Search Here

For most people, alcohol consumption is a part of their social life. People might choose to drink at a party, celebration or a night out. For some people, however, controlling how much they drink can be difficult. In a new study, researchers examined the role of genetics in people who become alcoholics. The team discovered a gene that regulates alcohol consumption. When this gene becomes faulty, it can lead to excessive drinking.

For this study, the researchers from the Imperial College London, Newcastle University, Sussex University, University College London, the University of Dundee and the Medical Research Council Mammalian Genetics Unit (MGU) at Harwell, used mice models and identified the gene, Gabrb1. The team randomly introduced mutations to this particular gene and observed the mice's alcohol preference. The mice were offered diluted alcohol and water and were allowed to choose which one they wanted to drink.

The researchers found that a mutation increased the mice's preference to alcohol with some of them becoming intoxicated within the first hour. These genetically altered mice were also more likely to work for the alcohol. The team observed that the mice continued to push a lever over long periods in order to get access to alcohol. The researchers analyzed the effects of the genetic mutation on the brain and found that the mutation triggered a receptor to activate without the help of the usual GABA trigger.

"It's amazing to think that a small change in the code for just one gene can have such profound effects on complex behaviors like alcohol consumption," Dr. Quentin Anstee, Consultant Hepatologist at Newcastle University and joint lead author said. "We are continuing our work to establish whether the gene has a similar influence in humans, though we know that in people alcoholism is much more complicated as environmental factors come into play. But there is the real potential for this to guide development of better treatments for alcoholism in the future."

The study was published in Nature Communications.