Recent studies demonstrated that alcohol dependence and excessive alcohol consumption are associated with increased rates of obesity. In healthy light-drinkers, we and others have observed associations between elevated body mass index (BMI) and reductions in brain volumes, lower concentrations of N-acetyl-aspartate (NAA, marker of neuronal viability) and choline-containing compounds (Cho, involved in membrane turnover), and lower glucose utilization, particularly in frontal lobe—a brain region that is particularly vulnerable to the effects of alcohol dependence.
Here, we evaluated whether BMI in alcohol-dependent individuals was independently associated with regional measures of brain structure, metabolite concentrations, and neocortical blood flow.
As part of a study on the effects of alcohol dependence on neurobiology, we analyzed retrospectively data from 54 alcohol-dependent males, abstinent from alcohol for about 1 month and with BMI between 20 and 37 kg/m2 by structural MRI, perfusion MRI (blood flow), and proton magnetic resonance spectroscopic imaging.
After correction for age, smoking status, and various measures of alcohol consumption, higher BMI was associated with lower concentrations of NAA, Cho, creatine and phosphocreatine (Cr, involved in high energy metabolism), and myo-inositol (m-Ino, a putative marker of astrocytes) primarily in the frontal lobe, in subcortical nuclei, and cerebellar vermis
.The results suggest that BMI, independent of age, alcohol consumption, and common comorbidities, is related to regional NAA, Cho, Cr, and m-Ino concentrations in this cohort of alcohol-dependent individuals.
Additionally, as some common comorbid conditions in alcohol dependence such as cigarette smoking are associated with BMI, their associations with regional brain metabolite levels in alcohol-dependent individuals may also be influenced by BMI.
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