Abstract
Binge drinking is an increasing social problem, particularly in adolescents. Cognitive deficits may occur as a result of such drinking patterns, although the biochemical processes involved in such changes are unclear. Recent studies in a rat model of binge drinking have shown that the innate immune system is activated in both the periphery and a specific brain region, the hippocampus. It was therefore of interest to ascertain whether a) inflammatory markers were present in the blood of University students, N=24, identified as binge drinkers for at least 2 years, and b) whether cognitive function was impaired, by comparison to controls, N=24. There was a significantly increased mean plasma TNFα value in male binge drinkers by comparison to controls, P>0.007, while the female binge drinkers showed a significantly lower mean value for TNFα, A¯Â€Â P<0.05,A¯Â€Â¬ by comparison to controls. An inflammatory profile, as assessed by increased plasma values of IL-6, was evident in binge drinkers, although the values did not reach significance. Although there were significant differences between the controls and binge drinking individuals with respect to the Trail-Making test and semantic fluency, both of which were increased, (possibly indicating a compensation mechanism), no gross neuropsychological changes were identified in the binge drinking group. This may relate to the fact that such individuals were University students with high cognitive capacity. Continued activation of the innate immune system in such ‘binge drinking’ individuals may ultimately contribute to neuropsychiatric deficits.
Highlights
Intermittent alcohol abuse, ‘binge drinking’ is a commonly used regime of ethanol drinking by adolescents where excessive amounts of alcohol are consumed over a short period of time (1-2 days) followed by a period of abstinence
The mean level of plasma TNFα was significantly elevated in male binge drinkers by comparison to the controls, while a lower mean level of this cytokine was evident in female binge drinkers (Figure 1)
Monocytes isolated from the blood of each group showed a robust response in the release of IL-6 and TNFα after ex vivo stimulation with LPS, no significant differences in activation were discernible between the binge drinkers and controls (Figure 2)
Summary
Intermittent alcohol abuse, ‘binge drinking’ is a commonly used regime of ethanol drinking by adolescents where excessive amounts of alcohol are consumed over a short period of time (1-2 days) followed by a period of abstinence. The potential harm to the brain has been of major concern since there is active neurogenesis during this period of development, which could be impaired by such alcohol abuse, leading to various cognitive deficits which include visual perception and memory [1]. The biochemical processes which underlie the pathogenesis have been the subject of various animal studies, in rats and mice, as yet, there have been few investigations of adolescents actively engaged in binge drinking. Rat studies have shown that binge drinking will induce an inflammatory state, both in the periphery, alveolar macrophages [2] as well as in specific brain areas, such as the nucleus accumbens [2] and the dentate gyrus in the hippocampus [3]. As a result of each binge drinking period, may lead to the release of damaging pro-inflammatory cytokines, as well as glutamate, which could reduce cell proliferation as well as the survival and function of new neurons
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