The majority of MRS studies in alcoholism have focused on the 3 major metabolites: NAA, Cho, and tCr. Reduced NAA/tCr and Cho/tCr ratios relative in chronic alcoholics relative to normal controls have been reported in the frontal and medial temporal lobes, cerebellum, and thalamus (Bendszus et al., 2001; Ende et al., 2005; Jagannathan, Desai, & Raghunathan, 1996). Lower NAA levels are typically interpreted as reflecting neuronal compromise (Petroff, Pleban, & Spencer, 1995). Various interpretations for Cho changes in alcoholism have been suggested (e.g., undetected, subclinical pathologies such as thiamine deficiency or liver cirrhosis) (Zahr et al., 2010). Further challenging the interpretation of changes in Cho in alcoholism is that acute alcohol intake in healthy individuals is associated with elevations of Cho (Ende et al., 2006; Tunc-Skarka, Weber-Fahr, & Ende, 2015). Metabolic changes associated with AUD appear to normalize upon discontinuation of alcohol consumption (Bartsch et al., 2007; Bendszus et al., 2001; Durazzo, Gazdzinski, Rothlind, Banys, & Meyerhoff, 2006; Parks et al., 2002).
