The number of therapeutic drugs available for the treatment of alcohol use disorders (AUDs) is limited, and a well-tolerated, self-administrable drug is much needed. Subgroups of alcohol-dependent individuals, for example, individuals with heredity for AUD, may respond differently to pharmacological treatments, particularly to drugs affecting the serotonergic system in the brain.
Clinical observations and case reports indicate that mirtazapine, a widely used and well-tolerated antidepressant drug, which increases both noradrenaline and serotonin release but simultaneously blocks serotonergic (5-hydroxytryptamine)3 receptors, reduces alcohol consumption. Moreover, drugs affecting serotonergic (5-hydroxytryptamine)3 receptors have been shown to work differently in individuals with heredity for AUD.
This double-blind, randomized, placebo-controlled, 2-armed clinical trial aimed to establish whether mirtazapine lowers alcohol consumption in male high consumers. The study population was also subgrouped in accordance with heredity for AUD. After 2 lead-in weeks of single-blind placebo, 59 males were randomly assigned to receive 8 weeks of treatment with 30-mg mirtazapine daily (n = 29) or placebo (n = 30). The main outcome was self-reported alcohol consumption (drinks per day) measured by an alcohol diary. The alcohol consumption was calculated as weekly mean during the study period compared with baseline. The data were analyzed in accordance with intention to treat and per protocol.
The results suggest that high consumers of alcohol with a heredity for AUD benefit from treatment with mirtazapine.
The results of this study did not support an advantage of mirtazapine over placebo on alcohol consumption in the intention-to-treat analysis. However, mirtazapine could be an alternative to available treatments for alcohol dependence in patients with heredity for AUD.
From the *Addiction Biology Unit, Section of Psychiatry and Neurochemistry, Institute of Neuroscience and Physiology, The Sahlgrenska Academy, University of Gothenburg; and †Sahlgrenska University Hospital Beroendekliniken, Gothenburg, Sweden.
Received February 15, 2012; accepted after revision September 10, 2014.
Reprints: Andrea de Bejczy, MD, Addiction Biology Unit, Department of Psychiatry and Neurochemistry, Institute of Neuroscience and Physiology, The Sahlgrenska Academy, University of Gothenburg, Blå Stråket 15, 413 45 Göteborg, Sweden (e-mail: email@example.com).