Just as clear are some changes in the big picture of body weight. Not long ago, obesity was revered as a sign of wealth. Sons were encouraged to marry heavy women because it meant they were well cared for, and came from well-to-do families. In some cultures that still exists.
But in the 1900s, the ideal body type began to get thinner, especially after World War II. The impact was felt primarily on women and somehow, their success in life became linked to how thin they were. No wonder Cindy Crawford and Kate Moss became bigger female role models than Indira Gandhi or Margaret Thatcher. Then there was a fundamental change in an old belief that obesity was an emotional problem that emanated from the bad habits you had as a kid. Now, science is grasping the fact that biology plays a major role in body weight. One easy way to prove this point was the fact that psychologists who treated obese patients had little success. The idea sunk in that it wasn't the failure of all these psychologists--the psychological model was all wrong.
"Only in the past decade has the U.S. government embraced the idea that genetic makeup plays a key role in weight gain," says Woods. "Until then it had been thought that people were somehow weak or had emotional problems that lead to weight gain and obesity. The Food and Drug Administration has finally realized the role biology plays. That is a big change."
One of the biggest breakthroughs was the discovery of the hormone called leptin. Originally identified late in 1994 after an eight-year search by Rockefeller University researchers, leptin is a protein produced by the obesity gene of mice. Animals with defects in both copies of this gene act as if they are in a state of perpetual starvation, unable to reproduce, stay warm, grow normally and restrain their appetites. Thus, they get grossly fat, weighing as much as three times more than normal animals.
While this is exciting news, mutations in those genes don't seem to be at fault in human obesity. The now-obese, diabetes-wracked Pimas were found to have low leptin levels but most overweight and obese people have high leptin levels. The large fat stores in people seem to be pumping out the hormone normally, which implies that leptin itself won't work as an obesity cure. Instead, something must be going wrong in obese people's response to the hormone, although the difficulty doesn't seem to be in their leptin receptors.
The problem could be that leptin can't quite make its way from the bloodstream into the brain, Schwartz has found. In any event, strong evidence shows leptin keeps the peptide called neuropeptide Y in check. This peptide is known as the signal that travels to the brain to stimulate appetite and reduce energy expenditure when it is told that a person's fat stores seem to be decreasing. When leptin is removed, the NPY system goes nuts, the animal will eat nonstop until he reaches obesity. Drug companies are likely to try to come up with an artificial version of leptin for human regulation of the peptide.
Meanwhile, other hormones, such as insulin, are being scrutinized in the very complicated web of biochemical and brain-signaling circuits that transmit signals such as when to stop eating. Scientists say finding the magic hormone and turning it into a pill to fool your brain could provide one solution to the problem. But beware: all the biology, biochemistry, genetics and pharmaceuticals in the world may be no match for visual cues (that cheesecake looks scrumptious), senses like smell and taste (that pizza is driving me wild), emotional factors (I'm so angry, where is that pint of Haagen Dazs?) and habits (is it 6 o'clock? Dinnertime!).
In other words, science still has an awful lot to digest.* Jon Marmor, '94, is associate editor of Columns.
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