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Study IDs Brain Area That May Be Key to Alcohol Addiction, Treatment

(Fall 2018) A new study from Sweden suggests that there is a biological reason for alcoholism and that taking this into account could result in the development of a medication-based treatment.

Barring caffeine, alcohol is the most prevalent drug in the world. We know most people do not develop a substance abuse disorder with alcohol, while a smaller percent does. Recent research with lab rats may now shed some light upon why this is the case.

Mammals are hardwired to like sweetness, as the sugar turns into energy quickly and increases the chances of survival. Armed with this information, the researchers gave a group of rats the option between a calorie-free sweetened liquid or alcohol. Most of the subjects picked the sweet solution; however, approximately 13% of the rats, when allowed to pick between the two, regularly chose alcohol. (It is interesting to note here that the general occurrence of human alcohol addiction is near 15%—very similar to the portion of rats who grew to prefer alcohol.) Rats who became “addicted” still opted for alcohol, even when it was paired with an electric shock to the foot.

Researchers found that a gene called GAT-3 was not strongly expressed in the “addicted” rats. The gene usually works to help control the amount of GABA in the brain, which is a chemical confirmed to be associated with alcohol dependence. Co-researchers at the University of Texas at Austin discovered through the examination of brain samples from deceased humans with alcohol use disorder that the amount of GAT-3 was noticeably less than normal in the amygdala, which is thought to be the area of the brain that processes emotions. It’s theorized that the gene’s malfunction would also affect the brain’s reward system related to pleasurable things such as food, gambling and sex.

The Swedish researchers think they have pinpointed a potential addiction treatment founded on their study and have partnered with a drug maker. They anticipate testing the substance, which lowers levels of GABA, on humans in the near future.

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