GHB Stats & Data
SJZRECIVHVDYJC-UHFFFAOYSA-NInteraction Warnings
This combination can result in an increased risk of vomiting during unconsciousness and death from the resulting suffocation. If this occurs, users should attempt to fall asleep in the recovery position or have a friend move them into it.
It is dangerous to combine GHB, a depressant, with stimulants due to the risk of excessive intoxication. Stimulants decrease the sedative effect of GHB, which is the main factor most people consider when determining their level of intoxication. Once the stimulant wears off, the effects of GHB will be significantly increased, leading to intensified disinhibition as well as other effects. If combined, one should strictly limit themselves to only dosing a certain amount of GHB per hour.
Pharmacology
DrugBankDescription
Gamma hydroxybutyric acid, commonly abbreviated GHB, is a therapeutic drug which is illegal in multiple countries. It is currently regulated in the US and sold by Jazz Pharmaceuticals under the name Xyrem. However, it is important to note that GHB is a designated Orphan drug (in 1985). Today Xyrem is a Schedule III drug; however GHB remains a Schedule I drug and the illicit use of Xyrem falls under penalties of Schedule I. GHB is a naturally occurring substance found in the central nervous system, wine, beef, small citrus fruits and almost all other living creatures in small amounts. It is used illegally under the street names Juice, Liquid Ecstasy or simply G, either as an intoxicant, or as a date rape drug. Xyrem is a central nervous system depressant that reduces excessive daytime sleepiness and cataplexy in patients with narcolepsy.
Mechanism of Action
GHB is present at much higher concentrations in the brain, where it activates GABA-B receptors to exert its sedative effects. With high affinity, GHB binds to excitatory GHB receptors that are densely expressed throughout the brain, including the cotex and hippocampus. There is some evidence in research that upon activation of GHB receptors in some brain areas, the excitatory neurotransmitter glutamate is released. GHB stimulates dopamin release at low concentrations by acting on the GHB receptor, and the release of dopamine occurs in a biphasic manner. At higher concentrations, GHB inhibits dopamine release by acting on the GABA-B receptors, which is followed by GHB receptor signaling and increased release of dopamine. 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. It is proposed that overtime, the level of GHB in the brain decreases below the threshold for significant GABA-B receptor activation, leading to preferential activation of GHB receptor over GABA-B receptors and enhanced wakefulness.
Pharmacodynamics
GHB predominantly works at two distinct binding sites in the central nervous system: it works as an agonist at the newly-characterized excitatory GHB receptor, while acting as a weak agonist at the inhibitory GABAB receptor. Since it is a naturally occurring substance, its physiological action is similar to that of some endogenous neurotransmitters in mammalian brain. GHB is probably synthesized from GABA in GABAergic neurons, and released when the neurons fire.
Indication
Used as a general anesthetic, to treat conditions such as insomnia, clinical depression, narcolepsy, and alcoholism, and to improve athletic performance.
Elimination
Animal studies indicate that metabolism is the major elimination pathway for sodium oxybate, producing carbon dioxide and water via the tricarboxylic acid (Krebs) cycle and secondarily by beta-oxidation. Succinic acid enters the Krebs cycle where it is metabolized to carbon dioxide and water. Fecal and renal excretion is negligible. 5% renal elimination.
Clearance
* apparent oral cl=9.1 mL/min/kg healthy adults receiving a single oral dose of 25 mg/kg * 4.5 mL/min/kg cirrhotic patients without ascites receiving a single oral dose of 25 mg/kg * 4.1 mL/min/kg cirrhotic patients with ascites receiving a single oral dose of 25 mg/kg
History & Culture
1874–1960s
The chemical family to which GHB belongs was first explored by Russian chemist Alexander Zaytsev, who published work on related compounds in 1874. The compound itself was first synthesized in the 1920s, though it would remain largely unexamined for several decades. Extended research into GHB and its applications in humans began in the early 1960s when French researcher Henri Laborit investigated the compound as part of his studies on the neurotransmitter GABA. During this period, GHB was examined for numerous potential medical applications including use during obstetric surgery, childbirth, and as an anxiolytic agent. Researchers also noted anecdotal reports suggesting antidepressant and aphrodisiac properties. The compound was studied as an intravenous anesthetic and began being marketed for this purpose in Europe starting in 1964. However, this application never achieved widespread adoption due to the compound's propensity to induce seizures. GHB and its pharmaceutical form, sodium oxybate, were also investigated for treating narcolepsy and alcohol addiction from the 1960s onward.
1980s–1990
Throughout the 1980s, GHB was sold openly as a weight loss and muscle development aid, gaining particular popularity within the bodybuilding community due to its reputed positive effects on growth hormone levels. In May 1990, the compound was formally introduced as a dietary supplement and marketed to bodybuilders as a sleep aid and as a replacement for L-tryptophan, which had been removed from the market in November 1989 following contamination concerns. The unregulated availability of GHB soon led to health concerns. Dozens of illness cases were reported to the Centers for Disease Control and Prevention, with users having consumed up to three teaspoons of the substance. While no deaths occurred during this period, several individuals required intensive care. The FDA issued a warning in November 1990 declaring the sale of GHB to be illegal, though the compound continued to be manufactured and distributed through illicit channels.
1990s–present
Following its removal from the dietary supplement market, GHB transitioned into recreational use and was adopted as a club drug during the 1990s. Users sought the substance for its disinhibiting, pro-social, and sedative properties at lower doses, as well as its reputation for enhancing libido. The drug became a fixture in nightclub and rave scenes throughout this period, appealing to users seeking an alternative to alcohol with a shorter duration of effects.
late 1990s–present
By the late 1990s, GHB had gained significant public notoriety as a date-rape drug following sustained media coverage. The compound's colorless and odorless properties made it particularly concerning, as it was described as very easy to add to drinks without detection. Several high-profile cases brought national attention to this issue. In early 1999, fifteen-year-old Samantha Reid of Rockwood, Michigan, died from GHB poisoning after unknowingly consuming the drug. Her death, along with that of Hillory J. Farias, directly inspired federal legislation—the Hillory J. Farias and Samantha Reid Date-Rape Drug Prohibition Act of 2000—which led to GHB being placed on Schedule I of the Controlled Substances Act. In the United Kingdom, serial killer Stephen Port administered GHB to victims by adding it to their drinks, committing sexual assaults and murdering four individuals in his flat in Barking, East London.
2007–present
In November 2007, an unusual public health incident brought renewed attention to GHB and its precursors. A popular children's toy marketed as Bindeez in Australia and Aqua Dots in the United States was discovered to contain 1,4-butanediol, a compound that metabolizes into GHB when ingested. The toxic chemical had been substituted for the intended non-toxic plasticizer 1,5-pentanediol during the bead manufacturing process. Three young children were hospitalized after consuming large quantities of the beads, prompting a product recall by Melbourne-based manufacturer Moose and a nationwide ban in Australia.
Subjective Effect Notes
physical: The physical effects of GHB can be broken down into several components which progressively intensify proportional to dosage.
cognitive: The cognitive effects of GHB can be broken down into several components which progressively intensify proportional to dosage.
study ranking various drugs (legal and illegal) based on statements by drug-harm experts. GHB was found to be the ninth overall most dangerous drug.]] 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.
Carcinogenicity
No indication of carcinogenicity to humans (not listed by IARC).
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.
Organ-specific toxicity
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.
Toxicity (DrugBank)
High doses of GHB may lead to nausea, dizziness, drowsiness, agitation, visual disturbances, depressed breathing, amnesia, unconsciousness, and death in some cases.
Community Effects
TripSitTolerance & Pharmacokinetics
drugs.wikiTolerance Decay
Acute tolerance: develops within a single session — the reset numbers above apply after sustained heavy use, not after one binge. Within-session tachyphylaxis usually resets largely overnight.
Tolerance builds quickly with daily/continuous use but decays over 1–3 weeks with abstinence, based on GHB patterns; values are approximate and intended for HR planning, not exact prediction.
Cross-Tolerances
Demographics
Gender Distribution
Age Distribution
Reports Over Time
Effect Analysis
Erowid + BluelightEffects aggregated from 214 experience reports (193 Erowid + 21 Bluelight)
Effect Sentiment Distribution
Confidence Distribution
Positive Effects 32
Adverse Effects 40
Dosage Distribution
Dose distribution from experience reports
Real-World Dose Distribution
62K DosesFrom 221 individual dose entries
Oral (n=105)
Common Combinations
Most co-occurring substances in experience reports
Form / Preparation
Most common forms and preparations reported
Body-Weight Dosing
Dose relative to body weight from reports with weight data
Redose Patterns
Redosing behavior across 151 reports
Legal Status
| Country | Status | Notes |
|---|---|---|
| United Kingdom | Controlled substance | Scheduled as a controlled substance in 2003. Before this, the drug existed in a legal grey area following its emergence as a recreational substance in the late 1990s. |
| United States | Controlled substance | Became a scheduled controlled substance in 2000. Prior to scheduling, GHB was sold openly as a weight loss and muscle development aid during the 1980s and emerged as a recreational drug in the late 1990s. |
Harm Reduction
drugs.wikiReasoning and evidence for harm-reduction additions (with sources):
- Prodrug to GHB: Aceburic acid is the acetate ester at 4‑OH of GHB, expected to be rapidly hydrolyzed by esterases to active GHB. Community chemists have long noted this, explicitly calling it “4‑acetoxy‑GHB… metabolised pretty rapidly by esterases into GHB.” This supports treating dosing, interactions, and risks as GHB‑like.
- Steep dose–response and tight redose window: GHB has a very steep curve; TripSit warns even small overdoses can progress from euphoria to unrousable sleep/coma. Therefore, space redoses by at least 2 hours and avoid stacking. This is crucial because aceburic’s slightly delayed onset versus GBL increases premature redose risk.
- Accurate measurement: Liquids/powders should be measured with a precise scale or known‑concentration solution; poor measurement is a leading cause of G‑outs. Drugs‑Forum and Erowid emphasize accurate dosing and variability of liquids; do not swig from containers.
- Avoid depressant mixing: Alcohol, benzos, opioids, barbiturates markedly increase risk of respiratory depression, vomiting, and aspiration. TripSit lists these combinations as unsafe; SaferParty repeatedly warns of life‑threatening additive CNS/respiratory depression with GHB/GBL plus depressants.
- Stimulants caution: Uppers can mask sedation, leading to risk‑taking, mis‑timed redosing, and cardiovascular strain. SaferParty highlights this general risk with downer–upper mixes.
- Overdose management: There is no specific antidote; management is supportive with airway protection. Community HR stresses recovery position to reduce aspiration risk and to monitor breathing until help arrives. Do not give stimulants or more substances. Public‑domain reviews of GHB toxicity also emphasize supportive care and respiratory monitoring.
- Onset/kinetics framing: Compared with GHB salts, prodrugs like GBL have faster onset; aceburic appears intermediate (slower than GBL, near GHB). TripSit’s GHB timings (10–40 min onset, 1–3 h total) and the clinical review of GHB PK/PD justify conservative timing and spacing recommendations for the ester.
- Mucosal/GI irritation and pH: Acidic or strongly basic G‑related solutions can burn mucosa. Users and moderators on Bluelight report oral and cheek burns when solutions are not properly neutralized. For aceburic acid, dissolving and buffering to near‑neutral pH with food‑grade carbonate reduces throat irritation and likely discourages corrosive injury.
- Dependence & withdrawal risk: GHB dependence can develop rapidly with around‑the‑clock use; withdrawal can be severe and requires medical care (often benzodiazepines as first‑line). The clinical review and Drugs‑Forum resources document this. Set hard frequency limits (e.g., max 2–3 uses/week) to minimize risk.
- Legal risk context: EUDA reports GHB/GBL as depressants of concern; many jurisdictions control GHB and often its prodrugs/precursors. As an ester of a scheduled drug, aceburic may be considered controlled; check local law.
- Practical HR tips: Use timers (phone/app) to enforce redose spacing; community tools exist for G tracking. Keep a sober sitter, avoid driving for at least 6 hours after last strong dose, and lock up supply to prevent accidental ingestion.
Concise HR guidance:
- Treat aceburic doses cautiously as GHB‑equivalent after accounting for mass; start low, wait full onset. Use a 0.01 g scale or standardized solution; never drink from stocks. Keep redose spacing ≥2 h. Avoid all depressant mixes. If someone is unrousable, place in recovery position, monitor breathing, call emergency if apnea/bradycardia occur. Buffer acidic solutions to ~pH 7 to lower throat irritation. Frequent/round‑the‑clock use can cause severe dependence; seek medical help to taper. Because legal status is unclear, possession may carry risk.
References
Drugs.wiki References
- PubChem entry — Aceburic acid (CID 176865)
- Bluelight thread — Aceburic acid identified as 4‑acetoxy‑GHB prodrug
- Reddit r/researchchemicals — Aceburic acid availability/legal discussion
- TripSit GHB wiki — dose, duration, HR warnings
- Clinical review — GHB abuse: pharmacology, poisoning, withdrawal (Open‑access PMC)
- Drugs‑Forum GHB wiki — dosing accuracy, combinations HR
- SaferParty (Zurich) — warnings about mixing depressants incl. GHB/GBL
- Bluelight/EADD & GHB/GBL discussions — pH burns/neutralization reminders
- EUDA European Drug Report 2025 — section covering GHB among ‘other drugs’