Gene Mutation May Cause Alcohol Abuse and Excessive Drinking

Have a problem with drinking? A certain gene may be responsible. Scientists have discovered a gene that regulates alcohol consumption and when faulty can cause excessive drinking. The findings could reveal a little bit more about alcohol abuse and could potentially help researchers develop new treatments.

In order to examine alcohol abuse a little more closely, the researchers studied mice. They introduced subtle mutations into the genetic code at random throughout the genome of the mice and then tested the rodents for alcohol preference. In the end, the scientists found that the gene Gabrb1 changes alcohol preferences so strongly that mice carrying either of two single base-pair point mutations in this gene preferred drinking alcohol over water.

In fact, the researchers showed that mice carrying the mutation were willing to work to obtain an alcohol-containing drink by pushing a lever. Unlike normal mice, these mutated mice continued to do so over long periods. In addition, they would also voluntarily consume sufficient alcohol in an hour to become intoxicated and even have difficulty coordinating their movements.

"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," said Quentin Anstee, one of the researchers, in a news release. "But there is the real potential for this to guide development of better treatments for alcoholism in the future."

So what exactly does this mutation do? The mutation of the gene Gabrb1 codes for the beta 1 subunit, which is an important component of the GABA A receptor in the brain. The mutation of the beta1 containing receptor actually alters its structure and creates spontaneous electrical activity in the brain in this pleasure zone, the nucleus accubens.

The findings could be huge for better understanding how alcoholism impacts not just mice, but also humans. Currently, the researchers are looking forward to the future in order to determine whether a similar gene could also be responsible in humans.

The findings are published in the journal Nature Communications.