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Charles P. O’Brien, MD, PhD

Arch Gen Psychiatry. 2008;65(2):132-133.

	Since this article does not have an abstract, we have provided the first 150 words of the full text and any section headings.

The article in this issue of the Archives by Anton et al¹ is the latest chapter in the story of a treatment translated from animal models to successful clinical trials that, now with genomic evidence, may refine patient selection and improve outcome. A seminal alcoholism discovery was that alcohol significantly activates the endogenous opioid system in some but not all animal and human subjects, so that part of the reward from alcohol ingestion is mediated via opioid peptides. The evidence for this is that pharmacological blockade of opioid receptors reduces alcohol drinking in a dose-related fashion and blocks the increase in dopamine in the ventral striatum associated with alcohol ingestion. Altshuler et al² reported the dose-related effect of naltrexone on decreasing ethanol drinking in 10 of 21 rhesus monkeys that were willing to self-administer alcohol. This report led to dose-ranging studies in persons with alcoholism . . . [Full Text of this Article]

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