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.
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
The idea that a virus might be partly responsible for weight gain "is sort of a fringe idea as opposed to a cutting-edge idea," Heymsfield said. "But Doctors Atkinson and Dhurandhar have done their homework. There's nothing to suggest that their observations are not valid to this point."
As Heymsfield noted, "they've gone from animals, looked at humans, found associations, and are now shoring up their work with populations. That's the usual and important thing to do."
If all goes as planned, Atkinson's new company -- Obetech, based in that biotech park in Richmond -- will begin offering the first lab blood test for AD 36 in September. The test is expected to cost about $125 to $150. It will take two to four weeks for a patient's results to be ready.
Atkinson's plan is to look for the virus not just in patients referred by physicians but also in large populations. He's been approached both by West Virginia state health officials and by the Air Force to test blood collections for the virus and compare findings with weight records for those populations.
If the link between obesity and AD 36 "pans out, it would be very powerful evidence that the virus is contributing to the problem of obesity, and that might help change a lot of things," Atkinson said. Chief among them: proving that obesity is a disease, not just a marker for lack of willpower. "What we hope is that if we can demonstrate that the virus is causing obesity, it will be more difficult for Medicare and health insurance companies to deny treatment to these people." [Recent changes in Medicare may soon make it easier for obese people to receive some coverage for weight control treatment.]
Those who know they are infected with the fat virus could also take additional steps to avoid weight gain, although researchers don't expect that it will necessarily lead to ground-breaking treatment.
"Having the fat virus doesn't guarantee that a person will become obese," Atkinson said. "But we know that a high percentage of animals infected with the virus became obese. It will alert people that they are going to have to be more careful than the average person to prevent weight gain. At least that is what we think."
Exactly how AD 36 may promote weight gain is still not understood. Infection with the virus "does not appear to cause very severe illness," Atkinson said, so people aren't likely to know they've had it unless they get tested.
One theory is that infection prompts fat cells to pull more triglyercides and cholesterol from the blood -- an idea that fits with the lower levels of these substances in the blood of those who have had the virus.
Other research points to the possibility that infection may significantly reduce the amount of leptin produced by fat cells. And still more studies suggest that AD 36 may prompt fat cells to mature more quickly and start storing fat.
"It's really not clear what may be going on," Atkinson said.
Still: a fat virus?
"If you told people 20 years ago that ulcers are caused by a bacterial infection, you would have been laughed at," Heymsfield noted. "But it turns out that ulcers are caused by infectious disease. So we scientists have learned to have open minds."
And so should you. But in the meantime, if you'd like to control your weight, eat less and move more.
Share Your Tips or ask questions about healthy nutrition and activity when Sally Squires hosts the Lean Plate Club online chat, from 1 p.m. to 2 p.m. today, on www.washingtonpost.com. Can't join live? E-mail firstname.lastname@example.org anytime.
New To The Club? The Lean Plate Club is devoted to healthy eating and boosting activity. To learn more, and subscribe to our free e-newsletter, visit www.washingtonpost.com/leanplateclub.