Binge drinking in adolescence increases the risk of cortical thinning – News Block

Throughout adolescence, the brain undergoes extreme development and is especially vulnerable to the harmful effects of alcohol consumption. According to the results of a study, young people whose excessive alcohol consumption began in adolescence have reduced the thickness of cortical gray matter and altered neurotransmission.

Previous studies have indicated that recurrent heavy drinking in adolescence is related to central nervous system changes in adulthood, such as increased inhibitory neurotransmission and reduced gray matter volume. The current study looked at the connection between neurotransmission and gray matter thickness.

The study involved 26 young adults with a history of heavy drinking, as well as a group of 21 controls who drank little or no alcohol. They were monitored for 10 years, from ages 13 to 18 to approximately 25 years.

Changes in gray matter volume were measured using magnetic resonance brain imaging, and cortical activity was measured using electroencephalography and simultaneous transcranial magnetic stimulation.

In adolescents who had a history of heavy drinking, there was a reduction in average gray matter thickness in some brain areas, as well as higher average N45 potential, compared with adolescents who drank little or no alcohol.

The N45 potential is indicative of the inhibitory activity of the GABA and glutamate excitatory neurotransmitter systems. In the high alcohol intake group, reduced gray matter thickness was associated with elevated N45 potential, specifically in the parietal and frontal lobes.

The results suggest that the thinning of the cerebral cortex seen in young adults with a history of heavy drinking since adolescence is related to impaired neurotransmission, particularly in the parietal and frontal lobes. However, further studies are required to assess the mechanisms underlying these results.

Binge drinking in adolescence increases the risk of cortical thinning

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