Marker in Blood Has the Potential to Predict Who Will Benefit from a Treatment for Alcohol Dependence
Marker in Blood Has the Potential to Predict Who Will Benefit from a Treatment for Alcohol Dependence
From The Quarterly, Summer 2015
For people struggling to overcome an alcohol use disorder, there are a handful of medications that may help. One of these is acamprosate (sold as Campral), which seems to reduce cravings by modifying signaling in the brain. But the drug doesn’t work for everybody, and while the U. S. Food and Drug Administration approved its use for treating alcohol dependence in 2004, it has not been widely prescribed.
Acamprosate might be used more often if health professionals could predict which patients would benefit from treatment. Encouragingly, new research reported August 18th in the journal Translational Psychiatry suggests the prospect of identifying those people who are likely to respond to acamprosate with a simple blood test.
Glutamate is involved in many metabolic processes in the body, and acts as the main excitatory neurotransmitter in the brain. Alcohol dependence is triggered partly by an imbalance in excitatory and inhibitory signaling in the brain. Acamprosate is thought to help restore balance by acting on excitatory signaling pathways that use glutamate as a neurotransmitter.
In their study, the researchers collected blood samples from 120 alcohol-dependent people before they had 12 weeks of treatment with acamprosate. A second blood sample was collected at the end of the 12 weeks. Seventy-one of the participants (59 percent) abstained from alcohol throughout the treatment period. Those who consumed any alcohol during the period were considered “non-responders.”
The researchers performed tests to identify potential biomarkers that might gauge the effectiveness of acamprosate. They measured the levels of 36 substances in the blood called amino acid metabolites, comparing responders and non-responders. During the 12 weeks before treatment, glutamate was present in higher levels among responders than non-responders. As the treatment progressed, glutamate levels dropped in responders, although not in non-responders.