GHB, also known as G and liquid ecstasy, is a central nervous system depressant with effects similar to alcohol and MDMA. After its synthesis in the 1960s, GHB began to be evaluated for a variety of medicinal applications, including use in anesthesia, obstetrics, alcohol/opiate dependence, and as a treatment for narcolepsy. Its use became more widespread in the 1980s when it was widely available over the counter as a bodybuilding supplement and sleep aid. By the next decade, it was being used recreationally as a “club drug” for its euphoric and pro-sexual effects. Eventual reports of abuse and GHB-related deaths, coupled with its acquired status of a “date-rape” drug, eventually led to its federal scheduling in 2000.
Table of Contents
- Legal Status
- GHB Today
GHB is a sedative commonly used as a recreational drug due to its euphoriant, empathogenic, and aphrodisiacal effects. It’s an endogenous compound found in trace amounts in the brains of humans and other animals. In the brain, it’s a putative neurotransmitter and regulator of energy metabolism.
What is GHB (Gamma Hydroxybutyric Acid)
Gamma Hydroxybutyric Acid is both a precursor and metabolite of the endogenous neurotransmitter GABA. It can also be found in trace amounts in beef, small citrus foods, and fermented beverages like wine, but not in sufficient quantities to render it psychoactive.
GHB is easily manufactured by non-professional “kitchen” chemists using GHB precursors, namely GBL. GBL is an industrial solvent that’s found in floor cleaning products, paint strippers, and nail polish removers. GHB is synthesized from GBL under strongly alkaline conditions by the addition of lye (sodium hydroxide). GBL is also considered a “prodrug” of GHB. After ingestion, the body converts it to GHB within minutes. Another precursor, called 1,4–butanediol, is not as easily converted to GHB but is also metabolized within the body to GHB.
- Gamma Oh
- Georgia Home Boy
- Grievous Bodily Harm
- Liquid X
- Liquid Ecstasy
GHB, or γ-hydroxybutyric acid, is a short-chain fatty acid with a chemical formula of C4H8O3. It is typically found as its sodium salt, which has a chemical formula of C4H7NaO3. It is a small, polar 4-carbon compound with a chemical structure that closely resembles the inhibitory neurotransmitter GABA (gamma-aminobutyric acid). The only chemical difference between the two occurs on the 4th carbon, where GABA’s amino group is replaced by a hydroxyl group. GHB is both a metabolite and precursor to GABA. It is also a precursor to the excitatory neurotransmitter glutamate and the inhibitory neurotransmitter glycine in certain brain areas.
Forms & Ways of Consumption
Although it does exist as a free acid, GHB is mostly encountered as salts that are known as oxybates. It is most commonly encountered as its sodium salt (sodium oxybate, brand name Xyrem), but also exists as a potassium salt (K-GHB, or potassium oxybate). The salts are highly soluble in both water and alcohol. Recreationally, they are almost exclusively consumed orally, but in medical settings for anesthesia can be given intravenously.
In pure form, GHB exists as a white powder. The salts are “hygroscopic,” meaning they retain moisture from the air. For this reason, GHB is less commonly consumed in tablet, capsule, or powder form. This method of ingestion can also be impractical, considering the number of capsules or tablets that would be required for a dose (usually exceeding 1 gram).
For these reasons, pure GHB powder is often placed in water before being consumed orally. Liquid GHB is clear and odorless and has an oily consistency. It has a soapy, salty taste that is sometimes masked by adding it to flavored beverages.
When prescribed as Xyrem, the sodium salt comes in an oral solution with a dosage of 0.5g/mL. Recreationally, GHB is diluted into a liquid with a concentration that varies, making dosing more difficult. When the concentration is known, a measuring spoon, dropper, or syringe can be used to accurately measure a dose each time. It’s important to shake the bottle each time it is dosed, as GHB has a tendency to settle onto the bottom, which can make later doses more potent.
GHB was first synthesized in the late 19th century, but its therapeutic applications weren’t revealed until the mid-19th century. Its use increased in the 1980s as a bodybuilding supplement and sleep aid. By the 1990s, it was used as a recreational intoxicant, leading to its federal scheduling in 2000.
Modern Day Discovery
GHB was first synthesized in 1874 by the Russian chemist Alexander Zaytsev, but substantial research with humans didn’t occur until nearly 90 years later. GHB was synthesized in the early 1960s by Dr. Henri Laborit, a French researcher who was attempting to create a GABA analog that would cross the blood-brain barrier.
Soon after Laborit published a paper in 1964 describing GHB’s pharmacological properties, numerous researchers began investigating it for a variety of uses. Initially, they studied it as an intravenous anesthetic, particularly for surgeries in children and to aid in childbirth by dilating the cervix. However, enthusiasm for this purpose waned once researchers discovered it produced undesirable effects such as vomiting and seizure-like activity.
In the 1960s, studies also focused on its anti-anxiety, antidepressant, and sexual-enhancing properties. By the next decade, investigation began into its potential for the treatment of sleep disorders like narcolepsy, and a few decades later, for alcohol and opiate withdrawal. GHB’s medical uses have declined in recent times in parallel with recognition of its abuse potential and the development of newer drugs, but it is still used today for narcolepsy and, less often, alcoholism.
Important Events, Findings, Studies
GHB became a popular dietary supplement in the late 1980s among bodybuilders and dieters to promote muscle growth and fat reduction. These anabolic effects became known once studies demonstrated that GHB raises growth hormone and prolactin levels in humans. The health food industry also marketed and sold GHB as a sleep aid and replacement for L-tryptophan, an amino acid removed from the market in response to contaminated batches.
With the increasing use of GHB came reports of misuse and intoxications, eventually leading the Food and Drug Administration (FDA) to prohibit the over-the-counter sale of GHB in November of 1990.
GHB Labeled a “Date-Rape” Drug
By the late 1990s, GHB gained notoriety within the general public as a “date-rape”drug, one of a class of drugs that are sometimes used in drug-facilitated sexual assault (DFSA). While alcohol and benzodiazepines (particularly flunitrazepam) appear to be the most common date-rape drugs, the press has reported on stories of perpetrators secretly adding GHB into the drinks of victims at nightclubs and bars. The perpetrators exploit the fact that liquid GHB is colorless, odorless, and water soluble. its ability to produce amnesia, suggestibility, passivity, and increased libido at lower doses have also contributed to its use in this fashion.
Most of the evidence that GHB is used for this purpose is anecdotal. Between 1996 to 1999, 22 reports of GHB’s role in drug-facilitated sexual assault were made to the Drug Enforcement Administration. Since GHB is quickly metabolized by the body, it makes screening difficult in sexual assault cases unless it is done immediately after the assault.
Important Legislation Passed
In response to the sexual assault cases, Congress passed an amendment to the Controlled Substances Act called the Drug-Induced Rape Prevention and Punishment Act. Passed in 1996, this act provided criminal penalties of up to 20 years imprisonment and fines for the use of GHB or other substances to aid in sexual assault.
Then in 1999, national attention was drawn to a fatal GHB or GBL poisoning of a 15-year-old girl named Samantha Reid. The incident inspired a piece of legislation called the Hillory J. Farias and Samantha Reid Date-Rape Prohibition Act of 2000. This legislation eventually made GHB a schedule I controlled substance in March 2000.
Shortly after federal scheduling, GHB manufacturing and sales continued within the “gray market.” In particular, the GHB analogs GBL and 1,4-butanediol rose in popularity, as these chemicals evaded federal scheduling. On the internet, kits could be purchased that contained these precursor chemicals and recipes to produce GHB. In the early 2000s this led to a campaign by the DEA called Operation Webslinger that aimed to take down the illicit internet trafficking of GHB and its analogs.
3. Laws and Legal Status
As described previously, GHB received an increasing amount of negative press relating to its abuse potential and alleged use in drug-facilitated sexual assaults. These reports led to swift changes in its legal status, first on a state-wide and then on a federal basis.
Legality in the United States
GHB has been a Schedule I substance under the Controlled Substances Act since March of 2000. This means it is illegal to manufacture, buy, possess, or distribute without a DEA license.
However, the sodium salt of GHB, which goes by the prescription brand name of Xyrem, is listed as a Schedule III controlled substance when prescribed and used legally under a limited distribution program. Its Schedule III classification means it has the potential for moderate physical dependence and high psychological dependence, but also carries valid medical uses. When Xyrem is illicitly trafficked or used recreationally, it converts to a Schedule I substance.
GHB precursors such as GBL and 1,4-butanediol are not scheduled federally, but they are controlled in a number of states, including California, New York, Hawaii, Oklahoma, and Oregon. If GBL or 1,4-butanediol are consumed recreationally, they may be punishable as a Schedule I substance under the Federal Analog Act.
Around the world, GHB and its precursors are controlled in a manner similar to that in the United States. In 2001, the Commission on Narcotic Drugs placed GHB in Schedule IV of the 1971 Convention on Psychotropic Substances, making it a controlled substance in all UN member states. The WHO and the UN are more recently considering moving GHB from Schedule IV to Schedule II.
In the UK, GHB, GBL, and 1,4-butanediol are all Class C drugs under the Misuse of Drugs Act 1971, making it illegal to possess or sell them for human ingestion.
In Canada, GHB has been a Schedule I controlled substance since November 6, 2012. However, it is not illegal for an individual to possess GBL there.
In New Zealand and Australia, GHB, GBL, and 1,4-butanediol are all Class B illegal drugs, which prohibits their importation, sale, and possession.
In Norway and Switzerland, GHB is considered a narcotic and is only available as the prescription drug Xyrem.
For a more detailed breakdown of international legality, visit this page.
Unlike GABA, GHB freely crosses the blood-brain barrier and achieves peak plasma concentration in 20–60 minutes. Once in the body, it has a short half-life of 30–60 minutes and is ultimately metabolized into nontoxic metabolites, namely carbon dioxide and water.
Mechanism of Action
At low doses, GHB binds to and activates excitatory GHB receptors that are found in many brain regions, including the hippocampus, cortex, and in dopaminergic brain regions such as the olfactory tracts, striatum, and substantia nigra. These receptors inhibit the release of GABA and stimulate the release of dopamine and the excitatory neurotransmitter glutamate. Taken together, these mechanisms account for its stimulatory and rewarding effects.
At higher doses, GHB increasingly binds to and activates the inhibitory GABAB receptors, an action that inhibits dopamine release and is responsible for its sedative/hypnotic effects. This mechanism differs from other sedative and hypnotic drugs—including ethanol, benzodiazepines, and barbiturates—which activate GABAA receptors.
This dual mechanism of action on GHB and GABAB receptors accounts for the “rebound effect,”, in which it’s common for GHB users to abruptly sleep for 2–3 hours and then wake up feeling refreshed. GHB initially causes sedation and sleep via GABAB receptors, but later stimulation and arousal via GHB receptors once the body metabolizes GHB and its concentration in the body drops.
Toxicity is based on the levels of exposure or dose required for a substance to cause harm to a human or animal. The lethality of a compound is measured by the median lethal dose or LD50. This is the dose of a drug that will kill 50% of the animals that are being tested.
In animal studies, the LD50 of GHB ranges from 1–2 g/kg, with the cause of death being respiratory depression. The lethal dose in humans isn’t precisely known and varies depending on factors such as body weight, tolerance levels, the co-ingestion of other substances, and idiosyncratic reactions. Fatal overdoses of GHB used orally have occurred with just 5.4 g, while subjects have survived as much as 29 g. Overall, the LD50 is well above the active dosage, approximately 5–15 times higher than the dose that produces a coma.
GHB is generally nontoxic when used responsibly and/or under medical supervision, but like other drugs, its toxicity is dose-dependent. Doses of 20–30 mg/kg (1.4–2.1 g for a 70 kg individual) result in euphoria, drowsiness, and sleep, but just twice this amount can put the user in a comatose state followed by an abrupt awakening after several hours. Many individuals have a quick and uneventful recovery from an overdose of GHB, but the toxicity is heightened dramatically when it is combined with other sedative drugs, particularly alcohol. Combining with sedative drugs dangerously exacerbates both CNS and respiratory depression. This can lead to rapid unconsciousness and the risk of aspirating on vomit if the user isn’t placed in the recovery position.
According to several animal studies, GHB may produce neurotoxic effects with prolonged abuse. One 2009 rodent study found that GHB administration resulted in spatial and working memory deficits. These deficits were correlated with neuronal damage in the hippocampus and prefrontal cortex, possibly due to increased levels of oxidative stress in these areas. An earlier study from 2004 administered GHB for five days to adolescent rats and found that exposure to the drug resulted in impaired spatial learning on the Morris Water Maze, a common test of spatial memory in rodents. These deficits were associated with reduced expression of the NMDA receptor in the frontal cortex.
GHB and Other Substances
Never combine GHB with alcohol. GHB is synergistic with alcohol and the combination can result in hypotension, respiratory depression, and a potentially life-threatening overdose.
Do not combine GHB with opioids. Opioids such as fentanyl, heroin, and morphine strongly potentiate the effects of GHB, and can rapidly lead to unconsciousness, vomiting, and aspiration.
Avoid using GHB with MXE, nitrous, ketamine, and DXM. These combinations can increase the chance of ataxia (loss of motor control), vomiting, and unconsciousness. In addition, it is not advised to take GHB with MDMA. A large dose of GHB can overpower the effects of MDMA on the comedown.
GHB should not be consumed with stimulants such as cocaine and amphetamines. These drugs can initially mask the symptoms of a GHB overdose, but once they wear off, the GHB can overtake the effects and cause an overdose.
GHB and Medications
GHB should not be used with other CNS depressants, sedatives, and hypnotics.
- Benzodiazepines (such as Valium, Klonopin, and Xanax)
- Z-drugs (zolpidem, zaleplon, and zopiclone)
- Phenothiazine antipsychotics (such as Thorazine and Stelazine)
- Painkillers (barbiturates and opiates)
- Anticonvulsants (including Dilantin, phenobarbital, gabapentin, and others)
- Muscle relaxants (such as Soma, Flaxedil, Banflex, and others)
Combining GHB with these drugs can result in dangerous CNS and respiratory depression, unconsciousness, nausea, vomiting, and aspiration. Additionally, combining GHB with many over-the-counter allergy and sleep remedies is also not recommended without direct medical supervision.
Lastly, GHB should not be used by individuals who are taking protease inhibitors, a class of antiviral drugs. These compounds alter GHB’s metabolism, potentially resulting in a life-threatening overdose even when small doses of GHB are consumed.
GHB and Psychological Conditions
GHB should not be used in those with a history of depressive psychiatric disorders. Users with depression may find GHB exacerbates the condition and potentially causes suicidal ideation.
GHB and Physical Conditions
GHB should not be used by individuals with severe illness of any kind, including severe cardiovascular disease, hypertension, bradycardia (slow heart rate), hyperprolactinemia (high amounts of prolactin), and Cushing syndrome (high levels of cortisol).
In addition, GHB should not be used by those with epilepsy or a history of seizures. GHB, especially at high doses, can cause seizure-like activity.
Women should avoid GHB during pregnancy or breastfeeding, as its effects on prenatal development and babies are not well understood and possibly harmful.
In Europe, GHB overdose and coma is the third most common drug-related cause for emergency medical attendance, after heroin and cocaine. The biggest safety concerns involve frequent use (which can lead to dependence and withdrawals), taking too high of a dose, and combining GHB with other substances. A 2011 study of 226 GHB-related deaths found 65% of the fatal GHB overdoses involved combinations with other substances, most commonly alcohol and MDMA. CNS depressants have dangerous additive effects with GHB, which can rapidly lead to unconsciousness and cardiorespiratory arrest, especially at high doses.
When taken alone, GHB can cause unarousable sleep for several hours in the 3–5+ gram range, about twice a normal dose. There is a risk of death in the 7–10+ gram range, or approximately 3–4 times a normal dose. Overdoses can quickly lead to vomiting (with the risk of aspiration), convulsions, unarousable coma, respiratory depression, and sometimes death. However, if GHB was the only drug ingested, overdoses commonly lead to a spontaneous awakening and full recovery in 5–8 hours.
GHB’s narrow margin of safety underscores the importance of accurate and intentional measurement. Always be sure of the concentration of the solution before carefully measuring out a dose, and start with a low dose to gauge individual reaction.
Another preventable factor relating to GHB overdosing is the potential for accidental dosing. Given that GHB is colorless and odorless, it can be easily mistaken for water if it is placed in a drinking container like a water bottle. These accidental intoxications can be easily avoided by labeling the storage container and adding blue food coloring to the liquid.
If a GHB Overdose is Suspected
- Make sure the person is breathing. When users are in a GHB coma, they will often show “Cheynes-Stokes” breathing, where users alternate between slow, shallow breaths and deep, rapid breaths.
- Turn the person onto their side (the recovery position). This will keep their airway open so that if they vomit while unconscious, they won’t choke.
- Constantly monitor the person until help arrives or they regain consciousness. Try to figure out what else they’ve taken as well.
Due to GHB’s steep dose-response curve, its effects are very dose-dependent. When taken orally, GHB is quickly absorbed into the bloodstream and readily crosses the blood-brain barrier. The effects come on within 10–20 minutes and last between 1.5 to 2.5 hours. There may be aftereffects for 2–4 hours; users may feel drowsy or sleepy, but sometimes alert and refreshed, especially after sleeping, given that GHB enhances slow-wave (SWS) and REM sleep.
Note: the following dose-dependent effects are for pure GHB powder, and not liquid. The mL dosages are meaningless without knowing the concentration of the solution, which can vary dramatically from batch to batch.
At low doses (0.5–1.5 g), GHB’s physiological effects resemble mild to moderate alcohol inebriation, and may include:
- Slightly decreased motor skills
- Muscle relaxation
- Physical stimulation
At medium doses (1–2.5 g), GHB can produce:
- Slurred speech
- Pupil dilation
- Increased salivation
- Impaired motor coordination
- Increase in tactile sensitivity
- Heightened and prolonged orgasm
- Enhanced erectile capacity
Heavy doses (2.5g+) can lead to all the previous physiological effects, in addition to:
- Physical sedation
- Optical sliding
- Respiratory depression
- Bradycardia (slow heart rate)
- Potential unconsciousness
A heavy dose can easily lead to an overdose, depending on one’s body weight, tolerance levels, and individual sensitivity. These complications can be further compounded by difficulties in knowing the purity and concentration of the drug. For this reason, always start with a low dose and slowly titrate up to avoid the overdose range.
At low doses (0.5–1.5 grams), GHB produces effects similar to 1–3 alcoholic drinks. These include:
- Mild relaxation
- Enhanced sociability
- Mild dizziness
At medium doses (1–2.5 g), the psychological effects can include:
- Deep relaxation
- Mood enhancement
- Decreased anxiety
- Increased intensity of emotions
- Increased appreciation for talking and dancing
- Disinhibition (this can result in impaired decision-making and risky sex)
- Music enhancement
- Increased libido
- Heightened awareness of one’s body and sensations
Heavy doses (2.5+g) of GHB can lead to:
- Strong euphoria
- Entactogenic effects (increased empathy, affection, and sociability)
- Pro-sexual effects
- Feelings of disequilibrium
- Potential loss of consciousness
Common Side Effects
At recreational doses, GHB is associated with a multitude of undesirable side effects. These effects are more likely with higher doses, and can include:
- Muscle cramps
- Slow heartbeat
- Shallow breathing
The possibility of adverse effects with GHB increase with increasing dosage. Some of these adverse effects may be mild, while others are potentially life-threatening. In addition to these adverse effects, the reduced level of consciousness produced by high doses can leave users vulnerable to situational dangers such as robberies or sexual assaults.
Some of GHB’s many potential adverse effects include:
- Bradycardia (slowed heart rate)
- Clonic seizure-like activity (uncontrollable muscle contractions or twitches)
- Memory loss and amnesia (“blackouts”)
- Decreased body temperature
- Lack of bladder control
- Potential cardiac arrest (high doses)
- Coma (high doses)
While the same dose can produce widely different effects among individuals, generally speaking, 3–4 g can lead to unconsciousness within minutes, and doses of more than 4–5 g (however, doses up to 30 g have been described) to a deep (but reversible) coma that lasts several hours. In this dangerously high dose range, it’s common for users to unexpectedly wake up in the hospital, not knowing what happened.
Addiction, Withdrawal, and Tolerance
Given that GHB activates dopaminergic brain regions within the reward pathway, it is known to be moderately addictive, and regular use can lead to dependence. In users who are dependent, serious emotional and physical withdrawal symptoms can start 1–6 hours after abruptly stopping use. Withdrawal symptoms are characterized by insomnia, tremors, irregular heart rate, anxiety, sweating, and agitation, In severe cases of withdrawal, delirium, hallucinations, and psychosis have been reported. The acute withdrawal phase can last up to two weeks, but emotional problems and insomnia can persist for months.
Tolerance to GHB’s effects can develop after several weeks of prolonged use. The development of tolerance can lead to extremely high doses that would be life-threatening for non-tolerant users. Narcoleptics have been known to take daily doses of 9 grams or more as a result of tolerance. Without further dosing, tolerance normally returns to baseline within 2 weeks. GHB presents cross-tolerance with alcohol and its precursors, namely GBL and 1,4-butanediol.
The recreational use of GHB as a “club drug” began in the 1990s before it was federally controlled. Nowadays, recreational sourcing is clandestine via grey and black market production, which can commonly produce GHB of questionable quality and purity. On the other hand, the sodium salt of GHB is prescribed medically for narcolepsy and, less commonly, alcohol and opiate dependence. Sodium oxybate is the active ingredient in the prescription drugs Xyrem, from Jazz Pharmaceuticals, and Alcover, from D&A Pharma.
The GHB salts (which are powders) are commonly mixed with water for recreational use. The effects come on within 10–20 minutes and last 1.5–2.5 hours, but this is prolonged by repeated dosing. However, small dose increases can lead to a dramatic intensification of effects, so recreational users must be extremely cautious when dosing.
People find GHB to be a desirable alcohol replacement, producing feelings of euphoria, disinhibition, increased sex drive, empathy, and sociability without a characteristic alcohol hangover the next morning. It’s commonly used by young people in their 20s and 30s, especially in party environments like clubs and raves. GHB is also used as a “chemsex” drug to enhance sexual performance and desire, particularly among the gay population
The sodium salt of GHB, under the brand name Xyrem, is approved by the US Food and Drug Administration (FDA) for the treatment of narcolepsy. For narcoleptics, Xyrem helps to prevent excessive daytime sleepiness and attacks of cataplexy, or brief episodes of muscle weakness brought on by strong emotions. It alleviates symptoms of narcolepsy by increasing slow-wave sleep and reducing the number of nighttime awakenings, which can help daytime functioning the next day.
In addition, Xyrem is sometimes used off-label to treat symptoms of fibromyalgia, including insomnia, fatigue, and chronic pain. Apart from its potential side effects, one drawback of GHB’s use for these conditions relates to its short half-life. Users commonly have to wake up in the middle of the night to readminister a second dose.
Sodium oxybate is also used for anesthesia in France and Germany, where it is known under the brand names of Gamma-OH and Somsanit, respectively. In addition, it is approved in Italy and Austria for the treatment of alcoholism and opiate dependence. Specifically, it is used as an adjuvant medication for withdrawal symptoms, initial detoxification, and to maintain abstinence in dependent users.
7. GHB Today
Compared to other club drugs like MDMA, GHB has a relatively low prevalence of use in the United States and around the world. It appears to be most popular among young people that attend raves, festivals, and parties. Its popularity stems partly from its affordability. A single dose typically costs a couple of dollars, while its bulk price is even cheaper, approximately 10 to 50 dollars per 100 grams.
Trends in Use
According to the 2018 National Survey on Drug Use and Health, approximately 1.4 million people aged twelve or older have used GHB in their lifetime. After GHB was listed as a controlled substance in 2000, its use significantly declined, according to data from local poison control centers. Between 1999 and 2003, The California Poison Control System (CPCS) reported a 76% decrease in GHB exposures. Similarly, in 2018, the National Poison Data System (NPDS) reported 392 single exposures and no deaths.
Around the World
The prevalence of GHB/GBL use is relatively low around the world. However, there are limited data concerning its prevalence because the drugs aren’t often listed on national surveys. According to the 2016 National Drug Strategy Household Survey, only 0.1% of Australians report GHB use in the previous 12 months. Similarly, in 2015, Norway reported a prevalence rate of 0.1% in adults between the ages of 16 and 64. In the United Kingdom, GHB use peaked between 1994 and 2002, followed by a falling trend.
More recently, a 2017 study found that the number of GHB-related deaths in London increased by 119% from 2014 to 2015. The authors claim the rise could be the result of its increased use for chemsex. A similar trend was seen in Victoria, Australia between 2012 and 2019, where GHB-related ambulance attendances increased 147% to 5,866 attendances over the seven-year period. The growing number of GHB overdoses requiring emergency attention in recent years underscores the importance of careful dosing, measuring, and storing.
Does GHB Show Up in a Drug Test?
GHB and its metabolites are not detected on a standard drug test. It’s possible to detect GHB with specialized drug tests (such as GC/MS). Testing is difficult, however, due to its short detection window. Its metabolites are excreted from the body within 24 hours.
How to Store GHB
GHB will last indefinitely when stored in a bottle (glass or plastic) in the refrigerator. Store the GHB in a container that can’t be mistaken for a drinking container, such as a dark-brown medicine bottle. To be extra cautious, you can add blue food coloring to the bottle to distinguish it from other liquids like water. If GHB is in powdered form, it should be kept in a cool, dark space in an airtight container.
Can Dogs Smell GHB?
Yes, drug sniffer dogs can be trained to detect GHB, though the actual extent of this happening is unclear.
What Does GHB Taste Like?
GHB has a chemical taste that has been described as salty or soapy.
Disclaimer: GHB is potentially categorized as an illegal drug. Reality Sandwich is not encouraging the use or growth of this drug where it is prohibited. However, we believe that providing information is imperative for the safety of those who choose to explore this substance. This guide is intended to give educational content and should in no way be viewed as medical recommendations.