There's a pair of new books that take a radical view of being overweight. It's not your fault, they claim; you're a prisoner of your genes. The outlook—biology is all—is diametrically opposed to the prevailing behaviorist theory of weight, which holds that learning new eating behavior, buttressed with willpower and discipline, is what it takes to drop pounds.

Both camps agree that debiting calories daily or weekly—taking in fewer than the body needs to maintain itself—is the key to losing weight. However, Gina Kolata, a New York Times medical reporter, claims we can't keep weight off because of biochemical forces against which willpower is all but powerless. This, she says, explains the huge recidivism rate—which some experts put as high as 90 percent—among those who manage to lose weight. The other author, Gary Taubes, an award-winning science writer, claims that far from being a dieter's secret weapon, exercise can actually sabotage weight loss.

The new books could be dismissed if they were works of pop science. But Kolata's Rethinking Thin and Taubes's Good Calories, Bad Calories are based on extensive reviews of more than 50 years of obesity research, done at leading universities and examining the effects of diet and exercise on weight. Both books reflect a new tilt toward biology and genetics in the study of weight, an outgrowth of the mapping of the human genome.

Your Body in Charge

Here's Kolata's argument: Being overweight is not simply the result of too many Twinkies; it's also the product of having the wrong genes. She argues that our bodies—through the manipulation of hunger and satiety hormones—keep themselves at a specific weight, or "set point." If you're overweight, this set point is too high. There's nothing groundbreaking in this: Set-point theory has been around for a while. "It appears some people are genetically favored toward being obese, and they do have a greater physiological challenge to stay at a healthy weight," agrees Wendy Bazilian, Ph.D., the nutrition specialist at the Golden Door, adding that precious few of us are so physiologically gifted we can eat anything we want. "People who never have to deal with weight issues are a minority, and probably they've already adopted behaviors that support a healthy weight." In other words, there's no free lunch; if you're thin, you probably don't overeat.

Where Kolata's theory diverges from the mainstream is in its contention that it's virtually impossible to battle your set point, much less change it to a lower weight. "The research shows that individuals have a range of weights, often spanning as much as 20 or 30 pounds, that they can achieve and sustain," she writes in Rethinking Thin. "Being at the bottom of your range usually means constant vigilance." If people manage to lose weight, "they become obsessed with food, they are always hungry, they find themselves bingeing and gorging despite their best intentions, and the pounds come back." Her theory is based on Rockefeller University research that found that when overweight people diet down to a normal weight, their bodies react as if they're starving, sending physiological signals—hunger hormones and brain chemicals—that urge the body to conserve calories and the person to eat more.

Some recent discoveries regarding the biology of hunger suggest that there are indeed potent chemicals at work. On a molecular level, we now know that leptin, a satiety hormone produced in our fat cells, and grehlin, a hunger hormone produced in our stomachs, influence appetite. Leptin decreases it; grehlin increases it. The balance between these hormones is governed—you guessed it—by our genes. For Kolata, this helps explain why pounds we take off pile right back on.

Analysis of the human genome lends some support to Kolata's thesis. According to a 2007 New York Times article (not by Kolata), there's a genetic sequence that enables people to eat fatty foods without gaining weight—I'll take a double strand of that—and another one (a GG sequence at the gene location rs3751812) that makes its owner weigh six pounds less on average than someone whose sequence reads AA. The science is still emerging, but it's a tantalizing tilt toward biology and away from willpower. And it finds an echo in the experience of thousands of women who battle down to their dream weight (over and over again), only to have the pounds creep back.

But there's a big, fat hole in Kolata's reasoning: the obesity epidemic. In the late '70s, less than half (47 percent) of the U.S. population was overweight or obese; today two-thirds of us are. The explanation has to be environmental—we're inundated by fattening food—because it takes millennia for DNA to reformat itself. But what? Gary Taubes thinks he knows the answer.

Wrong Foods, Not Wrong Genes

Looking at the same obesity research Kolata analyzed, Taubes draws a similar conclusion—we're prisoners of our metabolism—but offers a different culprit: carbohydrates. He claims that consuming carbs stimulates the production of insulin, which in turn leads the body to accumulate fat. "The more carbohydrates you eat, the more fat you'll store," Taubes contends. The insulin-carbs theory succeeds where Kolata's analysis fails, in offering an explanation for the obesity epidemic: "When the government announced in the late 1970s that a low-fat diet was healthy—and a low-fat diet is by definition high in carbs—suddenly we were told to eat carbs," says Taubes, who lost 20 pounds on the Atkins diet, a high protein?high fat regimen.