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Gamma-hydroxybutyrate

Gamma-hydroxybutyrate (4-hydroxybutanoic acid, C₄H₈O₃) is both a drug and a naturally occurring compound found in the central nervous system as well as in other organs such as the liver, kidneys, heart and bones. GHB is structurally similar to the ketone body beta-hydroxybutyrate. As a drug it is used most commonly in the form of a chemical salt (Na-GHB or K-GHB). The sodium salt is commercially known as sodium oxybate. more...

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Uses

Endogenous

The precise function of GHB in the body is not clear. It is an immediate precursor to GABA, a neurotransmitter which regulates awakeness, physical activity and sleep. As GABA cannot cross the blood-brain barrier, GHB obtained from food may be used for converting to GABA. GHB prevents cells from oxygen starvation, which might explain presence of the compound in vital organs. GHB was also found to have neuroprotective capabilities.

Medical

It has been used as a general anesthetic, and a hypnotic in the treatment of insomnia. GHB has also been used to treat clinical depression, and improve athletic performance. In the United States, the Food and Drug Administration permits the use of GHB under the trade name Xyrem to reduce the number of cataplexy attacks in patients with narcolepsy. In Italy, under the trade name Alcover, GHB is used in the treatment of alcoholism (50 to 100 milligrams per kilogram per day, in 3 or more divided doses), both for acute alcohol withdrawal and medium to long term detoxification.

Recreational

GHB is an intoxicant. It may be known as G, Liquid X, Liquid E. It is less commonly known as GHB, Gamma-oh, Georgia Homeboy, Georgia Hillbilly, Blue Verve, Gamma-G, Qi, scoop, or goop.

Its potential for use as a date rape drug in the 1990s led to it being placed in the US on Schedule I of the Controlled Substances Act in March, 2000. On March 20, 2001, the Commission on Narcotic Drugs placed GHB in Schedule IV of the 1971 Convention on Psychotropic Substances. In the UK it was made a class C drug in June 2003.

The sodium salt of GHB has a thin, very salty, chemical taste. At low doses, GHB can cause a state of euphoria, increased sociality and intoxication. This kind of use is particularly common at rave parties. At higher doses, GHB may induce nausea, dizziness, drowsiness, visual disturbances, depressed breathing, amnesia and unconsciousness. The effects of GHB can last from 1.5 to 3 hours.

Some chemicals convert to GHB in the stomach and blood. GBL, or gamma-butyrolactone, is one such precursor. It is 1,6 times less potent than GHB, so 1ml of GBL is equivalent to 0,4g of GHB. GBL has also a shorter onset and is longer acting than GHB. GBL has an extremely bad taste and is also known to irritate innards and skin.

Other precursors include 1,4-butanediol. There may be additional toxicity concerns with these precursors.

Mode of action

The action of GHB has yet to be fully elucidated. GHB clearly has at least two sites of action, stimulating the newly characterized and aptly named "GHB receptor" as well as the GABA_B. GHB, if it is indeed a neurotransmitter, will only reach concentrations high enough to act at the GHB receptor, as it only has weak affinity fo the GABA_B. However, during recreational usage, GHB can reach very high concentrations in the brain, relative to basal levels, and can act at the GABA_B receptor . GHBs action at the GABA_B is probably responsible for its sedative effects. GHB-mediated GABA_B receptor stimulation inhibits dopamine release as well as causes the release of natural sedative neurosteroids (like all other GABA_B agonists e.g. Baclofen). In animals GHBs sedative effects can be stopped by GABA_B antagonists (blockers).

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Gamma-Hydroxybutyrate and Withdrawal Syndrome
From American Family Physician, 9/15/01 by Richard Sadovsky

Gamma-hydroxybutyrate (GHB), originally introduced in 1960 as an anesthetic agent, has recently been abused as a nutritional supplement for bodybuilding, for euphoria, and as a sexual enhancer and an incapacitator for assault. It is illegal to possess or prescribe GHB in the United States, but it is easily available through a variety of sources. Its precursors are sold as dietary supplements. The acute effects are coma, myoclonus and bradycardia, which generally resolve rapidly without complication. Many patients presenting to the emergency department with symptoms of GHB ingestion can be discharged within a few hours. Unfortunately, discontinuation of GHB after long-term use can cause prolonged illness. Dyer and associates conducted a retrospective review of poison center records in California and identified seven consecutive cases of excess GHB use. An additional case was brought to the authors' attention by a medical examiner. The authors describe the characteristics, course and symptoms of this syndrome.

The patients all had exhibited a consistent abuse pattern of frequently ingesting large amounts of GHB. Early withdrawal symptoms include insomnia, tremor, confusion, nausea and vomiting. A patient might delay seeking medical attention until the onset of more severe symptoms that include agitation and hallucinations. The withdrawal syndrome progresses over the first two or three days with mild autonomic instability resulting in tachycardia, hypertension, tremor and diaphoresis. Central nervous system symptoms include vivid hallucinations and anxiety, as well as confusion, disorientation, delirium with agitation and combative behavior (often requiring four-point constraints and sedation). These symptoms can become episodic as the syndrome wanes, and symptoms do not always progress from mild to severe in a predictable fashion. When patients are examined in the emergency department, the differential diagnoses that must be considered include other sedative, hypnotic or alcohol withdrawal syndromes, as well as intoxication by sympathomimetic agents, serotonin syndrome and neuroleptic malignant syndrome. Metabolic causes of symptoms include thiamine deficiency and endocrine abnormalities (e.g., thyroid storm, pheochromocytoma and steroid psychoses).

Management of patients experiencing GHB withdrawal syndrome is symptomatic and supportive with a stress on sedation. Benzodiazepines and barbiturates have demonstrated efficacy in these patients.

GHB dependence is rare, probably because of its rapid absorption and elimination. Frequent dosing (every one to three hours around the clock) is required to maintain levels sufficient for physiologic adaptation and dependence. GHB appears to modulate both GAMAA and GABAB receptors, actually resulting in neuroinhibition with physiologic tolerance developing over time. This down regulation of inhibitory GABA receptors releases excitatory neurotransmitters and pathways from inhibition, playing an important role in the withdrawal syndrome that threatens whenever GHB use is discontinued.

The authors conclude that the GHB withdrawal syndrome is becoming more common, develops after frequent ingestion and is manifested by anxiety, insomnia and tremor. Early recognition of these signs, as well as the later development of severe delirium and autonomic instability, will identify patients who would benefit from in-patient medical detoxification.

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