Adolescence is a critical period of brain development that is particularly vulnerable to the harmful effects of alcohol use. Heavy drinking during adolescence can lead to changes in the structure and function of the brain that persist into adulthood.
In this article, we review the findings from a recent study by Juntunen et al. (2023) that examined the association between cortical thickness and cortical activity in young adults who had a history of heavy drinking since adolescence.
Cortical thickness is a measure of the thickness of the outer layer of the brain, called the cerebral cortex, which is responsible for many cognitive functions such as memory, attention, language, and reasoning. Cortical activity is a measure of the electrical activity of the neurons in the cortex, which reflects the communication between different brain regions.
Cortical activity can be measured using transcranial magnetic stimulation (TMS) and electroencephalography (EEG). TMS is a technique that uses magnetic pulses to stimulate specific areas of the brain, while EEG records the brain’s response to the stimulation.
Juntunen et al. (2023) conducted a follow-up study of 26 young adults who had a history of heavy drinking since adolescence, and 21 young adults who consumed little or no alcohol at all. The study participants were followed for 10 years, from the age of 13–18 until around the age of 25.
The researchers measured cortical thickness from magnetic resonance images (MRI) of the brain, and cortical activity from TMS-EEG recordings. They focused on a specific component of the cortical response called the N45 potential, which reflects the balance between inhibitory and excitatory neurotransmission in the cortex. Inhibitory neurotransmission is mediated by gamma-aminobutyric acid (GABA), while excitatory neurotransmission is mediated by glutamate.
The results showed that young adults who had a history of heavy drinking since adolescence had lower cortical thickness in several regions of the brain, especially in the frontal and parietal lobes, compared to young adults who consumed little or no alcohol at all. Moreover, young adults who had a history of heavy drinking since adolescence had higher N45 potentials, indicating greater inhibitory neurotransmission, especially in the frontal lobe, compared to young adults who consumed little or no alcohol at all.
Furthermore, lower cortical thickness was associated with higher N45 potentials in certain brain regions, suggesting that cortical thinning and altered neurotransmission are correlated in young adults who had a history of heavy drinking since adolescence.
These findings provide evidence that adolescent drinking is associated with cortical thinning and altered neurotransmission in young adults, which may have implications for their cognitive functioning and mental health. However, more research is needed to understand the causal mechanisms underlying these associations, and whether they are reversible or not.
The study also has some limitations, such as the small sample size, the lack of information on other factors that may influence brain development (such as genetics, nutrition, stress, etc.), and the use of self-reported alcohol consumption data.
In conclusion, Juntunen et al. (2023) have conducted a novel study that sheds light on the effects of adolescent drinking on brain development in young adulthood.
Their findings suggest that heavy drinking during adolescence can lead to cortical thinning and altered neurotransmission in young adults, which may affect their cognitive and emotional functioning.
These findings highlight the importance of preventing and reducing alcohol use among adolescents, as well as providing support and treatment for young adults who have a history of heavy drinking since adolescence.
Juntunen A., Määttä S., Könönen M., Kallioniemi E., Niskanen E., Kaarre O., Kivimäki P., Vanninen R., Tolmunen T., Ferreri F., Kekkonen V. (2023). Cortical thickness is inversely associated with transcranial magnetic stimulation-evoked N45 potential among young adults whose heavy drinking began in adolescence. Alcohol: Clinical and Experimental Research . DOI: 10.1111/acer.15119