Spanagel et al (2014) argue that calcium ion alone is the active moiety of acamprosate. This finding contravenes the conventional wisdom on the action of acamprosate in relapse prevention in alcoholism (Littleton, 1995). In closing, the authors request that their findings be independently replicated; in particular, there is a need for validation in humans. To this end, we analyze the impact of calcium levels on drinking behavior in the framework of a large RCT, the PREDICT study (Mann et al, 2012).

The paper by Spanagel et al is based on three preclinical studies that support the conclusion that calcium rather than N-acetylhomotaurinate is the active moiety of acamprosate. The authors argue that, compared with calcium, the sodium salt of N-acetylhomotaurinate is ineffective at reducing excessive alcohol drinking, alcohol-seeking, or relapse-like drinking behavior. In addition, they show animal brain profiles 30 min after single i.p. injections of both calcium and sodium N-acetylhomotaurinate, each dosed at 200 mg/kg. As similar concentrations of each compound reached the entire brain, the authors argue that differences of bioavailability do not have a role in the observed behavioral effects.

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