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GAMBIA-L  January 2004

GAMBIA-L January 2004

Subject:

Can a virus make you fat?

From:

"Morrie K. Kebbeh" <[log in to unmask]>

Reply-To:

The Gambia and related-issues mailing list <[log in to unmask]>

Date:

Mon, 26 Jan 2004 23:43:13 -0800

Content-Type:

text/plain

Parts/Attachments:

Parts/Attachments

text/plain (182 lines)

New York Daily News - http://www.nydailynews.com
Can a virus
make you fat?
By LIZ NEPORENT
Sunday, November 2nd, 2003

Jim Thornton, a 51-year-old health columnist for the
magazine Field & Stream, is an identical twin.
Although he and his brother, John, have always
exercised about the same amount and have similar
eating patterns, Jim is 40 pounds heavier. "Neither of
us is by any means overweight," he's quick to point
out, "but I always wondered about that weight
difference."
Perhaps Thornton has something in common with
chickens.

In the 1970s, Dr. Nikhil Dhurandhar, an obesity
researcher who holds the William Hardy Chair in
obesity research at Wayne State University in
Michigan, began studying a viral disease that was
killing chickens by the thousands in India. He noticed
that infected birds didn't waste away as they got
sicker, but instead, packed on pounds  up to 50% more
fat tissue than uninfected birds.

Oddly, the sick chickens tested low for levels of
cholesterol and triglycerides (fat in the
bloodstream). "Normally, obesity in any species is
associated with high levels of cholesterol and
triglycerides," Dhurandhar says.

Dhurandhar noticed something even stranger about the
infected birds: They did not seem to eat more as they
gained weight.

Eventually Dhurandhar and his research team identified
the cause of the birds' sickness as adenovirus-36, or
Ad-36, a highly infectious microbe that affects
animals as well as people. It was first isolated in
humans in 1978 in the fecal matter of a 7-year-old
diabetic girl. Based upon the discovery of Ad-36,
Dhurandhar began to theorize that it might be a
contributing factor to the skyrocketing obesity
epidemic in humans.

To test his theories, Dhurandhar performed a series of
studies while at the University of Wisconsin at
Madison, where he looked at the blood samples of
numerous subjects for the existence of Ad-36
antibodies. An antibody is a chemical produced by the
body to fight a particular condition; its presence is
a sort of biological thumbprint that proves a person
was infected by the virus that causes the condition at
some point.

More than 30% of the obese subjects tested positive
for Ad-36 antibodies compared to only 5% of
normal-weight individuals.

When the researchers factored out 29 other possible
sources of weight gain, such as genetics, family
history and lifestyle, subjects did not differ in any
other respects. The Ad-36-positive subjects were among
the most obese in the study, but paradoxically had low
cholesterol and triglyceride levels - just like the
chickens in India.

Another group of investigations done in Germany looked
at nearly 100 pairs of identical twins. Researchers
found that when one twin tested positive for Ad-36
antibodies, he always weighed more and had a higher
percentage of body fat than the uninfected twin.

In fact, several years ago Thornton sent blood samples
from both him and his twin brother to Dhurandhar when
he was researching an article on obesity-causing
viruses. Thornton tested positive for the Ad-36
antibody, while his svelte-by-comparison twin did not.


"It freaked me out to think that there's a possibility
that a microbe could be messing with my metabolism,"
he says. He does observe, however, that his
cholesterol levels are fairly high and that at
6-foot-1, 175 pounds, he's far from obese.

How might one catch a case of heftiness from Ad-36?
Dhurandhar says that the most likely transmission
method is airborne. "In animal experiments, when
infected animals were kept in the same room with
noninfected animals, the noninfected animals became
infected in a matter of days, even though there was no
direct contact," he says.

Dhurandhar strongly warns that more work, particularly
by virologists, needs to be done. "You certainly
cannot reliably translate the results of animal
experiments to humans," he says.

However, the notion that obesity could, in some cases,
be caught like a common cold is not so farfetched.
Researchers have blamed many chronic health conditions
on infections. Ulcers, for example, were once thought
to be caused by high stress and poor diet, but now the
ulcer bug, Helicobacter pylori, is an accepted medical
reality and ulcers are most commonly treated with
antibiotics. Ongoing studies are focusing on microbial
causes for everything from heart disease to
depression.

Looking at cause and effect

Scientists speculate that Ad-36 amplifies fatness by
increasing the number and size of adipocytes (fat
cells) and by stimulating immature adipocytes to bloom
more quickly. Animals infected with Ad-36 may wind up
with three times more fat cells than uninfected
animals, as well as vastly decreased metabolisms.

"We also found that Ad-36-infected fat cells have
reduced leptin levels," says Dhurandhar. Leptin is a
recently discovered hormone that seems to regulate fat
storage, metabolism and appetite.

When you gain weight, leptin levels should rise,
signaling the body to put the breaks on fat
accumulation. Dhurandhar speculates that those who are
Ad-36-positive may not be able to produce enough
leptin to normalize fat metabolism.

But not all scientists are convinced that you should
edge away from that portly gentleman in the elevator
when he sneezes. "We don't know whether the virus
causes weight gain or shows up after you've already
gained the weight," says Dr. Steven Heymsfield,
Departmental Director of the Obesity Research Center
at St. Luke's Roosevelt Hospital.

In other words, Ad-36 could be a marker that shows up
after fat cells multiply, rather than the cause of the
excess adipose itself. Still, Heymsfield admits that
the research is compelling and he'd like to see if
further investigation will establish a
cause-and-effect relationship.

If Ad-36 is shown to cause excessive weight gain in
humans, even when they don't overeat, it's not clear
how contagious it may be, especially once the carrier
has already reached full corpulence.

It's also unclear how many other viruses may have
similar effects. And certainly scientists are not
suggesting that all obesity is communicable, though
many experts don't think the worldwide spread of
obesity can be totally explained by supersized
portions and a couch-potato lifestyle. Viruses and
other infectious entities may well be a contributing
factor.

The Wayne State University research team, led by
Dhurandhar, recently received a National Institutes of
Health grant to further study the concept of
"infectobesity."



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