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Death may occur when GABAergic substances are combined with other depressants such as opiates, benzodiazepines, barbiturates, gabapentinoids, thienodiazepines or alcohol.[1]

It is strongly discouraged to combine these substances, particularly in common to heavy doses.

Summary sheet: GHB
Chemical Nomenclature
Common names GHB, G, Xyrem, Sodium oxybate
Substitutive name gamma-Hydroxybutyric acid
Systematic name 4-Hydroxybutanoic acid
Class Membership
Psychoactive class Depressant
Routes of Administration

WARNING: Always start with lower doses due to differences between individual body weight, tolerance, metabolism, and personal sensitivity. See responsible use section.

Light 0.5 - 1 g
Common 1 - 2.5 g
Strong 2.5 - 4 g
Heavy 4 g + Warning: Risk of death above 10 g[2]
Total 1.5 - 2.5 hours
Onset 10 - 30 minutes
Peak 45 - 90 minutes
Offset 15 - 30 minutes
After effects 2 - 4 hours

DISCLAIMER: PW's dosage information is gathered from users and resources for educational purposes only. It is not a recommendation and should be verified with other sources for accuracy.

gamma-Hydroxybutyric acid (also known as and 4-hydroxybutanoic acid and GHB) is a naturally occurring depressant substance. GHB is found naturally in the human central nervous system as well as in wine, beef, some citrus fruits, and in almost all animals (in small amounts).[3]

GHB as the sodium salt, known by the trade name Xyrem,[4] is a prescription sleep-aid which is used to treat various medical conditions such as cataplexy[5] and excessive daytime sleepiness in patients with narcolepsy.[6] It has also been used in a medical setting as a general anesthetic to treat conditions such as insomnia, clinical depression, and alcoholism,[7] and to improve athletic performance.

GHB is used as a recreational substance for its alcohol-like effects. While a common recreational dose is 3 grams, a dose of 5 - 10 grams can result in convulsions, unconsciousness (a coma-like state) and vomiting. Doses above 10 grams are associated with a risk of death.[2] As a result, users are commonly advised to start with a low dose and work their way up slowly by increasing the dose in small increments.

GHB, along with GBL, has acquired a reputation as a "date rape drug," in which it is purportedly secretly placed into alcoholic drinks.[citation needed] There is very limited evidence to suggest that this actually happens but care should always be taken when accepting drinks from strangers.


GHB, or gamma-Hydroxybutanoic acid, is a carboxylic acid substituted with an additional hydroxy group. GHB contains a four carbon chain with a terminal carbon bonded to a hydroxy group (OH-) and double bonded to an oxygen group to form a carboxyl unit; this is butanoic acid. At the other end of the four carbon change at Rγ, GHB is substituted with a hydroxy group.


GHB has at least two distinct binding sites[8] in the central nervous system. GHB is an agonist at the newly characterized GHB receptor, which is excitatory.[9][10] It is also a weak agonist at the GABAB receptor, which is inhibitory.[11]

However, at therapeutic doses, GHB reaches much higher concentrations in the brain and activates GABAB receptors, which are primarily responsible for its sedative effects.[12] GHB's sedative effects are blocked by GABAB antagonists. As the GABA system is the most prolific inhibitory receptor set within the brain, its modulation results in the sedating (or calming effects) of GHB on the nervous system. While research into the GHB receptor is limited, there is evidence that activation of the GHB receptor in some brain areas results in the release of glutamate, the principal excitatory neurotransmitter.[13] Drugs that selectively activate the GHB receptor cause absence seizures in high doses, as do GHB and GABAB agonists.[14]

Activation of both the GHB receptor and GABAB is responsible for the addictive profile of GHB. GHB's effect on dopamine release is biphasic.[15] This means that while low concentrations stimulate dopamine release via the GHB receptor,[16] higher concentrations inhibit dopamine release via GABAB receptors.[17] After an initial phase of inhibition, dopamine release is then increased via the GHB receptor.

GHB induces the accumulation of either a derivative of tryptophan or tryptophan itself, possibly by increasing tryptophan transport across the blood–brain barrier. GHB-induced stimulation may be due to this 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.

These findings may explain the paradoxical mix of sedative and stimulatory properties of GHB as well as the so-called "rebound" effect reported by individuals using GHB as a sleeping agent wherein they awake suddenly after several hours of GHB-induced deep sleep. 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.

Subjective effects

The effects listed below are based upon the subjective effects index and personal experiences of PsychonautWiki contributors. These effects should be taken with a grain of salt and will rarely (if ever) occur all at once, but heavier doses will increase the chances of inducing a full range of effects. Likewise, adverse effects become much more likely on higher doses and may include serious injury or death.

Physical effects

Cognitive effects

Experience reports

There are currently no anecdotal reports which describe the effects of this compound within our experience index. Additional experience reports can be found here:

Toxicity and harm potential

Radar plot showing relative physical harm, social harm, and dependence of GHB[18]

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 be 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.[19]

One publication investigated 226 deaths attributed to GHB.[20] 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.

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.[21] 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.[22] In one European study, no adverse effects were reported after several years of regular recreational use.[23]

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.

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


In multiple studies, GHB has been found to impair spatial memory, working memory, learning and memory in rats with chronic administration.[24][25][26][27] These effects are associated with decreased NMDA receptor expression in the cerebral cortex and possibly other areas as well.[28]

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.


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 3g, a dose of 5g - 10g can result in convulsions, unconsciousness and vomiting. Doses above 10 grams are associated with a risk of death.[2] One must also factor in the added difficulty of knowing the purity of the product (among other problems like its hygroscopy may lower the concentration of GHB in one solution, which is the form which is commonly bought and sold in the illicit market). This makes it hard for even the experienced user to dose properly.[29]

Tolerance and addiction potential

This table compares the withdrawal symptoms of GHB, benzodiazepines, and alcohol.[30]

GHB is moderately physically and 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.[31][32] 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.[33][30]

Although there have been reported fatalities due to GHB withdrawal, reports are inconclusive and further research is needed.[34]

Tolerance will develop to the sedative-hypnotic effects within several weeks 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.

Dangerous interactions

Although many psychoactive substances are safe to use on their own, they can quickly become dangerous or even life-threatening when combined with other substances. The following lists some known dangerous combinations, but may not include all of them. A combination that appears to be safe in low doses can still increase the risk of injury or death. Independent research should always be conducted to ensure that a combination of two or more substances is safe to consume.

A review of the details of 194 deaths attributed to or related to GHB over a ten-year period found that most were from respiratory depression caused by interaction with alcohol or other drugs.[35] In humans, GHB has been shown to inhibit the elimination rate of alcohol. This may explain the respiratory arrest that has been reported after ingestion of both drugs.[36]

  • Stimulants - It can be dangerous to combine depressants with stimulants due to the risk of accidental excessive intoxication. Stimulants mask the sedative effect of depressants, which is the main factor most people use to gauge their level of intoxication. Once the stimulant effects wear off, the effects of the depressant will significantly increase, leading to intensified disinhibition, motor control loss, and dangerous black-out states. This combination can also potentially result in severe dehydration if one's fluid intake is not closely monitored. If choosing to combine these substances, one should strictly limit themselves to a pre-set schedule of dosing only a certain amount per hour until a maximum threshold has been reached.

Legal status

  • Austria: GHB is illegal to possess, produce and sell under the SMG (Suchtmittelgesetz Österreich).[citation needed]
  • Australia: GHB, 1,4-B and GBL are all Class B illegal drugs, along with any possible esters, ethers and aldehydes.[citation needed]
  • Chile: GHB is a controlled drug under the law "Ley de substancias psicotropicas y estupefacientes" (psychotropic substances and narcotics).[citation needed]
  • Hong Kong: GHB is regulated under Schedule 1 of Hong Kong's Chapter 134 Dangerous Drugs Ordinance.[citation needed]
  • New Zealand: GHB, 1,4-B and GBL are all Class B illegal drugs, along with any possible esters, ethers and aldehydes.[citation needed]
  • Norway: GHB is considered a narcotic and is only available by prescription under the trade name Xyrem.[citation needed]
  • Switzerland: GHB is considered a narcotic and is only available by prescription under the trade name Xyrem.[citation needed]
  • United Kingdom: GHB was made a Class C drug in June 2003.[citation needed]
  • United States: GHB was placed on Schedule I of the Controlled Substances Act in March 2000. However, when sold as sodium oxybate, it is considered a Schedule III substance but with Schedule I trafficking penalties.[37] It is one of several drugs that are listed in multiple schedules.[citation needed]

See also

External links


  1. Risks of Combining Depressants (Tripsit) |
  2. 2.0 2.1 2.2 GHB Dosage by Erowid |
  3. Weil, Andrew; Winifred Rosen (1993). "Depressants". From Chocolate to Morphine (2nd ed.). Boston/New York: Houghton Mifflin Company. p. 77. ISBN 0-395-66079-3.
  5. Sodium Oxybate |
  6. United States Patent | Patent Number: US4738985 | Pharmaceutical composition and treatment of narcolepsy (Erowid) |
  7. United States Patent | Patent Number: US4983632 | Use of Gamma-Hydroxybutyric Acid Salts for Preparing Pharmaceutical Compositions for Use in the Treatment of Alcoholism, and the Compositions Obtained (Erowid) |
  8. Gammahydroxybutyrate: An endogenous regulator of energy metabolism (ScienceDirect) |
  9. γ-Hydroxybutyric acid (GHB) and γ-aminobutyric acidB receptor (GABABR) binding sites are distinctive from one another: molecular evidence (ScienceDirect) |
  10. A mechanism for γ-hydroxybutyrate (GHB) as a drug and a substance of abuse |
  11. A mechanism for γ-hydroxybutyrate (GHB) as a drug and a substance of abuse |
  12. Drosophila GABAB receptors are involved in behavioral effects of γ-hydroxybutyric acid (GHB) (ScienceDirect) |
  13. Selective γ-hydroxybutyric acid receptor ligands increase extracellular glutamate in the hippocampus, but fail to activate G protein and to produce the sedative/hypnotic effect of γ-hydroxybutyric acid |
  14. Selective γ-hydroxybutyric acid receptor ligands increase extracellular glutamate in the hippocampus, but fail to activate G protein and to produce the sedative/hypnotic effect of γ-hydroxybutyric acid |
  15. Drosophila GABAB receptors are involved in behavioral effects of γ-hydroxybutyric acid (GHB) (ScienceDirect) |
  16. A specific gamma-hydroxybutyrate receptor ligand possesses both antagonistic and anticonvulsant properties ( / NCBI) |
  17. Tonic GABA-ergic modulation of striatal dopamine release studied by in vivo microdialysis in the freely moving rat (ScienceDirect) |
  18. Development of a rational scale to assess the harm of drugs of potential misuse (ScienceDirect) |
  19. | Erowid. "GHB Overdoses & Poisonings: An Experience with GHB (ID 1926)". Jun 19, 2000.
  20. | Zvosec DL, Smith SW, Porrata T, Strobl AQ, Dyer JE (2011). "Case series of 226 gamma-hydroxybutyrate-associated deaths: lethal toxicity and trauma". The American Journal of Emergency Medicine 29 (3): 319–32.
  21. Psychotherapeutic Drugs. 1340-1375. Bibliographic information missing.
  22. Ferrara, SD. Zotti, S. Tedeschi, L. Frison, G. Palatini, P. et al.. "Pharmacokinetics of gamma-hydroxybutyric acid in alcohol dependent. . .". British Journal of Clinical Pharmacology. 1992. 34. 231-235. R 31 B 93. .
  23. 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 ga. RESEARCH COMMUNICATIONS IN CHEMICAL PATHOLOGY AND PHARMACOLOGY. 1972. 3(1).
  24. Adolescent γ-hydroxybutyric acid exposure decreases cortical N-methyl-d-aspartate receptor and impairs spatial learning (ScienceDirect) |
  25. Effects of subchronic administration of gammahydroxybutyrate (GHB) on spatial working memory in rats ( / NCBI) |
  26. γ-Hydroxybutyric Acid–Induced Cognitive Deficits in the Female Adolescent Rat |
  27. Neurotoxic effects induced by gammahydroxybutyric acid (GHB) in male rats |
  28. ( / NCBI) |
  30. 30.0 30.1 GHB Withdrawal Syndrome | Texas Commission on Alcohol and Drug Abuse |
  31. Systematic Assessment of Gamma Hydroxybutyrate (GHB) Effects During and After Acute Intoxication ( / NCBI) |
  32. Illicit gamma-hydroxybutyrate (GHB) and pharmaceutical sodium oxybate (Xyrem®): differences in characteristics and misuse ( / NCBI) |
  33. | Gamma-hydroxybutyrate withdrawal syndrome.
  34. Gamma-hydroxybutyrate: an emerging drug of abuse that causes physical dependence |
  36. The role of gamma-hydroxybutyric acid in the treatment of alcoholism: from animal to clinical studies ( / NCBI) |