercise, but because its body partitions fuel to its lean tissue, not to its fat.
It may be easier to believe that we remain lean because we’re virtuous and we get fat because we’re not, but the evidence simply says otherwise. Virtue has little more to do with our weight than with our height. When we grow taller, it’s hormones and enzymes that are promoting our growth, and we consume more calories than we expend as a result. Growth is the cause—increased appetite and decreased energy expenditure (gluttony and sloth) are the effects. When we grow fatter, the same is true as well.
We don’t get fat because we overeat; we overeat because we’re getting fat.
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The tendency in popular science and medical writing is to make it appear that one researcher did all the work, so as not to clutter up the prose by having to keep repeating phrases like “Wade and his students.” I’m doing the same here. Wade did these experiments with various undergraduates and graduate students. The work was collaborative, as science almost always is.
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This is how
Williams Textbook of Endocrinology
, a well-respected textbook on hormones and hormone-related diseases, describes this same concept: “The activity of LPL within individual tissues is a key factor in partitioning triglycerides [i.e., fat] among different body tissues.”
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The Wikipedia entry for “obesity” in July 2009, when I wrote this chapter, included no discussion of the regulation of fat issue, although that could be found in the entry for “adipose tissue.” The implicit assumption would be that the regulation of fat tissue is not relevant to a disorder of excess fat accumulation.
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When I use the phrase “almost assuredly,” what I mean is that I believe this to be the case with such conviction that I would stake my reputation on it. But I’ve been writing about science so long, and am such a firm believer in the process of science, that I find I can’t remove the “almost.” We can never say anything for certain in science until it has survived rigorous tests, particularly when we’re challenging accepted beliefs. When people do, it’s a good reason not to trust them, whether they are diet-book authors or academic experts. Nonetheless, if you prefer to read “almost assuredly” as “assuredly,” you’ll almost assuredly be justified in doing so.
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The camel’s hump is another example of a large fat mass that exists for a purpose: the hump provides a reservoir of fat for survival in the desert, without the camel’s having to keep that fat in subcutaneous deposits, as we do, where the insulation would present problems in the desert heat. The same goes for fat-rumped and fat-tailed sheep, and fat-tailed marsupial mice, all desert dwellers that carry their fat almost exclusively in the eponymous locations.
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This is only in summer. During the rest of the year, whales apparently live off their stored fat, like hibernating rodents.
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To be more precise, every animal model of obesity that researchers study in the laboratory (to the best of my knowledge) can be divided into two categories: (1) those in which this same cause and effect holds true, and (2) those in which the researchers never thought to do the experiments to find out (put the animals on a calorie-restricted diet and see if they get fat anyway), because the researchers never imagined that their animals might get fat for any reason other than eating too much.
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These researchers typically don’t measure energy expenditure in these rodents, so I’m assuming this is true.
A Historical Digression on “Lipophilia”
This way of thinking about why we get fat is by no means original, as I’ve suggested. It dates to 1908, when the German internist Gustav von Bergmann evoked the term “lipophilia”—“love of fat”—to explain why parts of the body differ in their affinity for stockpiling fat. (One of the highest honors awarded today by the German Society of Internal Medicine is in honor of von Bergmann.) In essence, I’m doing little more in this book than taking von Bergmann’s ideas and updating the science.
Von Bergmann’s approach to obesity was straightforward: he considered it a disorder of excess fat accumulation and then set out to learn what he could about the regulation of our fat tissue. His observations—many of which I cited earlier—led him to the conclusion that some tissue is obviously “lipophilic” and avidly accumulates fat, and other tissue is not. This attribute, he noted, differs not only from tissue to tissue but from person to person. Just as some parts of the body have an affinity for growing hair and others don’t, and some people are hairier than others, some have an affinity for accumulating fat and others don’t, and some people are fatter (their bodies are more lipophilic) than others. These people fatten easily, and it often seems there’s nothing they can do about it. Others, whose bodies are not lipophilic, are lean; they find it difficult to put on weight, even if they make a concerted effort.
In the late 1920s, von Bergmann’s lipophilia idea was taken up and championed by Julius Bauer of the University of Vienna. Bauer was a pioneer in the application of genetics and endocrinology to clinical medicine, at a time when these sciences were in their infancy.
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Few physicians of that era could imagine how genes might bestow lifelong characteristics on people and, with them, a predisposition for disease. Bauer knew more about this relationship between genes and disease than anyone, and he spent considerable effort trying to get physicians in the United States to see the errors in Louis Newburgh’s “perverted appetite” hypothesis.
Whereas Newburgh argued that genes, if they did anything (which he doubted),
might
bestow on the obese an uncontrollable urge to eat too much, Bauer explained that the only way genes could logically cause obesity is by directly influencing the regulation of the fat tissue itself. They “regulate lipophilia,” he said, and then this regulation, in turn, determines “the general feelings ruling the intake of food and the expenditure of energy.”
Bauer considered the fat tissue in obesity akin to malignant tumors. Both have their own agendas, he explained. Tumors are driven to grow and spread and will do so with little relation to how much the person who has that tumor might be eating or exercising. In those who are predisposed to grow obese, fat tissue is driven to grow, to expand with fat, and it will accomplish this goal, just as the tumor does, with little concern about what the rest of the body might be doing. “The abnormal lipophilic tissue seizes on foodstuffs, even in the case of undernutrition,” Bauer wrote in 1929. “It maintains its stock, and may increase it independent of the requirements of the organism. A sort of anarchy exists; the adipose tissue lives for itself and does not fit into the precisely regulated management of the whole organism.”
By the late 1930s, von Bergmann and Bauer’s lipophilia hypothesis had become “more or less fully accepted” in Europe.
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It was catching on in the United States as well, where Russell Wilder of the Mayo Clinic wrote in 1938, “This conception deserves attentive consideration.”
Within a decade, though, it had vanished. Those European physicians and researchers who hadn’t died in the Second World War or fled the continent (as Bauer did in 1938) had far more pressing issues to deal with than obesity. In the United States, a new generation of physicians and nutritionists came along after the war to fill the void, and they were enamored with Newburgh’s “perverted appetite” logic, perhaps because it played to their preconceptions about the penalties of gluttony and sloth.
Anti-German sentiment in the postwar medical community, understandable as it may have been, assuredly didn’t help matters. The authorities writing about obesity in the United States after the war treated the German medical literature as though it didn’t exist, even though it was Germans and Austrians who had founded and done most of the meaningful research in the fields of nutrition, metabolism, endocrinology, and genetics, which means all the fields relevant to obesity. (The one notable exception was Hilde Bruch, a German herself, who discussed this prewar literature extensively.) Once the psychologists took over in the 1960s and obesity officially became an eating disorder—a character defect but in kinder words—any hope that these authorities would pay attention to how the fat tissue was regulated effectively vanished.
Still, a few research-oriented physicians occasionally came to the same conclusions after the war. Bruch, who remained the leading authority on childhood obesity through the 1960s, continued to suggest that a defect in the regulation of fat tissue was the
likely cause of obesity and professed amazement that her colleagues were so completely uninterested in the idea. Even Jean Mayer, as late as 1968, was pointing out that “different body types and fat contents” were associated with “different concentrations of hormones in the blood” and suggesting that slight differences in “relative or absolute hormone concentrations” might be the reason why some get fat and others stay effortlessly lean. In other words, as von Bergmann and Bauer would have said, these hormone concentrations might be determining whether or not fat tissue is lipophilic. (Mayer paid no attention to what von Bergmann and Bauer had written, or neglected to credit them if he did.)
The postwar expert who had the most perceptive take on why we get fat happened to be the one who had the most expertise in hormones and hormone-related disorders—Edwin Astwood of Tufts University. In 1962, Astwood was president of the Endocrinology Society when he gave a lecture called “The Heritage of Corpulence” at its annual meeting. Astwood attacked the notion that obesity was caused by overeating—“the primacy of gluttony,” as he described this way of thinking—and his presentation was as good a description as any I know on the subject of how we can think about obesity if we simply focus on the fat and the fat tissue, attend to the actual evidence (always a good idea), and do so with no preconceptions (also a good idea).
The first point that Astwood made was that a predisposition to fatten easily or remain lean is obviously determined in large part by our genes—a heritage, something passed down from generation to generation. If genes determine our height and our hair color and the size of our feet, he said, then “why can’t heredity be credited with determining one’s shape?”
But if genes control our shape, how do they do it? By 1962, biochemists and physiologists had gone a long way toward establishing exactly how body fat is regulated, as I will discuss shortly, and Astwood considered this to be the obvious answer, just as von Bergmann, Bauer, and Bruch had before him. Dozens of enzymes and multiple hormones had already been identified that
influence fat accumulation, Astwood explained. Some work to liberate fat from the fat tissue; others to put it there. Ultimately, the amount of fat that would be stored in any single person or at any single location on the human body would be determined by the balance of these competing regulatory forces.
“Now just suppose that any one of these … regulatory processes were to go awry,” Astwood said.
Suppose that the release of fat or its combustion [burning it for fuel] was somewhat impeded, or that the deposition or synthesis of fat was promoted; what would happen? Lack of food is the cause of hunger and, to most of the body, [fat] is the food; it is easy to imagine that a minor derangement could be responsible for a voracious appetite. It seems likely to me that hunger in the obese might be so ravaging and ravenous that skinny physicians do not understand it.…
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This theory would explain why dieting is so seldom effective and why most fat people are miserable when they fast. It would also take care of our friends, the psychiatrists, who find all kinds of preoccupation with food, which pervades dreams among patients who are obese. Which of us would not be preoccupied with thoughts of food if we were suffering from internal starvation? Hunger is such an awful thing that it is classically cited with pestilence and war as one of our three worst burdens. Add to the physical discomfort the emotional stresses of being fat, the taunts and
teasing from the thin, the constant criticism, the accusations of gluttony and lack of “will power,” and the constant guilt feelings, and we have reasons enough for the emotional disturbances which preoccupy the psychiatrists.