GHB and bodybuiling

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TweetAlthough 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 (gamma-hydroxybutyrate)
by John Morgenthaler and Dan Joy

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 (see Figure 1). 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.

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.

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 [1969] 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.”
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 stimules 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 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.

GHB also stimulates the release of acetylcholine in the brain [Gallimberti, 1989].

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