In a study involving mice, researchers have found a gene that regulates alcohol consumption. When this gene is faulty, the mice are prompted to drink excessive amounts of alcohol, suggesting a potential genetic component at play in human alcohol consumption.
The research was undertaken by researchers from five universities in the UK and was funded by the Medical Research Council (MRC), Wellcome Trust and the European Foundation for Alcohol Research (ERAB).
Results of the findings were published in the journal Nature Communications.
Researchers observed that normal mice showed no interest in alcohol presented to them, choosing a bottle of water over a bottle of diluted alcohol.
But when mice with a mutated Gabrb1 gene were offered alcohol, they consistently opted for alcohol over water, consuming nearly 85% of their daily fluid intake as alcohol.
“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,” says Dr. Quentin Anstee, consultant hepatologist at Newcastle University and joint lead author.
He notes their work is ongoing, as they want to establish whether the gene has a similar effect in humans, though he says they “know that in people alcoholism is much more complicated, as environmental factors come into play.”
A team from Imperial College London, led by Prof. Howard Thomas, introduced the subtle mutations into the genetic code of the mice at random, testing them subsequently for their alcohol preference.
This is how they isolated the gene Gabrb1, which they say changes alcohol preference so much that mice who carry one of two single “base-pair point mutations” in the gene prefer drinking alcohol about the strength of wine instead of water.
Additionally, the mice with this mutation worked extra hard to get their paws on the alcohol, by pushing a lever to obtain it.
The researchers say the mice even continued this over long periods of time, voluntarily consuming enough alcohol in 1 hour to become intoxicated and have difficulty moving.
Looking closely at the gene mutation, the team found that it caused a receptor in the brain – the GABAA receptor – to activate randomly, even when its usual trigger – an inhibitory chemical messenger called GABA – was not present.
Dr. Anstee explains that these changes were strong in the part of the brain that controls positive emotions and reward:
“The mutation of the beta1 containing receptor is altering its structure and creating spontaneous electrical activity in the brain in this pleasure zone, the nucleus accumbens. As the electrical signal from these receptors increases, so does the desire to drink to such an extent that mice will actually work to get the alcohol, for much longer than we would have expected.”
Prof. Thomas says the team knew from earlier studies in humans that the GABA system was involved in alcohol consumption, but their mouse studies reveal that a particular part of the GABAA receptor has a substantial impact, allowing them to look closely at the underlying mechanism.
“This is important when we come to try to modify this process first in mice and then in man,” he adds.
Prof. Hugh Perry, chair of the MRC’s Neurosciences and Mental Health Board, notes that addiction to alcohol puts a substantial burden on the individual and society, adding:
“There’s still a great deal we don’t understand about how and why consumption progresses into addiction, but the results of this long-running project suggest that, in some individuals, there may be a genetic component. If further research confirms that a similar mechanism is present in humans, it could help us to identify those most at risk of developing an addiction and ensure they receive the most effective treatment.”
Despite previous assumptions, a recent study showed that alcohol neither causes nor prevents depression. Medical News Today also reported on another study that suggested eating disorders and alcohol abuse share genetic factors.