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Gene Boosts Drinkers’ Colon Cancer Risk


FRIDAY, Dec. 19 (HealthDay News) — About a fifth of white Americans carry a gene mutation that leaves them at higher risk of colon cancer if they become chronic drinkers, a new study finds.

“If people drink alcohol chronically and have a certain genetic background, then they have an increased risk for large intestinal cancer — colorectal cancer — if they drink over a certain amount of alcohol every day,” explained study co-author Dr. Helmut K. Seitz, a professor of medicine at Heidelberg University in Heidelberg, Germany.

Seitz and his colleagues were expected to publish their findings in the March issue of Alcoholism: Clinical and Experimental Research. The study was posted online Dec. 19.

Describing his team’s work, Seitz said scientists have long known that chronic drinking ups risks for a wide range of cancers including breast, liver, esophageal and laryngeal malignancies.

In fact, the American Cancer Society already recommends limiting alcohol consumption to no more than one or two drinks per day for women and men, respectively, as a means of reducing overall cancer risk.

The new study focused on colon cancer. The team examined how disease risk might be affected by the varying speeds with which white individuals convert ethanol (alcohol) into a particularly metabolite called acetaldehyde.

This ethanol-to-acetaldehyde conversion process can be particularly rapid among those whites who carry a particular gene variant labeled ADH1C*1, the researchers noted.

“Acetaldehyde is a very toxic compound which changes and damages our DNA,” Seitz noted. “And the speed of the change from ethanol to acetaldehyde is different in different individuals. So the idea is that if people have that gene which is responsible for a faster metabolism to acetaldehyde, then more of it would be produced in a shorter period of time, and more of would bind to our DNA. And that could increase colon cancer risk.”

To explore this notion, the research team conducted genetic testing on 173 colon cancer patients, and compared their findings with tests conducted on 788 healthy people.

The result: Those men and women who possessed the ADH1C*1 gene were, in fact, at a genetically higher risk for developing colorectal cancer, although only when consuming more than 30 grams (about two drinks) of alcohol per day.

This translates to about a twofold to threefold increase in the risk for colon cancer for chronic drinkers with this particular genetic marker, Seitz said.

“But I have to state that, even so, the general risk is not tremendous,” he noted. “Yes, it’s certainly a significantly higher risk for those with the gene [about 20 percent of the general population] than for those without. But it’s not an extremely huge risk.”

“However, in any case, the message is very simple,” added Seitz. “To be on the safe side, if you don’t know your genetic background, be moderate in your alcohol consumption. That means you can have two drinks. But then be careful.”

Dr. Marc Galanter, director of the division of alcoholism and substance abuse at New York University Langone Medical Center/Bellevue in New York City, noted that the current work serves to highlight another negative consequence of heavy alcohol use.

“Some develop liver disease,” he said. “Others develop cardiac disease and, apparently, based on this study, some are more vulnerable to developing colorectal cancer. Research like this will help us understand which people are most vulnerable to the ill consequences of heavy drinking.”

More information

There’s more on the alcohol-cancer link at the American Cancer Society.

SOURCES: Helmut K. Seitz, M.D., professor, medicine, Heidelberg University, Heidelberg, Germany; Marc Galanter, M.D., professor, psychiatry, and director, division of alcoholism and substance abuse, New York University’s Langone Medical Center/Bellevue, New York City; January 2009, Alcoholism: Clinical and Experimental Research

By Alan Mozes
HealthDay Reporter

Last Updated: Dec. 19, 2008

Copyright © 2008 ScoutNews, LLC. All rights reserved.


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