New research in Sweden found that the inhibition of impulse control may be related to the lack of a significant brain enzyme.
The study, published in the journal Molecular Psychiatry, was the first to find a specific molecule in the brain that could explain why a drinker’s control impulses become impaired. Prior to this study, the hypothesis for alcohol dependence was thought to be due to damage in the brain’s frontal lobe, which is linked to impulsivity and decision-making. This new data may allow scientists to design improved therapies to aid alcoholics and combat excessive drinking.
The research showed that the brain enzyme, PRDM2, may be the cause of impairment. Enzymes are molecules in living cells of organisms that activate reactions. The researchers hypothesized that PRDM2 came into play regarding impulse control in the nerve cells of the frontal lobe of the brain. This hypothesis was based on the idea that PRDM2 impacts the way in which impulse control signals are delivered throughout the brain.
As quoted by The Fix, the study’s lead author, Markus Heilig, told the Times, “PRDM2 controls the expression of several genes that are necessary for effective signaling between nerve cells. When too little enzyme is produced, no effective signals are sent from the cells that are supposed to stop the impulse.”
In order to test their theory, researchers stalled the production of PRDM2 in alcohol dependent brains of test rats. This disruption caused the rats to consume higher volumes of alcohol, despite bad side effects. Test rats were highly prone to alcohol dependence when this enzyme was turned off in the brain’s nerve cells, and those who were previously dependent, but not presently, often relapsed once the enzyme was disrupted.
To verify that PRDM2 reduction was the cause and not an effect of alcohol dependence, the same study was repeated on non-alcohol dependent rats. Again, once PRDM2 production was turned off in the brains of these rats, they demonstrated less impulse control.
Past research on addiction and the brain focused on the frontal lobe, particularly in relation to cocaine addiction. In 2011, a study done by Cambridge examined 120 human brains, half of them cocaine dependent. This research found that the cocaine-dependent brains’ frontal lobes included abnormal structures, likely linked to their compulsive behaviors related to cocaine use.
The study, led by Dr. Karen Ersche, demonstrated the cyclical nature of both the cause and effect of addiction. The amount of grey matter lost in the brain was caused by the duration of cocaine use. Moreover, the more grey matter that was lost led to greater compulsion to use cocaine.
At the time of this 2011 study, Ersche expressed the significance of these findings, in that the research showed a direct relationship between the duration of cocaine abuse and the users’ compulsion and dependence on the drug. She also suggested that the study’s findings would aid innovators to create the proper treatment needed for drug addicts.
In the long run, this most recent discovery may help pinpoint specific brain chemistry that relates to addiction, allowing psychologists and scientists to produce better treatment programs and medications to help addicts or anyone who is drug or alcohol dependent. But for now, the research team’s head researcher, Heilig, says this new study shows that addiction shouldn’t be stigmatized, due to its scientifically proven biological foundation.
“We see how a single molecular manipulation gives rise to important characteristics of an addictive illness,” said Heilig. “Over the long term, we want to contribute to developing effective medicines, but over the short term the important thing, perhaps, is to do away with the stigmatization of alcoholism.”