Gamma Hydroxybutyrate: An Ethnographic Study of Recreational Use and Abuse (Report‪)‬

Gamma hydroxybutyrate (GHB) is a neuroactive substance that is currently used clinically under the name sodium oxybate (brand name Xyrem[R]), for the treatment of nareolepsy, and its use is being investigated for the treatment of other causes of excessive daytime sleepiness. GHB was originally synthesized in 1961 by Henri Laborit in an attempt to create a substance structurally similar to gamma-amino butyric acid (GABA) that could cross the blood-brain barrier (Laborit 1964). GHB has been considered for use as a general anesthetic (Laborit, Larcan & Kind 1962) and a treatment for alcohol and other chemical addictions (Gallimberti et al. 1992; Fadda et al. 1989), as well as nareolepsy (Scharf et al. 1985). In the 1980s and 1990s when GHB was sold legally in health food stores as a sleep-promoting agent, data showing that GHB increases endogenous secretions of growth hormone (Takahara et al. 1977) led bodybuilders to use it as a supplement to try to gain muscle mass. However, significant anabolic effects have never been clinically demonstrated. GHB occurs naturally in the brain, being found in the substantia nigra, thalamus, hypothalamus, cerebellum, and certain areas in the cerebral cortex (Vayer et al. 1988; Bessman & Fishbein 1963; Snead & Morlet 1981). GHB has several different actions in the brain. Most significantly it is a potent central nervous system (CNS) depressant, binding to GABA-B receptors in the brain, though not in the spinal cord (Ito, Ishige & Zaitsu 1995; Bernasconi, Lauber & Marescaux 1992; Marescaux, Vergnes & Bernasconi 1992). It also causes elevations of acetylcholine (Giarman & Schmidt 1963), serotonin (Waldmeier & Dehr 1963), and dopamine (Godbout et al. 1995; Cheramy, Nieoullon & Glowinski 1977; Bustos & Roth 1972) in distinct parts of the brain though various direct and indirect pharmacologic actions. With respect to dopamine, GHB has a biphasic effect, inhibiting dopamine release at low doses and enhancing dopamine release at higher doses (Hechler, Peter & Gobaille 1993; Hechler, Gobaille & Bourguignon 1991). GHB is also associated with increased release of an opioid-like substance in the striatum (Cheramy, Nieoullon & Glowinski 1977) and decreased norepinephrine release in the hypothalamus (Miguel, Aldegunde & Duran 1988). Both effects are likely involved in GHB's sedating and euphorogenic effects.