No connection ......

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BILL GATES: Burger .... BAD!

Joel

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A Molecular Explanation of Why Burgers Are Bad For You

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Researchers identify cholesterol-forming mechanism
By Ed Edelson, HealthDay Reporter

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THURSDAY, Jan. 27 (HealthDayNews) -- Researchers say they have
discovered the molecular switch that turns the bad fats in food into
the cholesterol that clogs your arteries.

It is a molecule designated PGC-1 beta, biochemically classified as a
co-activator, and it plays a role in liver metabolism, according to a
report in the Jan. 28 issue of Cell by scientists at Harvard's
Dana-Farber Cancer Institute.

When the saturated fats and trans-fatty acids in meat, whole-milk
dairy products and other foods on cardiologists' crime sheet arrive at
the liver, PGC-1 beta begins a cascade of biochemical signals that
direct liver cells to produce LDL cholesterol, the "bad" kind that
clogs arteries, as well as triglycerides, another family of
artery-blocking substances, the researchers report.

"This gives us a target for drug development," said study author Bruce
Spiegelman, a professor of cell biology at Harvard Medical School. "It
might be possible to develop agents for people who can't be treated
with current drug regimens. It also is a way to understand better why
some foods have deleterious effects and some don't."

Scientists and cardiologists have known for a long time which foods
are bad for people. Study after study has shown that diets rich in
saturated fats and trans fats -- most notoriously, the
burger-and-fries meal so popular in this country -- increase blood
levels of LDL cholesterol, while foods rich in unsaturated fats are
associated with HDL cholesterol, the "good" kind that helps keep
arteries clear.

"We knew these saturated and trans-fatty acids had bad effects,"
Spiegelman said. "We had no idea, in molecular terms, what they did to
set up the bad pathways. What we have found is a missing link, a
mechanism by which saturated fats and trans fats can do their dirty
work."

As an exercise in pure science, the discovery is another example of
the natural selection process that is at the center of Charles
Darwin's theory of evolution, Spiegelman said.

Until recently in human history, PGC-1 beta did no particular harm to
humans because "most of our evolution did not occur in times of great
nutritional abundance," he explained. "In addition, its bad effects
are mostly felt in older people, after the child-bearing years, so
there has been no selection pressure."

Now that people are living longer, the evil effects of PGC-1 beta have
become a target of medical practice, Spiegelman said.

Research to develop compounds that block the activity of PGC-1 beta
could provide new cholesterol-lowering treatments, he added.

"I am hopeful that this paper will stimulate interest on the part of
pharmaceutical companies to do that," he said.

"This is a very important finding that sheds a great deal of light on
the molecular pathways for production of fats," said Dr. Ronald
Krauss, director of atherosclerosis research at the Children's
Hospital Oakland Research Center in California.

Some findings do require follow-up research, Krauss added. For
example, in humans, consumption of fat-rich foods is believed to
suppress the activity of LDL cholesterol receptors on cells, thus
raising LDL cholesterol blood levels. The new study, done in mice,
found increased activity of LDL cholesterol receptors.

"There might be some details that are different between mice and
humans," Krauss said.

More information

The cholesterol story, good and bad, is outlined by the American Heart
Association.

content by:

SOURCES: Bruce Spiegelman, Ph.D, professor, cell biology, Dana-Farber
Cancer Institute, Boston; Ronald Krauss, M.D., director,
atherosclerosis research, Children's Hospital Oakland Research Center,
Oakland, Calif.; Jan. 28, 2005, Cell
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