Brain damage can occur in as little as 24 hours after binge drinking, according to a new study. Researchers at the Universities of Kentucky and North Carolina have found that a protein called vimentin indicates damage to the hippocampus after heavy drinking episodes.
“We know that the extent of damage following alcohol exposure depends heavily on the manner in which it is consumed,” says Kimberly Nixon, associate professor of pharmaceutical sciences at The University of Kentucky as well as corresponding author for the study. “Human studies suggest that binge-pattern drinking is more closely associated with brain damage. One study, for example, reported that binge drinking at least once per month in adulthood significantly increases the risk of developing dementia later in life. Animal models help provide the critical information that binge drinking, which produces high blood alcohol levels, directly causes damage.”
Nixon and her colleagues administered a nutritionally complete liquid diet to adult male Sprague-Dawley rats that additionally contained either alcohol (25% w/v) or isocaloric dextrose every eight hours for either one or two days. The rodents were sacrificed immediately following, two days after, or seven days after alcohol exposure and their brain tissues were examined.
“This was really a simple study that took advantage of some new tools to look for evidence of brain damage,” explains Nixon. “We didn’t look for dying cells themselves, but we looked at more indirect indices of damage by looking at what happens to astroglia, one of the supporting cells for neurons. Astroglia react to brain damage by expressing several proteins that they do not normally express under healthy, happy conditions, one of which is an intermediate filament protein called vimentin. We saw a remarkable number of cells expressing this marker. It is one of those ‘here is your brain, here is your brain on drugs’ kind of findings where the expression was obvious to the naked eye in many brains with as little as 24 hours of high blood alcohol levels.”
Nixon adds that, because rodents metabolize alcohol significantly faster than humans do, it is important to look at the actual concentration of alcohol in the blood in order to translate this to the human condition. “These rats had blood alcohol levels that were more than four times the legal driving limit, which for humans would require excessive drinking in the nature of a 12-pack of beer, a couple bottles of wine, or half of fifth of whisky. Unfortunately, drinking self-reports and blood alcohol level data from emergency rooms confirm that this level of drinking is common in those with alcohol use disorders.”
“Rodent brain damage can model human damage,” notes Fulton T. Crews, John Andrews distinguished professor and director of the center for alcohol studies at the University of North Carolina. “Vimentin seems to be a good marker of glial activation that shows that one day of binge drinking can cause some brain damage that persists and grows after a week of abstinence. However, both rodent and human brain damage generally require long-term alcohol consumption that models alcoholism and not the acute responses studied in this manuscript.”
Nixon agrees. “The lack of overt neuronal deterioration suggests that a single, short-term, high-level binge probably does not result in functional changes and/or cognitive deficits,” she says. “However, since alcoholics experience multiple binges throughout their lifetime, it is important to consider that each successive binge, starting with the very first one, affords some level of damage to the brain. Therefore, theoretically, with multiple binges comes a cumulative detrimental effect where pronounced cognitive, behavioral, and structural effects are observed.”
Results will be published in the March 2013 issue of Alcoholism: Clinical & Experimental Research and are currently available at Early View.