Scientists have discovered that drinking alcohol releases feel-good chemicals in an area of the human brain often referred to as the “pleasure centre”.

The rush of chemicals released in specific brain locations after drinking produce feelings of pleasure and reward.

Previously scientists had deduced from animal studies that the pleasurable effects of alcohol come from the release of endorphins in the brain.

A new research used scanning technology to “light up” the brain regions of drinkers, showing where it has the biggest impact.

A study from the Ernest Gallo Clinic and Research Centre at the University of California marks the first time that endorphin release in two regions of the brain, the nucleus accumbens and orbitofrontal cortex, in response to drinking alcohol has been directly observed in humans.

Research leader Jennifer Mitchell, assistant professor of neurology, said: “This is something that we’ve speculated about for 30 years, based on animal studies, but haven’t observed in humans until now.

“It provides the first direct evidence of how alcohol makes people feel good.”

The researchers used PET imaging (positron emission tomography) to observe the immediate effects of alcohol in the brains of 13 heavy drinkers and 12 matched “control” subjects who were not heavy drinkers.

Scientists have discovered that drinking alcohol releases feel-good chemicals in an area of the human brain often referred to as the “pleasure centre”

According to researchers, drinking led to a release of endorphins in all those taking part. The more endorphins released in the nucleus accumbens, the greater the feelings of pleasure reported by each drinker.

However, as levels of endorphins released in the orbitofrontal cortex went up, heavy drinkers felt more intoxicated – but not those in the control group.

Prof. Jennifer Mitchell said: “This indicates that the brains of heavy or problem drinkers are changed in a way that makes them more likely to find alcohol pleasant, and may be a clue to how problem drinking develops in the first place.

“That greater feeling of reward might cause them to drink too much.”

Before drinking, the volunteers were given injections of radioactively tagged carfentanil, an opiate-like drug that binds to sites in the brain called opioid receptors, where endorphins also bind.

This allowed researchers to map what happened in the brain as the receptor sites “lit up” on PET scans, says a report in the journal Science Translational Medicine.

Volunteers were then each given a drink of alcohol, followed by a second injection of radioactive carfentanil, and scanned again with PET imaging. As the natural endorphins released by drinking were bound to the opioid receptor sites, they prevented the carfentanil from being bound.

By comparing areas of radioactivity in the first and second PET images, the researchers were able to map the exact locations – areas of lower radioactivity – where endorphins were released in response to drinking.

The researchers found endorphins released after drinking bind to a specific type of opioid receptor, the Mu receptor, which they claim could be a target for developing drugs to treat or prevent alcohol addiction.

Senior study author Howard Fields said the result suggests a possible way to improve on existing medication.

Although it is effective, the drug naltrexone – which prevents binding at several opioid receptor sites – is not widely accepted as a treatment for alcohol dependence since it can make people feel depressed.

Howard Fields said: “Some people stop taking it because they don’t like the way it makes them feel.

“Naltrexone blocks more than one opioid receptor, and we need to know which blocking action reduces drinking and which causes the unwanted side effects.

“If we better understand how endorphins control drinking, we will have a better chance of creating more targeted therapies for substance addiction.”

Scientists say low to moderate doses of alcohol release feel-good chemicals, while high doses appear to fail to release them and may stimulate other systems in the brain leading to anxiety and depression.