GHB, or gamma-hydroxybutyrate, is a nutrient that is part of the metabolism process in mammalians. It can be found in every cell of the human body. The greatest quantities can be found in the kidney, heart, skeletal muscles, and brown fat tissues (Chin and Kreutzer, 1992). Chin and Kruetzer also believe it to be a neurotransmitter, however that has not yet been proven. GHB is known to be a metabolite and also a precursor of the inhibitory neurotransmitter GABA (gamma-aminobutyric acid). GHB and GABA have a close structural relationship, but GHB does not act on GABA receptor sites.

GHB was first synthesized about thirty years ago. A french researcher, Dr. H. Laborit, was exploring the effects of GABA in the brain. Laborit had to synthesize GHB because very little or no GABA crosses the blood-brain barrier. The difference in the two allowed GHB to cross this barrier where some of it is metabolized into GABA (Vickers, 1969).

What happened was GHB exhibited a range of effects beyond what was expected from GABA. In the years to follow, the effects of GHB have been extensively researched. It has come to be used in Europe as a general anesthetic, a treatment for narcolepsy, an aid in child birth, and also as a treatment for alcoholism and withdrawal syndrome. Then in the 80’s, it was available over the counter in health food stores. It was used by body builders for its ability to stimulate growth hormone release which aided in fat reduction and muscle building. However, in the last few years it has become a popular recreational drug. It gives a pleasant, alcohol like, hangover free “high” with prosexual effects.

For the thirty years prior to 1990, all research papers on GHB were unanimous in reporting numerous beneficial physiological effects and the absence of long term negative effects. Vickers called it “a truly nontoxic hypnotic” and emphasized its “lack of toxicity.” Vickers also showed evidence that GHB demonstrates “no toxic effects on the liver and kidney.” As recent as 1989, the consensus was unchanged. Gallimberti’s study from that year on its uses in treating alcohol withdrawal in humans notes that “GHB’s action…seems to be without serious side effects.” Gallimberti’s reference to the “safety of GHB” shows how well-established this property of the nutrient had become.

Then, on November 8, 1990, the FDA banned the over the counter sale of GHB in the United States. In 1991, two scientists from the California Department of Health Services wrote a report on ten “poisonings” associated with GHB. Chin and Kreutzer had warned of GHB’s potential for abuse. They observed that “all interviewed patients reported a pleasurable sensation or a ‘high’. Several of them..continued taking [GHB] because it made them ‘feel good’.”

If the ten “poisonings” are looked at more closely, four involved “unknown doses,” four featured the “coingestion” of other drugs, (usually alcohol), one involved unmedicated epilepsy, and another a history of grand mal seizures. Since alcohol and other central nervous system depressants are not recommended with GHB, and because it is contraindicated for epileptics, such cases are not unexpected.

One point of the poisonings needs to be addressed–the use of the terms “coma” and “seizures” are used in the description of these ten cases. If a high dose of GHB is consumed it can cause clonus, a rapid, rhythmic contraction and relaxation of muscles which would be better described as muscle spasm or uncontrollable twitching than a seizure. GHB has also been known to cause intense drowsiness, abrupt sedation, and deep sleep which is probably better described as unarrousability or deep sedation rather than coma.

The authors of these ten reports confirmed that “there have not been any reported deaths” and that “if product use is discontinued, full recovery with no long term side effects is universal.”

Some of the concerns that are related with GHB are some of the side effects that are present when large doses are consumed. A dose twice the recommended for relaxation can put you to sleep in a very short amount of time after consumption. In this respect it is similar to alcohol: if you drink twice as much as you normally would, you probably wouldn’t function very well.

Most of the people that take it find that it gives a pleasant state of relaxation and tranquility. There can also be feelings of placidity, sensuality, mild euphoria, and can also give a tendency to talk. Worries tend to fade into feelings of emotional warmth, well being, and pleasant drowsiness. The morning after is unlike that of alcohol or other drugs that induce similar feelings. Most people claim to feel refreshed and even energized the next day. The effects can be felt in as quick as five minutes to as long as twenty minutes after ingestion. It lasts for anywhere from an hour to three hours. These feelings can be prolonged by more doses when it starts to wear off. Higher levels can be reached by just small doses after the initial dose. One may experience giddiness, silliness, trouble walking and speaking, and may become dizzy. Even higher doses can induce sleep in just a matter of minutes.

GHB temporarily inhibits the release of dopamine in the brain. This leads to a build up of dopamine and later increased dopamine release when the GHB wears off (Chin and Kreutzer, 1992). This releasing of the dopamine may explain the middle-of- the-night wakings which are common with higher doses, and for the energized feeling the next day.

GHB also stimulates pituitary growth hormone release. One rigorous Japanese study reported nine-fold and sixteen-fold increases in growth hormone 30 and 60 minutes respectively after an intravenous administration of 2.5 grams of GHB in six healthy men between the ages of twenty five and forty (Takahara, 1977). Growth hormone levels were still at seven-fold higher at two hours.

GHB induces muscle relaxation and is growing in France and Italy as an aid to child birth. It causes “spectacular action on the dilation of the cervix,” decreased anxiety, greater intensity and frequency of uterine contractions, increased sensitivity to oxytocic drugs, which are used to induce contractions, preservation of reflexes, a lack of respiratory depression in the fetus, and protection against fetal cardiac anoxia (Vickers, 1969; Laborit, 1964).

GHB is completely metabolized onto carbon dioxide and water, leaving absolutely no residue of toxic metabolites (Vickers, 1969; Laborit, 1972). It is so efficient that it can no longer be detected in the urine four to five hours after injected (Laborit, 1964).

It also activates a metabolic process known as the “pentose pathway” which plays an important role in the synthesis of protein within the body (Laborit, 1972). GHB also creates a “protein sparing” effect (Laborit, 1964) which reduces the rate at which the body breaks down its own proteins. It is because of this and its effect on the growth hormone, that it is used in muscle building and fat loss.

At extremely large doses GHB is used as an anesthetic. The large doses are followed by a small increase in blood sugar levels, and a significant decrease in cholesterol. Respiration becomes slower and deeper. Blood pressure may rise or fall slightly, or remain stable, but a mild slowing of the heart is consistent (Vickers, 1969; Laborit, 1964).

Smart Drugs II called GHB “almost an ideal sleep inducing substance.” Due to the relaxation experienced from small doses it is easier to fall asleep naturally. Then from larger doses sleep will be induced within five to ten minutes (Laborit, 1964). Most other hypnotics interfere with the various stages of the sleep cycle and prevents the body from getting a complete rest. GHB induced sleep is characterized by increased levels of carbon dioxide in the arteries, as in normal sleep (Vickers, 1969). During normal and GHB sleep, the central nervous system continues to be responsive to pain and other stimuli, which limits GHB’s use as an anesthetic (Vickers, 1969). It also facilitates REM sleep, and non-REM (slow-wave) sleep, the stage of sleep featuring increased release of growth hormone (Laborit, 1972). And unlike the unconsciousness produced by other anesthetics, that triggered by GHB does not feature a systemic decrease in oxygen consumption (Laborit, 1964).

In laboratory rats that are addicted to alcohol, withdrawal symptoms closely resemble those that are exhibited by humans. These symptoms include: tremors, convulsions, and hypersensitivity to sound. All symptoms were blocked by large doses of GHB (Fadda, 1989). Administration of GHB has also been found to prevent alcohol consumption among rats that voluntarily ingest alcohol (Fadda, 1989; Gallimberti, 1989).

In a rigorous, double-blind, placebo-controlled study conducted of human alcoholics, “nearly all withdrawal symptoms disappeared within two to seven hours” after administration of GHB. On a severe-moderate-mild-or-none scale, withdrawal symptoms remained below moderate during the entire period. The only side effects observed was slight, occasional, and transient dizziness. The researchers concluded, “the results clearly indicated that GHB is effective for the suppression of withdrawal symptoms in alcoholics” (Gallimberti, 1989).

GHB’s efficacy for treating anxiety has been positively demonstrated in tests involving schizophrenic subjects (Laborit, 1964). Its sedative properties have earned it a role as a pyschotherapeutic adjunct (Vickers, 1969). It has also been used to assist the process of “abreaction,” or the release, usually through verbalization, of repressed emotion (Vickers, 1969). Unlike other anti-anxiety drugs, it’s effect is non-toxic. And it encourages verbalization, and the typical lack of fear during the GHB experience would seem to provide and ideal context for the verbal exploration of difficult emotions during therapy.

GHB is growing in popularity and seems to be widely available in the underground “gray market.” Since most of the GHB available through such means is of the “bootleg” variety, made by those other than professionals. So there are concerns about quality and purity.

As has been emphasized, the overall safety of GHB is well established, and no deaths linked to GHB have been reported in over the thirty years that it has been in use (Vickers, 1969; Chin and Kreutzer, 1992). Actually, as of 1990, there had only been forty six adverse reactions that had been reported in the United States. All which were followed by a rapid and complete recovery (Chin and Kreutzer, 1992). Unlike a large number of other drugs, GHB has no toxic effects on the liver, kidney, or other organs (Vichers, 1969; Chin and Kreutzer, 1992). Vickers in 1969 even reports that doses as high as twenty to thirty grams per twenty four hour period have been used for several days without negative consequences. Canadien studies of narcolepsy there is a use of roughly 2.5 grams for several years which resulted in no reports of long term adverse effects, or problems with issues of addiction or dependence. And in France, sub-anesthetic oral doses were used by “a large number of patients for about six years” without unfavorable effect (Laborit, 1972).

The most common side effects are dizziness, nausea, and sometimes vomiting. Also there may be muscle spasms, headache, moderate slowing of the heart rate, and small changes in blood pressure can occur. And at higher doses cardiac and respiratory depression can occur. Also at these higher doses sudden sedation and loss of consciousness are expected. Some of the more unusual adverse reactions may include: diarrhea, lack of bladder control, temporary amnesia, and sleep walking.

Vickers reports that there are “remarkably few” contraindications. However, those who suffer from any of the following conditions should not use GHB: severe illness of any kind, epilepsy, convulsions, slowed heart rate due to conduction problems, Cushing’s syndrome, severe cardiovascular disease, hyperprolactinemia, and severe hypertension (Gallimberti, 1989; Vickers,1969).

GHB should not be used with benzodiazepines, phenothiazines, various painkillers (barbiturates and opiates), alcohol, anticonvulsants, and even many other over the counter allergy and sleep remedies.

The amount required for a given level of effect will vary from person to person. Once the amount is found it will stay the same, in that a tolerance does not build up. Most people find that a dose in the range of .75-1.5 grams is suitable for the prosexual effects, and that a quantity around 2.5 grams will be sufficient to force sleep.

So should GHB be used for uses such as a sleep aid for those with mild sleep disorders, those in therapy sessions, those with alcoholism, and possibly those with anxiety disorders. If a drug comes along that has so many good uses and is for the most part safe, why shouldn’t it be used. There are many more drugs out there that are on the shelves in the pharmacy that can not do even half of what this drug can do and that are much more dangerous. This is not a plea to legalize the drug, but instead a plea just to look at the possibilities of the drug. With no toxicity and uses that range from anesthesia to child birth to weight loss to sleep aids, how can one just label it as a “date rape” drug and forget about it. It has too much to offer on the good side than it does on the bad. New studies are coming out all the time. Possibly more is truly known about the drug than what they are telling us. However, from the information that I have gathered it seems that this could be a renaissance drug of sorts. GHB was recently put on the control list as a schedule 1 drug. Possibly now some of its uses can be examined a little more closely, for possible use in the abnormal psychology as well as other areas of medicine.


Chin MY, Kreutzer RA and Dyer JE. Acute poisoning from gamma-hydroxybutyrate in California. West J Med (United States). 156(4): 380-4, April 1992.

Fadda F, Colombo G, Mosca E and Gessa GL. Suppression by gamma-hydroxybutyrate acid of ethanol withdrawal syndrome in rats. Alcohol and Alcoholism [Great Britain]. 24(5): 447-51, 1989.

Gallimberti L, Gentile N, Cibin M, Fadda F, Canton G, Ferri M, Ferrara SD and Gessa GL. Gamma-hydroxybutyric acid for treatment of alcohol withdrawal syndrome.

The Lancet, 787-9, 30 September 1989.

Laborit H. Correlations between protein and serontin 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 3(1): January 1972.

Laborit H. Sodium 4-Hydroxybutyrate. Int J Neuropharmacology [Great Britain]. 3: 433-52, 1964.

Takahara J, Yunoki S, Yakushiji W, Yamauchi J and Ofuji T. Stimulatory effects of gamma-hydroxybutyric acid on growth hormone and prolactin release in humans. J Clin Endocrinal Metab 44: 1014, 1977.

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William Anderson (Schoolworkhelper Editorial Team)
William completed his Bachelor of Science and Master of Arts in 2013. He current serves as a lecturer, tutor and freelance writer. In his spare time, he enjoys reading, walking his dog and parasailing. Article last reviewed: 2022 | St. Rosemary Institution © 2010-2024 | Creative Commons 4.0

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