Adolescence is a period of social and environmental changes and dramatic biological development, including of the brain. During adolescence, the brain undergoes significant growth and remodeling, which raises concerns about alcohol's effects on normal brain development. It is also the time of life during which drinking, binge drinking, and heavy drinking (binge drinking five or more times in the past 30 days) all ramp up significantly. To address this critical public health issue NIAAA currently supports two consortia: one studying animals, the other studying human adolescents. Collectively, early results from both consortia suggest that alcohol can negatively impact the developing adolescent brain.
In FY 2013 the NIAAA-supported National Consortium on Alcohol and Neurodevelopment in Adolescence (NCANDA) launched a multisite study using an accelerated longitudinal design to investigate whether persistent changes in neural and behavioral functioning result from adolescent alcohol use; whether the same processes that confer adaptability of the adolescent brain to its environment also make it more vulnerable to alcohol-induced changes in structure and/or functioning; and whether such changes may increase risk for future substance use disorder. To date, the five NCANDA sites collectively have enrolled approximately 800 youth, ages 12 to 21, and will capture brain images as well as psychological and behavioral data from these participants before and after they start to drink. In a recent analysis, NCANDA researchers used high resolution magnetic resonance imaging to assess the brain structure of 40 healthy adolescents, ages 12-17, half of whom initiated heavy drinking during a three year follow up. The researchers found that youth who transitioned from no or minimal substance use to heavy drinking, compared to youth who did not initiate drinking, had certain structural anomalies at baseline, prior to the initiation of alcohol use. These included smaller left cingulate, pars triangularis, and rostral anterior cingulate volume, and less right cerebellar white matter volumes in the right cerebellar frontal cortex, an area important for executive functioning. In addition, over time, participants who initiated heavy drinking compared to non-drinking youth showed significantly greater volume reduction in the left ventral diencephalon, left inferior and middle temporal gyrus, and left caudate and brain stem. These differences, which did not predate the transition to heavy drinking, occurred in regions important for sensory integration, feedback processing, motor control, habit learning, visual object recognition, and language comprehension. Whereas some reduction in brain volume over time is normal and the result of synaptic pruning during adolescent brain development, adolescents who transitioned to heavy drinking during the study showed significantly larger reductions in brain volumes in the identified areas than non-drinking control subjects.
In FY2010, NIAAA launched the Neurobiology of Adolescent Drinking in Adulthood (NADIA) initiative, which currently supports animal studies to understand the neurobiological mechanisms by which adolescent alcohol exposure affects brain function and behavior into adulthood. Findings from NADIA have and will continue to inform research to help us understand the changes we see in humans. For example, NADIA researchers have demonstrated that intermittent adolescent alcohol exposure produces higher voluntary drinking, increased risky choice behavior, and reduced behavioral flexibility in adulthood, as well as hippocampal impairments, persistent alterations in amygdala function, and decreased cholinergic markers in the adult brain. In a recent study, researchers used rodent models of adolescent binge drinking and adult alcohol dependence to gain insight into how alcohol affects white matter integrity in the frontal cortex of the brain. They found that adolescent binge drinking reduced the size of anterior branches of the corpus callosum and this neuropathology correlated with higher relapse to drinking in adulthood. The researchers also demonstrated that adolescent binge drinking was associated with damaged myelin, the insulating sheath that forms around the nerve cells that comprise white matter, in the medial prefrontal cortex in adulthood, as well as reduced density of myelin in the medial prefrontal cortex in adolescence. Heavier drinking in adolescence also predicted worse performance on a working memory task in adulthood. These results suggest that adolescent binge drinking may affect white matter integrity in the medial prefrontal cortex through reduction of myelin, and these changes may contribute to deficits in executive function in adulthood.
Results such as these have spurred, NIDA, NIAAA, NCI, and NICHD to propose the Adolescent Brain Cognitive Development (ABCD) study through the Collaborative Research on Addiction at NIH (CRAN) initiative. Informed by NCANDA, the proposed longitudinal study of approximately 10,000 adolescents will recruit participants prior to the initiation of any substance use and follow them over 10 years using imaging and neurocognitive testing to study the risks and long-term effects of adolescent use of alcohol and other substances of abuse, including tobacco, alone and in combination, on health and well-being.