Author: 
Dr. George Koob, NIAAA Director

NIAAA-Funded Study Explores the Brain Mechanisms Mediating the Potential Harmful Effects of Teen Binge Drinking

As CADCA coalitions know all too well, underage drinking and its consequences remain a major public health challenge.  Fortunately, research advances continue to improve our understanding of this seemingly intractable problem.  For example, according to a new study supported by the National Institute on Alcohol Abuse and Alcoholism, underage binge drinking can interfere with normal gene processes during adolescence and can disrupt brain development in ways that lead to excessive drinking in adulthood.  The new findings contribute to our understanding of the alcohol-induced brain changes that lead to alcohol problems in adulthood.

Previous studies have shown that people who start drinking before the age of 15 are four times more likely to meet the criteria for alcohol dependence at some point in their lives than those who started drinking at age 21.  Patterns of drinking also matter, especially since young people consume more than 90 percent of their alcohol by binge drinking.

The new study, published in the journal Neurobiology of Disease, was led by Subhash C. Pandey, Ph.D., at the University of Illinois at Chicago. To model adolescent binge-drinking in humans, the researchers gave rats alcohol intermittently throughout adolescence.  The animals exhibited changes in behavior that lasted into adulthood, for example, increased anxiety-like behaviors and increased alcohol intake.

Prior research has shown that a brain structure known as the amygdala is involved in anxiety and alcohol-drinking behaviors.  When researchers analyzed the alcohol-exposed rats, they found that DNA and proteins within amygdala cells were modified in a way that made genes within the amygdala DNA less active.

In particular, they found reduced activity of two genes that nerve cells need to form new connections with each other, brain-derived neurotrophic factor and activity-regulated cytoskeleton-associated protein,. The diminished activity of these genes persisted in adulthood, long after alcohol exposure stopped, and the researchers also observed fewer nerve connections in the amygdala of these affected adult rats.  The researchers also showed that a drug that blocks the activity of the protein, histone deacetylase class 2, HDAC2, could restore the activity of these genes and promote nerve cell connectivity.  The treated animals also exhibited less anxiety and reduced alcohol intake.

The researchers plan additional studies of this brain neurochemical target to investigate its possible use in reversing the persistent harmful effects of adolescent alcohol exposure.

While laboratory research studies like this may seem miles away from the schools and playing fields of our neighborhoods, the information they provide about the adolescent brain may help us develop future treatments for adults with alcohol use disorder.