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The Lean Plate Club: Sally Squires

A Question From the Edge: Is Fat Contagious?

By Sally Squires
Tuesday, August 3, 2004; Page HE01

The continuing battle against the obesity epidemic moves this week to a biotech park affiliated with Virginia Commonwealth University in Richmond. That's where physician and scientist Richard Atkinson, president of the American Obesity Association, starts assembling a new lab designed to test blood for a fat virus.

Yes, that's right. A fat virus.


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While eating less and moving more remains the standard treatment for obesity, scientists are eager to unravel the disease's underlying mechanisms. Among the key questions: Why do some obese people bear extra weight with fewer medical consequences than others? What is the best way to identify which slender young adults are most likely to wage waistline wars in middle age? And what about leptin and those dozen or so other recently discovered hormones that influence body weight by regulating calorie use and storage. What role might they play in controlling weight?

Most of those questions are far from being answered. But the discovery of leptin 10 years ago provided some hope -- and disappointment. Finding leptin and the dozen or so similar hormones that help to control weight "was totally unexpected and like a shot heard 'round the world," said Steven B. Heymsfield, deputy director of the St Luke's-Roosevelt Hospital Obesity Research Center in New York. Scientists guessed that mutations in these genes might help account for obesity. But that excitement faded when studies showed that few obese people had major mutations in leptin or other related genes.

Nevertheless, these findings suggest that "the system regulating weight is probably determined by multiple genes interacting with the environment in a way that is extremely complicated," Heymsfield said. "Nothing is simple."

Or being overlooked. Which brings us back to that fat virus. About 15 years ago an Indian researcher named Nikhal Dhurandhar found a virus that left infected chickens fatter, but with lower blood cholesterol and triglyceride levels, than uninfected poultry.

Dhurandhar teamed with Atkinson, then at the University of Wisconsin-Madison, to expand the research into other animals and to humans. Along the way, the two identified this "fat virus" as adenovirus (AD) 36, one of 50 such viruses that "are quite common" in humans, Atkinson said.

In a series of studies involving chickens, rats, mice and monkeys, the team injected AD 36 into healthy animals and observed that it caused them to become fat compared with control groups. Just like Dhurandhar's chickens, the infected animals had blood cholesterol and triglyceride levels that remained lower than those in uninfected animals.

Researchers usually don't inject viruses into people. So Atkinson and Dhurandhar did the next best thing: They screened blood from obese U.S. residents looking for antibodies against the virus, the best way to detect previous infection. They also tested blood from healthy-weight people and measured blood cholesterol and triglyceride levels in both groups.

The study found that about 30 percent of the obese participants had antibodies against AD 36, compared with just 10 percent of the healthy-weight controls. And just as in the animal studies, people who had been infected with the virus had significantly lower blood cholesterol and triglyceride levels than their uninfected counterparts. On average, their total blood cholesterol was about 35 milligrams lower than the uninfected. And most of that difference was due to lower levels of low-density lipoprotein (LDL), a damaging form of cholesterol


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