Abstract
Alcohol-use disorders are thought to be heterogeneous in etiology, pathophysiology and response to treatment. One hypothesized contributor to this variability is the common A118G polymorphism of the µ-opioid receptor gene, OPRM1. This article critically evaluates the evidence that the A118G substitution affects subjective, behavioral and neurobiological responses to alcohol and the opioid receptor antagonist, naltrexone. Although screening of patients in a clinical setting remains premature, results suggest the A118G substitution may influence one etiological pathway to alcoholism, for which naltrexone pharmacotherapy is more effective.
Financial & competing interests disclosure
M Leyton received research funds from GlaxoSmithKline (Ontario, Canada) in 2006–2007 to carry out a study on naltrexone. The authors have no other relevant affiliations or financial involvement with any organization or entity with a financial interest in or financial conflict with the subject matter or materials discussed in the manuscript apart from those disclosed.
No writing assistance was utilized in the production of this manuscript.