Alcoholism & Addiction

Study Examines Response to Alcohol in Development of AUDs

It can be difficult to identify those at risk of developing alcohol use disorders (AUDs) as they are influenced by multiple genetic, environmental and behavioral factors. According to a recent Science Daily release, a new study has examined how a person’s level of response (LR) to alcohol – which is closely linked to the development of AUDs – is related to “gene sets” rather than individual genes.

Findings from this study show that glutamate receptor signaling genes that enable brain cells to respond to chemicals, and then to communicate a response, are involved in a person’s LR.

"Alcohol dependence (AD) is a very complex disorder," said Geoff Joslyn in the Science Daily, Joslyn is a senior scientist at the Ernest Gallo Clinic and Research Center and corresponding author for the study.

"We know that inherited genes account for about half of a person’s risk of becoming AD but this genetic risk is spread across many genes. To simplify the genetic risk, we took advantage of clinical and epidemiological studies that have shown that a person’s innate response to alcohol is related to their risk of becoming AD.

Individuals that have a low response to alcohol, that is people who must drink more than the average person to become drunk, are at a greater risk of becoming AD. We studied this alcohol response because we think it is a sub-component of AD and is much less genetically complex."

Joslyn and colleagues analyzed data on subjects from a long-term study called the San Diego Sibling Pair investigation. All subjects were tested for their LR to alcohol, and a Gene Set Enrichment Analysis (GSEA) was done to determine if a gene set demonstrates a greater genetic association than would normally be found.

Joslyn noted the study suggests that natural, inherited variability in glutamate signaling may contribute to variability in alcohol response. It is hypothesized that it is possible to alter alcohol response through therapies that target altering glutamate signaling.
 

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