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Depressant

GHB

Also called G, Xyrem, Sodium oxybate, γ-Hydroxybutyric acid

Original Wikipedia articleen.wikipedia.org/wiki/Γ-Hydroxybutyric_acid revision used (24 October 2026)

Why a "revision used" link? Anyone can edit Wikipedia at any time, so the article you open today may not say what it said when we read it. This link opens the exact version we read on 24 October 2026, frozen as it was. It is the only way to check that every quote on this page matches its source word for word. Newer versions may correct or change things. When we re-check this page against a newer version, the edit log records it. How we cite

Common dose · Oral1–2.5 g PW
Onset5–30 minutes PW
Total1.5–2.5 hours PW
After-effects2–4 hours PW

Dosage

When sources disagree, both rows are shown as published. Nothing is averaged or merged.

Oral

SourceThresholdLightCommonStrongHeavy
PsychonautWiki0.5 g PW0.5–1 g PW1–2.5 g PW2.5–4 g PW4 g+ Warning: Risk of death above 10 g[8] PW
TripSit–0.5–1.5 g TS1–2.5 g TS2–3.5 g TS3.5–5 g TS

NOTE: Tends to induce heavy sedation from about the 3g mark. TS

TripSit dose text

TripSit's factsheet also states its doses as text.

Oral Light: 0.5-1.5g Common: 1-2.5g Strong: 2-3.5g Heavy: 3.5-5g Dangerous: 7g+ | NOTE: Tends to induce heavy sedation from about the 3g mark. TS

What dose are you on? (self-reported, unverified)
Read this first. These numbers come from anonymous visitors typing in a box. Nobody checks them. People misjudge, mistype, troll, or take untested products of unknown strength. They are not a dose guide and never override the sourced table above. They exist only so the sourced ranges can be compared with what people say they take. If you are deciding what to take, use the sourced table, start low, and read the risks section.
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Duration

Route · sourceOnsetCome-upPeakOffsetTotalAfter-effects
Oral · PsychonautWiki5–30 minutes PW10–20 minutes PW45–90 minutes PW15–30 minutes PW1.5–2.5 hours PW2–4 hours PW

TripSit factsheet

Onset
20-60 minutes TS
Duration
1.5-2.5 hours TS
Aftereffects
2-4 hours TS

Mixing

Acute combinations: what happens when these are taken close together. Entries backed by a medical journal or agency are listed first.

Backed by medical journals

Awaiting sourcePeer-reviewed reports on acute combinations, from PubMed and the journals the harm reduction sites cite.

Other documented combinations

  • Dangerous Ketamine - Both substances cause ataxia and bring a risk of vomiting and unconsciousness. If the user falls unconscious while under the influence there is a severe risk of vomit aspiration if they are not placed in the recovery position. PW
  • Dangerous MXE - Both substances cause ataxia and bring a risk of vomiting and unconsciousness. If the patient falls unconscious while under the influence there is a severe risk of vomit aspiration if they are not placed in the recovery position. PW
  • Dangerous DXM - Both substances cause ataxia and bring a risk of vomiting and unconsciousness. If the patient falls unconscious while under the influence there is a severe risk of vomit aspiration if they are not placed in the recovery position. This combination is hard to predict. PW
  • Dangerous PCP - Details of this combination are not well understood but PCP generally interacts in an unpredictable manner. PW
  • Dangerous Alcohol - Even in very low doses this combination rapidly leads to memory loss, severe ataxia and unconsciousness. There is a high risk of vomit aspiration while unconscious. PW
  • Dangerous Opioids - The two substances potentiate each other strongly and unpredictably, very rapidly leading to unconsciousness. While unconscious, vomit aspiration is a risk if not placed in the recovery position. PW
  • Dangerous Tramadol - The sedative effects of this combination can lead to dangerous respiratory depression. PW
  • Dangerous Benzodiazepines - The two substances potentiate each other strongly and unpredictably, very rapidly leading to unconsciousness. While unconscious, vomit aspiration is a risk if not placed in the recovery position. PW
  • Uncertain Nitrous - Both substances potentiate the ataxia and sedation caused by the other and can lead to unexpected loss of consciousness at high doses. While unconscious, vomit aspiration is a risk if not placed in the recovery position. Memory blackouts are likely. PW
  • Uncertain Amphetamines - Stimulants increase respiration rate allowing a higher dose of sedatives. If the stimulant wears off first then the GHB may overcome the patient and cause respiratory arrest. PW
  • Uncertain MDMA - Large amounts of GHB/GBL may overwhelm the effects of MDMA on the comedown. PW
  • Uncertain Cocaine - Stimulants increase respiration rate allowing a higher dose of sedatives. If the stimulant wears off first then the GHB may overcome the patient and cause respiratory arrest. Likewise the GHB can wear off and leave a dangerous concentration of Cocaine behind. PW

TripSit combination chart

TripSit rates each pairing. Only pairings with a number carry a citation from TripSit. See the whole chart, with TripSit's note for every pairing.

Dangerous

alcohol TSdextromethorphan TSdiphenhydramine[9–12] TSketamine TSmxe TSpcp TStramadol TS

Caution

cocaine TSmdma TSnitrous TS

Low Risk & Synergy

cannabis TS

Low Risk & No Synergy

caffeine TS

Low Risk & Decrease

amt TSdmt TSlsd TSmescaline TSmushrooms TS

Risks and toxicity

GHB is considered to be a safe and non-toxic substance when used responsibly or medically. The LD₅₀ is above the active dosage, and there is no danger of acute toxicity. However, it can become dangerous when used as a recreational drug or abused. There have been many negative reports from recreational users who have overdosed, combined GHB with alcohol or other drugs, or accidentally dosed themselves unexpectedly.[13] PW

One publication investigated 226 deaths attributed to GHB. Seventy-one deaths (34%) were caused by GHB alone while the other deaths were from respiratory depression caused by interaction with alcohol or other drugs.[14] PW

As an endogenous regulator of energy metabolism and a natural neurotransmitter, GHB is well-known to the brain and organs which are used to its effects and have highly efficient systems for metabolizing it safely. The substance is eliminated (that is, back to baseline levels) in 2-4 hours and continues to be so even after twice-daily doses for a week. In one European study, no adverse effects were reported after several years of regular recreational use.[15][16] PW

Accidental ingestions of GHB have also occurred due to inadequate storage methods. If GHB is put into a clear liquid, glass, or bottle, it can be easily mistaken for water. It is recommended to clearly label your GHB in writing and dye the liquid with blue food coloring so it no longer resembles a drinkable beverage. It is also recommended to store your GHB in a container that no one would drink out of. PW

It is recommended to dilute GHB with a non-alcoholic liquid in the ratio of at least 1:100 (e.g., 200ml of water for 2ml of GHB), in order to avoid potential burns to the intestines and mouth.[17] PW

It is strongly recommended that one use harm reduction practices when using this substance. PW

Neurotoxicity

A 2022 review compared 43 studies on GHB-induced cognitive impairment in humans and animals. The analysis suggests that moderate or clinical use may result in acute cognitive impairment. Working memory, short-term memory, and impaired performance on cognitive tasks were impaired after doses as low as 10mg/kg, but these effects appear to be temporary. Conversely, one study found that a dose of 20mg/kg improved social and non-social cognition, but did not affect base cognitive functions, such as visual or verbal memory recall. However, chronic heavy use of GHB, especially if accompanied by GHB-induced comas appear to cause long-term cognitive impairment and are likely neurotoxic.[18] PW

In multiple studies, GHB has been found to impair spatial memory, working memory, learning and memory in rats with chronic administration. These effects are associated with decreased NMDA receptor expression in the cerebral cortex and possibly other areas as well.[19–22] PW

One study found that repeated administration of GHB to rats for 15 days drastically reduced the number of neurons and non-neuronal cells within the hippocampus and in the prefrontal cortex. With doses of 10 mg/kg of GHB, they were decreased by 61% in the hippocampus region and 32% in the prefrontal cortex, and with 100 mg/kg, they were decreased by 38% and 9%, respectively. This paper demonstrates contradicting effects on neuronal loss, with lower doses (10 mg/kg) producing the most neurotoxicity, and higher doses (100 mg/kg) producing less. PW

Overdose

To avoid a possible overdose of GHB, it is important to start with a low dose and work your way up slowly by increasing the dosage in small increments. While a common recreational dose is 2g, a dose of 5g - 10g can result in convulsions, unconsciousness and vomiting. Doses above 10 grams are associated with a risk of death. Recreational users must also consider the different potency of different GHB preparations available on the illicit market. Thus, even an experienced user should start with a lower than normal dose, if trying a new product for the first time.[8][23] PW

Tolerance and addiction potential

GHB is moderately to highly physically and moderately psychologically addictive. The frequent use of GHB can cause withdrawal symptoms similar to those caused by other depressants such as alcohol and benzodiazepines if abruptly discontinued. These symptoms seem to depend on the dosage and the length of time the drug was used for. Light to moderate users often experience anxiety, insomnia, sleep-related problems, and tremors whereas heavy use can cause severe withdrawal symptoms like delirium, psychosis, and hallucinations.[24–27] PW

GHB, when used medicinally (two medicinal doses per day, four hours apart), creates little to no dependance while the more frequent one uses GHB, it causes exponentially more dependance and withdrawal symptoms.[28] PW

Although there have been reported fatalities due to GHB withdrawal, reports are inconclusive and further research is needed.[29] PW

Tolerance will develop to the sedative-hypnotic effects within several days of continuous use. After cessation, the tolerance returns to baseline in 7 - 14 days. Withdrawal symptoms or rebound symptoms may occur after ceasing usage abruptly following a few weeks or longer of steady dosing, and may necessitate a gradual dose reduction to minimize neurotoxicity from withdrawal. It is proposed that GHB and especially GBL can lead to dependence at a significantly faster rate than longer-acting depressants. PW

GHB presents cross-tolerance with 1,4-Butanediol and GBL, since these act as prodrugs for GHB. Cross-tolerance with alcohol and baclofen has been shown in rats, and is likely with other GABAB-agonists.[30][31] PW

TripSit factsheet

Avoid
Alcohol, benzos and other depressants[1][2] TS

Testing

Awaiting sourceReagent reactions and test kit guidance from a harm reduction testing service.

Effects

Similar to alcohol, but subjectively 'cleaner' TS

Overview

gamma-Hydroxybutyric acid (also known as 4-hydroxybutanoic acid and GHB) is a depressant substance. It is found naturally as a neurotransmitter and is also a precursor to GABA, glutamate, and glycine in certain brain areas. It acts on the GHB receptor and is a weak agonist at the GABAB receptor. PW

A euphoric depressant which is prescribed as a sleep aid and sometimes to help with Alcohol detox. Also used as a recreational depressant, as a non-toxic alternative to Alcohol. Despite not having Alcohol's toxicity it is risky due to among other things inconsistent concentration in commonly sold solution form, and can be very dangerous if taken with other depressants.[1][2] TS

γ-Hydroxybutyric acid (GHB), also known as 4-hydroxybutanoic acid, is a naturally occurring neurotransmitter and a depressant drug. It is a precursor to GABA, glutamate, and glycine in certain brain areas. It acts on the GHB receptor and is a weak agonist at the GABAB receptor. GHB has been used in medicine as a general anesthetic and as treatment for cataplexy, narcolepsy, and alcohol use disorder. It is also used illicitly for performance enhancement, date rape, and recreation.[3][4][5] WP

It is commonly used in the form of a salt, with the conjugate base of GHB being called γ-hydroxybutyrate or oxybate. The sodium (NaGHB, sodium oxybate, or Xyrem) and potassium (KGHB, potassium oxybate) salts are common. GHB is produced as a result of fermentation, and is found in small quantities in some beers and wines, beef, and small citrus fruits.[6][7] WP

Succinic semialdehyde dehydrogenase deficiency causes GHB to accumulate in the blood. WP

History

History

Alexander Zaytsev worked on this chemical family and published work on it in 1874. The first extended research into GHB and its use in humans was conducted in the early 1960s by Henri Laborit to use in studying the neurotransmitter GABA. It was studied in a range of uses including obstetric surgery and during childbirth and as an anxiolytic; there were anecdotal reports of it having antidepressant and aphrodisiac effects as well. It was also studied as an intravenous anesthetic agent and was marketed for that purpose starting in 1964 in Europe but it was not widely adopted as it caused seizures; as of 2006 that use was still authorized in France and Italy but not widely used. It was also studied to treat alcohol addiction; while the evidence for this use is weak; however, sodium oxybate is marketed for this use in Italy.[32–36] WP

GHB and sodium oxybate were also studied for use in narcolepsy from the 1960s onwards.[34] WP

In May 1990 GHB was introduced as a dietary supplement and was marketed to body builders, for help with weight control and as a sleep aid, and as a "replacement" for l-tryptophan, which was removed from the market in November 1989 when batches contaminated with trace impurities were found to cause eosinophilia–myalgia syndrome, although eosinophilia–myalgia syndrome is also tied to tryptophan overload. In 2001 tryptophan supplement sales were allowed to resume, and in 2005 the FDA ban on tryptophan supplement importation was lifted. By November 1989 57 cases of illness caused by the GHB supplements had been reported to the Centers for Disease Control and Prevention, with people having taken up to three teaspoons of GHB; there were no deaths but nine people needed care in an intensive care unit. The FDA issued a warning in November 1990 that sale of GHB was illegal. GHB continued to be manufactured and sold illegally and it and analogs were adopted as a club drug and came to be used as a date rape drug, and the DEA made seizures and the FDA reissued warnings several times throughout the 1990s.[37–44] WP

At the same time, research on the use of GHB in the form of sodium oxybate had formalized, as a company called Orphan Medical had filed an investigational new drug application and was running clinical trials with the intention of gaining regulatory approval for use to treat narcolepsy.[34][45] WP

A popular children's toy, Bindeez (also known as Aqua Dots, in the United States), produced by Melbourne company Moose, was banned in Australia in early November 2007 when it was discovered that 1,4-butanediol (1,4-B), which is metabolized into GHB, had been substituted for the non-toxic plasticiser 1,5-pentanediol in the bead manufacturing process. Three young children were hospitalized as a result of ingesting a large number of the beads, and the toy was recalled.[46] WP

Pharmacology

Detection of use

GHB may be quantitated in blood or plasma to confirm a diagnosis of poisoning in hospitalized patients, to provide evidence in an impaired driving, or to assist in a medicolegal death investigation. Blood or plasma GHB concentrations are usually in a range of 50–250 mg/L in persons receiving the drug therapeutically (during general anesthesia), 30–100 mg/L in those arrested for impaired driving, 50–500 mg/L in acutely intoxicated patients and 100–1000 mg/L in victims of fatal overdosage. Urine is often the preferred specimen for routine drug abuse monitoring purposes. Both γ-butyrolactone (GBL) and 1,4-butanediol are converted to GHB in the body.[68–71] WP

A method of detecting GHB in saliva was developed in 2016.[72] WP

Pharmacology

GHB is very similar to the important inhibitory neurotransmitter GABA, with an amino group of GABA being replaced by a hydroxy group. If taken orally, GABA does not effectively cross the blood–brain barrier while GHB does.[73] WP

GHB has at least two distinct binding sites in the central nervous system. It acts as an agonist at the excitatory GHB receptor and as a weak agonist at the inhibitory GABAB receptor. GHB is a naturally occurring substance that acts in a similar fashion to some neurotransmitters in the mammalian brain. GHB is probably synthesized from GABA in GABAergic neurons, and released when the neurons fire.[74–77] WP

GHB has been found to activate oxytocinergic neurons in the supraoptic nucleus.[78] WP

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.[79][80][81] WP

However, at therapeutic doses, GHB reaches much higher concentrations in the brain and activates GABAB receptors, which are primarily responsible for its sedative effects. GHB's sedative effects are blocked by GABAB antagonists.[82][83] WP

The role of the GHB receptor in the behavioural effects induced by GHB is more complex. 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. Drugs that selectively activate the GHB receptor cause absence seizures in high doses, as do GHB and GABAB agonists.[84][85][86] WP

Activation of both the GHB receptor and GABAB is responsible for the addictive profile of GHB. GHB's effect on dopamine release is biphasic. Low concentrations stimulate dopamine release via the GHB receptor. Higher concentrations inhibit dopamine release via GABAB receptors as do other GABAB agonists such as baclofen and phenibut. After an initial phase of inhibition, dopamine release is then increased via the GHB receptor. 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.[85][87–91] WP

This explains the paradoxical mix of sedative and stimulatory properties of GHB, as well as the so-called "rebound" effect, experienced by individuals using GHB as a sleeping agent, wherein 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 below the threshold for significant GABAB receptor activation and activates predominantly the GHB receptor, leading to wakefulness.[92] WP

Recently, analogs of GHB, such as 4-hydroxy-4-methylpentanoic acid (UMB68) have been synthesised and tested on animals, in order to gain a better understanding of GHB's mode of action. 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 (γ-hydroxyvaleric acid, GHV) and a prodrug form γ-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.[93] WP

Other prodrug ester forms of GHB have also rarely been encountered by law enforcement, including 1,4-butanediol diacetate (BDDA/DABD), methyl-4-acetoxybutanoate (MAB), and ethyl-4-acetoxybutanoate (EAB), but these are, in general, covered by analogue laws in jurisdictions where GHB is illegal, and little is known about them beyond their delayed onset and longer duration of action. The intermediate compound γ-hydroxybutyraldehyde (GHBAL) is also a prodrug for GHB; however, as with all aliphatic 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.[94] WP

Only a minor portion (1–5%) of the administered GHB dose is excreted unchanged in the urine. Studies have shown that the maximum concentration of GHB in urine appears within 1 hour and rapidly declines thereafter. The vast majority (95–98%) undergoes extensive metabolism in the liver. GHB is broken down through a series of enzymatic pathways. The primary route involves conversion to succinic semialdehyde (SSA) by either GHB dehydrogenase (ADH) or GHB transhydrogenase. SSA is further oxidized by succinic semialdehyde dehydrogenase (SSADH) to succinic acid, which enters the Krebs cycle and is ultimately converted into carbon dioxide and water.[85][94][95][96] WP

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 recreational or health promotion 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. WP

Chemistry

Formula
C4H7O3- PC
Formula (Wikipedia infobox)
C4H8O3 WP⚠ Wikipedia and PubChem give different formulas. Both are shown as each source has it.
Note
⚠ The PubChem record carries a charge, so it may describe an ion or salt of this substance rather than the substance itself.
Molar mass (g/mol)
103.10 PC
IUPAC name (computed by PubChem)
4-hydroxybutanoate PC
SMILES
C(CC(=O)[O-])CO PC
InChIKey
SJZRECIVHVDYJC-UHFFFAOYSA-M PC
PubChem CID
3037032

User reports

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Listings

Erowid Experience Vault listing TS

Link as published on TripSit's factsheet.

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Pop culture

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References

  1. Journal / agency The presence of gamma-hydroxybutyric acid (GHB) and gamma-butyrolactone (GBL) in alcoholic and non-alcoholic beverages
  2. Journal / agency Pharmacological aspects of the combined use of 3,4-methylenedioxymethamphetamine (MDMA, ecstasy) and gamma-hydroxybutyric acid (GHB): a review of t
  3. Journal / agency Sodium Oxybate: MedlinePlus Drug Information. 28 July 2010
  4. Other Benzer TI, Cameron S. Toxicity, Gamma-Hydroxybutyrate. 8 January 2007
  5. Other US Drug Enforcement Administration. GHB, GBL and 1,4BD as Date Rape Drugs
  6. Journal / agency Roth, T. Therapeutic Use of γ-Hydroxybutyrate: History and Clinical Utility of Oxybates and Considerations of Once- and Twice-Nightly Dosing in Narcolepsy. CNS drugs. March 2025. doi:10.1007/s40263-024-01150-8 · PMID 40111735 · PMC11950157
  7. Other Weil A, Winifred R. From Chocolate to Morphine. 1993
  8. Harm reduction site Erowid GHB Vault : Dosage
  9. Journal / agency William J Tharion, Donna J. McMenemy, Terry M. Rauch. Antihistamine Effects on the Central Nervous System, Cognitive Performance and Subjective States
  10. Journal / agency Sicari V, Zabbo CP. Diphenhydramine. Diphenhydramine
  11. Journal / agency Couper FJ, Marinetti LJ. γ-Hydroxybutyrate (GHB) - Effects on Human Performance and Behavior
  12. Journal / agency Busardò FP, Jones AW. GHB Pharmacology and Toxicology: Acute Intoxication, Concentrations in Blood and Urine in Forensic Cases and Treatment of the Withdrawal Syndrome
  13. Harm reduction site GHB - Erowid Exp - “GHB Overdoses & Poisonings”
  14. Journal / agency Zvosec, D. L., Smith, S. W., Porrata, T., Strobl, A. Q., Dyer, J. E. Case series of 226 γ-hydroxybutyrate-associated deaths: lethal toxicity and trauma. The American Journal of Emergency Medicine. March 2011. doi:10.1016/j.ajem.2009.11.008
  15. Journal / agency Ferrara, S., Zotti, S., Tedeschi, L., Frison, G., Castagna, F., Gallimberti, L., Gessa, G., Palatini, P. Pharmacokinetics of gamma-hydroxybutyric acid in alcohol dependent patients after single and repeated oral doses. British Journal of Clinical Pharmacology. September 1992. doi:10.1111/j.1365-2125.1992.tb04129.x
  16. Journal / agency Laborit, H. Correlations between protein and serotonin synthesis during various activities of the central nervous system (slow and desynchronized sleep, learning and memory, sexual activity, morphine tolerance, aggressiveness, and pharmacological action of sodium gamma-hydroxybutyrate). Research Communications in Chemical Pathology and Pharmacology. January 1972
  17. Other https://sidekicks.berlin/en/ghb-gbl/#beratung
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  19. Journal / agency Sircar, R., Basak, A. Adolescent γ-hydroxybutyric acid exposure decreases cortical N-methyl-d-aspartate receptor and impairs spatial learning. Pharmacology Biochemistry and Behavior. 1 December 2004. doi:10.1016/j.pbb.2004.09.022
  20. Journal / agency García, F. B., Pedraza, C., Arias, J. L., Navarro, J. F. Effects of subchronic administration of gammahydroxybutyrate (GHB) on spatial working memory in rats. Psicothema. August 2006
  21. Journal / agency Sircar, R., Basak, A., Sircar, D. γ-Hydroxybutyric Acid-Induced Cognitive Deficits in the Female Adolescent Rat. Annals of the New York Academy of Sciences. October 2008. doi:10.1196/annals.1432.044
  22. Journal / agency Pedraza, C., García, F. B., Navarro, J. F. Neurotoxic effects induced by gammahydroxybutyric acid (GHB) in male rats. The International Journal of Neuropsychopharmacology. October 2009. doi:10.1017/S1461145709000157
  23. Harm reduction site https://www.erowid.org/chemicals/ghb/ghb_health.shtml
  24. Journal / agency Kim, S. Y., Barker, J. C., Anderson, I. B., Dyer, J. E., Earnest, G., Blanc, P. D. Systematic Assessment of Gamma Hydroxybutyrate (GHB) Effects During and After Acute Intoxication. The American journal on addictions / American Academy of Psychiatrists in Alcoholism and Addictions. 2008. doi:10.1080/10550490802138988
  25. Journal / agency Carter, L. P., Pardi, D., Gorsline, J., Griffiths, R. R. Illicit gamma-hydroxybutyrate (GHB) and pharmaceutical sodium oxybate (Xyrem®): differences in characteristics and misuse. Drug and alcohol dependence. 1 September 2009. doi:10.1016/j.drugalcdep.2009.04.012
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  27. Harm reduction site GHB Withdrawal Syndrome | Texas Commission on Alcohol and Drug Abuse
  28. Harm reduction site https://drugs-forum.com/threads/important-ghb-gbl-addiction-withdrawal.43390/page-4
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  31. Journal / agency Smith, M. A., Gergans, S. R., Lyle, M. A. The motor-impairing effects of GABAA and GABAB agonists in γ-hydroxybutyrate (GHB)-treated rats: Cross-tolerance to baclofen but not flunitrazepam. European Journal of Pharmacology. 15 December 2006. doi:10.1016/j.ejphar.2006.08.080
  32. Other Lewis DE. Early Russian organic chemists and their legacy. 2012
  33. Journal / agency Saytzeff A. Über die Reduction des Succinylchlorids. Liebigs Annalen der Chemie. 1874. doi:10.1002/jlac.18741710216
  34. Journal / agency Critical review of gamma-hydroxybutyric acid (GHB). 2012
  35. Journal / agency Laborit H, Jouany JM, Gerard J, Fabiani F. Generalities concerning the experimental study and clinical use of gamma hydroxybutyrate of Na. Agressologie. October 1960. PMID 13758011
  36. Other Alcover: Riassunto delle Caratteristiche del Prodotto. 31 March 2017
  37. Journal / agency Ito J, Hosaki Y, Torigoe Y, Sakimoto K. Identification of substances formed by decomposition of peak E substance in tryptophan. Food and Chemical Toxicology. January 1992. doi:10.1016/0278-6915(92)90139-C · PMID 1544609
  38. Journal / agency Smith MJ, Garrett RH. A heretofore undisclosed crux of eosinophilia-myalgia syndrome: compromised histamine degradation. Inflammation Research. November 2005. doi:10.1007/s00011-005-1380-7 · PMID 16307217
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