Age of onset of adolescent binge drinking is differentially associated with cortical thickness in post‐9/11 adult Veterans

Abstract

Background Adolescence is a critical period for neural development and has been associated with high rates of alcohol abuse. This research examined potential long‐term brain and behavioral effects of early versus late‐onset adolescent binge drinking in an adult sample of post‐9/11 Veterans. Methods We compared cortical thickness measures in Veterans with a history of binge drinking that began before the age of 15 (n = 50; mean age = 32.1 years) to those with a history of binge drinking with onset after the age of 15 (n = 300; mean age = 32.1 years). Data processing was conducted with FreeSurfer. A targeted neuropsychological battery (Digit Span test, Delis‐Kaplan Executive Function System Color‐Word Interference Test, California Verbal Learning Test‐II) was used to examine the relationships between cortical thickness and attention, memory, and inhibition. A reference group of social drinkers with no history of early binge drinking (n = 31) was used to provide normative data. Results Early‐onset adolescent binge drinkers (EBD) had greater cortical thickness in several regions than late‐onset adolescent binge drinkers (LBD); both binge‐drinking groups had greater cortical thickness than the reference group. There was a stronger negative association between cortical thickness and age in EBDs than LBDs in the (i) lateral orbitofrontal cortex, (ii) supramarginal gyrus, (iii) paracentral lobule, and (iv) anterior caudal cingulate. Poorer performance on the attention and inhibition tasks in the EBDs was also associated with thicker cortices. Conclusions This study demonstrates greater cortical thickness across frontoparietal regions in adults who began binge drinking in early versus late adolescence. A stronger negative association between cortical thickness and age in the EBDs suggests that early‐onset adolescent binge drinking may be associated with accelerated cortical thinning. Thicker cortex in these regions, which are known to mediate inhibitory control, may increase impulsive behavior and contribute to the risk of alcohol addiction.

Adolescent Alcohol and Stress Exposure Rewires Key Cortical Neurocircuitry

“…Retrospective analyses conducted during adulthood may also provide clarity on cortical changes. An examination of cortical thickness and drinking patterns of United States veterans conducted after September 11, 2001, revealed that individuals with early onset binge drinking (defined as having first binge drinking episode before age 15) had thicker PFCs than post-9/11 veterans who started binge drinking in later adolescence (defined as first binge drinking episode at age 15 or later), and the early onset binge drinkers were at a higher risk for later development of AUD as well as other mental illnesses, as well as having poorer performance on attention and inhibition tests ( Bedi et al, 2021 ). Both groups had thicker PFCs than an age-matched reference group of social drinkers.…”

“…As shown in Bedi et al (2021) , adolescent alcohol consumption also poses concern for present and future psychological illness. Several longitudinal studies demonstrate that drinking alcohol in early adolescence predicts higher risk of alcohol use in late adolescence and early adulthood ( Duncan et al, 1997 ; Enstad et al, 2019 ; Magee and Connell, 2021 ).…”