Interaction 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.
Toxicity
High doses of GHB may lead to nausea, dizziness, drowsiness, agitation, visual disturbances, depressed breathing, amnesia, unconsciousness, and death in some cases.
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.
Community Effects
TripSitTolerance & Pharmacokinetics
drugs.wikiTolerance Decay
Tolerance and dependence patterns are inferred from clinical withdrawal reports and community harm‑reduction guidance. Consecutive‑day or round‑the‑clock dosing rapidly escalates tolerance and produces severe withdrawal. Recovery of baseline sensitivity likely takes 1–2+ weeks after repeated daily use. Data quality: mixed clinical case series plus community reports; treat as conservative guidance.
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.wikiHarm‑reduction justifications and key cautions: 1) Steep dose–response: the gap between desired effects and unrousable sleep/coma is small; small misestimations or redoses can cause loss of consciousness and respiratory depression. Therefore, start low, measure precisely, and avoid redosing for at least 2 hours; set a timer to prevent ‘stacking’. Community and agency guides consistently emphasise this risk. 2) Liquids vary in strength: illicit GHB/GBL solutions differ widely and sellers often cannot state concentration. Dose by mass where possible; if using liquid, use a 1–3 ml oral syringe to 0.1 ml, never caps or swigs. Always label and keep your dose with you to avoid accidental ingestion by others. 3) Prodrugs differ: GBL and 1,4‑BD convert to GHB but generally have faster onset and, for GBL, more potency by volume; never substitute ml‑for‑ml with GHB. Always dilute GBL; it is an industrial solvent and can irritate mucosa. 4) Absolutely avoid mixing with other depressants (alcohol, benzos, opioids, Z‑drugs, sedating antihistamines): combinations greatly increase risk of vomiting, aspiration, respiratory arrest, coma, and death. 5) Redose discipline: despite a short plasma half‑life, functional effects and risk persist several hours; impulsive redosing to chase euphoria or to force sleep is a common pathway to overdose and dependence. 6) Chemsex context and consent: GHB/GBL can cause amnesia and incapacitation; use only with trusted people, avoid unlabeled communal drinks, and plan for explicit consent. 7) Overdose first aid: if someone becomes unresponsive, place in the recovery position, keep airway clear, monitor breathing, and call emergency services; do not give caffeine or stimulants or additional substances. Vomit aspiration is a key danger while unconscious. 8) Tolerance/dependence: use on consecutive days or frequent ‘around‑the‑clock’ dosing can produce rapid tolerance and severe, potentially life‑threatening withdrawal; limit use to no more than 2–3 days per week and avoid overnight patterns of dosing unless prescribed/clinically supervised. 9) Food and timing: taking on a full stomach can blunt/delay onset; alcohol is metabolised before GHB, so co‑use can lead to accumulation and delayed overdose. 10) Driving and machinery: impairment can persist beyond subjective effects; avoid for the rest of the day after use.
References
Drugs.wiki References
- TripSit Wiki: GHB (dosage, duration, harm‑reduction notes)
- Hi‑Ground: GHB substance page (redosing interval, measuring liquids, after‑effects)
- DrugWise: GHB/GBL (risks, overdose, dependence/withdrawal)
- EUDA/EMCDDA: Risk assessment of GHB (steep dose–response; public‑health risks)
- EUDA: Drug‑facilitated sexual assault paper (sedation/amnesia; consent risks)
- DrugBank DB01440: gamma‑Hydroxybutyric acid (half‑life, pharmacology, depressant warning)
- Erowid (DEA 2011 Resource Guide excerpt hosted by Erowid): variability of illicit liquids; street names; timing
- Saferparty.ch warnings (general ‘don’t mix downers’ incl. GHB/GBL)