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The Metabolism of Alcohol: Risk and Protective Factors

Abstract

Purpose: Abstract for poster submission to VCU Poster Symposium for Undergraduate Research and Creativity Title: The Metabolism of Alcohol: Risk and Protective Factors Background: In 2002, it was reported by the National Institutes of Health that 60.3% of college aged students (18-22) drank alcohol in the past month of being asked, as compared to 51.9% of those not in college. They also found that 20% of college students met the criteria for at least one alcohol use disorder (AUDs)1. Many genes have been linked to an increased risk for AUDs and how individuals with various ethnic backgrounds respond to alcohol. Genes that metabolize alcohol are obvious candidate genes for alcohol-related phenotypes. The purpose of this presentation is to synthesize information about the key genes involved in alcohol metabolism, as documented in the literature. Methods: The information about each gene was found through a literature search using databases including PubMed, Google Scholar, and cited references from relevant papers. For database searches, the names of the genes were used as well as terms such as AUDs, alcohol metabolism, and alcohol and aldehyde dehydrogenase. The focus of the presentation will be relevant to college-aged students, but rely on research done in college and adult populations due to a lack of sufficient college- aged gene-based studies in this area. Results: Alcohol metabolism genes affect how individuals process and respond to alcohol. The main genes that have been studied are alcohol and aldehyde dehydrogenase genes. Alcohol dehydrogenase genes, like ADH1B and ADH1C, first metabolize ethanol (alcohol) into the by-product acetaldehyde and acetaldehyde is then metabolized by aldehyde dehydrogenase genes, like ALDH2, into the waste product acetate2. Many of the adverse effects associated with alcohol consumption are due to the build up of acetaldehyde. Some of these effects include facial blushing, nausea, headaches, and other similar alcohol sensitivity symptoms3,6. Acetaldehyde builds up in an individuals body after alcohol consumption if he or she has a super- active isoenzyme from the ADH1B and/or ADH1C genes and/or a slow ALDH2 enzyme. Individuals with the super-active alcohol dehydrogenase isoenzyme and slow aldehyde dehydrogenase enzyme are less likely to develop AUDs due to the negative effects from excess acetaldehyde in the body4,5,6. However, this also implies that individuals who do not exhibit the described protective phenotype are more likely to endorse increased drinking behaviors and AUDs. Spit for Science: the VCU Student Survey is currently investigating these genes and their association with alcohol consumption and alcohol use disorder symptoms. Due to the diverse nature of the sample, the researchers are able to explore ethnic differences in these alcohol metabolism genes and their effects. Implications: In general, the more public knowledge about these genes and research findings, the more at-risk individuals can get help and diagnosis. A better understanding of aggregate effects of alcohol metabolism genes, as well as more information regarding ethnic differences in the distribution of genetic variants which impact alcohol processing, will assist researchers and health professionals working with those at risk for AUDs.https://scholarscompass.vcu.edu/uresposters/1137/thumbnail.jp

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