activity also makes us tired; it wears us out. We expend less energy when the activity is over.
In short, the energy we consume and the energy we expend are dependent on each other. Mathematicians would say they are
dependent
variables, not
independent
variables, as they have typically been treated. Change one, and the other changes to compensate. To a great extent, if not entirely, the energy we expend from day to day and week to week will determine how much we consume, while the energy we consume and make available to our cells (a key point, as I will discuss later) will determine how much we expend. The two are that intimately linked. Anyone who argues differently is treating an extraordinarily complex living organism as though it were a simple mechanical device.
In 2007, Jeffrey Flier, dean of Harvard Medical School and his wife and colleague in obesity research, Terry Maratos-Flier, published an article in
Scientific American
called “What Fuels Fat.” In it, they described the intimate link between appetite and energy expenditure, making clear that they are not simply variables that an individual can consciously decide to change with the only effect being that his or her fat tissue will get smaller or larger to compensate.
An animal whose food is suddenly restricted tends to reduce its energy expenditure both by being less active and by slowing energy use in cells, thereby limiting weight loss. It also experiences increased hunger so that once the restriction ends, it will eat more than its prior norm until the earlier weight is attained.
What the Fliers accomplished in just two sentences is to explain why a hundred years of intuitively obvious dietaryadvice—eat less—doesn’t work in animals. If we restrict the amount of food an animal can eat (we can’t just tell it to eat less, we have to give it no choice), not only does it get hungry, but it actually expends less energy. Its metabolic rate slows down. Its cells burn less energy (because they have less energy to burn). And when it gets a chance to eat as much as it wants, it gains the weight right back.
The same is true for humans. I don’t know why the Fliers said “an animal” instead of “a person,” since the same effects seen in animal studies have been demonstrated repeatedly in humans. One likely answer is that the Fliers (or the magazine’s editors) didn’t want the implication to be quite so obvious: that the diet advice that our doctors and public-health authorities are invariably giving us is misconceived; that eating less and/or exercising more is not a viable treatment for obesity or overweight and shouldn’t be considered as such. It might have short-term effects but nothing that lasts more than a few months or a year. Eventually, our bodies compensate.
8
Head Cases
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
In short, the energy we consume and the energy we expend are dependent on each other. Mathematicians would say they are
dependent
variables, not
independent
variables, as they have typically been treated. Change one, and the other changes to compensate. To a great extent, if not entirely, the energy we expend from day to day and week to week will determine how much we consume, while the energy we consume and make available to our cells (a key point, as I will discuss later) will determine how much we expend. The two are that intimately linked. Anyone who argues differently is treating an extraordinarily complex living organism as though it were a simple mechanical device.
In 2007, Jeffrey Flier, dean of Harvard Medical School and his wife and colleague in obesity research, Terry Maratos-Flier, published an article in
Scientific American
called “What Fuels Fat.” In it, they described the intimate link between appetite and energy expenditure, making clear that they are not simply variables that an individual can consciously decide to change with the only effect being that his or her fat tissue will get smaller or larger to compensate.
An animal whose food is suddenly restricted tends to reduce its energy expenditure both by being less active and by slowing energy use in cells, thereby limiting weight loss. It also experiences increased hunger so that once the restriction ends, it will eat more than its prior norm until the earlier weight is attained.
What the Fliers accomplished in just two sentences is to explain why a hundred years of intuitively obvious dietaryadvice—eat less—doesn’t work in animals. If we restrict the amount of food an animal can eat (we can’t just tell it to eat less, we have to give it no choice), not only does it get hungry, but it actually expends less energy. Its metabolic rate slows down. Its cells burn less energy (because they have less energy to burn). And when it gets a chance to eat as much as it wants, it gains the weight right back.
The same is true for humans. I don’t know why the Fliers said “an animal” instead of “a person,” since the same effects seen in animal studies have been demonstrated repeatedly in humans. One likely answer is that the Fliers (or the magazine’s editors) didn’t want the implication to be quite so obvious: that the diet advice that our doctors and public-health authorities are invariably giving us is misconceived; that eating less and/or exercising more is not a viable treatment for obesity or overweight and shouldn’t be considered as such. It might have short-term effects but nothing that lasts more than a few months or a year. Eventually, our bodies compensate.
8
Head Cases
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
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