A Molecular Explanation of Why Burgers Are Bad For You

Researchers identify cholesterol-forming mechanism

Please note: This article was published more than one year ago. The facts and conclusions presented may have since changed and may no longer be accurate. And "More information" links may no longer work. Questions about personal health should always be referred to a physician or other health care professional.

En Español

By
HealthDay Reporter

THURSDAY, Jan. 27, 2005 (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.

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

Last Updated: