Binge drinking ‘is in your GENES’: Scientists blame a genetic fault for making some people consume ‘much more’ alcohol to feel good (Excerpt)

Scientists have discovered a pathway in the brain that causes the neurons in the ‘pleasure centre’ to release dopamine when we drink alcohol

Some may genetically have a weaker pathway and at risk of binge drinking

‘Extremely exciting’ findings could lead to treatment for alcohol use disorders

Source: https://www.dailymail.co.uk/

By VANESSA CHALMERS

25 October 2018

Unable to ever stop at one drink? Well, now science may finally have the answer – and your parents could be to blame.

Researchers claim binge drinking could be triggered by a genetic fault that means some people need more alcohol to enjoy themselves.

Scientists already know alcohol causes the neurons in a region called the ventral tegmental area (VTA) to release dopamine.

But now the exact pathway alcohol uses to cause the reaction has been uncovered by researchers at the University of Illinois at Chicago.

However, some people naturally have less of the KCNK13 channel – meaning they need to drink ‘much more’ to get the same pleasure.

Professor Mark Brodie, author of the research, told MailOnline this would lead to an ‘increased predisposition to binge drink’.

The study, published in the journal Neuropharmacology, used mice in a range of experiments to test their hypothesis.

In one experiment, the scientists genetically reduced the KCNK13 channel in their VTAs by about 15 per cent compared with normal mice.

The KCNK13-deprived mice drank 20-30 per cent more alcohol than their normal counterparts.

Professor Brodie said: ‘We believe mice with less KCNK13 in the VTA drank more alcohol in order to achieve the same reward from alcohol as normal mice.’

He said this was ‘presumably because alcohol was triggering the release of less dopamine in their brains’.

However, Professor Brodie admitted they ‘don’t know’ how much more alcohol a person with reduced KCNK13 expression may drink.

Another test observed the neuronal response to alcohol in the VTA region for mice with less KCNK13 compared to normal mice.

Neurons of the genetically modified mice were 50 per cent less responsive to alcohol than those from the normal mice.

Professor Brodie said the research offers hope of an ‘extremely exciting’ target for drugs that could help alcoholics.

‘Theoretically, there may be several ways to target this protein pharmacologically to treat alcohol use disorders’, he said.

‘A drug that prevented alcohol from binding to this ion channel may be useful in blocking some of the rewarding properties of alcohol.’

Targeting this channel would only dampen the effects of alcohol and not the brain’s response to pleasure in general.

Globally, more than three million people die from alcohol-attributed deaths each year.

In England alone, 337,000 hospital admissions were due to alcohol in the year 2016-2017, and there were 5,507 alcohol-specific deaths, according to the NHS.

In the US, an estimated 88,000 people die from alcohol-related causes annually, according to figures.

Researchers are unsure how many people may have a reduced KCNK13 channel. They plan to conduct further trials to investigate.