Are the effects of gamma-hydroxybutyrate (GHB) treatment partly physiological in alcohol dependence?

Am J Drug Alcohol Abuse. 2008;34(2):235-6; author reply 237-8. doi: 10.1080/00952990701877177.


It has been hypothesized that the therapeutic effects of Gamma-hydroxybutyrate (GHB) in alcohol dependence could be related to ethanol-mimicking action of the drug and that GHB could reduce alcohol craving, intake and withdrawal by acting as a "substitute" of the alcohol in the central nervous system. Nevertheless, alcohol being the strongest trigger of craving and intake, it is difficult to ascribe reduction of craving and intake to ethanol-mimicking activity of GHB. I have recently proposed that alcohol/substance dependence could result from a GHB-deficiency-related dysphoric syndrome in which alcohol/substances would be sought to "substitute" for insufficient GHB effect. GHB is the sole identified naturally occurring gamma-aminobutyric acid B (GABA (B)) receptor agonist. Here, I propose that exogenous GHB might in fact "substitute" for deficient endogeneous GHB and represent true substitutive treatment for GHB-deficiency. And that baclofen and GHB could both compensate for deficient effect of the physiological GABA (B) receptor agonist(s).

Publication types

  • Comment
  • Letter

MeSH terms

  • Alcoholism / metabolism*
  • Alcoholism / rehabilitation
  • Baclofen / pharmacology
  • GABA Agonists / pharmacology
  • GABA-B Receptor Agonists*
  • Humans
  • Sodium Oxybate / blood*
  • Sodium Oxybate / pharmacology*


  • GABA Agonists
  • GABA-B Receptor Agonists
  • Sodium Oxybate
  • Baclofen