Altered Anterior Cingulate Neurochemistry in Emerging Adult Binge Drinkers with a History of Alcohol-Induced Blackouts
Article first published online: 11 FEB 2014
Copyright © 2014 by the Research Society on Alcoholism
Alcoholism: Clinical and Experimental Research
Volume 38, Issue 4, pages 969–979, April 2014
How to Cite
Silveri, M. M., Cohen-Gilbert, J., Crowley, D. J., Rosso, I. M., Jensen, J. E. and Sneider, J. T. (2014), Altered Anterior Cingulate Neurochemistry in Emerging Adult Binge Drinkers with a History of Alcohol-Induced Blackouts. Alcoholism: Clinical and Experimental Research, 38: 969–979. doi: 10.1111/acer.12346
- Issue published online: 9 APR 2014
- Article first published online: 11 FEB 2014
- Manuscript Accepted: 22 NOV 2013
- Manuscript Received: 16 JUL 2013
- MMS. Grant Numbers: K01 AA014651, R01 AA018153
- Emerging Adult;
- Magnetic Resonance Spectroscopy;
- Gamma Amino-Butyric Acid;
- Anterior Cingulate Cortex;
- Binge Alcohol
Binge alcohol consumption is associated with multiple neurobiological consequences, including altered neurophysiology, brain structure, and functional activation. Magnetic resonance spectroscopy (MRS) studies have demonstrated neurochemical alterations in the frontal lobe of alcohol users, although most studies focused on older, alcohol-dependent subjects.
In this study, neurochemical data were acquired using MRS at 4.0 Tesla from emerging adults (18 to 24 years old) who were binge alcohol drinkers (BD, n = 23) or light drinkers (LD, n = 31). Since binge drinking is also associated with increased prevalence of experiencing an alcohol-induced blackout, BD were stratified into alcohol-induced blackout (BDBO) and non-blackout (BDN) groups.
Overall, BD had significantly lower gamma amino-butyric acid (GABA) and N-acetyl-aspartate (NAA) in the anterior cingulate cortex (ACC) than LD. When stratified by blackout history, BDBO also had lower ACC glutamate (Glu) than LD. No group differences in MRS metabolites were observed in the parietal-occipital cortex. Lower ACC GABA and Glu remained significant after accounting for lower gray matter content in BD, however, NAA differences were no longer evident. In addition, low ACC GABA levels were associated with greater alcohol use consequences, and worse response inhibition and attention/mental flexibility in BD.
These data indicate that binge drinking affects frontal lobe neurochemistry, more so in those who had experienced an alcohol-induced blackout. Characterization of the neurochemical profiles associated with binge alcohol consumption and blackout history may help identify unique risk factors for the later manifestation of alcohol abuse and dependence, in young individuals who are heavy, frequent drinkers, but who do not meet the criteria for alcohol abuse disorders.