Protein May Reduce One’s Craving for Alcohol

SONY DSCNew research suggests that targeting a particular protein may reduce one’s craving for alcohol, while simultaneously protecting against alcohol-induced heart and liver damage, Medical New Today reports. A new study from researchers at the University of Iowa has found that a protein, called RGS6 (regulator of G protein signaling 6), functions through two separate mechanisms to control alcohol-seeking behavior and alcohol-induced cell death in organs.

“Given the prevalence of alcohol abuse worldwide there is a clear need for more effective therapeutics,” says lead researcher, Rory Fisher, Ph.D., professor of pharmacology in the UI Carver College of Medicine. “We propose that inhibiting this RGS6 protein could represent a new approach to counteract alcohol dependence and at the same time protect against the cell-killing actions of alcohol in the heart and liver.”

While a miracle drug may be far off, the goal of one day developing drugs to mitigate the pernicious effects of alcohol on the human body is of the utmost importance. The researchers believe that the RGS6 protein shows great promise. Research tests, according to the article, showed that mice lacking the RGS6 protein consumed less alcohol, were less susceptible to alcohol-induced reward, and had less severe alcohol withdrawal symptoms. The protein lacking mice also experienced less damage to heart and liver as well as the lining of the gut.

“To our knowledge RGS6 is the only gene with a demonstrated ability to promote alcohol-seeking behaviors while simultaneously worsening the damaging effects of alcohol consumption on the heart, stomach, intestine and liver,” Fisher says.

The researchers point out that separate drugs may need to be created to address both alcohol cravings and alcohol related organ damage, because the protein works through multiple biological pathways the article notes.

The findings were published in the online Early Edition of the Proceedings of the National Academy of Sciences (PNAS).