A recent study suggests that teenage drinking may cause anxiety in later life, and predispose a person to alcohol abuse in adulthood.
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Alcohol and anxiety, a two-way relationship
While much research has previously tied anxiety problems during adolescence with alcohol abuse later in life due to alcohol being used as a coping mechanism for the mental health issue, new studies are showing that the relationship also works in reverse.
A new study published in the online journal eNeuro has presented findings showing that drinking alcohol during adolescence can modify gene expression in the brain, leading to susceptibility to anxiety and alcohol abuse in adulthood.
Alcohol alters gene expression
Earlier this year, researchers at the University of Illinois at Chicago uncovered that adolescent binge drinking increases the risk of developing anxiety problems later in life. Their research, which was conducted with animals, highlighted that early alcohol abuse caused abnormal epigenetic programming.
They noted that adolescent alcohol use modified neural connectivity, particularly in the brain area associated with anxiety, the amygdala. While they understood that the small bits of RNA that determine gene expression, microRNA, were involved in these brain modifications caused by early drinking habits, they were unsure of how the mechanism worked.
To get to the route of this, a team also based at the University of Illinois at Chicago, led by Evan Kyzar, investigated the impact of alcohol on the microRNA within the amygdala of rats. They administered alcohol to the adolescent rats and measured the changing levels of a specific microRNA known as miR-137. The levels of miR-137 were found to increase in rats who consumed alcohol.
This increment in the microRNA led to a lower expression of the proteins fundamental to the development of healthy neuron growth and branching. Further to this, in adulthood, these rats demonstrated a marked increase in anxious behaviors in comparison to control rats, as well as an increased preference for alcohol.
Researchers then inhibited miR-137 in the amygdala and found that the anxious behaviors and alcohol preference reduced, showing that the detrimental impact of adolescent alcohol consumption was reversible through amending its impact on the microRNA.
The findings are significant in adding to the understanding of how mental health and substance abuse problems manifest. While these issues are complex, and a multitude of factors play a role in their establishment, development, and regarding how people respond to treatment, the Chicago team’s findings are an essential piece of the entire picture of mental health.
The results show that teenage drinking has the power to modify gene expression in the amygdala, leading to abnormalities in connectivity and potentially structure. Given that this impact has been found to be long-lasting, it needs to be explored further to understand how it can influence not only anxiety and alcohol abuse but other mental health disorders also.
A route to new therapies
This research has strong implications for potential new therapies for both anxiety disorder, alcohol abuse problems, and potentially other mental health disorders. In identifying the role of microRNA, and demonstrating that by inhibiting miR-137 symptoms can be reversed, a potential new avenue of therapy has opened up for exploration.
The findings also emphasize the detrimental and long-lasting impact of drinking alcohol in adolescence, which has implications for preventative methods that would be valuable to explore.
While these early findings are promising in elucidating new therapeutic pathways, much more research will need to be done to corroborate these findings in humans, given that they have so far only been demonstrated in animal models. Further to this, the development of a new therapeutic method that targets the microRNA would also require significant study in the lab before trialing it on humans.
Adolescent drinking increases anxiety, alcohol abuse later in life. Eurekalert. Available from: https://www.eurekalert.org/emb_releases/2019-11/sfn-adi111219.php