Like your meat well done—perhaps with a slightly charred flavor? Then have a beer. The reason: A new study shows that, at least in mice, beer limits the DNA damage triggered by exposure to the carcinogens that form in overcooked meat.
Researchers at Okayama University administered locally purchased beer—minus its alcohol—to the rodents. Alcohol was excluded because it alone can be carcinogenic. Some mice got the nonalcoholic beer in place of drinking water. Others got solids extracted from the beer, added to their chow.
After a few days of administering the beer diets, the scientists laced some of the animals' food with either of two heterocyclic amines (HCAs)—the carcinogens from cooked meat. Some animals received one compound known as MeIQx. Others' food was treated with trace quantities of Trp-P-2. Such HCAs were just recently added to the list of potential human carcinogens compiled by the National Toxicology Program (see Carcinogens in the Diet).
After a few more days of giving the mice HCA-supplemented diets, Sakae Arimoto-Kobayashi and his colleagues removed key organs and scanned their cells for HCA-induced DNA changes known as adducts. These genetic changes, in which bits of a chemical inappropriately bind to DNA, often serve as a first step in the development of cancer.
As expected, both HCAs triggered adducts. Trp-P-2's adducts appeared in the liver while those caused by MeIQx developed not only there, but also in the lungs and kidneys. However, beer diminished by some 40 to 75 percent the number of HCA adducts that formed, depending on the type of tissue and quantity of beer ingredients ingested, the researchers report in the Feb. 9 Journal of Agricultural and Food Chemistry. Good news for beer drinkers: Both light-colored lager and a darker stout proved protective.
The Okayama scientists also conducted test-tube experiments to determine how beer affected the chemical activation of Trp-P-2 to a form capable of mutating cells—another means by which those cells might turn cancerous. The team found that incubating cells with beer or its ingredients cut the activation by about 75 percent.
These results haven't been confirmed in people or human cells. But the new study does stoke the imagination, especially in light of research that the Okayama group published 2 years ago. At that time, they showed a similar inhibition of HCAs' potentially carcinogenic changes—in insect DNA—by a naturally occurring antioxidant isolated from green tea: epigallocatechin gallate (EGCG).
So what? Just 2 months ago, researchers with a Japanese tea company reported not only that EGCG and related tea catechins can help people lose weight, but that their company had begun adding the compounds to one of its commercial green-tea products, making it a diet aid (see Trimming with Tea). It's not much of a stretch to envision brewers fortifying beer with compounds from green tea.
A cancer-fighting diet beer—now, wouldn't that be a pub-crawler's dream?
Department of Pharmaceutical Sciences
Tsushima, Okayama 700-8530
National Toxicology Program
Department of Health and Human Services
P.O. Box 12233
Research Triangle Park, NC 27709
Web site: [Go to]
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