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The Scientist and the Stairmaster

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The key is that among the many things regulated in this homeostatic system—along with blood pressure and blood sugar, body temperature, respiration, etc.—is the amount of fat we carry. From this biological or homeostatic perspective, lean people are not those who have the willpower to exercise more and eat less. They are people whose bodies are programmed to send the calories they consume to the muscles to be burned rather than to the fat tissue to be stored—the Lance Armstrongs of the world. The rest of us tend to go the other way, shunting off calories to fat tissue, where they accumulate to excess. This shunting of calories toward fat cells to be stored or toward the muscles to be burned is a phenomenon known as fuel partitioning.

The job of determining how fuels (glucose and fatty acids) will be used, whether we will store them as fat or burn them for energy, is carried out primarily by the hormone insulin in concert with an enzyme known technically as lipoprotein lipase—LPL, for short. (Sex hormones also interact with LPL, which is why men and women fatten differently.)

In the eighties, biochemists and physiologists worked out how LPL responds to exercise. They found that during a workout, LPL activity increases in muscle tissue, and so our muscle cells suck up fatty acids to use for fuel. Then, when we’re done exercising, LPL activity in the muscle tissue tapers off and LPL activity in our fat tissue spikes, pulling calories into fat cells. This works to return to the fat cells any fat they might have had to surrender—homeostasis, in other words. The more rigorous the exercise, and the more fat lost from our fat tissue, the greater the subsequent increase in LPL activity in the fat cells. Thus, post-workout, we get hungry: Our fat tissue is devoting itself to restoring calories as fat, depriving other tissues and organs of the fuel they need and triggering a compensatory impulse to eat. The feeling of hunger is the brain’s way of trying to satisfy the demands of the body. Just as sweating makes us thirsty, burning off calories makes us hungry.

This research has never been controversial. It’s simply been considered irrelevant by authorities, all too often lean, who have been dead set on blaming fatness on some combination of gluttony, sloth, and perhaps a little genetic predisposition thrown in on the side. But contemplating the means by which we might lose weight without considering the hormonal regulation of fat tissue is like wondering why children grow taller without considering the role of growth hormones. Or, for that matter, like trying to explain the record-breaking triumphs of modern athletes—Barry Bonds, say—and never considering the possibility that steroid hormones (or human growth hormone or insulin) might be involved.

If it’s biology, and not a lack of willpower, that explains why exercise fails so many of us as a weight-loss tool, then we can still find reason for optimism. Since insulin is the primary hormone affecting the activity of LPL on our cells, it’s not surprising that insulin is the primary regulator of how fat we get. “Fat is mobilized [from fat tissue] when insulin secretion diminishes,” the American Medical Association Council on Foods and Nutrition explained back in 1974, before this fact, too, was deemed irrelevant to the question of why we gain weight or the means to lose it. Because insulin determines fat accumulation, it’s quite possible that we get fat not because we eat too much or exercise too little but because we secrete too much insulin or because our insulin levels remain elevated far longer than might be ideal.

To be sure, this is the same logic that leads to other unconventional ideas. As it turns out, it’s carbohydrates—particularly easily digestible carbohydrates and sugars—that primarily stimulate insulin secretion. “Carbohydrates is driving insulin is driving fat,” as George Cahill Jr., a retired Harvard professor of medicine and expert on insulin, recently phrased it for me. So maybe if we eat fewer carbohydrates—in particular the easily digestible simple carbohydrates and sugars—we might lose considerable fat or at least not gain any more, whether we exercise or not. This would explain the slew of recent clinical trials demonstrating that dieters who restrict carbohydrates but not calories invariably lose more weight than dieters who restrict calories but not necessarily carbohydrates. Put simply, it’s quite possible that the foods—potatoes, pasta, rice, bread, pastries, sweets, soda, and beer—that our parents always thought were fattening (back when the medical specialists treating obesity believed that exercise made us hungry) really are fattening. And so if we avoid these foods specifically, we may find our weights more in line with our desires.

As for those people who insist that exercise has been the key to their weight-loss programs, the one thing we’d have to wonder is whether they changed their diets as well. Rare is the person who decides the time has come to lose weight and doesn’t also decide perhaps it’s time to eat fewer sweets, drink less beer, switch to diet soda, and maybe curtail the kind of carb-rich snacks—the potato chips and the candy bars—that might be singularly responsible for driving up their insulin and so their fat.

For the rest of us, it may be time to take a scientific or biological view of our excesses rather than a biblical one. The benefits of exercise include the joys of virtuousness. I worked out today, therefore I can eat fattening foods to my heart’s content. But maybe the causality is reversed here too. Maybe it’s because we eat foods that fatten us that the workout becomes a necessity, the best we can do in the battle against our own fat tissue.

Gary Taubes is the author of Good Calories, Bad Calories: Challenging the Conventional Wisdom on Diet, Weight Control, and Disease (Knopf, October 2), from which this article is adapted.


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