GHB

Prosexual uses of GHB:
Men: ease of erection; stability of erection; postponement of ejaculation.
Women: greater intensity of orgasm; increase in vaginal sensitivity.
Men & Women: disinhibition; increased interest in sex; increased tactility; increased bonding; emotional intensity; intimacy.

GHB, or gamma-hydroxybutyrate, is a normal constituent of mammalian biochemistry. It is found naturally in every cell in the human body. In the brain, the highest amounts occur in the hypothalamus and basal ganglia [Gallimberti, 1989]. GHB is found in even greater concentrations in the kidney, heart, skeletal muscles, and brown fat [Chin, 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, 1992]. It is both a metabolite and precursor of the inhibitory neurotransmitter GABA (gamma-aminobutyric acid), to which it bears a close relationship of chemical structure. GHB, however, does not act on GABA receptor sites [Chin, 1992].

GHB was first synthesized about thirty years ago by H. Laborit, a French researcher interested in exploring the effects of GABA in the brain. Direct administration of GABA would not be effective for this purpose because it does not cross the blood-brain barrier. Laborit's alternative was to administer GHB, which does cross the blood-brain barrier, and some of which, once inside the brain, metabolizes into GABA [Vickers, 1969].

Independently of its relationship to GABA, however, GHB turned out to be a drug with its own range of effects. It has since been widely used and researched, finding applications in obstetrics and general anesthesia and in the treatment of alcohol withdrawal syndrome, narcolepsy, insomnia, and other arenas.

During the 1980s, GHB was widely available over-the-counter in health-food stores, purchased largely by body-builders for its ability to aid 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" and potent prosexual effects.

The Demonization of GHB

A long-lived media truism holds that "all publicity is good publicity." The recent history of GHB might serve as a case in point. Most of those who've heard of GHB probably first became aware of it by way of a widespread rumor-unsupported by the subsequent coroner's report-that it played a role in the death of actor River Phoenix in the Fall of 1993. An article in the December 6th issue of Newsweek reported that this piece of hearsay-despite its alarming nature-inspired a groundswell of demand for GHB in the nightclub drug underground. Newsweek reported: "The hunt was on. 'I'd never heard of GHB before. No one in New York had,' said a Manhattan drug user. 'This month it's the only drug'" [Rogers, 1993].

The facts were widely misrepresented in the popular media, which vastly exaggerated GHB's so-called "dangers"- and usually left them unspecified. For instance, Newsweek sensationally described GHB as "an obscure and dangerous steroid substitute occasionally gulped down by West Coast thrillseekers" [Rogers, 1993]. (Although it can be used to increase muscle mass, GHB is neither a "steroid" nor in any other way "steroid-like," as it was often rendered in even more distorted reports.) And a guide to aphrodisiacs published in 1993 made a vague reference to "dangerous side effects" in the first sentence of its description of the drug [Watson, 1993].

In 1992, a report written by epidemiologist Ming-Yan Chin and Richard A. Kreutzer, MD, both staff members of the California Department of Health Services, warned sternly of GHB's "tremendous potential for abuse." Nonetheless, the authors went on to conclude: "there are no documented reports of long term [detrimental] effects. Nor is there any evidence for physiologic addiction." (See "Addictive potential" in the "Safety Issues" section.) [Chin, 1992.]

What, then, was the source of their concern? By way of explanation for "sounding the alarm," Chin and Kreutzer offered only the following statement: "All interviewed patients reported a pleasurable sensation or a 'high.' Several of them explicitly noted that one reason they continued taking the drug was because it made them 'feel good.'" It would seem that the authors construed "feeling good"-in and of itself-as a threat to the public health in whose service they were ostensibly employed. For whatever reasons, the FDA banned the over-the-counter sale of GHB on November 8th, 1990 [Chin, 1992].

Setting the Record Straight

More than twenty-five years of scientific research into the effects of GHB-right up to 1989, one year prior to the FDA ban-clearly contradicts GHB's U.S. media image as a menacing poison. It will become clear as this chapter unfolds that numerous beneficial physiological effects-in the absence of significant negative physiological consequences-are well-documented in the scientific literature. Additionally, there is strong anecdotal evidence for psychological and sexual benefits. In fact, prior to the FDA ban, GHB's high degree of safety was practically taken for granted in the scientific literature. A 1964 report lists "very low toxicity" as one of the "principle elements" of the GHB's pharmacology [Laborit, 1964]. A 1969 summary of its anesthetic uses called GHB "a truly nontoxic hypnotic," repeatedly emphasized its "lack of toxicity," and cited evidence that it demonstrates "no toxic effects on the liver and kidney" [Vickers, 1969]. In describing the way GHB is metabolized, a 1972 paper mentions "the absence of any need of detoxication by the organism" [Laborit, 1972].

As recently as 1989, this scientific picture of GHB's benign nature remained unchanged. A study from that year on its uses in treating alcohol withdrawal in humans notes that "GHB action...seems to be without serious side effects." The same report's almost off-hand reference to the "safety of GHB" shows how well-established this property of the drug had become [Gallimberti, 1989].

Worst-case Scenarios

Chin and Kreutzer's 1992 document, summarizing ten cases of "Acute poisonings associated with gammahydroxybutyrate in California," thus represented a radical departure from the previous consensus. (It is worth noting that "poisoning" was never defined in this paper.) Four of the cases reported involved "unknown doses." Four featured the "coingestion" of other drugs, usually alcohol. One involved unmedicated epilepsy and another a history of grand mal seizures-conditions specifically contraindicated for GHB. Chin and Kreutzer acknowledged 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."

The two most severe incidents of adverse reaction out of the ten included in Chin and Kreutzer's document are by far the most extreme cases encountered in the wide-ranging research on GHB performed for this book. Both of these cases involved the ingestion of central nervous system depressants in addition to GHB. (Combining GHB with central nervous system depressants, such as alcohol or tranquilizers, is generally considered inadvisable.) They are included here as "worst case scenarios" to guarantee that the complete spectrum of GHB's potential effects is represented.

One of Chin and Kreutzer's case histories relates the story of a "previously healthy 39-year old Caucasian woman." During the period of her experimentation with GHB, she was also using Vicodin, a prescription painkiller containing a central nervous system depressant. She "experienced numbing of the legs, dizziness, and a tight chest" after her first dose of GHB (consisting of one teaspoon) purchased from a health-food store. Nonetheless, this woman resumed taking GHB three weeks later. For one month thereafter, she took one-half teaspoon of GHB on a near-daily basis without negative consequence.

However, after the last of "three or four doses" consumed on a day during which she departed from this regimen, "she experienced a 'high'...the 'jabbers' (pressured speech and ebullience), intense drowsiness, confusion, trouble breathing, and uncontrollable twitching in her arm. Her children found her and reported that her eyes were rolled back, her body was tense, and"-although no mention is made as to how the children were able to make such a determination-"she was hallucinating."

She was admitted to a hospital for a night, where, despite the disturbing nature of the symptoms recounted above, it was determined that "her pulse, blood pressure, and respiration were normal." Her physical exam was deemed "unremarkable except for alternating wakeful and sleepy states with irregular leg twitches." Her case history concludes: "she experienced a full recovery with no lasting symptoms."

The second case involves a "28-year old Caucasian woman" who took an unspecified quantity of GHB in addition to "some mixed drinks" at a nightclub. The report continues: "she experienced confusion and uncontrollable shaking followed by a seizure and then coma. A witness states that she was banging her head on a wall before becoming unconscious. Patient vomited and was suctioned before transport. Paramedics reported that she alternated between combativeness and unresponsiveness as she was taken to the emergency room. She arrived...with good respiratory effort but with long apneic periods [lapses of breathing]." Her recovery was complete, with "no adverse side effects" since the incident.

Several points regarding this case are worth keeping in mind. The woman's blood alcohol level was assessed at the hospital and was found to be quite high. Furthermore, it seems likely from the context of Chin and Kreutzer's presentation that the GHB may have been acquired at the nightclub where the incident took place. Under such circumstances, and in light of the severity of the woman's reaction, the possibility must be taken into account that the substance in question may in fact not have been GHB at all. Lastly, the report of "seizure and then coma" need not be the great cause for alarm that it at first seems-as will be explained shortly. (And in any case, this woman's "coma" must have been rather short-lived in order for her to be able to behave in a "combative" manner towards paramedics.)

Another of Chin and Kreutzer's cases is worthy of mention not for its severity but for its mildness. In this incident, a "39-year-old Caucasian man" took a rather large quantity of GHB (one and a half teaspoons, or nearly four grams) along with twenty-five milligrams of diphenhydramine hydrochloride (another central nervous system depressant, marketed over-the-counter both for allergies and as an aid to sleep). The only reported symptom is that he became "lethargic." This effect hardly seems disturbing given that he had just taken two known hypnotics (although it apparently disturbed his wife, who called 911 and had him taken to an emergency room- from which he was released in two hours). It is especially difficult to understand why this case is included among so-called "poisonings."

Despite their alarmist tone, the authors acknowledge 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."

Summarizing the results of Canadian research into GHB as a treatment for narcolepsy, authors Chin and Kreutzer further undermine their own stated position on GHB's abuse potential by reporting that:

"Several researchers...consistently describe the beneficial clinical effects...One Canadian researcher has noted adverse effects no worse than abrupt sedation, ataxia [lack of coordination], sleepwalking, unarousability, and decreased inhibition in normals [meaning persons free of narcolepsy or other major disease conditions] taking two to six teaspoons twice a night for several years. One patient who accidentally took fifteen teaspoons on one occasion suffered no adverse reactions other than deep sedation and a headache the next day. No investigator reported any long-term adverse effects, addictive or dependent qualities associated with discontinued usage of the drug." (See "Addictive potential" in the Safety section.)

Chin and Kreutzer acknowledge that "Researchers working with narcoleptics consider GHB a relatively harmless and effective drug" [Chin, 1992].

"Comas and Seizures" or "Sleeping and Twitching"?

Negative press on GHB frequently mentions the possibility of "seizures" and "coma." These are certainly frightening words-until their meaning is closely examined in context.

With regard to GHB, "coma" refers merely to the state of deep sleep or unconsciousness induced by higher doses, from which people often cannot be aroused until the GHB has worn off. This "coma" is of short duration-one to two hours-and provides the basis for GHB's use as a general anesthetic. In fact, one researcher even described it as a "nontoxic coma," [Vickers, 1969] a phrase that in itself defuses much of the fear inspired by the use of the word.

This state of "coma" could just as easily-and accurately-be described as one of "unarousability" (the key term in the definition of "coma") or "deep sedation." In fact, these are the words used by Chin and Kreutzer themselves in their summary of research results from Canada, quoted above.

Their phrases "adverse effects no worse than...unarousability" and "no adverse reactions other than deep sedation" would have quite a different impact if the word "coma" was inserted in place of its synonyms. In fact, the alternate phrases created thereby-"adverse effects no worse than...coma" and "no adverse reactions other than coma"-appear blatantly self-contradictory. Nevertheless, there is no significant difference here in meaning, only in choice of terminology.

The point here is that the wording chosen by the major media and other sources in public discourse about GHB has carried a substantial negative load.

Like "coma," the word "seizure" becomes much less frightening when it is replaced by alternatives that are considerably less "loaded" but nonetheless equally accurate in terms of GHB's actual observed side effects. The "seizures" sometimes associated with GHB are usually described as being of the "clonic" variety [Vickers, 1969; Chin, 1992]. This word refers to "a forced series of alternating contractions and partial relaxations of a muscle" [Webster's 7th New Collegiate], as in one researcher's statement that "During the onset of [GHB] coma...random clonic movements of the limbs or face are frequently seen." This activity could alternatively-and correctly-be described as "muscle spasms" or "twitching."

Thus, a dire-sounding warning such as "a large dose of GHB can cause coma and seizures" could be translated into the relatively innocuous statement that "a sufficient dose of GHB may result in a few hours of deep sleep from which the user cannot be aroused, and the entry into unconsciousness may be accompanied by some twitching of the face or limbs."

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 drug neither scheduled by the DEA nor approved by the FDA for prescription use. (The latter status requires considerable expenditure of time and money on the part of a pharmaceutical firm in an investment that can usually be recovered only when the company in question holds an exclusive U.S. patent. In the case of GHB, no such patent exists.) As physician Ward Dean has put it, "the FDA doesn't like drugs that people use just to 'feel good' or unwind after a hard day's work. In fact, the aphrodisiac properties of GHB may well have been part of the motivation for the ban" [Dean, 1993].

What Are the Real Concerns?

The purpose of this section has been to make clear that the dangers widely attributed to GHB have been greatly exaggerated. Were this not the case-and were not the benefits offered by GHB both substantive and well-documented-a drug so controversial, and so ambiguous in legal status, would not have been included in this book. Such an argument having been made, it must be emphasized that, as with most substances, unpleasant-although not ultimately dangerous-side effects can be associated with GHB. Furthermore, there is one potentially significant hazard that must be taken into account when self-administering GHB: a sufficient dose-usually only about twice the amount required for a pleasant prosexual effect-can, as one user put it, "knock you out, but fast." (To keep things in perspective, remember that alcohol-a drug of exponentially greater toxicity and health risk than GHB-and many approved prescription drugs can also function in this manner.)

Durk Pearson and Sandy Shaw's book Life Extension: A Practical Scientific Approach features a chapter entitled "Is There Anything Perfectly Safe?" The entire text of this chapter consists of a single capitalized word: "NO" [Pearson & Shaw, 1982]. This succinct statement applies to GHB. In spite of its general safety and lack of toxicity, the intelligent use of GHB requires preparation, information, care, caution, and good judgement. These issues will be fully discussed in the sections called "Safety Issues" and "Self-Administration."

How Does It Feel?

Most users find the "high" induced by GHB to be a pleasant state of relaxation and tranquility. Many compare it to the state afforded by alcohol; others mention "Quaaludes," minor tranquilizers such as Valium or Xanax, or marijuana. Others draw parallels with their experiences in meditation or following sessions of deep massage. Those who experience emotional release, heart-opening qualities, and facilitation of intimate verbal communication are sometimes reminded of MDMA ("Ecstasy"). The morning after effects of GHB lack the unpleasant or debilitating characteristics associated with some of these other drugs. In fact, many users report feeling particularly refreshed, even energized, the next day. As one woman put it, "I look at it as like being really high on alcohol, without the body poisoning."

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. Placidity, sensuality, mild euphoria, and a tendency to verbalize often characterize the "high." Anxieties and inhibitions tend to dissolve into a feeling of emotional warmth, well-being, and pleasant drowsiness. A forty-one year old female singer-songwriter describes the GHB state in terms of "...a certain sensual, very blissful quality. It also gives you reduced inhibitions."

The effects of GHB are very dose-dependent. This means that small increases in the amount ingested lead to significant intensification of the effect. Higher levels feature greater giddiness, silliness, interference with mobility and verbal coherence, and sometimes dizziness. Doses slightly higher than those required for such effects will usually induce sleep.

The nature of the GHB "high" will be further discussed in the section entitled "GHB and Sex." Control and modulation of the "high," and its relationship to dosage, will be further elaborated in the section on "Self-Administration." Unpleasant sensations and effects that can sometimes arise will be discussed under "Precautions, Side Effects, and Contraindications."

The Action of GHB in the Body

GHB significantly alters concentrations of the neurotransmitter dopamine and levels of two hormones released by the pituitary gland: growth hormone and prolactin. It also features several other benign metabolic, biochemical, and physiological effects.

Dopamine

GHB can double concentrations of dopamine in the brain. This dopamine increase is specific to certain brain regions [Laborit, 1972], including the substantia nigra, a major center of dopamine manufacture [Chin, 1992]. (For more information on dopamine and its functions, see the chapters "Bromocriptine" and "Some Basic Physiology.") It is possible to inhibit this effect with other substances, including naloxone, caffeine, and amphetamines [Chin, 1992].

Oddly enough, this heightening of brain dopamine levels does not, at least initially, lead to increased activity of the brain's dopamine system. Rather, GHB increases dopamine concentrations by inhibiting the release of dopamine from nerve endings. This creates higher levels of the neurotransmitter within the brain cells where it is stored. Some scientists have speculated that this buildup of dopamine may be released into the synapses after GHB wears off [Chin, 1992]. This could lead to feelings of increased well-being, alertness, and arousal associated with greater dopamine activity the next day.

Growth hormone

GHB is a potent stimulator of the release of growth hormone by the pituitary. One article notes that the "increased GH [growth hormone] secretion produced by GHB administration is far in excess of any other previously available GH stimulator" [Fowkes, 1993]. As discussed in the chapter on bromocriptine, growth hormone, which stimulates the body to burn its own fat for fuel and to grow new muscle tissue, is attributed with life-extending, immune-enhancing, and prosexual effects.

One Japanese study reported in 1977 involved six healthy men between the ages of twenty-five and forty. Blood levels of growth hormone were tracked across a period of two hours after intravenous injection of 2.5 grams of GHB, and compared to control or baseline levels assayed in the same men across a similar period of time after injection of placebo (saline solution). Growth hormone levels increased by a factor of nine within thirty minutes, and peaked at sixty minutes at a level sixteen times that of baseline. Thereafter, growth hormone levels began to decline gradually, but were still seven to eight times higher than normal at the two-hour point [Takahara, 1977].

The mechanism by which GHB stimulates growth-hormone release is not known. As described in the chapters "Some Basic Physiology" and "Bromocriptine," dopamine activity in the hypothalamus stimulates pituitary release of growth hormone. Thus, many dopaminergic drugs function as growth-hormone releasers. However, as has been noted, GHB actually inhibits the release of dopamine from nerve terminals, leaving its growth hormone stimulating effects-which must take place through an entirely different route-something of a mystery [Takahara, 1977].

Prolactin

The same Japanese study discussed above also assayed the response of blood prolactin levels to GHB injection. Serum prolactin levels increased along a curve contoured similarly to that for growth hormone, peaking at the sixty-minute point at a level more than five times greater than baseline [Takahara, 1977]. This effect, unlike the release of growth hormone, is entirely consistent with GHB's inhibition of dopamine. Other compounds which dampen dopamine activity in the brain, such as the neuroleptic Thorazine, have been shown to result in pituitary prolactin release.

GHB is thus a clear exception to the rule stated by Durk Pearson and Sandy Shaw in Life Extension that "Most drugs that increase GH [growth hormone] decrease prolactin and vice versa." In fact, as also noted in Life Extension, the effects of these two hormones are often diametrically opposed [Pearson & Shaw, 1982]. For instance, growth hormone is an immune stimulant, whereas excessive levels of prolactin have been attributed with anti-immune effects; where growth hormone is associated with fat reduction, prolactin is associated with fat increase; and where growth hormone is thought to have prosexual effects, the sex-negative consequences of high prolactin concentrations have been well documented.

However, it is probably safe to assume that, in the case of GHB, the effects of growth hormone release overwhelm those of prolactin release in those areas where the actions of the two hormones are opposed. While an intravenous dose of 2.5 grams of GHB can increase prolactin levels by as much as a factor of five, the same dose induces a much greater surge of growth hormone-an increase by a factor of sixteen.

It has been suggested that GHB's seemingly contradictory function as a simultaneous stimulator of growth hormone and prolactin release might be resolved through a mechanism, consistent with its inhibition of dopamine release, that involves the serotonin system. As of this time, however, such notions-extrapolated from observations involving the nervous system of a certain species of mussel-are entirely speculative [Takahara, 1977].

Other physiological effects

In addition to its effects on concentrations of dopamine, growth hormone, and prolactin, several other aspects of GHB's physiological action are worthy of note. GHB induces what has been called "remarkable hypotonia," or muscle relaxation [Fowkes, 1993; Vickers, 1969]. GHB is completely metabolized into carbon dioxide-the primary constituent of normal human exhalation-and water, leaving the body with absolutely no residue of toxic metabolites [Vickers, 1969; Laborit, 1972]. Because of the efficiency with which it is metabolized, 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], including muscle tissue. It also features what has been called a "protein sparing" effect [Laborit, 1964], meaning that it reduces the rate at which the body breaks down its own proteins (for example, those in muscle). These properties, along with GHB's role as a growth hormone releasing agent, underlie its use as an aid to muscle building and fat loss.

Anesthetic 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 common [Vickers, 1969; Laborit, 1964]. A slight drop in body temperature also occurs [Laborit, 1964]. While these effects have been observed at anesthetic levels, it is probably safe to assume at least some similar activity takes place in response to smaller doses, if to a lesser degree. Indeed, a ten to thirteen percent decrease in heart rate has been observed among patients administered GHB in sufficiently low dosage for them to remain conscious [Gallimberti, 1989].

GHB also stimulates the release of acetylcholine in the brain [Gallimberti, 1989]. This chemical is a neurotransmitter credited with an important role in memory.

GHB, Sleep, and Narcolepsy

GHB has been called "almost an ideal sleep inducing substance" [Dean, 1993]. A sufficient 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 [Fowkes, 1993]. 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 central nervous system 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, considered "the most restful sleep" [Dean, 1993], 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 decrease in consumption of oxygen [Laborit, 1964].

No doubt due in large part to its resemblance to natural sleep, GHB-induced sleep lacks the morning-after "hangover" and grogginess often associated with other sleep-inducing agents. To the contrary, people usually experience a rapid-even sudden-and complete awakening from GHB sleep that leaves them feeling unusually refreshed and invigorated [Fowkes, 1993].

The primary difference between normal and GHB sleep is the length of the sleeping phase. GHB sleep tends to be more brief-from two to six hours-than what most people consider a normal night's sleep. Thus many people who use GHB for sleep awaken in the middle of the night in an alert state. Some have called this pattern the "dawn effect" and have speculated that it is related to the release of the dopamine build-up that is stored during the GHB sleep cycle. Some who experience the "dawn effect" have found that they can avoid it by decreasing their initial bedtime dose. Others merely take a second dose when they awaken in the middle of the night, which puts them back to sleep. Some of those for whom the GHB-initiated sleep cycle is five or six hours long find themselves more than adequately refreshed by GHB sleep of such duration. They may therefore choose to take advantage of this "built-in alarm clock" by using GHB to shorten the total amount of sleep they need.

It should be noted that not everyone can be put to sleep by GHB. The authors have spoken to three men who have never achieved sleep even with the doses normally used for such purposes. In addition, Takahara [1977] 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.

Outside of the United States, GHB's ability to induce deep and restful sleep has afforded this compound a role in the treatment of narcolepsy. Narcoleptics are sometimes given stimulants during the day to prevent spontaneous episodes of sleep. GHB treatment for narcolepsy approaches the problem from the opposite perspective. When taken orally at bedtime, GHB provides narcoleptics with deeper sleep and greater frequency of REM cycles, leading to fewer daytime narcoleptic episodes [Fadda, 1989; Chin, 1992]. Some of the "auxiliary" symptoms of narcolepsy-which GHB is also of assistance in treating-are associated with dopamine deficiency. It's possible that the daytime release of the dopamine buildup caused by use of GHB at night is the mechanism by which these symptoms are alleviated [Chin, 1992].

GHB as a Smart Drug?

It seems unlikely that the GHB "high"-at least at greater levels of intensity-would be conducive to disciplined cognitive activity. Rather, the question regarding GHB's potential as a "smart drug" is whether or not its use for recreational, sleep-inducing, or growth hormone-related purposes in the evening or at night might facilitate cognitive and learning processes during the next day.

REM sleep and protein synthesis-processes which may be linked, and which are both facilitated by GHB-have been correlated with periods of intensive learning [Laborit, 1972]. As mentioned earlier, GHB has also been shown to stimulate the release of acetylcholine, one of the brain's own "smart chemicals" [Gallimberti, 1989]. These effects suggest a possible role for GHB as a cognition-enhancer.

Beyond possible specific mechanisms is a more general route by which GHB might improve cognitive function. A good night's sleep improves cognitive ability while sleep deprivation impairs it. Since GHB facilitates and deepens sleep, it seems likely that it would also promote mental acuity.

The authors have encountered only one study directly relevant to GHB and cognition. Here, subjects under the influence of GHB scored "no worse" than controls on a word fluency test. (At least GHB didn't make them dumber.) This result is particularly interesting since most sedative drugs impair cognition.

GHB, Fat Reduction and Muscle Building

Both activation of the pentose pathway and release of growth hormone offer means by which GHB could be expected to increase the ratio of lean tissue to fat. While there is a great deal of anecdotal evidence that GHB can be used effectively both for weight loss and muscle building, on-line database searches performed for this book produced no documentation of scientific studies on GHB and weight loss.

According to articles in body-building magazines, athletes have experienced increases in strength and decreases in fat as a result of GHB. And one man in his thirties interviewed for this book shared his enthusiasm for the results of his girlfriend's use of GHB for muscle-building and fat-loss purposes: "It's made a huge difference in her breasts. They're higher, and it's made her pectoral muscles hard and firm. And it's given her great back muscles. All of this even though she doesn't really work out that much." Such reports are not unusual among those using GHB for its growth hormone effects.

More