"Food is not the boss in my life. I am stronger than the temptation of any food."
--from the Richard Simmons home page
Then again, maybe not. Americans spend $30 billion a year on weight-loss programs, but obesity resists treatment more tenaciously than do viruses--90 percent to 95 percent of people who lose weight eventually regain it.
Why is that? We've learned much in the last few years about the role that hunger plays in obesity. Drug companies have capitalized on that knowledge to create powerful new appetite suppressants. But these "cures" come with serious risks. Researchers linked the popular diet-drug combination "fen-phen" to a rare heart disease a year ago. But doctors continued to prescribe it to millions, arguing that the health risks associated with obesity justified fen-phen's wide use. Now reports of new heart abnormalities in women on fen-phen raise fresh questions about using pills for obesity before all the facts are in.
Scientists didn't always view appetite as a cause of obesity. The dominant thinking for more than two decades was that the obese gained weight because they burned fewer calories. In experiments, overfed or underfed volunteers always returned to their original weight--the "setpoint"--when they ceased their diets. Also, when obese dieters lost weight, their metabolism slowed, conserving calories and driving their weight back to the setpoint. It seemed that obese people's only option was a combination of starvation and exercise, while skinny people got to feast and watch television. In the late '60s, amphetamine, which increases metabolism, became the rage for dieters. But it didn't keep the weight off, and proved to be addictive.
As it turned out, thin people didn't have higher metabolic rates. On high-calorie diets, they gained weight just as easily as obese people. (In fact, obese people had to eat more to put on a given amount of weight.) The metabolism of obese dieters never slowed enough to explain how quickly their weight bounced back. They were also eating more. Put simply, even at their baseline weight, obese people eat more than thin people.
Swedish studies of pregnant women demonstrate this observation. Women weighed about a pound more one year after delivery than at the start of pregnancy. Some gained more than a pound, and many returned to their old weight. How were the gainers different from the non-gainers? Mainly, they ate more total calories, especially in the form of snacks. Although gainers ate lunch less often, their snacking increased to three or more times per day.
The study also demonstrated another frustrating fact about setpoints--they're easier to increase than decrease. Experts believe that once you've put on extra weight for six months to a year, the setpoint resets, as it does after pregnancy. To permanently lower the setpoint, you must keep weight off for about three years, perhaps longer. Until recently, nothing short of has kept the seriously obese from eating as much as they want to.
The big breakthrough in understanding obesity came in 1994, when experiments on lab mice revealed that the hormone leptin controls the setpoint by controlling satiety. When your weight falls, leptin decreases, hunger increases, and you eat more--until you return to your weight setpoint. This year, researchers in Cambridge, England, found an inbred family whose members all lacked the gene for producing leptin. Without leptin to signal satiety, the children in this family eat ravenously. The 2-year-old weighs 64 pounds and the 8-year-old, 189 pounds.
These leptin findings imply that hormones and neurotransmitters control the instinctual desire to eat, overwhelming willpower in the process. In evolutionary terms, this makes sense. The drive to find and eat food was integral to the survival of our early ancestors. People who gorged themselves survived winter famines and reproduced more than others. But this behavior became "maladaptive" when access to round-the-clock hamburgers and ice cream became the norm. Now, as we gain weight and push our setpoints upward, we are reprogrammed to eat even more.
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