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Specifying alcohol-related brain-damage among heavy social drinkers

School of Medicine, "in that they're looking at changes that may occur prior to patients being sick enough to be hospitalized. If you take this to mean that these are people who are earlier in the course of their alcoholism, then it becomes very valuable, as they have studied a population that has not yet been studied, and it complements what's already in the literature."

Meyerhoff and his colleagues examined 46 chronic, heavy drinkers (38 males, 8 females) and 52 light drinkers (32 males, 20 females) recruited from the general community via newspaper advertisements and flyers. Researchers compared measures of regional brain structure using magnetic resonance imaging (MRI), as well as measures of common brain metabolites in both gray and white matter of the major cerebral lobes, subcortical nuclei, brainstem, and cerebellum using short-echo time MR spectroscopic imaging. Regional levels of N-acetylaspartate (NAA), myo-inositol (mI), and creatine- and choline-containing metabolites were also compared as a function of the groups' drinking practices, including binge drinking, and family history of alcoholism.

Meyerhoff said that the cumulative lifetime alcohol consumption among the heavy drinkers was about 60 percent of that typically found among treatment populations. Nonetheless, they found that frontal white matter NAA generally considered to be a marker of neuronal damage was lower in heavy drinkers than light drinkers, and was associated with lower executive and working memory functions.

"Although the men and women who drank heavily for many years demonstrated fewer changes in brain metabolites than do alcoholics in treatment," he said, "the abnormalities that we found are nonetheless associated with lower brain function." Lower cognitive functioning, he said, can affect daily living routines in not-so-obvious ways the changes may be too gradual or too weak to be noticeable but they may still interfere with basic
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14-Apr-2004


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