GHB has been used in a medical setting as a general anesthetic and as a treatment for cataplexynarcolepsyand alcoholism. GHB is also produced as a result of fermentation, and is found in small quantities in some beers and wines, beef and small citrus fruits. Succinic semialdehyde dehydrogenase deficiency is a disease that causes GHB to accumulate in the blood. The only common medical use for GHB today are in the treatment of narcolepsy and more rarely alcoholism.
GHB is the active ingredient in Is ghb legal in the us prescription medication sodium oxybate Xyrem. Sodium oxybate is approved by the U. Food and Drug Administration FDA for the treatment of cataplexy associated with narcolepsy  and excessive daytime sleepiness EDS associated with narcolepsy.
GHB has been shown to reliably increase slow-wave sleep    and decrease the tendency for REM sleep in modified multiple sleep latency tests  . GHB is a central nervous system depressant used as an intoxicant. Its effects have been described anecdotally as comparable with ethanol alcohol and MDMA use, such as euphoriadisinhibition, enhanced libido and empathogenic states.
At higher doses, GHB may induce nauseadizzinessdrowsinessagitationvisual disturbances, depressed breathingamnesiaunconsciousnessand death. When death is associated with GHB, it is sometimes in conjunction with other drugs, such as alcohol or benzodiazepine which influence the same neurotransmitter gamma-aminobutyric acidGABA.
The effects of GHB can last from 1. Recreational doses of g generally provide a feeling of euphoria, and larger doses create deleterious effects such as reduced motor function and drowsiness. Other prodrugs, such as 1,4-butanediol 1,4-Balso have their own toxicity concerns. GBL and 1,4-B are normally found as pure liquids, but they may be mixed with other more harmful solvents when intended for industrial use, e.
GHB can be manufactured with little knowledge of chemistry, as it involves the mixing Is ghb legal in the us its two precursors, GBL and an alkali hydroxide such as sodium hydroxideto form the GHB salt. Due to the ease of manufacture and the availability of its precursors, it is not usually produced in illicit laboratories like other synthetic drugs, but in private homes by low level producers.
While available as a prescription for the rare and severe forms of sleep disorder narcolepsy in most of Europe, GHB was banned in the U. However, on 17 JulyGHB was approved for treatment of cataplexyoften associated with narcolepsy. GHB is "colourless and odorless".
GHB has been used as a club Is ghb legal in the usapparently starting in the s, as small doses of GHB can act as a euphoriant and are believed to be aphrodisiac.
Some athletes have used GHB or analogs because they have been marketed as being anabolic agents, although there is no evidence that it builds muscle or improves performance in athletes. GHB became known to the general public as a date rape drug by the late s. Consequently, the evidence and the identification of the perpetrator of the rape is often difficult. It is also difficult to establish how often GHB is used to facilitate rape as it is difficult to detect in a urine sample after a day, and many victims may only recall the rape some time after its occurrence.
There have been several high-profile cases of GHB as a date rape drug that received national attention in the United States. This is the law that made GHB a Schedule 1 controlled substance. GHB can be detected in hair. In humans, GHB has been shown to reduce the elimination rate of alcohol.
This may explain the respiratory arrest that has been reported after ingestion of both drugs. One publication has investigated deaths attributed to GHB. One report has suggested that sodium oxybate overdose might be fatal, based on deaths of three patients who had been prescribed the drug. Levels lower than this may be due to GHB or to postmortem endogenous elevations. A UK parliamentary committee commissioned report found the use of GHB to be less dangerous than tobacco and alcohol in social harms, physical harm and addiction.
In multiple studies, GHB has been found to impair spatial memoryworking memorylearning and memory in rats with chronic administration.
Although there have been reported fatalities due to GHB withdrawal, reports are inconclusive and further research is needed. Rats forced to consume massive doses of GHB will intermittently prefer GHB solution to water but, after experiments on rats, it was noted that "no rat showed any sign of withdrawal when GHB was finally removed at the end Is ghb legal in the us the week period" or during periods of voluntary abstinence.
GHB has also been associated with a withdrawal syndrome of insomniaanxiety, and tremor that usually resolves within three to twenty-one days. Baclofen has been suggested as an alternative or adjunct to benzodiazepines based on anecdotal evidence and some animal data.
GHB withdrawal is not widely discussed in textbooks and some psychiatrists, general practitioners, and even hospital emergency physicians may not be familiar with this withdrawal syndrome. Overdose of GHB can sometimes be difficult to treat because of its multiple effects on the body.
The greatest life threat due to GHB overdose with or without other substances is respiratory arrest. People are most likely to vomit as they become unconscious, and as they wake up. It is important to keep the victim awake and moving, who must not be left alone due to the risk of death through vomiting. Frequently they will be in a good mood but this does not mean they are not in danger. GHB overdose is a medical emergency and immediate assessment in an emergency department is needed.
Convulsions from GHB can be treated with the benzodiazepines diazepam or lorazepam. GHB may be quantitated in blood or plasma to confirm a diagnosis of poisoning in hospitalized patients,  provide evidence in an impaired driving arrest or to assist in a medicolegal death investigation. Urine is often the preferred specimen for routine drug abuse monitoring purposes.
In Januaryit was announced scientists had developed a way to detect GHB, among other things, in saliva. This enzyme appears to be induced by cAMP levels,  meaning substances that elevate cAMP, such as forskolin and vinpocetinemay increase GHB synthesis and release.
Conversely, endogeneous GHB production in those taking valproic acid will be inhibited via inhibition of the conversion from succinic acid semialdehyde to GHB.
It is important to note, however, that direct administration of GHB or endogenous GHB already present in the body will not be affected by valproic acid. The precise function of GHB in the body is not clear. It is known, however, that the brain expresses a large amount of receptors that are activated by GHB.
It is a precursor to GABAglutamate, and glycine in certain brain Is ghb legal in the us. GHB has neuroprotective properties and has been found to protect cells from hypoxia. GHB is also produced as a result of fermentation and so is found in small quantities in some beers and wines, in particular fruit wines.
The amount found in wine is pharmacologically insignificant and not sufficient to produce psychoactive effects. GHB has at least two distinct binding sites  in the central nervous system. GHB has been found to activate oxytocinergic neurons in the supraoptic nucleus. If taken orally, GABA itself does not effectively cross the blood—brain barrier. GHB induces the accumulation of either a derivative of tryptophan or tryptophan itself in the extracellular space, possibly by increasing tryptophan transport across the blood—brain barrier.
The blood content of certain neutral amino-acids, including tryptophan, is also increased by peripheral GHB administration. GHB-induced stimulation of tissue serotonin turnover may be due to an increase in tryptophan transport to the brain and in its uptake by serotonergic cells.
As the serotonergic system may be involved in the regulation of sleep, mood, and anxiety, the stimulation of this system by high doses of GHB may be involved in certain neuropharmacological events induced by GHB administration. However, at therapeutic doses, GHB reaches much higher concentrations in the brain and activates GABA B receptors, which are primarily responsible for its sedative effects.
GHB receptors are densely expressed in many areas of the brain, including the cortex and hippocampus, and these are the receptors that GHB displays the highest affinity for.
There has been somewhat limited research into the GHB receptor; however, there is evidence that activation of the GHB receptor in some brain areas results in the release of glutamate, the principal excitatory neurotransmitter.
GHB's effect on dopamine release is biphasic. Both the inhibition and increase of dopamine release by GHB are inhibited by opioid antagonists such as naloxone and naltrexone. Dynorphin may play a role in the inhibition of dopamine release via kappa opioid receptors.