History Of Illicit Use Of

In 1977, a study was published that would permanently change the relative obscurity of GHB, GBL and 1,4BD. Takahara et al. (1977) administered GHB to six healthy adult males and showed an approximately 10-fold increase in plasma growth hormone concentration that peaked at 45 min post-dose. This effect persisted for about 15 min and then the growth hormone concentration declined towards the pretreatment level. The growth hormone concentration at 120 min post-dose was still above baseline but significantly (two-thirds) below the peak concentration. Based on this report, bodybuilders assumed that they could increase growth hormone concentration by using GHB and thereby optimize their muscle-building potential. A more recent study by Van Cauter et al. (1997) showed that the increase in growth hormone secretion was correlated with the enhancement of slow wave sleep and growth hormone release did not occur prior to sleep onset. The growth hormone stimulating effect of a 2-3 g dose of GHB was seen during the first 2h of sleep as an increase in amplitude and duration of the normal growth hormone secretory pulse associated with sleep onset as opposed to an increase in the number of growth hormone release pulses.

The use of GHB by bodybuilders seemed harmless in theory until emergency room reports associated with GHB toxicity started to accumulate (Centers for Disease Control, 1990). Users soon discovered that GHB had a definite mood elevating quality and introduced

Table 11.1 Common street names for GHB

Gamma OH

Liquid ecstasy

Sodium oxybate

Easy Lay

Natural Sleep 500

Salt water


Vita G


Georgia Home Boy


Grievous bodily harm


Great Hormones at Bedtime


Liquid X

GHB into the party drug scene, where it remains today. GHB is known by numerous street/ slang names (Table 11.1). Most of these slang names utilize the letters G, H and B, such as 'Georgia Home Boy' or 'Great Hormones at Bedtime'. The slang name 'liquid ecstasy' can be confusing, as 'ecstasy' or XTC is the slang name commonly associated with methylene-dioxymethamphetamine (MDMA), which is not in the same class of compounds as GHB. In November 1990, the US Food and Drug Administration (FDA) warned consumers of the danger of GHB, but the incidents of poisonings continued to rise. GHB and products containing GHB were removed from the market and GHB moved underground. Users soon discovered that GHB could easily be synthesized from readily available precursors. The industrial solvent g-butyrolactone (GBL), when made basic with lye and heated, would yield GHB. With addition of an acid such as vinegar to adjust the pH, the solution of GHB was ready to consume. This illicit GHB is especially dangerous because its concentration is unknown and can vary greatly from batch to batch. Coupled with the fact that GHB has a very steep dose response curve, it is easy to overdose accidentally. Also, contaminants may be introduced in the clandestine manufacturing process. Toxicity of GHB is characterized by euphoria, dizziness, visual disturbances, decreased level of consciousness, nausea, vomiting, suppression of the gag reflex, bradycardia, hypotension, acute delirium, confusion, agitation, hypothermia, random clonic muscle movements (twitching), coma, respiratory depression and death. Although there have been some reports of seizures associated with GHB intoxication, there is no evidence of true seizure activity as measured by EEG in humans (Entholzner et al., 1995). However, only GHB doses consistent with safe anesthesia have been evaluated in these EEG studies. Clonic muscle movements and severe parasympathomimetic activity, including profuse salvation, defecation and urination, have been documented in dogs treated with large doses (toxic and lethal) of GHB (Lund et al., 1965). The clonic muscle movement was so prominent in the dogs that at anesthetic doses a barbiturate was also administered to effect convenient anesthesia. Another complicating factor is that GHB used outside a clinical setting is frequently used in combination with other drugs. This could affect the pharmacology of GHB in many ways depending upon which additional drug(s) are consumed and their dose. By far the most common drug taken in combination with GHB is ethanol (Louagie et al., 1997; Li et al., 1998; Centers for Disease Control and Prevention, 1999). This combination is especially dangerous because ethanol potentiates GHB's Central Nervous System (CNS) depressant effects, as demonstrated by depression of the startle response (a measure of sensory responsiveness) in rats (Marinetti and Commissaris, 1999). GHB has been implicated in fatalities both when administered alone (Marinetti et al., 2000) and when used in combination with other drug(s) (Ferrara et al., 1995). The use of GHB has been implicated in sexual assault. In fact, a common slang name for GHB is 'date rape drug', although it is not deserving of this title. Actual confirmed cases where GHB has been used in this capacity do exist but they are not common in comparison with other drugs more frequently chosen for this crime, namely ethanol, cannabinoids and benzodiazepines (ElSohly and Salamone, 1999). The most likely negative outcome of chronic GHB use is addiction. A GHB withdrawal syndrome has been documented with chronic GHB use (Hernandez et al., 1998; Craig et al., 2000; Dyer et al., 2001). The clinical presentation of GHB withdrawal ranges from mild clinical anxiety, agitation, tremors and insomnia to profound disorientation, increasing paranoia with auditory and visual hallucinations, tachycardia, elevated blood pressure and extra-ocular motor impairment. Symptoms, which can be severe, generally resolve without sequelae after various withdrawal periods, although one documented death has occurred. Treatment with benzodia-zepines has been successful for symptoms of a mild withdrawal syndrome.

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