April 12, 1997
The hottest topic in obesity, this week, is whether some share of America's growing epidemic of expanding waistlines might be driven by viruses related to some of those responsible for the common cold.
At a meeting in New Orleans, Monday, Nikhil V. Dhurandhar and Richard L. Atkinson of the University of Wisconsin Medical School reported finding antibodies for an adenovirus known as AD-36 in 15 percent of the 154 obese volunteers that they had recruited from entrants at two university weight-loss centers, one in Wisconsin, the other in Florida (SN: 4/12/97, p. 220). Not only does AD-36 cause coughing, sneezing, and other cold-like respiratory symptoms, but, more intriguingly, it also induces obesity in chickens.
Dhurandhar's team has previously shown in three separate studies that within 3 weeks of the initial infection, chickens develop 60 to 75 percent more fat than uninfected birds. The mechanism behind this rapid weight gain remains a mystery, Dhurandhar says, but would appear to trace to some derangement of the animals' metabolism.
Indeed, infected birds get fatter while eating the same amount of feed as svelter, uninfected broodmates. Explains Atkinson, it appears that the adenovirus infection effectively flips some biochemical switch within the birds so that they begin preferentially accumulating fat instead of lean tissue.
A follow-up study by the researchers, scheduled to be presented at a June meeting in Dublin, has fueled their confidence that the virus-induced obesity may also occur in people. Their yet-unpublished data show that AD-36 infection also fosters a rapid fattening in mice.
The infection appears to turn the animals into couch potatoes, Dhurandhar says. For instance, "chickens who get the virus sit in a lump all day long," while the uninfected birds scratch about normally
A finding that some fat humans carry antibodies to the AD-36 germ would probably do little more than raise a few eyebrows were it not for the fact that volunteers possessing these telltale markers of earlier infection also had an unusual ratio of fats in their blood -- the same atypical ratio seen in chickens and mice that have the virus-induced obesity.
Heavy people tend to possess high concentrations of cholesterol and triglycerides in their blood. Yet total-cholesterol levels in the blood of obese volunteers with the AD-36 antibodies fell solidly under 200 milligrams per deciliter (mg/dl) of blood -- the common cutoff for normal levels. Indeed, the average for this group of portly souls, all weighing in around 250 pounds, was about 189 mg/dl. By contrast, obese volunteers without the antibodies harbored cholesterol concentrations averaging 217 mg/dl. No similar comparison can be made among lean individuals, because none of the 45 who were assayed carried the antibodies.
Dhurandhar and Atkinson also observed a similar variation in triglyceride concentrations in the blood of the two groups of obese volunteers. Those with AD-36 antibodies had about 110 mg/dl, compared to 155 mg/dl in people without the antibodies. In general, "we basically use 150 [mg/dl] as the upper limit of normal," explains Atkinson, an obesity specialist and director of the university's clinical nutrition center.
Like a cold virus, AD-36 seems to remain infectious for only a short time. In laboratory studies, Dhurandhar has been able to isolate the live germ from animals 7 days after they had been deliberately infected. Three weeks later, no viable virus could be obtained from the animals, Atkinson says.
"Whatever damage has occurred appears to have been done during the acute infection," he explained, "so we want to make sure that people don't start shunning obese people, thinking they'll catch a virus.
"If you're concerned," he says, "you really want to shun the skinny person with a cold, because [by the time they gain weight] the damage has been done and the virus will be gone."
Because the virus doesn't appear to stick around very long, is there any advantage to learning who might have been infected? Absolutely, Atkinson believes. At a minimum, he says, fat people "suffer enormous discrimination" by society. The stigma can hurt employment opportunities and devastate an individual's self esteem. "So if people can say [their heaviness] comes from having a virus, emotionally that can be important. It could offer some significant peace of mind."
Beyond that, men harboring the antibodies went on to shed considerably more pounds during weight-loss counseling -- some 17.8 percent of their initially body weight versus just 11 percent in men without antibodies. (Alas, women derived no comparable benefit.) So identifying men whether men carry the antibodies may offer some gauge of how well they will respond to weight-loss programs, Atkinson says.
Currently, his assay for the antibodies is available for use only in an experimental setting. However, that could soon change. His team has set up a separate company to perform the screening, pending approval from the Food and Drug Administration.
How about a vaccine?
"It is very clear that if there were a vaccine for this [germ] that it would be a very important product," Atkinson says. Currently, perhaps 100 million people in the United States are seriously overweight, he notes. "If we can make a vaccine to prevent up to 15 percent of this, you would have an enormous impact upon the health and mental status of a huge number of people," he says.
While acknowledging that his team lacks conclusive proof that the virus causes obesity in humans, he notes that because it does promote a significant fattening in two animal models -- one of them a rodent frequently used to model human health -- argues strongly that humans are not immune to the phenomenon.
Toward that end, he told Science News Online, the Wisconsin team plans to begin work on such a vaccine almost immediately. At the same time, it will continue to probe how the virus influences obesity. For now, he notes, the adenovirus appears to act through some mechanism other than that of canine distemper virus or tuberculosis—both viruses that have been shown capable of promoting weight gain by damaging the brain's satiety center. He points out that neither of those viruses suppressed the normal elevation of cholesterol and triglycerides that tends to accompany obesity.
References:
Dhurandhar, N.V., and R.L. Atkinson. 1997. Evidence for an association of a virus with obesity in humans (abstract #1335). The FASEB Journal 11(Feb. 28):A230.
_____. 1996. Development of obesity in chickens after infection with a human adenovirus. Obesity Research 4, Supplement 1(October):24S.
Raloff, J. 1997. Viruses may leave a weighty legacy. Science News 151(Apr. 12):220.
Related Readings:
Bower, B. 1996. Gene pair may incite obesity, depression. Science News 150(Sept. 21):181.
Fackelmann, K. 1996. Lose a gene, lose some weight -- in mice. Science News 150(Aug. 24):125.
Raloff, J. 1995. Obesity, diet linked to deadly cancers. Science News 147(Jan. 21):39.
Seachrist, L., and J. Travis. 1995. Hormone triggers cells to turn to fat. Science News 148(Dec. 9):390.
Travis, J. 1996. Obesity researchers feast on two scoops. Science News 149(Jan. 6):6.
Sources:
Richard L. Atkinson
Beers Clinical Nutrition Center
University of Wisconsin Medical School
Nutritional Sciences Building
1415 Linden Dr.
Madison, WI 53706
Phone: 888-408-4787
Nikhil V. Dhurandhar
University of Wisconsin Medical School
Nutritional Sciences Building
1415 Linden Dr.
Madison, WI 53706
This week's Food for Thought is prepared by Janet Raloff, senior editor of Science News.
Illustration: Wendy Temple.
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