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[MAY 27, 2004]  URBANA -- "Life is so lonely when you are obese," writes one woman on the website of the American Obesity Association. The woman is 25, has lived with obesity all her life and is afraid of losing her mother, who is morbidly obese and about to undergo gastric bypass surgery.

Without the surgery, her mother could die within the year because obesity is escalating her lung problems and causing many other conditions, such as diabetes and sleep apnea.

This woman also believes her obesity is a disease, but is she right? Is obesity on a par with diabetes? Or is obesity a risk factor that leads to illnesses?

These questions are the center of controversy among doctors, health advocates, insurance companies and others. And the answers could have long-range implications, particularly for insurance coverage of certain treatments for obesity.

"I think obesity meets all of the criteria of a chronic disease," said Richard L. Atkinson, president of the American Obesity Association. "But it's not a single disease; it's not monolithic. It's a collection of diseases."

The crux of the matter, Atkinson said, is that obese people have a different biochemistry than thin people -- an abnormal biochemistry that meets the definition of disease.

What obese people share in common, according to Atkinson, is "an abnormality of sensing excess energy stores." To explain, he said that when obese people lose a significant amount of weight, the enzymes in the body that store fat in the adipose tissue (fat tissue) go up. The body goes into a starvation mode, which means that most of the fat coming into the body goes directly into storage in the fat cells instead of being burned. The body doesn't sense that there is already plenty of excess fat being stored in the adipose tissue.

In contrast to the skinny person, Atkinson said, "You're now poised so that any extra molecule of fat that comes in gets stored. It doesn't get burned. You eat a few extra calories and wham! It gets stored in the fat cells because the biochemistry is not the same as a person who has never been obese. So the biochemistry favors gaining weight."

Donald Layman, a professor in the University of Illinois Department of Food Science and Human Nutrition, agrees that individuals have different metabolic efficiencies; they burn and store fat at different rates. But he said truly abnormal metabolisms are rare, affecting about 1 percent of obese subjects.

For the vast majority, Layman said, obesity is pure physiology. "Obesity has a lot of clinical pathology and negative outcomes," he said. "But my problem in considering it a disease is that I view obesity as a normal, expected outcome in an environment in which we eat too much and exercise too little."

If someone is obese at a young age, he said, there could be an inherent abnormality. "But when you find progressive weight gain over two or three decades at the rate of two or three pounds per year, that's not genetic. That's a calorie-balance issue."

However, Layman agreed that severe obesity can be difficult to correct.

 

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"If you take an individual and they become 20 percent overweight, can you correct that?" he asked. "I think you can. But if you take a 200-pound person and they go up to 400 pounds, can you correct that? Chances are that person has developed new fat cell populations. And most of the data suggest that once you develop new fat cell populations, you're not going to get rid of them easily."

But this level of obesity is not what's being seen in the population, he pointed out. "Everybody's not walking around at 400-plus pounds. Most are walking around at weights like 280."

Although Layman believes that overeating and under-exercising are behind most obesity, he said it doesn't work to simply say, "You're obese. Fix it." Making major changes is particularly tough in an environment where people work sedentary jobs, buy supersized meals and are encouraged to clean their plate no matter how much food is on it.

"In our environment, the profit incentive is that if I can give you bigger portion sizes, I can charge more money," Layman said. "If I can supersize it, I can make more money, and I don't care if you're overweight."

With bigger portion sizes, customers feel they are getting more bang for their buck. But in reality, they're simply getting more calories for their cash.

The question of whether obesity is the result of disease or an environment that promotes overeating (or both) is not just a matter of semantics. Some argue that defining it as disease would open the door for insurance coverage of drugs and treatments for obesity. But others argue that it would open that door too wide, causing insurance premiums to skyrocket.

Another issue is whether labeling obesity a disease would de-stigmatize the condition or whether it would send the wrong message by implying that overcoming obesity is out of a person's control.

However those questions are answered, Layman said one thing is certain. The dramatic increase in obesity over the past three decades is evidence that the trends are not being driven by genetics. The number of overweight adults in the United States increased from 46 to 64 percent between 1976 and 1999, while the number of obese adults increased from 14 to 30 percent.

"If you think it's genetic, we would have to have had a major change in the gene pool in the last 30 years," Layman noted.

Atkinson agrees that genetics obviously haven't changed in one generation, while "the environment has clearly changed," but he thinks these environmental changes have acted on the genetic predispositions of different people in different ways.

In other words, as he put it, "If you're destined to be thin, it's really hard to get fat. And if you're destined to be fat, it's really hard to stay skinny. If you are thin, thank your lucky stars and your parents."

[University of Illinois news release]

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