The Evolution of Fat
By Peter Jaret, EatingWell.com
The 18th century boasted the Age of Enlightenment, the 19th century the Age of Imperialism. By all accounts, ours may well be remembered as the Age of … Fat.
People are fat and getting fatter, experts say. More than 6 out of 10 Americans are now overweight or obese. And though we're still the plumpest people on the planet, waistlines are expanding almost everywhere in the developed world. Experts at the World Health Organization have begun to warn of an impending global epidemic of fat-related diseases, from gout and diabetes to high blood pressure and heart disease. In an unprecedented reversal in much of the world, more people suffer from overnutrition than undernutrition.
The biggest reason is simple. We eat too much. Food is available almost everywhere we turn, much of it in the form of high-calorie goodies like sugary drinks and fatty snacks. Advertisements constantly urge us to eat, eat, eat.
And we do. Women now eat 335 more calories a day than they did in 1971. Men scarf down an extra 168 calories daily. That translates into an astonishing average of 278 more pounds of food per person per year—and that's enough all by itself to explain the country's growing weight problem.
But not everyone's bellying up to the buffet table. "Look closely at the numbers and you find that people at the thin end of the spectrum have remained thin," says Jeffrey Friedman, an investigator at Howard Hughes Medical Institute. "People in the middle have gained 6 or 7 pounds. But it's really at the heavy end of the spectrum where people have gotten much, much fatter." They've put on an extra 25 to 30 pounds, according to researchers at the National Center for Health Statistics.
The reason some of us are fat and some thin lies in our genes, scientists say. "When we were hunter-gatherers, evolution favored people who could take in lots of food when times were good and store it in case of famine—people who could get fat," says Eric Ravussin, a scientist at the Pennington Biomedical Research Center in Baton Rouge, Louisiana. These people were considered to have "thrifty" genes. As some populations began farming, which allowed them to produce enough food to store for the winter, having such genes was no longer critical, but they stayed with most of us.
People without thrifty genes, who remain thin in today's land of plenty, are evolutionary oddities, says Ravussin. A majority of us are thought to possess some mix of thrifty genes—and their urgings are so powerful that even the most stubborn willpower won't keep many of us from getting pudgy if food is cheap and plentiful.
But obesity may well be more complicated than simple overconsumption. Researchers are beginning to decode the way thrifty genes work, and part of the explanation lies in the nature of fat cells themselves. Far from being passive storage pockets, these energy storehouses turn out to be highly active chemical factories. They churn out hormones like leptin and adiponectin: the first signals the brain to suppress hunger; the second triggers the body to burn fat for fuel. Together, they act as a check-and-balance system designed to keep the amount of body fat relatively stable. When fat stores increase, the hormones signal the body to stop eating and start burning fat.
"If everything works well, it's a beautifully balanced system," says William Banks, an obesity researcher at St. Louis University and the Veterans Affairs Medical Center. "As people become overweight and obese, unfortunately, the system breaks down."
With too many fat cells producing too much leptin, the body becomes resistant to leptin's appetite-suppressing signal. The result: People are hungry even when they have plenty of fat stores. They eat, they put on even more fat, and those additional fat cells churn out more leptin, which raises the levels high enough to overcome leptin resistance. Eventually weight stabilizes. But the set point at which it does is much higher for people with the thrifty genotype than for people who are genetically programmed to be thin. The higher set point also makes it devilishly difficult to lose weight.
To add to the problem of leptin resistance, excess fat cells also cause a decrease in adiponectin, the hormone that signals the body to burn fat. Because adiponectin affects the body's sensitivity to insulin, as levels fall people become insulin resistant, which increases their danger of developing diabetes.
Researchers are currently testing whether administering leptin will help obese people on diets lose weight by dampening their hunger. They are also looking for substances that might increase leptin sensitivity.
But thrifty genes and fat-cell biochemistry may not be the only reasons we stay fat. According to Wayne State University nutritional biochemist Nikhil Dhurandhar, the cause in some people may be a virus. "For years, we've known that certain viruses can cause dramatic weight gain in rats, mice and monkeys," says Dhurandhar. The most likely culprit in people is adenovirus-36, a human virus that has been shown to cause obesity in animals. In a study of 1,000 subjects, Dhurandhar found that obese people were much more likely than thin people to have antibodies to AD-36. If further research confirms that some cases of obesity are infectious, it may eventually be possible to create a vaccine to protect against the "fat bug."
The latest findings show why losing weight is easier for some people than others—and why it may prove almost impossible for those of us with the thriftiest genes. Future research may offer better understanding and possible remedies. For now, though, the only answer we have for winning the battle of the bulge is the advice we all know by heart—to eat less and move more.
From www.eatingwell.com © 2009 Eating Well Inc.
739 Irving Avenue - Suite 530 Syracuse, NY 13210 Tel: 315-478-1158 - Fax: 315-478-3014
site developed by laurieferger.com