Frontal Brain N-Acetylaspartate at Treatment Entry is Related to Future World Health Organization Risk Drinking...

The purpose of this study was to assess the viability of regional brain metabolite levels of individuals with alcohol use disorder (AUD) at treatment entry as a biomarker of posttreatment levels of alcohol use, categorized according to the World Health Organization risk drinking levels (WHO-RDL).

Eighty-five individuals initiating treatment for AUD (16 ± 13 days after last alcohol consumption) and 45 light/nondrinking controls completed a 1.5T proton multislice magnetic resonance spectroscopic imaging study. N-acetylaspartate (NAA), a marker of neuronal viability, and other metabolites were quantitated for cortical gray matter, white matter, and select subcortical regions. Individuals with AUD were classified according to their posttreatment alcohol consumption as abstainers (n = 42), low-risk (n = 20), or higher risk (n = 23) participants based on the WHO-RDL taxonomy.

Within frontal gray matter, higher risk participants exhibited significantly lower NAA levels than light/nondrinking controls and abstainers but did not differ from low-risk participants. Higher risk participants had significantly lower NAA concentration in frontal white matter than all groups who did not significantly differ from one another. Higher risk participants showed significantly lower parietal white matter NAA than light/nondrinking controls and abstainers; low-risk and higher risk participants did not differ from one another. Across higher risk and low risk, lower frontal gray matter and white matter NAA were related to shorter periods of abstinence before first posttreatment alcohol consumption and longer posttreatment duration of alcohol resumption. There were no significant group differences in myo-inositol or choline- or creatine-containing compound concentrations.

Frontal and parietal lobar NAA concentrations, near treatment entry, are associated with WHO-RDL categorized posttreatment alcohol consumption levels and may serve as predictive biomarkers of clinical outcomes following treatment for AUD.