thickness increases were observed in those with alcohol use disorder (AUD) during 7.3 months of abstinence.
A recent study, published in the journal Alcohol in August, delved into the effects of long-term abstinence on cortical thinning in the brains of individuals with alcohol use disorder (AUD). The researchers noted that previous studies have shown a link between AUD and widespread cortical thinning, but there is limited research on how cortical thickness changes during extended periods of abstinence.
According to the researchers, cortical thickness is a distinct measure from cortical volume and surface area, and it reflects the number and density of cells in the cortex. This includes factors such as cell size, number of spines and synapses, and myelination. They also pointed out that the ratio of glial cells to neurons in the cerebral cortex is approximately 0.7:1, making cortical thickness a potential marker for the overall health of the cells in the cortex.
The study focused on participants with AUD at one week, one month, and a little over seven months of abstinence. They also included a control group of individuals who had never smoked. Using magnetic resonance imaging, the researchers measured cortical thickness in 34 regions of interest in the brain. They found that over the course of 7.3 months of abstinence, there were significant linear increases in cortical thickness in 25 of the 34 regions.
Interestingly, the rate of change from one week to one month was greater than the rate of change from one month to 7.3 months in 19 of the regions. This suggests that the greatest changes in cortical thickness occur in the first month of abstinence. After 7.3 months of abstinence, individuals with AUD showed similar levels of cortical thickness as the control group in 24 of the 34 regions. However, there were still differences in cortical thickness in certain regions, such as the banks superior temporal gyrus, post central, posterior cingulate, superior parietal, supramarginal, and superior frontal cortices. These differences were primarily driven by thinner cortices in individuals with AUD who also had proatherogenic conditions compared to the control group.
The researchers also noted that in individuals with AUD who were actively smoking, there was a negative correlation between the number of pack-years smoked and cortical thickness recovery in the anterior frontal regions. This suggests that smoking may have a detrimental effect on cortical thickness recovery during abstinence.
Overall, the study found widespread increases in cortical thickness during 7.3 months of abstinence in individuals with AUD. This highlights the potential for the brain to recover from the effects of alcohol use disorder with extended periods of abstinence.
