<p>Alcohol consumption elevates circulating acetate. Prior studies showed that acute alcohol reduces brain glucose uptake and increases brain acetate oxidation. Previously we showed that heavy drinkers have elevated capacity to oxidize brain acetate. Here we repeat the study, adding individuals with alcohol use disorder (AUD). Four groups were enrolled. The analysis data set included Light Drinkers (LD, <i>n</i> = 13, female = 5), at-risk Heavy Drinkers (HD, <i>n</i> = 15, female = 7), AUD patients in long-term recovery (≥6 months; AUD_LTR, <i>n</i> = 6, female = 1), and a separate group of AUD treatment-seekers (AUD_Tx, <i>n</i> = 12, female = 1) underwent medically supervised detoxification, scanned at ~1 week abstinence (<i>n</i> = 9) and 1 month (<i>n</i> = 10). Seven AUD_Tx participants successfully completed scans at both time points. We infused participants with [2-¹³C]acetate during magnetic resonance spectroscopy (MRS) of ¹³C-glutamate (Glu) and ¹³C-glutamine (Gln) in the brain, to measure the cerebral metabolic rate for acetate (CMR_Ac) and the neuronal tricarboxylic acid cycle relative to glutamate-glutamine neurotransmitter cycling (V_tcaN/V_cycle; Energy Per Cycle: EPC). There was a group effect for CMR_Ac (<i>p</i> = 0.007) primarily owing to lower CMR_Ac in AUD_Tx at 1 week. Furthermore, higher CMR_Ac was observed among HD compared to LD participants, as previously reported. CMR_Ac was similar between the AUD_LTR and HD groups. In a separate within-subject comparison among AUD_Tx participants, CMR_Ac increased after 1 month to levels similar to those of LD. EPC was similar among the groups, representing normal glutamate-glutamine cycling versus energetics. In summary, abstinence reversed the lower acetate oxidation in early AUD, showing that just a few weeks of recovery can normalize this metabolic abnormality.</p>