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Alcohol Clin Exp Res. 2006 Mar;30(3):539-51.

Brain metabolite concentrations and neurocognition during short-term recovery from alcohol dependence: Preliminary evidence of the effects of concurrent chronic cigarette smoking.

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San Francisco Veterans Administration Medical Center, San Francisco, California 94121, USA.



Longitudinal studies of brain tissue metabolite recovery in short-term abstinent alcoholics have primarily investigated the frontal lobes and cerebellum with variable results. Preliminary proton magnetic resonance spectroscopic imaging (1H MRSI) suggested that chronic cigarette smoking exacerbates alcohol-induced brain injury in 1-week abstinent alcoholics. However, the potential effects of chronic cigarette smoking on the recovery of alcohol-induced brain injury have not been studied.


Multislice short-echo time 1H MRSI was used to measure longitudinal changes in common brain metabolites in 25 recovering alcohol-dependent individuals (RA), retrospectively assigned to smoking (n = 14) and nonsmoking (n = 11) subgroups. Recovering alcohol-dependent individuals in longitudinal analyses were studied after approximately 7 and 34 days of abstinence from alcohol. In cross-sectional analyses, 36 RA (19 smokers, 17 nonsmokers) with approximately 34 days of sobriety were compared with 29 light drinkers (LD). Relationships between neurocognition and metabolite concentrations in abstinent RA were also examined.


Over 1 month of abstinence from alcohol, RA, as a group, showed significant increases of regional N-acetylaspartate (NAA; marker of neuronal viability) and choline-containing compounds (Cho; marker of cell membrane synthesis/turnover) primarily in frontal and parietal lobes. These increases appeared to be driven by nonsmoking RA. Cross-sectional results indicate that metabolite levels in RA at 35 days of sobriety are not significantly different from those in LD in most regions, except for lower NAA and Cho in parietal WM and subcortical structures. However, metabolite levels at that time appear to be strongly modulated by smoking status. The patterns of metabolite-neurocognition relationships were different for nonsmoking and smoking RA.


Within the first weeks of sobriety, regional brain NAA and Cho levels increased, but metabolite levels did not normalize in all brain regions after 35 days of sobriety. Neurobiologic recovery in RA appeared to be adversely affected by chronic smoking. Greater consideration of the effects of continued cigarette smoking on the neurobiologic and neurocognitive recovery of alcohol-dependent individuals is warranted.

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