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GHB is also produced as a result of fermentation and so is found in small quantities in some beers and wines, particularly fruit wines such as that made from guavas. However, the amount of GHB found in wine is insignificant and not sufficient to produce any effects.
EndogenousCells produce GHB by reduction of succinic semialdehyde. People with the disorder known as succinic semialdehyde dehydrogenase deficiency, also known as gamma-hydroxybutyric aciduria, have elevated levels of GHB in their urine, blood plasma and cerebrospinal fluid.[1]
MedicalGHB 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 to improve athletic performance. In Italy, under the trade name Alcover (ATC code N07BB), 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.[citation needed] An author/scientist by the name of Gian Luigi Gessa has been researching alcoholism and the effects of various drugs to persons afflicted with said disease for the past ten years. His studies in 1998 note that GHB, as a pharmaceutical aid, can be much less toxic and much more effective than the leading pharmaceutical compound (disulfiram).[citation needed] 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 clinical trials Xyrem significantly reduced cataplexy attacks at a dose of 6000–9000mg per night. This is around three times the dose used recreationally, but almost all narcolepsy patients in the clinical trials were already stabilized on CNS stimulants such as modafinil; in patients not prescribed modafinil this dosage could be dangerous and should be reduced appropriately. Also the prescribing information for Xyrem states that patients should take the dose immediately before going to bed, and then a second dose 3–4 hours later. The maximum dose taken at one time should not exceed 4500 mg. Patients with hepatic insufficiency (compromised liver function) have slower clearance of GHB and require reduced doses, typically half the normal dose. Xyrem oral solution is standardised to 500 mg Na.GHB / 1 mL water, buffered to pH 7.5 with malic acid. When GHB is used in its sodium or potassium salt form, a significant quantity of excess sodium or potassium may be consumed, which should be taken into consideration by people with heart conditions, hypertension or compromised renal function. The bioavailability of sodium GHB is considerably reduced when it is consumed with food, and so it is advised to wait at least two hours after eating before consuming the dose. Because of its strong sedative effects, patients should not drive or operate heavy machinery for at least six hours after taking sodium GHB. Adverse effects from Xyrem in clinical trials included: headache, nausea, dizziness, nasopharyngitis, somnolence, vomiting, urinary incontinence, confusion, dyspnea, hypoesthesia, paresthesia, tremor, vertigo, and blurred vision. Out of the 717 patients and 182 healthy volunteers who took part in the trials (899 total), two of them died from drug overdoses, although only one of these involved GHB.[2] RecreationalImage:Gamma-hydroxybutyrate.jpg gamma-hydroxybutyrate powder GHB is a CNS depressant used as an intoxicant. It has many street names, including Gina, Georgia Home Boy, G, GB, GBH, Juice, Fantasy, Liquid Ecstasy, Liquid X, Gamma-OH and Jungle Juice. The drug is often represented as a date rape drug, much in the same way as alcohol and Rohypnol. It is sometimes referred to as liquid ecstasy due to its tendency to produce euphoria and sociability and its use in the dance party scene, however the effects of GHB are quite different from those of MDMA. The sodium salt of GHB has a thin, very salty, chemical taste. At low doses, GHB can cause a state of euphoria, increased libido, increased sociability and intoxication. This kind of use is particularly common at rave parties. At higher doses, GHB may induce nausea, dizziness, drowsiness, agitation, visual disturbances, depressed breathing, amnesia and unconsciousness. The effects of GHB can last from 1.5 to 3 hours, or even longer if large doses have been consumed or if it is mixed with alcohol. Use among athletes and bodybuilders is also known, as GHB is thought to increase growth hormone release; there is some evidence supporting these claims but actual efficacy for this purpose is unclear. In general the doses used recreationally are between 500 mg and 3000 mg, corresponding to approximately 0.5–3 mL of liquid if the concentration is 1 gram / 1 mL (which is not always the case). When used as a recreational drug, GHB may be found as a pure liquid, or as GHB salt dissolved in water, generally at a standardised concentration of 1 gram / 1 mL and so is twice the strength of the Xyrem solution sold legally for medical use. GHB salt dissolved in water is notoriously dangerous as the concentration of GHB may not be known, and so the actual dose of GHB being consumed can be difficult to judge accurately. Since GHB sold for recreational use is subject to no standardisation it can be impossible to verify the actual concentration of GHB solution bought on the illicit market. More than 1 gram of sodium GHB can be dissolved in 1 mL of water, and so sodium GHB solution can actually be stronger than pure GHB liquid. Other salt forms such as potassium GHB, calcium GHB and magnesium GHB have also been reported, but the sodium salt is by far the most common. Some chemicals convert to GHB in the stomach and blood. GBL, or gamma-butyrolactone, is one such prodrug. Other prodrugs include 1,4-butanediol. There may be additional toxicity concerns with these precursors. 1,4-B and GBL are normally found as pure liquids, although they may be mixed with other more harmful solvents when intended for industrial use, e.g. as paintstripper or varnish thinner. GHB (Gama Hydroxybutyric Acid) is a synthetic depressant produced in clandestine labs. While available as a prescription for sleep disorders in some other countries GHB was banned (in the U.S.) by the FDA in 1990 because of the dangers associated with its use. However, on July 17th, 2002, GHB was approved for treatment of a rare form of narcolepsy. Most of the GHB used in the U.S. is illegally manufactured within its borders. Like Rohypnol, GHB and its analogs are considered "date rape" drugs because they can be mixed with liquids (even water) and a victim wouldn't notice by smelling or looking at it. GHB, by itself, has a soapy or salty taste. It is often claimed that when mixed in a drink it may be difficult to detect. However, many recreational GHB users disagree with that claim:
Mode of actionThe 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 GABAB. GHB, if it is indeed a neurotransmitter, will normally only reach concentrations high enough to act at the GHB receptor, as it has relatively weak affinity for the GABAB. However, during recreational usage, GHB can reach very high concentrations in the brain, relative to basal levels, and can act at the GABAB receptor as well.[3] GHB's action at the GABAB is probably responsible for its sedative effects. GHB-mediated GABAB receptor stimulation inhibits dopamine release as well as causes the release of natural sedative neurosteroids (like other GABAB agonists e.g. Baclofen). In animals GHB's sedative effects can be stopped by GABAB antagonists (blockers). The relevance of the GHB receptor in the behavioural effects induced by GHB is more controversial. It seems hard to believe that the GHB receptor is not important when it is densely expressed in many areas of the brain, including the cortex, as well as it being the high affinity site of GHB action. There has only been limited research into the GHB receptor. However, evidence shows that it causes the release of glutamate, which is a stimulatory neurotransmitter. Drugs which selectively activate the GHB receptor but not the GABAB receptor, such as trans-4-hydroxycrotonic acid and 4-(p-chlorobenzyl)-GHB, cause convulsions in animals and do not produce GHB appropriate responding. It does not seem that activation of the GHB receptor alone explains GHB's addictive properties; indeed research using selective GABAB agonists and analogues of GHB which are selective agonists for the GHB receptor but do not activate GABAB, suggest that both the GHB receptor and the GABAB receptor are important for dopamine release and consequently abuse liability. Compounds which activate only one of the receptors but not both, do not seem to induce acute dopamine release or produce the abuse potential typical of GHB itself. One can propose a scheme where high doses of GHB are sedative through its action at the GABAB receptor, while a lower dose is stimulatory via activation of GHB receptors. This may explain the otherwise paradoxical mix of sedative and stimulatory properties typical of GHB intoxication, as well as the so-called "rebound" effect, experienced by individuals using GHB as a sleeping agent, where they awake suddenly after several hours of GHB-induced deep sleep. That is to say, that over time, the concentration of GHB in the system decreases (because of metabolism) below a threshold for stimulating GABAB receptor function, and simply stimulates the GHB receptor, leading to wakefulness. Recently, similar molecules to GHB, such as 4-hydroxy-4-methylpentanoic acid have been synthesised and tested on animals, in order to gain a better understanding of GHB's mode of action[4]. Analogues of GHB such as 3-methyl-GHB, 4-methyl-GHB and 4-phenyl-GHB have been shown to produce similar effects to GHB in some animal studies, but these compounds are even less well researched than GHB itself. Of these analogues, only 4-methyl-GHB (gamma-hydroxyvaleric acid, GHV) and its prodrug form gamma-valerolactone (GVL) have been reported as drugs of abuse in humans, and on the available evidence seem to be less potent but more toxic than GHB, with a particular tendency to cause nausea and vomiting. Other prodrug ester forms of GHB have also rarely been encountered by law enforcement, including 1,4-diacetoxybutane, methyl-4-acetoxybutanoate and ethyl-4-acetoxybutanoate, but these are generally covered by analogue laws in jurisdictions where GHB is illegal and little is known about them beyond their presumably delayed onset and longer duration of action. The intermediate compound 4-hydroxybutaldehyde is also a prodrug for GHB, however as with all aldehydes this compound is caustic and is strong-smelling and foul tasting; actual use of this compound as an intoxicant is likely to be unpleasant and result in severe nausea and vomiting. GHB is also metabolised into GABA by the enzyme GABA transaminase. This is only a minor route of metabolism and its significance to the pharmacological action of GHB is not known, although there is likely to be some increase in GABA levels when GHB is consumed in quantity. Also note that both of the metabolic breakdown pathways shown for GHB can run in either direction depending on the concentrations of the substances involved, so the body can make its own GHB either from GABA or from succinic semialdehyde. Under normal physiological conditions the concentration of GHB in the body is rather low, and the pathways would run in the reverse direction to what is shown here to produce endogenous GHB. However, when GHB is consumed for medical or recreational purposes its concentration in the body is much higher than normal, which changes the enzyme kinetics so that these pathways operate to metabolise GHB rather than producing it. DangersAs with pure alcohol, the dose-response curve is very steep, and proper dosing of illegal GHB can be difficult since it often comes as a salt dissolved in water, and the actual amount of GHB and/or other additives per "capful" can vary. Legal GHB comes in standardized doses and is free from contaminants, so it is much safer (cf. legal alcohol vs. bathtub gin). Also, like pure alcohol, small doses of GHB are considered safe, but high doses can cause unconsciousness, convulsions, vomiting, suppression of the gag reflex and respiratory depression. These effects vary between persons and are dose dependent. Synergy of its sedative effects are seen when combined with other CNS depressants such as alcohol, benzodiazepines (e.g. diazepam), barbiturates, and others. Another complication is the difference in pharmacokinetics between GHB and its two prodrugs, 1,4-B and GBL. 1,4-butanediol is converted into GHB in the body by two enzymes alcohol dehydrogenase and aldehyde dehydrogenase, which gives it a delayed onset of effects and a longer duration of action. GHB is then further metabolised, again by alcohol dehydrogenase and aldehyde dehydrogenase, into the inactive succinate. If alcohol has also been consumed this can saturate the dehydrogenase enzymes and so delays the conversion of 1,4-B into GHB, meaning that 1,4-B takes much longer to take effect and people may re-dose thinking it hasn't done anything, leading to an accidental overdose later on once it finally takes effect. 1,4-B itself can also contribute to the enzyme saturation, so when alcohol and 1,4-B are consumed together it produces a complex and somewhat unpredictable interaction between the varying levels of alcohol, 1,4-B and GHB present in the body. Alcohol also makes the GHB last longer in the body by competing for dehydrogenase enzymes and hence delaying the conversion of GHB into succinate. The other precursor gamma-butyrolactone (GBL) is rapidly converted into GHB by lactamase enzymes found in the blood. GBL is more lipophillic (fat soluble) than GHB and so is absorbed faster and has higher bioavailability; paradoxically this can mean that GBL has a faster onset of effects than GHB itself even though it is a prodrug. The levels of lactamase enzyme can vary between individuals and GBL is not active in its own right, so people who have never tried GBL before may have delayed or less effects than expected; however once someone has taken GBL a few times the production of lactamase enzymes is increased and they will feel the effects like normal. Because of these pharmacokinetic differences, 1,4-B tends to be slightly less potent, slower to take effect but longer acting than GHB, while GBL tends to be more potent and faster acting than GHB, and lasts around the same duration. The growth hormone releasing effects of GHB which have led to its use by bodybuilders are actually mediated by the metabolite succinate, and so these beneficial effects can be achieved by taking succinate instead of GHB which avoids the potential dangers, abuse potential and illegal status of GHB itself.[citation needed] Alcohol worsens both CNS depression and vomiting, so combination of alcohol with GHB or its precursors is a particularly dangerous combination. Another factor to be considered is that people who drink alcohol regularly tend to induce expression of their dehydrogenase enzymes and thus have higher levels of these enzymes than people who do not drink alcohol regularly; this means that regular alcohol drinkers will both convert 1,4-B into GHB more rapidly, and also break down GHB into succinate faster than people who don't drink alcohol. This multitude of different factors can make the interactions between 1,4-B, GHB and alcohol very complicated and highly variable between different individuals. Death while using GHB is most likely when it is combined with alcohol or other depressant drugs, however as with all substances, an overdose of GHB alone may be lethal. A review of the details of 194 deaths attributed to or related to GHB over a ten year period[4] found that most were from respiratory depression caused by interaction with alcohol or other drugs; several were from choking on vomit and asphyxiating; remaining causes of death included motor vehicle and other accidents. The review included 70 cases where high levels of GHB were found post-mortem without concomitant ingestion of other drugs or alcohol. Determining conclusively whether someone's death was caused by GHB is very difficult because a lab test will always detect the presence of some GHB in the human body, and levels of GHB can vary in the same individual depending on what part of the body is tested. GHB is a naturally occurring substance that is always present in everyone, but little research has been done on what levels are normal in what parts of the body at what times. There have been no systematic studies into the effects of GHB if taken chronically in humans, and hence whether prolonged use of GHB causes any bodily harm remains unknown. 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.[5] Treatment of overdoseOverdose of GHB can be difficult to treat because of its multiple effects on the body. GHB tends to cause rapid unconsciousness at doses above 3500 mg, with single doses over 7000 mg often causing life-threatening respiratory depression, and higher doses still can induce bradycardia and consequent heart failure. Because of the faster and more complete absorption of GBL relative to GHB, its dose-response curve is steeper, and overdoses of GBL tend to be more dangerous and problematic than overdoses involving only GHB or 1,4-B. As well as causing these depressant effects, GHB overdose also often produces twitches or convulsions, especially when combined with stimulants such as amphetamines. Also GHB tends to cause nausea and vomiting, particularly when combined with alcohol, and so a patient may be simultaneously unconscious, vomiting and convulsing all at the same time. Overdoses where the patient has consumed GHB along with both alcohol and amphetamine-based stimulants are often particularly problematic; the stimulants may cause the patient to slip in and out of consciousness and they may be confused and combative, fighting off medical staff while half-awake before lapsing back into unconsciousness again. Care should be taken when attempting to sweep foreign bodies out of the mouth of a patient who presents with a suspected GHB overdose. The patient may bite very hard, and sometimes will not let go. The most likely risk of death from GHB overdose is inhalation of vomit while unconscious. This risk can be partially prevented by laying the patient down in the recovery position. People are most likely to vomit as they become unconscious, and as they wake up. This is best managed in a hospital setting, but if the patient is not in a hospital, it is very important that someone stays with them until they become fully unconscious, to keep them in the recovery position and to check how deeply unconscious the person becomes. Then someone needs to stay with them to keep checking their pulse and breathing rate. Finally someone needs to stay with them until they fully wake up. This is important, because people tend to become conscious enough to roll onto their backs just before they start to vomit again, but often while they are still too deeply unconscious to protect their own airway. This makes the period while people are waking up particularly dangerous. Convulsions from GHB can be treated with diazepam or lorazepam, even though these are also CNS depressants they are GABAA agonists, whereas GHB is primarily a GABAB agonist so the benzodiazepines do not worsen CNS depression as much as might be expected. Most stimulants are not effective at counteracting the unconciousness from GHB, but intravenous injection of cholinergic drugs such as atropine, neostigmine and physostigmine can quickly reverse the effects of the GHB and cause rapid awakening; this can be dangerous however as these drugs lower the convulsion threshold and so can make convulsions worse. For this reason, these drugs are seldom used in most countries, although in France and Italy where there is a much longer history of medical use of GHB, physostigmine treatment for GHB overdose is more common. The best treatment of a more serious GHB overdose is co-administration of lorazepam with physostigmine, and the dose of both drugs must be carefully titrated to avoid worsening either the CNS depression or the convulsions. Overdoses with larger quantities of GHB or more particularly GBL (generally 10,000mg or more) can stop both heart and breathing, and may require restarting the heart with a defibrillator and mechanical ventilation, which often requires admission into an intensive care unit in a hospital. It can be very dangerous to look after someone who is unconscious as a result of drug overdose if the attending party does not have proper medical training. When an individual presents with a suspected GHB overdose and is unconscious, the first priority should be to check their pulse and breathing. If the patient is taking less than 8 breaths per minute, and if their pulse is less than 60 a minute (both numbers are for adults), then the appropriate course of action is to start CPR and call an ambulance. Unless the amount of GHB consumed by the unconscious patient is known to be 5000 mg or less, then calling an ambulance is appropriate in most cases. Medical staff cannot legally contact the police unless they have reason to believe that failure to do so will result in serious and imminent harm to the patient or to other people. It should be taken into consideration that if a non-medically trained person assumes responsibility themself for someone who has overdosed on GHB, rather than contacting trained professionals, then they could potentially face manslaughter charges if the patient died, wheras if they have contacted an ambulance as soon as it became apparent that medical attention was required they cannot be held to have been criminally negligent even if the patient dies before the ambulance arrives. A newer synthetic drug SCH-50911 which acts as a selective GABAB antagonist, quickly reverses GHB overdose in mice, however this treatment has yet to be tried in humans and it is unlikely that it will be researched for this purpose in humans due to the illegal nature of GHB making clinical trials unethical and the lack of medical indemnity coverage inherent in using an untested treatment for a life-threatening overdose. (1) Allen L, Alsalim W. Best evidence topic report. Gammahydroxybutyrate overdose and physostigmine. Emergency Medicine Journal. 2006 Apr;23(4):300-1. (2) Michael H, Harrison M. Best evidence topic report: endotracheal intubation in gamma-hydroxybutyric acid intoxication and overdose. Emergency Medicine Journal. 2005 Jan;22(1):43. (3) Carai MA, Colombo G, Gessa GL. Resuscitative effect of a gamma-aminobutyric acid B receptor antagonist on gamma-hydroxybutyric acid mortality in mice. Annals of Emergency Medicine. 2005 Jun;45(6):614-9. (4) http://www.emedicine.com/emerg/topic848.htm AddictionGHB can be physically addictive and may result in psychological addiction. Physical dependence develops when GHB is taken on a regular basis (i.e. every 2-4 hours for multiple consecutive days or weeks). Withdrawal effects may include insomnia, restlessness, anxiety, tremors, sweating, loss of appetite, edginess, tachycardia, chest pain and tightness, muscle and bone aches, sensitivity to external stimuli (sound, light, touch), dysphoria, and mental dullness. These side effects will subside after 2 - 21 days depending on frequency of usage and the size of the doses used. In particularly severe cases, withdrawal from GHB may cause symptoms similar to acute withdrawal from alcohol or barbiturates (delerium tremens) and can cause convulsions and hallucinations. Although there have been reported fatalities due to GHB withdrawal, reports are inconclusive and further research is needed. Unlike alcohol, there is no firm data that chronic use of GHB causes permanent damage to the body. In rats, no organ or brain damage was observed after chronic administration of GBL (a precursor to GHB).[6] In cases of regular or prolonged GHB use and addiction, an additional anecdotal symptom is sometimes noted, consisting of a form of dyskinesia similar to tardive dyskinesia, manifested in involuntary jaw-clacking, or a tick that presents in spontaneous clicking sounds.[citation needed] This symptom often takes longer to dissipate than the immediate GHB withdrawal symptoms, probably indicating a different mechanism of action from that of direct withdrawal.[citation needed] This is also supported by reports, of the dyskenesia occurring concurrently with active GHB use in regular users (especially in those who co administer the drug with amphetamines).[citation needed] Legal stateIn Hong Kong, GHB is regulated under Schedule 1 of Hong Kong's Chapter 134 Dangerous Drugs Ordinance. It can only be used legally by health professionals and for university research purposes. The substance can be given by pharmacists under a prescription. Anyone who supplies the substance without presciption can be fined $10000(HKD). The penalty for trafficking or manufacturing the substance is a $5,000,000 (HKD) fine and life imprisonment. Possession of the substance for consumption without license from the Department of Health is illegal with a $1,000,000 (HKD) fine and/or 7 years of jail time. In the United States it was placed on Schedule I of the Controlled Substances Act in March of 2000 although when sold as Xyrem it is considered Schedule III, making it the only drug to simultaneously occupy two different schedules.[7][8] On March 20, 2001, the Commission on Narcotic Drugs placed GHB in Schedule IV of the 1971 Convention on Psychotropic Substances.[9] In the UK it was made a class C drug in June 2003. In New Zealand and Australia, GHB, 1,4-B and GBL are all Class B illegal drugs, along with any possible esters, ethers and aldehydes. GABA itself is also listed as an illegal drug in these jurisdictions which seems unusual given its failure to cross the blood-brain barrier, but there was a perception among legislators that all known analogues should be covered as far as this was possible. Attempts to circumvent the illegal status of GHB have led to the sale of derivatives such as 4-methyl-GHB (gamma-hydroxyvaleric acid, GHV) and its prodrug form gamma-valerolactone (GVL), but these are also covered under the law by virtue of being "substantially similar" to GHB or GBL and so importation, sale, possession and use of these compounds is also considered to be illegal. HistorySynthesis of the chemical GHB was first reported in 1874 by A. Saizew,[10] but the first major research into its use in humans was conducted in the early 1960s by Dr. Henri Laborit to use in studying the neurotransmitter GABA.[citation needed] It quickly found a wide range of uses due to its minimal side effects and controlled action, the only difficulties being the narrow safe dosage range and the dangers presented by its combination with alcohol and other CNS depressants. GHB was widely used in France, Italy and other European countries for several decades as a sleeping agent and an anaesthetic in childbirth, but problems with its abuse potential and development of newer drugs have led to a decrease in legitimate medical use of GHB in recent times. The only common medical applications for GHB now days are in the treatment of narcolepsy and more rarely alcoholism. Typically GHB has been synthesized from GBL (gamma-butyrolactone) by adding sodium hydroxide (lye) in ethanol or water. As of late, GBL has become controlled and more circuitous routes have to be taken such as those starting with THF (tetrahydrofuran). GHB in popular cultureIn the "Murder In A Flash" episode of CSI: Miami, one of the victims, an 18 year-old boy, is found to have died from GHB intoxication. GHB is also named as "the date-rape drug" by one of the investigators who also relates the information that males often take the drug to get high. In the matter of the GHB-related death, however, the victim had received the GHB without noticing it. In the episode of Robot Chicken that featured Archie, when he walked onto a bus with his friends and after Betty says "Looks like Archie is going on his senior drug trip," Reggie says "Geez Archie, you're supposted to put the GHB in the girl's drink, not have it yourself." In the NCIS episode "Twisted Sister" GHB was used to drug Sarah McGee, Special Agent Timothy McGee's sister, into thinking that she committed a murder as a cover up. A classmate, whom she despises, drugged her by adding it to her peanut butter. In the pilot episode of Veronica Mars, Veronica tells us she was raped at a party when she was sixteen. At the end of episode 20, "M.A.D.", of season 1, Veronica discovers that she had been given GHB at the party and investigates that night in the following episode, "A Trip to the Dentist". This party is referenced throughout season one and is a major conflict for the character, which was revisited in the final episode of season 2 when she finally learned exactly who she was raped by that night. Additionally, the current season 3 of Veronica Mars centers around the main character's freshman year at Hearst College, where she investigates a string of GHB-related rapes on campus. An episode of Law and Order: Special Victims Unit involves a woman who is drugged with GHB by a vengeful colleague in hopes that the woman will be raped. In the Law and Order episode "Fools for Love" one of the victim's deaths is attributed to choking on vomit from a GHB overdose administered by her rapist/killer. The television series The West Wing featured GHB in a multi-episode story during the conclusion of season 4 and the beginning of season 5. The president's daughter consumes GHB that has been slipped into an alcoholic beverage without her knowledge, and as she feels the effects of the drug, her boyfriend implies she has consumed ecstasy. Later, she is kidnapped from a nightclub bathroom while barely or not conscious, setting off a massive manhunt. The president is told later by an FBI agent that the drug is created by mixing degreasing solvent and drain cleaner, and he finishes the agent's sentence by acknowledging he is aware the drug is known as a date-rape drug. The French activist and psychoanalytic theorist Félix Guattari used GHB recreationally in the early '70's, see The Anti-Oedipus Papers (2006:308,326) Near the end of the second season of the television series Everwood, leading character Amy Abbott is pressured into consuming a low dose of GHB dissolved in water with her then-boyfriend, allegedly-recovered addict Tommy Callahan. In a misguided effort to keep her from accidentally overdosing, he consumes most of the drugs before giving her the remainder, thus overdosing himself. Upon realizing he was unresponsive, Amy called her doctor father to come to his rescue, and while they succeeded in saving Tommy's life, this encounter with the controlled substance ended their relationship. In the movie Syriana, Arash refers to Tehran as the world capital of "liquid MDMA". An episode of the fifth series of Spooks sees Ros use a refined form of the drug to incapacitate targets for intelligence gathering. In the third episode of the American version of "Queer as Folk", the character Ted falls into a coma after being given a large dose of GHB by a date he brings home. In the song "What's Going On" by Zebrahead, found on their album Playmate of the Year (2000), GHB is referenced as a date rape drug: She takes another sip But has no clue of the spike from the G to the H to the B She wakes up in the morning bruised and raped in the street GHB features in the song Shores of California by The Dresden Dolls: And that is why the girl is called a tease / and that is why the guy is called a sleaze / and that's why God made escort agencies / one life to live and mace and GHB. References
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