Frequently Asked Questions about Gamma-hydroxybutyrate
v 1.0 - 1994
Erowid Note: This FAQ was not authored by Erowid. It may include out-of-date and/or incorrect information. Please check the version date to see when it was most recently revised. It appears on Erowid as part of our historical archives. For current information, see Erowid's summary pages in the substance's main vault.
|Table of Contents|
|1.||Introduction||2.||Scientific Reports on GHB|
|3.||Why was GHB banned?||4.||What are the real concerns?|
|5.||How does it feel?||6.||Actions of GHB in the body|
|7.||GHB and sleep||8.||GHB, Alcohol, and Alcoholism|
|9.||Other Uses of GHB||10.||GHB and sex|
|11.||Legal Status and Availability||12.||Safety Issues|
GHB, or gamma-hydroxybutyrate, is a normal component of mammalian metabolism. It is found naturally in every cell in the human body and is most properly considered a nutrient. In the brain, the highest amounts are found in the hypothalamus and basal ganglia [Gallimberti, 1989]. GHB is found in greater concentrations in kidney, heart, skeletal muscles, and brown fat tissues [Chin and Kreutzer, 1992]. It is believed to be a neurotransmitter, although the jury is still out as to whether it exhibits all of the properties required for fulfillment of this function [Chin and Kreutzer, 1992]. It is both a metabolite and precursor of the inhibitory neurotransmitter GABA (gamma-aminobutyric acid, or gamma-aminobutyrate), another nutrient to which it bears a close structural relationship. GHB, however, does not act directly on GABA receptor sites [Chin and Kreutzer, 1992].
GHB was first synthesized about thirty years ago by Dr. H. Laborit, a French researcher interested in exploring the effects of GABA in the brain. Because little or no GABA crosses the blood-brain barrier, Laborit synthesized GHB, which substitutes a hydroxy group for an amino group. This difference allows GHB to cross the blood brain barrier where some of it is metabolized into GABA [Vickers, 1969].
As it turned out, Laborit found that GHB exhibited a range of effects beyond those expected from GABA. Over the intervening years, numerous researchers have extensively studied GHB's effects. It is has come to be used in Europe as a general anesthetic, a treatment for insomnia and narcolepsy (a daytime sleeping disorder), an aid to childbirth (increasing strength of contractions, decreasing pain, and increasing dilation of the cervix), a treatment for alcoholism and alcohol withdrawal syndrome, and for many other uses.
During the 1980s, GHB was widely available over-the-counter in health-food stores, purchased largely by body-builders for its ability to stimulate growth hormone release which aids in fat reduction and muscle building. In the last few years it has been gaining popularity as a "recreational" drug offering a pleasant, alcohol-like, hangover-free "high" with potent prosexual effects.
Scientific Reports on GHB
For the thirty years prior to 1990, the scientific papers on GHB were unanimous in reporting numerous beneficial physiological effects and the absence of long-term negative effects. In 1964, Laborit listed "very low toxicity" as one of the "principle elements" of the compound's pharmacology. In a 1969 report on GHB's anesthetic uses, Vickers referred to GHB as "a truly nontoxic hypnotic" and repeatedly emphasized its "lack of toxicity." Vickers cited evidence that GHB demonstrates "no toxic effects on the liver and kidney." In 1972, Laborit described the body's metabolism of GHB and stressed "the absence of any need of detoxification by the organism." As recently as 1989, this scientific consensus on GHB's benign nature remained 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." His almost off-hand reference to the "safety of GHB" shows how well-established this property of the nutrient had become. Then, on November 8th, 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. The authors, Chin and Kreutzer, warned of GHB's "tremendous 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'." Apparently, the authors construed feeling good in and of itself as a potential threat to public health. Despite such dire language, the report acknowledged that "there are no documented reports of long-term [detrimental] effects. Nor is there any evidence for physiologic addiction."
Of the ten "poisonings" reported, 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 (CNS) depressants are not recommended with GHB, and because GHB is contraindicated for epileptics, such cases are not unexpected. Chin and Kreutzer acknowledge that the "more severe reactions...generally occurred when patients took an unmeasured dose, a particularly large dose, or several doses within a short period of time." Such problems are easily avoided by following the directions for GHB's use. Although the specific clinical details of these ten cases are too lengthy to go into here, one point needs addressing--the use of the terms "coma" and "seizures" in descriptions of these cases. At a sufficiently high dose, GHB 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 can also cause intense drowsiness, abrupt sedation, and deep sleep which is probably better described as unarrousability or deep sedation than coma. Vickers  described it as a "nontoxic coma," which blunts some of the inflammatory connotations of the term coma. Regardless of their alarmist tone, the authors confirm 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."
They concluded that "the prognosis for people who experience GHB poisoning is quite good." The degree to which the pleasant state of GHB euphoria may be psychologically addicting may not be fully appreciated. Anybody with known attraction or addiction to tranquilizers or alcohol should pay special heed to this possibility. In the few cases of GHB abuse that we have investigated, there were pre-existing use/abuse patterns with alcohol and/or tranquilizers. Ironically, it was GHB's lack of toxicity that led to increased frequency of use (numerous times per day) that characterized what can only be called classic cases of psychological addiction. Without the dehydration and CNS irritation of alcohol, or the side effects of tranquilizers, there was no incentive to moderate or curtail GHB use. Fortunately, few people seem to have such overwhelming attraction to the GHB state. Even Chin and Kreutzer minimize GHB's abuse potential by stating, "No investigator [has] reported any long-term adverse effects, addictive or dependent qualities associated with discontinued usage of the drug."
Why Was GHB Banned?
It seems likely, then, that at least some of the motives behind the 1990 FDA ban of GHB were other than those of public safety. Such a ban constitutes the only means of Federal control of a substance neither scheduled by the DEA nor approved by the FDA as a drug. In the absence of a genuine public-health concern, such control might have been motivated by a desire to protect the pharmaceutical industry (with which the FDA is closely intertwined) from competition from a safer, more effective and less expensive alternative to sleeping pills. Is it a coincidence that the FDA has also banned L-tryptophan, another nutrient that functions as a safe and effective sleep aid?
What Are the Real Concerns?
As with most substances, unpleasant and possibly dangerous side effects can be associated with excessive doses of GHB. A dose usually only about twice the amount required for relaxation or a prosexual effect can, as one user put it, "knock you out but fast." In this respect, GHB is probably comparable to alcohol: if you drink twice as much as you normally would, you probably wouldn't function very well. Despite its general safety and lack of toxicity, the safe use of GHB requires information, preparation, caution, and good judgment. In other words, follow the usage guidelines!
How Does It Feel?
Most users find that GHB induces a pleasant state of relaxation and tranquility. Frequent effects are placidity, sensuality, mild euphoria, and a tendency to verbalize. Anxieties and inhibitions tend to dissolve into a feeling of emotional warmth, wellbeing, and pleasant drowsiness. The "morning after" effects of GHB lack the unpleasant or debilitating characteristics associated with alcohol and other relaxation-oriented drugs. In fact, many users report feeling particularly refreshed, even energized, the next day. The effects of GHB can generally be felt within five to twenty minutes after ingestion. They usually last no more than one and a half to three hours, although they can be indefinitely prolonged through repeated dosing. The effects of GHB are very dose-dependent. SMALL INCREASES IN THE AMOUNT INGESTED LEAD TO SIGNIFICANT INTENSIFICATION OF THE EFFECT. Higher levels feature greater giddiness, silliness, and interference with mobility and verbal coherence, and maybe even dizziness. Even higher doses usually induce sleep.
The Actions of GHB in the Body
GHB temporarily inhibits the release of dopamine in the brain. This may cause increased dopamine storage, and later increased dopamine release when the GHB influence wears off [Chin and Kreutzer, 1992]. This effect could account for the middle-of-the-night wakings common with use of higher GHB doses, and the general feelings of increased well-being, alertness and arousal the next day.
GHB also stimulates pituitary growth hormone (GH) release. One methodologically rigorous Japanese study reported nine-fold and sixteen-fold increases in growth hormone 30 and 60 minutes respectively after intravenous administration of 2.5 grams of GHB in six healthy men between the ages of twenty-five and forty [Takahara, 1977]. GH levels were still seven-fold higher at 120 minutes. The mechanism by which GHB stimulates growth-hormone release is not known. Dopamine activity in the hypothalamus is known to stimulate pituitary release of growth hormone, but GHB inhibits dopamine release at the same time that it stimulates GH release. This suggests that GHB's GH-releasing effect takes place through an entirely different mechanism [Takahara, 1977]. At the same time GH is being released, prolactin levels also rise. Serum prolactin levels increase in a similar time-dependent manner as GH, peaking at five-fold above baseline at 60 minutes [Takahara, 1977]. This effect, unlike the release of GH, is entirely consistent with GHB's inhibition of dopamine. Other compounds which lessen dopamine activity in the brain (such as the neuroleptic Thorazine) have been shown to result in prolactin release. Although prolactin tends to counteract many of the beneficial effects of GH, the sixteen-fold increases in GH probably overwhelm the five-fold increases in prolactin.
GHB induces "remarkable hypotonia" (muscle relaxation) [Vickers, 1969]. It is now gaining popularity in France and Italy as an aid to childbirth. GHB causes "spectacular action on the dilation of the cervix," decreased anxiety, greater intensity and frequency of uterine contractions, increased sensitivity to oxytocic drugs (used to induce contractions), preservation of reflexes, a lack of respiratory depression in the fetus, and protection against fetal cardiac anoxia (especially in cases where the umbilical cord wraps around the fetus' neck) [Vickers, 1969; Laborit, 1964]. GHB is completely metabolized into carbon dioxide and water, leaving absolutely no residue of toxic metabolites [Vickers, 1969; Laborit, 1972]. Metabolism is so efficient that GHB can no longer be detected in urine four to five hours after it is taken by injection [Laborit, 1964]. GHB activates a metabolic process known as the "pentose pathway" which plays an important role in the synthesis of protein within the body [Laborit, 1972]. It also causes a "protein sparing" effect [Laborit, 1964] which reduces the rate at which the body breaks down its own proteins. These properties, along with GHB's effect on growth hormone, underlie its common use as an aid to muscle-building and fat loss.
Anesthetic (large) doses of GHB are accompanied 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 moderate bradycardia (slowing of the heart) is consistent [Vickers, 1969; Laborit, 1964]. A slight drop in body temperature also occurs [Laborit, 1964].
GHB also stimulates the release of acetylcholine in the brain [Gallimberti, 1989].
GHB and Sleep
GHB has been called "almost an ideal sleep inducing substance" [SMART DRUGS II, p245]. Small doses produce relaxation, tranquility and drowsiness which make it extremely easy to fall asleep naturally. Higher doses increase the drowsiness effect and decrease the time it takes to fall asleep. A sufficiently large dose of GHB will induce sudden sleep within five to ten minutes [Laborit, 1964].
Many other hypnotics interfere with various stages of the sleep cycle thus preventing the body from achieving a complete and balanced session of rest and recuperation. The most remarkable facet of GHB-induced sleep is its physiological resemblance to normal sleep. For instance, GHB sleep is characterized by increased levels of carbon dioxide in the arteries, as in normal sleep [Vickers, 1969]. During normal and GHB sleep, the CNS continues to be responsive to "noxious stimuli" (pain and other irritations), a factor which sets limits on GHB's uses in anesthesia [Vickers, 1969]. GHB facilitates both REM (rapid eye movement) sleep, and "slow-wave" (non-REM) sleep, the stage of sleep featuring increased release of growth hormone [Laborit, 1972]. And unlike the unconsciousness induced by other anesthetics, that triggered by GHB does not feature a systemic decrease in oxygen consumption [Laborit, 1964].
The primary disadvantage to GHB's use as a sleep aid is it's short-term influence--about three hours. During GHB's influence, sleep is deeper and more restful, but after the GHB has worn off, people have a tendency to wake up. The higher the dose, the greater is this tendency. Some have called this pattern the "dawn effect" and have speculated that it is related to the release of stored-up dopamine. Some people minimize this effect by taking minimal doses of GHB. Others take advantage of this effect by getting a couple of hours of work done in the middle of the night. Still others choose to take a second dose of GHB to sleep for another three hours. It should be noted that not everyone can be put to sleep by GHB. We have spoken to three men who have never achieved sleep even with the doses normally used for such purposes. In addition, Takahara  reported that one of the six men in the growth hormone study cited above remained conscious even though he had received two and a half grams of GHB intravenously, a dosage which rendered the rest of the participants unconscious.
GHB, Alcohol and Alcoholismv
GHB shows great promise in the treatment of alcoholism. In Europe, one of its primary uses is to relieve withdrawal symptoms, cravings, and anxiety among alcoholics.
In laboratory rats addicted to alcohol, withdrawal symptoms closely resemble those exhibited by humans, including tremors, convulsions, and hypersensitivity to sound. All of these symptoms were blocked by sufficiently high 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 effect 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].
Other Uses of GHB
GHB has a decades long track record of use as a general anesthetic. Administered intravenously, an anesthetic dose of GHB is in the range of 4-5 grams for a 150-pound person [Vickers, 1969]. Its advantages as an anesthetic include low toxicity, relatively few contraindications, slowing of the heart rate without loss of blood pressure, the absence of irritation to the veins with intravenous administration, muscle relaxation, absence of respiratory depression (usually), reduction of body temperature (hypothermia), and various protective and anti-shock actions [Laborit, 1964]. However, GHB can almost never be used in anesthesia without the additional administration of other drugs [Vickers, 1969] because it does not produce complete surgical anesthesia except in children [Laborit, 1964]. The autonomic nervous system remains active during GHB-induced anesthetic coma, and thus the body continues to respond to surgical stimuli through increases in heart rate, blood pressure, and cardiac output, as well as through sweating, peripheral vasoconstriction, vocalization, and reflex muscle action [Vickers, 1969]. Local anesthetics or other drugs which suppress these responses must therefore also be used, like the way a dentist or orthodontic surgeon might use Novocaine to kill pain along with nitrous oxide to render a patient unconscious. It is suspected that part of GHB's protective function involves a slowing of the metabolism of brain cells, thus reducing their requirements for oxygen and glucose [Chin and Kreutzer, 1992; Artru, 1980]. Another factor in GHB's anti-shock capability may be the marked vasodilation induced in the liver and kidney, thus increasing blood flow to those vital organs. 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 psychotherapeutic 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 "anxiolytic" (or anti-anxiety) drugs, GHB's effect is non-toxic. Furthermore, GHB's reduction of inhibitions, its tendency to encourage verbalization, and the typical lack of fear during the GHB experience would seem to provide an ideal context for the verbal exploration of difficult emotional territory during therapy.
GHB and Sex
Scientists and doctors have traditionally been reluctant to ascribe aphrodisiac properties to any substance, although this tendency may have abated somewhat in recent years. It is a testament, then, to the power the GHB's sexual effects that they were clearly acknowledged in the scientific literature by 1972. Dr. Laborit wrote:
"A last point should still be mentioned: the [GHB] action on Man
which could be called 'aphrodisiac.' We cannot present any animal
experiments on this subject. However, the oral form has now been
sufficiently used so that, as generally agreed, no doubt can
subsist as to its existence."
We have identified four main prosexual properties:
2) heightening of the sense of touch (tactility),
3) enhancement of male erectile capacity, and
4) increased intensity of orgasm.
Perhaps the foremost prosexual property of GHB is disinhibition. Some users suggest that GHB's other sexual benefits are secondary effects, made possible (or at least amplified) by this loosening of psychosomatic constraint. A number of people have commented that this disinhibition is particularly marked among women.
Women often report that GHB makes their orgasms longer and more intense, as well as more difficult or time-consuming to achieve, especially at higher doses. As with its other effects, GHB's impact on female orgasm seems highly sensitive to small adjustments in dosage.
Legal Status and Availability
GHB is not approved in the US and has been banned from over-the-counter sale by the FDA. GHB has not yet been "scheduled" as a "controlled substance" by the DEA, and therefore simple possession is not illegal. [became U.S. Federal Schedule I in March 2000] GHB continues to be sold to legitimate laboratories and scientists for research purposes, but selling it specifically for human consumption, especially while making claims about its health benefits, is a violation of current FDA regulations and policy.
In some European countries, GHB is an approved drug available by prescription. Local doctors, pharmacists and government bureaucrats should be able to provide country-by-country specifics.
GHB is growing in popularity and seems to be widely available in the underground "gray market." Since most of the GHB available through such channels is of the "bootleg" variety, manufactured by nonprofessional "kitchen" chemists, concerns about quality and purity should be kept in mind. Caveat emptor (buyer beware)!
As has been emphasized, the overall safety of GHB is well-established, and no deaths attributable to GHB have been reported over the thirty year period that this compound has been in use [Vickers, 1969; Chin and Kreutzer, 1992]. In fact, as of 1990, only forty-six adverse reactions had been reported in the United States surely constituting only an infinitesimal fraction of actual usage, all followed by rapid and complete recovery [Chin and Kreutzer, 1992]. Unlike a large proportion of other drugs including alcohol and even Tylenol, GHB has no toxic effects on the liver, kidney or other organs [Vickers, 1969; Chin and Kreutzer, 1992]. One program of sleep therapy using six to eight grams daily for a period of eight to ten days produced no side effects. Vickers  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 (don't do this at home kids!). In the Canadian studies of narcolepsy mentioned earlier, the nightly use of two to six teaspoons (one teaspoon equaling roughly 2.5 grams) for several years resulted in no reports of long-term adverse effects, or problems with issues of addiction or dependence. In one of these studies, one patient inadvertently ingested fifteen teaspoons without adverse consequence "other than deep sedation and headache the next day" [Chin and Kreutzer, 1992]. And in France, sub-anesthetic oral doses were used by "a large number of patients for about six years" without untoward effect [Laborit, 1972].
According to Dr. Gallimberti , the action of GHB is "without serious side effects." Some research programs have reported no side effects at all. Nonetheless, it's clear that some minor side effects can occur. Those most commonly experienced are drowsiness, dizziness, nausea, and sometimes vomiting. As a sedative-hypnotic, GHB's effects bear some similarity to those of alcohol and tranquilizers. GHB not only "may cause drowsiness" like these other drugs, IT WILL ALMOST INVARIABLY DO SO. Ataxia, or incoordination, can also be a side effect of GHB. DO NOT DRIVE A VEHICLE OR OPERATE DANGEROUS MACHINERY WHILE UNDER THE INFLUENCE OF GHB. As mentioned, clonic movements (muscle contractions or "seizures") have been observed during the onset of GHB-induced sleep. Headache is sometimes reported. A moderate slowing of the heart rate is a consistent effect, and small changes in blood pressure can take place. Likewise, orthostatic hypotension (a sudden drop in blood pressure caused by standing up quickly) has also been reported. Sometimes this is experienced as brief dizziness, and rarely people can briefly lose consciousness. At very high doses, cardiac and respiratory depression can occur. Sufficiently large doses of GHB can cause sudden sedation and loss of consciousness. Do not take such doses except when reclining on a bed or sofa. It is also a bad idea to take such doses in the presence of people who don't know anything about GHB. You may alarm your family or friends and wake up in an emergency room (with a large medical bill). More unusual and extreme reactions have included diarrhea, lack of bladder control, temporary amnesia, and sleepwalking. Whatever side effects may be noted, they are often much more severe when GHB is combined with other central nervous system depressants [Chin and Kreutzer, 1992, Gallimberti, 1989; Takahara, 1977; Vickers, 1969].
Although contraindications for GHB have been described as "remarkably few" [Vickers, 1969], those who suffer from any of the following conditions should not use GHB: severe illness of any kind, epilepsy, eclampsia (convulsions), bradycardia (slowed heart-beat) due to conduction problems [left-bundle-branch-block is an example of conduction difficulty], Cushing's syndrome, severe cardiovascular disease, hyperprolactinemia, and severe hypertension [Gallimberti, 1989; Vickers, 1969]. Severe alcoholism is sometimes mentioned as a contraindication for GHB [SMART DRUGS II, p244] even though GHB has been used quite successfully in the treatment of withdrawal symptoms. The explanation for this seeming contradiction probably lies in the likelihood that severe alcoholics may combine GHB with alcohol. GHB should not be used with benzodiazepines ("minor tranquilizers" such as Valium and Xanax), phenothiazines ("major tranquilizers" like Thorazine and Stellazine), various painkillers (barbiturates and opiates), alcohol, anticonvulsants (Dilantin and phenobarbital) and even many over-the-counter allergy and sleep remedies--without direct medical supervision.
Determining the ideal dose is probably the trickiest aspect of working with GHB. The amount required for a given level of effect will vary from person to person, and the dose-response curve is fairly steep. Overestimating the dose can have consequences ranging in seriousness from ruining your plans for the evening to waking up in the emergency ward as a result of panic on the part of concerned-but-uninformed friends or relatives. Once you have found the levels that give you the effects you desire, they will remain consistent. Tolerance to GHB does not develop. However, recent (not current) alcohol consumption may decrease the effect of a given dose of GHB [Fadda, 1989]. Most people find that a dose in the range of 0.75-1.5 grams is suitable for prosexual purposes, and that a quantity in the range of 2.5 grams is sufficient to force sleep.
Some people think that GHB might lower potassium levels and should therefore be taken with potassium supplementation. Some research papers have identified such an effect, others have not. If you want to play it safe, take a potassium supplement equal to 10% of the GHB dose.
Note 1: This article is excerpted and adapted from a 40-page special report on GHB written by the authors and available from:
Post Office Box 4667
Petaluma, California, 94955
To order send a check for $22.95 ($19.95 for the report and $3 for shipping). We do not accept credit cards.
(*) Note 2: This article was originally published in SMART DRUG NEWS [3(6): p1] and is copyright (c) 1994 by the Cognitive Enhancement Research Institute and the authors. For free information about CERI and SMART DRUG NEWS, telephone (415) 321-CERI or (415) 323-3864 FAX or e-mail to CERI's Executive Director Steven Wm. Fowkes at firstname.lastname@example.org. A small sidebar to this article written by Steven Wm. Fowkes and entitled "The Demonization of GHB" is also available for downloading from this directory.
Note 3: John Morgenthaler and Steven Wm. Fowkes (along with Ward Dean, M.D.) are coauthors of the book SMART DRUGS II: THE NEXT GENERATION (Smart Publications, 1993). This book is available from CERI and your local bookstores. It is a supplement to the first smart-drug book SMART DRUGS & NUTRIENTS, authored by Dr. Ward Dean and John Morgenthaler in 1990. The two books provide a comprehensive summary of smart drugs.
References Cited in this Article
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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-hydroxybutyric 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.
Kleimenova NN, Ostrovskaya RU and Arefolov VA. Effect of sodium hydroxybutyrate on the ultrastructure of the cross-striated muscle tissue myocytes during physical exercise. BYULL EKSP BIOL MED 88(9): 358-61, 1979.
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 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.
Ostrovskaya RU, Kleimenova NN, Kamisheva V, Molodavkin GM, Yavorskii AN and Boikko SS. Effect of sodium hydroxybutyrate on functional biochemical and morphological indexes of physical working ability. FARMAKOL REGUL PROTSESSOV UTOMLENIYA [Moscow, USSR] 39-56: 112-17, 1982.
Takahara J, Yunoki S, Yakushiji W, Yamauchi J, Yamane 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.
Vickers MD. Gamma-hydroxybutyric Acid. INT ANAESTHESIA CLINIC 7: 75-89, 1969.