Alcohol: the biggest gateway drug of them all.
Do you have a taste for £50 bags of teething powder cut with cocaine? Do you keep blowing your pay-cheque on blow? Well, it might be your functioning alcoholism that's fuelling your expensive cocaine habit – at least, according to a study done on rats.
A team at Columbia University Medical Center has found that just a ten day window of alcohol consumption is enough to make rats more vulnerable to compulsive cocaine use, even if that tasty white stuff comes with the price of a light electric shock. The research revealed that alcohol breaks down proteins in a region of the brain critical for reward-based memory (the nucleus accumbens), enabling addiction.
To assess the effects of alcohol on cocaine addiction, Dr Edmund Griffin and his colleagues studied a group of rats that was given alcohol in their cages for two hours a day, against a control group which was given a water bottle instead. Ten days later, both groups were given "voluntary cocaine access" and were presented with a lever. Five consecutive presses resulted in a cocaine reward, but only after receiving a mild electrical shock on the fourth press.
The researchers observed that test subjects in the alcohol-primed group sought cocaine with more tenacity than their teetotal counterparts. When drug access was cut off, alcohol primed rats pressed the lever in the hope of a bump an average of 58 times, while non-alcohol exposed rats pressed the lever 18 times.
"Most people who use an illicit drug do not go on to develop addiction," says Griffin, who believes their work can help us understand "how an early exposure to something like alcohol can actually tip the balance and increase a person's vulnerability to developing addiction".
Are you getting flashbacks of your mum telling you alcohol is a gateway drug yet?
You may be rolling your eyes, but observations of adolescent drug use patterns suggest that we try some drugs – i.e. "gateway drugs" like alcohol – prior to others. The million dollar question is if and how use of these drugs might increase the risk of using a different class of drugs.
These findings suggest that alcohol degrades the "molecular brake pads" inside the reward circuitry of the brain, specifically histone deacetylases 4 and 5, much like previous research has suggested nicotine has the same molecular effect on the brain.
Griffin hopes these findings will lead to the study of the interconnection of other drugs, as well as the development of more effective intervention methods. Their work, he believes, "gives us a handle, a way to start intervening and actually thinking about other molecular types of interventions".