GHB – safer and more valued than you are told

GHB   Articles of Interest

 

 

RE:  CONSIDER WHY GHB IS NOT DANGEROUS ADMINSTERED IN APNEA PATIENTS

 

Sleep. 2005 Apr 1;28(4):418-24.

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Effect of genetically caused excess of brain gamma-hydroxybutyric acid and GABA on sleep.

Arnulf I, Konofal E, Gibson KM, Rabier D, Beauvais P, Derenne JP, Philippe A.

Fédération des Pathologies du Sommeil, Hôpital Pitié-Salpêtrière. arnulf@stanford.edu

BACKGROUND: Exogenous gamma-hydroxybutyrate (GHB) increases slow-wave sleep and reduces daytime sleepiness and cataplexy in patients with primary narcolepsy. OBJECTIVE: To examine nighttime sleep and daytime sleepiness in a 13-year-old girl homozygous for succinic semialdehyde dehydrogenase (SSADH) deficiency, a rare recessive metabolic disorder that disrupts the normal degradation of 4-aminobutyric acid (GABA), and leads to an accumulation of GHB and GABA within the brain. METHODS: Sleep interview, nighttime polysomnography, Multiple Sleep Latency Tests, and continuous 24-hour in-lab recordings in the patient; overnight polysomnography in her recessive mother and in a 13-year-old female control. RESULTS: During quiet wakefulness, background electroencephalographic activity was slow and composed of 7-Hz activity. Sleep stage 3/4 was slightly increased (28.1% of total sleep period, norms 15%-28%), and the daytime mean sleep latency was short in the patient (3 minutes 42 seconds, norms > 8 minutes). Stage 2 spindles were infrequent in the child (0.18/minute, norms: 1.2-9.2/minute) and her mother (0.65/minute) but normal (4.6/minute) in the control. At the beginning of the second night, a tonic-clonic seizure occurred, followed by a dramatic increase in stage 3/4 sleep, that lasted 46.3 % of the total sleep period, double the normal value. The mother showed a reduced total sleep time and rapid eye movement sleep percentage.

 

DISCUSSION: This suggests that a chronic excess of GABA and GHB induces subtle sleep abnormalities, whereas increased slow-wave sleep evoked by a sudden event (here an epileptic seizure) may be caused by a supplementary increase in GABA and GHB.

 

Curr Opin Pharmacol. 2006 Feb;6(1):44-52. Epub 2005 Dec 20.

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Unravelling the brain targets of gamma-hydroxybutyric acid.

Crunelli V, Emri Z, Leresche N.

School of Biosciences, Cardiff University, Museum Avenue, Cardiff, UK. crunelli@cardiff.ac.uk

Gamma-hydroxybutyric acid (GHB) is a naturally occurring gamma-aminobutyric acid (GABA) metabolite that has been proposed as a neurotransmitter/neuromodulator that acts via its own receptor (GHBR). Its exogenous administration, however, elicits central nervous system-dependent effects (e.g. memory impairment, increase in sleep stages 3 and 4, dependence, seizures and coma) that are mostly mediated by GABAB receptors. The past few years have seen important developments in our understanding of GHB neurobiology: a putative GHBR has been cloned; a transgenic model of GHB aciduria has been developed; GABAB receptor knockout mice and novel GHB analogs have helped to characterize the vast majority of exogenous GHB actions mediated by GABAB receptors; and some of the cellular mechanisms underlying the dependence/abuse properties of GHB, and its ability to elicit absence seizures and an increase in sleep stages 3 and 4, have been clarified. Nevertheless, the physiological significance of a brain GHB signaling pathway is still unknown, and there is an urgent need for a well-validated functional assay for GHBRs. Moreover, as GHB can also be metabolized to GABA, it remains to be seen whether the many GABAB receptor-mediated actions of GHB are caused by GHB itself acting directly on GABAB receptors or by a GHB-derived GABA pool (or both).

 

RE  GHB ADMINISTRATION WITH DIAZEPAM

 

97: Clin Neuropharmacol. 1999 Jan-Feb;22(1):60-2.

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A case of gamma-hydroxybutyric acid withdrawal syndrome during alcohol addiction treatment: utility of diazepam administration.

Addolorato G, Caputo F, Capristo E, Bernardi M, Stefanini GF, Gasbarrini G.

Institute of Internal Medicine, Universitá Cattolica, Rome, Italy.

Gamma-hydroxybutyric acid (GHB) is an emerging drug for alcoholism therapy. We present a case of GHB withdrawal syndrome secondary to GHB addiction during alcoholism treatment. A complete disappearance of drug withdrawal syndrome was achieved with oral diazepam and the symptoms resolved without sequelae. GHB has been used for alcoholism therapy for only a few years now, but the trend is increasing, and other cases similar to this one are foreseeable. This risk could be higher in some countries in which GHB use is increasing not for alcoholism therapy, but for its euphoric and anabolic effects. The present experience indicates that administration of benzodiazepines would seem to be sufficient to achieve total regression of the withdrawal syndrome in a short time, at least if recognized early.

 COMMENT: DIAZEPAM   IS HELPFUL IN THE WITHDRAWL OF GHB

 

 

RE  SAFETY OF GHB   TISSUE PROTECTION

 

 

BRAIN

 

Vopr Biokhim Mozga. 1978;13:279-94.

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[Role of GABA and its derivatives in regulating cerebral circulation]

[Article in Russian]

Mirzoian SA, Akopian VP, Topchian AV.

GABA, its derivative — gamma-hydroxybuturic acid and metabolite –succinic acid have a pronounced dilatatory activity on cerebral circulation in various brain parts. GABA increases cerebral circulation by 25.3%, gamma-hydroxybutyric acid by 35.9% and sucinic acid by 20.4%. In ischaemia of the brain a relationship has been established between cerebral circulation, changes in the GABA system in brain and in the walls of cerebral arteries. The content of GABA increases following enhancement of GAD activity and inhibition of GABA-T. The increase of endogenous GABA level in brain during hypoxia of the brain brings to an improvement of blood circulation through increasing collateral vessels. Experiments with GABA-T inhibition by aminooxyacetic acid give direct evidence about the role of the GABA system in cerebral blood circulation. This mechanism is evaluated by us as an example of an autoregulatory system that is realized by a feed-back mechanism providing the adaptability and compensatory function of cerebral haemodynamics to changing conditions.

 

135: Biull Eksp Biol Med. 1982 Feb;93(2):42-4.

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[Mechanism of antihypoxic effect of depakine]

[Article in Russian]

Ostrovskaia RU.

It was shown that depakine (valproate) increases the lifespan of mice under hypoxic hypoxia, delays the appearance of rhythm disturbances and increases the total duration of ECG maintenance in rats in a low pressure chamber. Depakine was found to reduce the background level of lactate in brain and cardiac tissues and to prevent lactate accumulation characteristic of hypoxia, as well as the shift in its standard ratio with pyruvate. Comparison of depakine with other GABA-ergic compounds with the use of the tests cited revealed that as regards the nature of its protective effect in hypoxia, depakine is close to sodium hydroxybutyrate and succinic semi-aldehyde. By antihypoxic action depakine significantly exceeds piracetam. Analysis of the effects of the inhibitors of various reactions of the “GABA shunt” suggests that the inhibition of succinic semi-aldehyde dehydrogenase accompanied by the enhanced NAD-dependent reduction of succinic semi-aldehyde to gamma-hydroxybutyric acid plays an important part in depakine antihypoxic action.   COMMENT:  VALPROATE WORKS VIA CONVERSION TO  GHB

 

Yao Xue Xue Bao. 2007 Aug;42(8):838-42.

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[Effect of gamma-hydroxybutyric acid receptor on focal cerebral ischemia-reperfusion injury in rats]

[Article in Chinese]

Jin R, Jiang XY, Ma X, Gu SL, Dai TJ.

Department of Pharmacology, Xuzhou Medical College, Xuzhou 221002, China.

This study is to investigate the effect of gamma-hydroxybutyric acid receptor (GHBR) on focal cerebral ischemia-reperfusion injury in rats and its mechanism. NCS-356 (the agonist of GHBR) and NCS-382 (the antagonist of GHBR) were adopted as the tool medicine. The ripe male Sprague-Dawley rats weighing 240 – 280 g were randomly divided into seven groups: sham operation group (sham), ischemia-reperfusion group (Isc/R), NCS-356 160 microg x kg(-1) group (N1), NCS-356 320 microg x kg(-1) group (N2), NCS-356 640 microg x kg(-1) group (N3), NCS-382 640 microg x kg(-1) + NCS-356 640 microg x kg(-1) group (NCS-382 + N3), and nimodipine (Nim) 600 microg x kg(-1) group. The middle cerebral artery occlusion (MCAO) model referring to Longa’s method with modifications was adopted. The effect of GHBR on behavioral consequence of MCAO rats was studied after 2 h of ischemia-reperfusion. After 24 h of ischemia-reperfusion, part of animals were used to measure the cerebral infarction volume by TTC staining; ischemic cortex of another part of animals were used to measure the content of intracellular free calcium by flow cytometry, the tNOS, iNOS activity and the content of NO by spectrophotometric method, the content of cGMP by radioimmunoassay. The neurological function score and infarction volume rate in Isc/R group rats increased significantly than that in sham group; The content of intracellular calcium ([Ca2+]) of cortex neuron and cGMP, the activities of tNOS and iNOS, and the content of NO in Isc/R group were higher than that in sham group obviously (P < 0.01); These consequence we mentioned of N1, N2, N3 and Nim group were lower than that of Isc/R. NCS-382 + N3 group could significantly antagonize the above effect of N3. Thus, NCS-356 has protective effects against ischemia-reperfusion brain injury by activating GHBR. The neuroprotective effect of GHBR is related with decreasing the content of [Ca2+]i, NO, cGMP and tNOS, iNOS activity in MCAO rats.

COMMENT:   GHB IS NEUROPROTECTIVE OF BRAIN TISSUE

HEART TISSUE

Kardiologiia. 1982 Oct;22(10):38-44.

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[Prevention of heart damage of sodium oxybutyrate in terminal states caused by acute blood loss]

[Article in Russian]

Meerson FZ, Dolgikh VT.

After clinical death caused by acute blood loss, hearts of rats were essentially damaged. In isolated hearts, these damages were manifested in the decrease of major contractility parameters with the preferential disturbance of relaxation, increased loss of enzymes (lactate dehydrogenase and creatine phosphokinase) into the perfusate and a significant decrease of the cardiac muscle resistance to hypoxia. All these effects could be, to a large extent, prevented by gamma-hydroxybutyric acid, an endogenous metabolite having central inhibitory effect, which was administered to the animals before the loss of blood.

 


Biull Eksp Biol Med. 1980 Nov;90(11):531-3.

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[Prevention of disorders of cardiac muscle contractility developing after emotionally painful stress by gamma-hydroxybutyric acid and the antioxidant ionol]

[Article in Russian]

Meerson FZ, Trikhpoeva AM.

Studies on contractile function of the papillar muscles of the rat heart after exposure to emotional pain stress gave evidence of a significant decrease in the amplitude, rates of contraction and relaxation and in the index of contraction. These disturbances of contractile function of the heart muscle can be prevented by pretreatment of the animals with the endogenous inhibitory metabolite, gamma-hydroxybutyric acid, or by preliminary injection of the lipid hydroperoxidation inhibitor, antioxidant ionol–2,6-di(tret-butyl)-4-methylphenol.

 

RESPIRATION

 

J Dev Physiol. 1980 Dec;2(6):401-7.

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Respiratory depression by GABA-ergic drugs in the preterm rabbit.

Hedner J, Hedner T, Bergman B, Lundberg D.

Respiratory parameters were studied in preterm rabbits (gestational age 29 days) after intraperitoneal administration of the GABA-like drugs gamma-hydroxybutyric acid and muscimol. The animals were anaesthetized with 0.7% halothane in oxygen and studied in a closed body plethysmograph. Both drugs induced a decreased respiratory frequency and minute volume. Tidal volume decreased after muscimol, but not after gamma-hydroxybutyric acid administration. The present results indicate that an increased GABA-ergic activity causes respiratory depression in the preterm neonatal rabbit, presumably by an action on central nervous frequency and tidal volume modulating systems. Central GABA neurons may thus be involved in the pathogenesis of neonatal respiratory depression and irregular breathing.

 

 

ANTI STRESS  GENERAL

136: Biull Eksp Biol Med. 1981 May;91(5):537-9.

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[Evaluation of the protective effect of gamma-hydroxybutyric acid in stress]

[Article in Russian]

Malyshev VV, Treshchuk LI, Belykh NG.

Administration of GHBA during emotional stress reduces the stress syndrome that manifests in the lesser increase of the corticosterone content in blood plasma, while the noradrenaline level in the heart remains unchanged. GHBA prevents necrosis and contracture injuries of heart muscle cells during the stress. Quantitative evaluation of GHBA protective effect on the organism exposed to stress helped determine that the preliminary administration of GHBA reduces twofold the time necessary for the appearance of eosinophilia after eosinopenia. This indicates that GHBA a powerful antistress action.

 

 

DOSING

 

Encephale. 1980;6(1):93-9.

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Gamma-hydroxybutyric acid as hypnotic. Clinical and pharmacokinetic evaluation of gamma-hydroxybutyric acid as hypnotic in man.

Hoes MJ, Vree TB, Guelen PJ.

Gamma-Hydroxybutyric acid (GOH) was administered to three groups of four patients in 50, 75 or 100 mg/kg dose respectively, and sleep effects were scored, by sleep observation and questionnaire; GOH plasma levels were determined at 75-100 mg/kg, saliva and urine excretion at 100 mg/kg. Sleep induction was rapid and irresistible, subjects awoke at plasma levels of 90 micrograms/ml; sleep scores were good for 75 mg/kg, excellent for 100 mg/kg, notably on mood. For 75 or 100 mg/kg GOH had virtually disappeared from the blood eight hours after intake; twelve hours after intake no more GOH was detectable in urine; no correlation between plasma- and saliva levels was found. Plasma levels for 100 mg/kg dose were not at an anaesthetic level. So, GOH is a safe and good hypnotic at 75 or 100 mg/kg in clinical use.

COMMENT:   350 POUND MAN:    70-100MG/KG  =

 

 

 

 

SAFE TO DRIVE

 

Arch Int Pharmacodyn Ther. 1978 Aug;234(2):236-46.

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Actions and interactions with alcohol of drugs on psychomotor skills: comparison of diazepam and gamma-hydroxybutyric acid.

Mattila MJ, Palva E, Seppälä T, Ostrovskaya RU.

Effects of gamma-hydroxybutyric acid (GOBA) on psychomotor skills related to driving were studied in healthy student volunteers. The effects of oral GOBA 1.0 and 2.0 g, alone or in combination with 0.5 g/kg of ethyl alcohol, were compared in double-blind cross-over trials against oral diazepam 10 mg (D), alcohol 0.5 g/kg, and lactose placebo. Reactive and co-ordinative skills, attention, flicker fusion, proprioception, nystagmus, Maddox wing, and subjective estimations were included. The first single-dose trial with 12 volunteers revealed that neither GOBA 1.0 g nor D modified attention. D impaired reactive skills whilst co-ordinative skills remained largely uninfluenced by D or GOBA. Both D and GOBA impaired leg proprioception. Only D was experienced as a sedative drug. In the second trial with 12 volunteers, GOBA 1.0 g slightly increased reaction mistakes whereas GOBA 2.0 g next day did not. Either dose of GOBA was ineffective on co-ordinative skills, critical flicker fusion frequency, and proprioception. Alcohol alone (0.41 +/- 0.047 mg/ml) improved rather than impaired skills. GOBA 1.0 g + alcohol (0.36 +/- 0.027 mg/ml) impaired reactive skills more than GOBA 2.0 g did but no potentiation was seen. D impaired reactive and co-ordinative skills and flicker fusion. When D was given on two consecutive days, some tachyphylaxis to the D response was seen on co-ordinative skills but not on reactive skills or flicker fusion. It is concluded that in the recommended anxiolytic doses used GOBA neither deteriorates driving skills nor importantly increases the effects of low doses of alcohol.  COMMENT;   SAFE AND NOT POTENTIATING ALCOHOL

 

 

 

BENEFITS

 

 

HGH

 

J Clin Endocrinol Metab. 1977 May;44(5):1014-7.

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Stimulatory effects of gamma-hydroxybutyric acid on growth hormone and prolactin release in humans.

Takahara J, Yunoki S, Yakushiji W, Yamauchi J, Yamane Y.

A dose of 2.5 g of gamma-hydroxybutyric acid (GHB) was administered intravenously to 6 healthy male volunteers. A significant increase in plasma GH was observed at 30, 45, 60 and 90 min after injection. The plasma prolactin level increased significantly at 45 and 60 min after GHB injection. These responses were not found after the saline vehicle injection in the same subjects. It is conceivable that GHB could modify the release of serotonin from the nerve terminals and then stimulate the release of GH and prolactin.

 

ALCOHOLISM

Eur Neuropsychopharmacol. 2007 Dec;17(12):781-9. Epub 2007 Jul 3.

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Comparing and combining gamma-hydroxybutyric acid (GHB) and naltrexone in maintaining abstinence from alcohol: an open randomised comparative study.

Caputo F, Addolorato G, Stoppo M, Francini S, Vignoli T, Lorenzini F, Del Re A, Comaschi C, Andreone P, Trevisani F, Bernardi M, Alcohol Treatment Study Group .

G. Fontana Centre for the Study and Multidisciplinary Treatment of Alcohol Addiction, Department of Internal Medicine, Cardioangiology and Hepatology, University of Bologna, Via Massarenti 9, 40138 Bologna, Italy. fabio-caputo@libero.it

Maintaining abstinence from alcohol is the main goal in treating alcohol dependence. Our aim was to evaluate the efficacy of gamma-hydroxybutyric acid (GHB) and naltrexone (NTX), and their combination in maintaining abstinence. Fifty-five alcoholics were randomly enrolled in three groups and treated for 3 months with GHB, GHB plus NTX, and NTX, respectively. At the end of treatments, abstinence was maintained by 13 patients (72.2%) in combination group, 8 patients (40%; P=0.03) in GHB group, and one patient (5.9%; P=0.0001) in NTX group. Relapses in heavy drinking tended to occur more frequently in GHB group (15%) than in either combination group (no cases) or NTX group (5.9%), but such differences were not statistically significant. The GHB/NTX combination was more effective than either drug given alone; this suggests that the two drugs combine their different actions synergistically without suppressing the favourable effects of each other.

 

Clin Neuropharmacol. 2005 Mar-Apr;28(2):87-9.

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Suppression of craving for gamma-hydroxybutyric acid by naltrexone administration: three case reports.

Caputo F, Vignoli T, Lorenzini F, Ciuffoli E, Del Re A, Stefanini GF, Addolorato G, Trevisani F, Bernardi M; Alcoholism Treatment Study Group.

G. Fontana Centre for the Study and Multidisciplinary Treatment of Alcohol Addiction, Department of Internal Medicine, Cardioangiology and Hepatology, Alma Mater Studiorum, University of Bologna, Bologna, Italy. fabio-caputo@libero.it

Gamma-hydroxybutyric acid (GHB) is currently used to induce and maintain abstinence from alcohol. Cases of craving and desire to increase doses of GHB have been reported in both clinical trials and nonclinical self-administration. The enhancement of dopamine activity induced by GHB receptor activation might play a role in the euphoric effect and potential craving and the consequent abuse of this drug. Naltrexone (NTX), a mu-opioid antagonist, is effective in inducing and maintaining abstinence from alcohol, reducing relapses in heavy drinking and craving for alcohol in alcohol-dependent outpatients. Taking into account the alcohol antireward property of NTX, we tested its activity in reducing craving for GHB in 3 consecutive cases of alcoholics who manifested craving for this drug. In all patients the combination with NTX suppressed the craving for GHB. The antireward effect of NTX likely results from its interference with the GHB-induced dopamine release, leading to a partial blockade of the GHB reinforcing effect responsible of the craving for the drug. A combined therapy with GHB and NTX seems to be able to suppress craving for the former, thus improving the manageability and safety of treatment.

 

 

PROTECTS HEAD TRAUMA

 

Acta Anaesthesiol Scand. 2004 May;48(5):631-6.

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Effect of gamma-hydroxybutyric acid on tissue Na+,K- ATPase levels after experimental head trauma.

Yosunkaya A, Ustün ME, Bariskaner H, Tavlan A, Gürbilek M.

Department of Anesthesiology and Intensive Care, Faculty of Meram Medicine, University of Selçuk, Konya, Turkey. alpyos@superonline.com

BACKGROUND: A failure of the Na(+),K(+)-ATPase activity (which is essential for ion flux across the cell membranes) occurs in many pathological conditions and may lead to cell dysfunction or even cell death. By altering the concentration of specific opioid peptides, gamma-hydroxybutyric acid (GHB) may change ion flux across cell membranes and produce the ‘channel arrest’ which we assumed will inhibit the failure of Na+,K(+)-ATPase activity and therefore lead to energy conservation and cell protection. Therefore we planned this study to see the effects of GHB at two different doses on Na(+),K(+)-ATPase activity in an experimental head trauma model. METHODS: Forty New Zealand rabbits were divided equally into four groups: group I was the sham-operated group, group II (untreated group), group III received head trauma and intravenous (i.v.) 500 mg/kg GHB and group IV received head trauma and i.v. 50 mg/kg GHB. Head trauma was delivered by performing a craniectomy over the right hemisphere and dropping a weight of 10 g from a height of 80 cm. The non-traumatized (left) side was named as ‘a’ and the traumatized (right) side as ‘b’. One hour after the trauma in groups II and III and craniotomy in group I, brain cortices were resected from both sides and in group I only from the right side was the tissue Na-K-ATPase activity determined. RESULTS: The mean +/- SD of Na(+),K(+)-ATPase levels of each group are as follows: group I – 5.97 +/- 0.55; group IIa – 3.90 +/- 1.08; group IIb – 3.58 +/- 0.90; group IIIa – 5.53 +/- 0.60; group IIIb – 5.33 +/- 0.88; group IVa – 5.05 +/- 0.72; group IVb – 4.93 +/- 0.67. The Na(+),K(+)-ATPase levels of group IIa, IIb, IVa and IVb were significantly different from group S (P < 0.05). There were also significant differences between group IIa and groups IIIa and IVa; group IIb and groups IIIb and IVb (P < 0.05). CONCLUSIONS: We conclude that GHB is effective in suppressing the decrease in Na(+),K(+)-ATPase levels in brain tissue at two different dose schedules after head trauma.

 

 

ELIMINATES TREMOR

 

Drug Alcohol Depend. 2003 May 1;70(1):85-91.

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Gamma-hydroxybutyric acid versus naltrexone in maintaining alcohol abstinence: an open randomized comparative study.

Caputo F, Addolorato G, Lorenzini F, Domenicali M, Greco G, del RE A, Gasbarrini G, Stefanini GF, Bernardi M.

Department of Internal Medicine, Cardioangiology and Hepatology, ‘G. Fontana’ Centre for the Study and Treatment of Alcohol Addiction, University of Bologna, Via Massarenti no. 9, Bologna, 40138, Italy. fabio-caputo@libero.it

Maintaining abstinence from alcohol is the main goal in the treatment of alcohol dependence. Naltrexone (NTX) and gamma-hydroxybutyric acid (GHB) have proved able to maintain alcohol abstinence in alcoholic subjects. The aim of our study was to evaluate the efficacy of GHB compared with NTX in maintaining abstinence from alcohol after 3 months of treatment. A total of 35 alcohol-dependent outpatients were randomly enrolled in two groups: the GHB group consisted of 18 patients treated with oral doses of GHB (50 mg/kg of body weight t.i.d) for 3 months; the NTX group consisted of 17 patients treated with oral doses of NTX (50 mg/day) for 3 months. At the end of the study, a statistically significant difference (P=0.02) was found in the number of abstinent patients between the GHB and the NTX groups. In patients who failed to be abstinent, no relapses in heavy drinking were observed in the NTX group, while in the GHB group all patients relapsed. The results of the present study show that GHB is more effective than NTX in maintaining abstinence from alcohol in a short-term treatment period; on the other hand, NTX confirmed its ability to reduce alcohol relapses.

 

Mov Disord. 2005 Jun;20(6):745-51.

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Marked amelioration of alcohol-responsive posthypoxic myoclonus by gamma-hydroxybutyric acid (Xyrem).

Frucht SJ, Bordelon Y, Houghton WH.

Department of Neurology, Columbia University Medical Center, 710 West 168th Street, New York, NY 10032, USA. sf216@columbia.edu

We conducted an open-label, dose-finding, blinded-rating trial of gamma-hydroxybutyric acid (Xyrem) in a single patient with severe alcohol-responsive posthypoxic myoclonus refractory to treatment with standard antimyoclonic agents. Xyrem was given in divided doses during the day and was well tolerated. Intensity of myoclonus was measured using the Unified Myoclonus Rating Scale, and blinded videotape review demonstrated complete resolution of myoclonus at rest and stimulus-sensitive myoclonus. Action myoclonus and functional performance also improved in ways that were practically meaningful, allowing her to feed herself, to accomplish daily hygiene tasks, and to walk with assistance. The possible mechanisms of action and potential uses of this agent in other alcohol-responsive movement disorders are discussed. (c) 2005 Movement Disorder Society.

 

Naunyn Schmiedebergs Arch Pharmacol. 1976 Dec 17;295(3):203-9.

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Suppression of ethanol-induced locomotor stimulation by GABA-like drugs.

Cott J, Carlsson A, Engel J, Lindqvist M.

Ethanol (2.4 g/kg) was given intraperitoneally to mice and was found to cause a marked increase in spontaneous locomotor activity. When mice were pretreated with low doses of agents which mimic or augment the action of GABA (gamma-hydroxybutyric acid, baclophen, or aminooxyacetic acid) the ethanol-induced locomotor stimulation was completely eliminated; Baclophen (10 mg/kg) was found to cause an initial increase followed by a later decrease in synthesis of catecholamines, as measured by the accumulation of dopa after inhibition of central aromatic L-amino acid decarboxylase, in dopamine-rich areas of rat brain. These data are consistent with previous findings that baclophen, as well as other agents which enhance the activity of GABA systems, reduce the firing of dopamine neurons, thus causing enhanced synthesis of dopamine via feedback mechanisms. These findings also indicate a potential interaction between GABA-like drugs and alcohol in man, and may be of heuristic value in the treatment of chronic alcoholism. The possibility that the mechanism of the inhibition of ethanol-induced locomotor stimulation by GABA-like drugs may be due to a selective interference with ethanol-induced dopamine release is discussed.

 

 

Klin Padiatr. 2007 Jul-Aug;219(4):217-9.

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Gamma-hydroxybutyric acid sedation in neonates and children undergoing MR imaging.

Pöschl J, Kölker S, Bast T, Brüssau J, Ruef P, Linderkamp O, Bettendorf M.

Department of Neonatology, University Children’s Hospital, Heidelberg, Germany. johannes.Poeschl@med.uni-heidelberg.de

BACKGROUND: Insufficient sedation in pediatric magnetic resonance imaging (MRI) results in prolonged examination time. To describe the efficacy and side effects of sedation with Phenobarbital short-time infusion followed by continuous gamma-hydroxybutyric acid (GHB) infusion in neonates and children for MRI examinations in a retrospective study. PATIENTS: With Institutional Review Board approval 94 children (Group I: 1-4 weeks; Group II: >1 to 6 months; Group III: >6 months) were sedated with phenobarbital 10 mg/kg (maximum 200 mg) intravenously 30 min prior to examination. Than intravenous sedation was maintained with GHB 10 mg/kg/h after a priming dose of 30 mg/kg in 20 min. RESULTS: In group 1 all neonates (n=8) were well sedated without side effect. One of 21 infants in group 2 showed restlessness and the MRI failed. Two of 65 patients of group 3 were not sufficiently sedated and one of them vomited. CONCLUSIONS: Non-invasive diagnostic procedures in neonates and children may be managed by phenobarbital and GHB sedation with side effects or failure of 3%. 

COMMENT: SAFE ENOUGH TO USE IN INFANTS…..

 

 

SLEEP

 

Expert Rev Neurother. 2006 Aug;6(8):1139-46.

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Sodium oxybate for narcolepsy.

Scharf MB.

The Center for Research in Sleep Disorders, 1275 Kemper Road Cincinnati, OH 45246-3901, USA. mscharf@tristatesleep.com

Sodium oxybate (Xyrem), also known as gamma-hydroxybutyric acid, is the only therapeutic specifically approved in the USA for the treatment of cataplexy in narcolepsy. The US FDA has recently expanded its indication to include excessive daytime sleepiness associated with narcolepsy. In contrast to the antidepressants and stimulants commonly used to treat the disorder, sodium oxybate is the only compound that addresses both sets of symptoms and, when used properly, is less likely to lead to the development of tolerance and other undesirable side effects. In this review, the results of clinical trials and the place of sodium oxybate in narcolepsy treatment are discussed.

 

 

PROZAC EYES
Eksp Klin Farmakol. 2005 Nov-Dec;68(6):30-5.

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[Effects of lithium hydroxybutyrate and vagotomy on respiratory arrest caused by systemic serotonin administration in rats]

[Article in Russian]

Tarakanov IA, Tarasiva NN, Safronov VA.

The role of gamma-hydroxybutyric acid (GHBA) and gamma-aminobutyric acid (GABA) in the mechanisms of respiratory arrest after systemic serotonin administration has been studied in anaesthetized outbred male rats. Under normal conditions, serotonin (5-HT) administration (20 – 60 microg/kg, i.v.) leads to specific changes in the respiratory pattern, whereby a short (approximately 5 sec) increase in the respiratory rate is followed by a longer (up to approximately 20 sec) respiratory arrest. Pretreatment with Li-GHBA salt (750 mg/kg, i.v.) did not significantly change the first stage of the respiratory response to serotonin administration, but excluded or significantly reduced the stage of respiratory arrest. The effect of bilateral vagotomy on the respiratory pattern upon serotonin administration was very similar to the action of GHBA. It is suggested that GHBA as a neuromodulator probably participates in the mechanisms of respiratory control after serotonin administration.

 

GHB BLOCKS COCAINE CRAVING

 

Pharmacol Biochem Behav. 1998 Mar;59(3):697-702.

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Gamma-hydroxybutyric acid decreases intravenous cocaine self-administration in rats.

Martellotta MC, Balducci C, Fattore L, Cossu G, Gessa GL, Pulvirenti L, Fratta W.

B. B. Brodie Department of Neuroscience, University of Cagliari, Italy.

Gamma-hydroxybutyric acid (GHB) is an endogenous compound present in mammalian brain suggested as a putative neurotransmitter, which has been shown to affect several aspects of dependence from various classes of drugs of abuse. In the present study, two sets of experiments were performed to investigate the effects of acute pretreatment with GHB on intravenous cocaine self-administration in rats. In the first experiment GHB was administered intragastrically at the doses of 175, 350, and 700 mg/kg to Long-Evans rats trained to self-administer cocaine using nose-poke as operandum. In the second experiment, GHB was administered intraperitoneally at the doses of 100, 200, and 400 mg/kg to Wistar rats trained to self-administer cocaine intravenously using lever-pressing as operandum. In both experiments acute pretreatment with GHB significantly and dose dependently reduced cocaine self-administration. The effectiveness of GHB was similar in both experiments, indicating that the effect of GHB on cocaine self-administration is independent of animal strain. route of administration, and type of operant response required. These results indicate that GHB reduces cocaine-seeking behavior in rats, modulating the acute reinforcing effect of cocaine. The clinical effectiveness of GHB in dependence from various classes of abused drugs warrants further studies to evaluate the possibility that GHB might represent a useful therapeutic agent for cocaine addiction in humans.

 

Psychopharmacology (Berl). 1997 Jul;132(1):1-5.

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Rewarding properties of gamma-hydroxybutyric acid: an evaluation through place preference paradigm.

Martellotta MC, Fattore L, Cossu G, Fratta W.

B.B. Brodie Department of Neuroscience, University of Cagliari, Italy.

Gamma-hydroxybutyric acid (GHB), a putative neurotransmitter or neuromodulator found in the mammalian brain, has been successfully used in clinical practice to alleviate both alcohol and opiate withdrawal symptoms. In the present study we used a conditioned place preference (CPP) paradigm to investigate whether GHB possesses rewarding properties in rats. In order to exclude possible artifacts due to experimental design, we evaluated the possibility of a shift in preference when rats are conditioned either on their non-preferred side or on a randomly assigned side of conditioning. In both experiments GHB was seen to induce CPP. Although to date the physiological role of this compound still remains unclear, there is no doubt that GHB, further to its proven effect on alcohol and opiates, possesses rewarding properties of its own. The abuse liability afforded by this drug suggests the use of particular caution in handling GHB as a clinically useful drug.

 

 

Behav Pharmacol. 2006 Mar;17(2):119-31.

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Gamma-hydroxybutyric acid affects the acquisition and reinstatement of cocaine-induced conditioned place preference in mice.

Maldonado C, Rodríguez-Arias M, Castillo A, Aguilar MA, Miñarro J.

Department of Psychobiology, Faculty of Psychology, University of Valencia, Avda Blasco Ibáñez 21, 46010 Valencia, Spain.

Cocaine addicts very often use different combinations of cocaine and other drugs of abuse such as gamma-hydroxybutyric acid. The objective of the present work was to evaluate the impact of gamma-hydroxybutyric acid administration on the rewarding actions of cocaine, using the conditioned place preference procedure. Cocaine-induced conditioned place preference (50 mg/kg) was studied after pairing this drug with different gamma-hydroxybutyric acid doses (6.25, 12.5, 25, 50 and 100 mg/kg) during either the acquisition or the expression phase of the procedure. After conditioned place preference had been established, and the preference was extinguished, a reinstatement was induced by a dose of cocaine half of that used to produce conditioning, or by gamma-hydroxybutyric acid alone or by both drugs together. The doses of 12.5 and 100 mg/kg of gamma-hydroxybutyric acid blocked the acquisition of cocaine-induced conditioned place preference, and no dose affected the expression of this conditioning. Reinstatement was abolished only with the dose of 25 mg/kg gamma-hydroxybutyric acid, which did not reinstate the preference by itself. This is the first study evaluating the effects of gamma-hydroxybutyric acid on the rewarding properties of cocaine using the conditioned place preference procedure. The principal conclusion of the study is that gamma-hydroxybutyric acid does not enhance the rewarding effect of cocaine, and within a narrow margin of effective doses, blocks the acquisition and reinstatement of cocaine-induced preference.

 

MELLOW

 

Prog Neuropsychopharmacol Biol Psychiatry. 2007 Mar 30;31(2):337-42. Epub 2006 Oct 13.

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Anti-aggressive effects of GHB in OF.1 strain mice: involvement of dopamine D2 receptors.

Pedraza C, Dávila G, Martín-López M, Navarro JF.

Department of Psychobiology, Faculty of Psychology, Campus de Teatinos, University of Málaga 29071 Málaga, Spain. mdpedraza@uma.es

Numerous studies indicate that gamma-hydroxybutyric acid (GHB) influences the endogenous dopamine system. Both GHB and most dopaminergic D(2) receptor antagonists are effective anti-aggressive agents in animal models. The present study aimed to investigate the effects of GHB on agonistic behaviour and to implicate D(2) dopamine receptor on these behaviours. For this purpose, the effects of GHB (80, 120 and 160 mg/kg, IP) and tiapride (60 mg/kg) administered alone or in combination were examined on agonistic behaviour elicited by ‘isolation’ in male mice. Individually housed mice were exposed to anosmic “standard opponents” 30 min after drug administration, and the encounters were videotaped and evaluated using an ethologically based analysis. The administration of 80 and 120 mg/kg of GHB reduced threat without impairing motor activity, but the administration of 160 mg/kg of GHB or the co-administration of GHB+tiapride (a selective D(2) receptor antagonist) significantly reduced threat and attack but concomitantly increased immobility. The co-administration of GHB+tiapride had different effects to those observed by the administration of these drugs separately. It is concluded that the anti-aggressive effect of GHB appears to be mediated, at least in part, by D(2) dopamine receptors. This anti-dopaminergic activity is an indirect effect, probably induced by the activation of GHB receptors of low affinity, and in this way, this compound would reduce levels of dopamine without blockading of D(2) postsynaptic dopamine receptors.

 

Alcohol Withdrawl

Acta Med Austriaca. 2003;30(3):83-6.

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Gamma-hydroxybutyric acid in the treatment of alcohol withdrawal syndrome in patients admitted to hospital.

Korninger C, Roller RE, Lesch OM.

Lorenz Böhler Trauma Unit, Donaueschingenstrasse 13, A-1200 Wien. Christian.Korninger@auva.sozvers.at

Gamma-hydroxybutyric acid is a gamma-aminobutyric acid analogue which can be found in the human brain and is believed to be a neurotransmitter in the central nervous system. In animal experiments as well as in humans gamma-hydroxybutyric acid has been shown to alleviate the symptoms of the alcohol withdrawal syndrome.   299 patients, who were admitted to hospital for reasons primarily unrelated to their alcohol dependence, were treated with gamma-hydroxybutyric acid when symptoms of the alcohol withdrawal syndrome occurred. Gamma-hydroxybutyric acid was usually given at a daily dose of 50 mg/kg in 3 divided doses, the clinical course of the patients was followed for 7 days or until discharge from hospital. Patients were 214 men and 82 women aged 18-87 years. The reasons for admission to hospital were frequently internal diseases, neurological/psychiatric problems, trauma or surgery. At the start of gamma-hydroxybutyric acid treatment, tremor was present in 81% of patients, sweating in 76% and unrest in 92%. Symptoms occurred 1-72 hours after admission. The efficacy of gamma-hydroxybutyric acid to ameliorate or suppress the symptoms of the alcohol withdrawal syndrome was judged to be excellent in 57%, good in 34%, fair in 18%, insufficient in 3% of patients. Drug tolerance was judged to be excellent in 79%, good in 17%, fair in 2% and poor only in 1% of patients. Adverse events were rare and mild. It is concluded that gamma-hydroxybutyric acid is an attractive alternative to tranquilizers in the management of the alcohol withdrawal syndrome in hospital.

 

Ann Neurol. 2003;54 Suppl 6:S3-12.

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GABA, gamma-hydroxybutyric acid, and neurological disease.

Wong CG, Bottiglieri T, Snead OC 3rd.

Institute of Medical Sciences, University of Toronto, Faculty of Medicine and Brain and Behavior Research Program, Hospital for Sick Children, Ontario, Canada.

gamma-Aminobutyric acid (GABA) is the primary inhibitory neurotransmitter in the central nervous system. GABA is converted from glutamic acid by the action of glutamic acid decarboxylase (GAD) of which two isoforms exist GAD65 and GAD67. GABA then is broken down, both within the cell and in the synaptic cleft by GABA transaminase to form succinic semialdehyde. In turn, succinic semialdehyde is converted either to succinic acid by succinic semialdehyde dehydrogenase or into gamma-hydroxybutyric acid (GHB) by succinic semialdehyde reductase. Because GABA modulates the majority of inhibition that is ongoing in the brain, perturbations in GABAergic inhibition have the potential to result in seizures. Therefore, the most common disorder in which GABA is targeted as a treatment is epilepsy. However, other disorders such as psychiatric disease, spasticity, and stiff-person syndrome all have been related to disorders of GABAergic function in the brain. This review covers the roles of GABAergic neurotransmission in epilepsy, anxiety disorders, schizophrenia, stiff-person syndrome, and premenstrual dysphoric disorder. In the final section of this review, the GABA metabolite GHB is discussed in terms of its physiological significance and its role in epilepsy, sleep disorders, drug and alcohol addiction, and an inborn error of GABA metabolism, succinic semialdehyde dehydrogenase deficiency.

 

BACLOFEN

Curr Drug Targets CNS Neurol Disord. 2003 Aug;2(4):248-59.

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GABA(B) receptors as potential therapeutic targets.

Vacher CM, Bettler B.

Pharmazentrum, University of Basel, Department of Physiology, Klingelbergstr. 50-70, CH-4056 Basel, Switzerland. bernhard.bettler@unibas.ch

gamma-Aminobutyric acid-B (GABA(B)) receptors are broadly expressed in the nervous system and have been implicated in a wide variety of neurological and psychiatric disorders. To date the only GABA(B) drug on the market is the agonist baclofen (Lioresal((R))) that is used to treat severe spasticity of cerebral and spinal origin. In addition baclofen is effective in animal models for many central and peripheral disorders, but side-effects and the development of tolerance prohibited a more widespread use of this drug in man. Similarly GABA(B) antagonists show great therapeutic promise but their shortcomings, e.g. the lack of brain penetration or some proconvulsive potential, prevented clinical development. The cloning of GABA(B) receptors in 1997 revived interest in these receptors as drug targets. The long-awaited availability of the tools that were necessary to develop more selective and safer drugs stimulated an impressive activity in the field. The demonstration that GABA(B) receptors needed to heteromerize for function provided new insights into the structure of G-protein coupled receptors in general and enabled to identify allosteric GABA(B) drugs. Gene knockout mice revealed neuronal systems that are under tonic GABA(B) control and therefore best suited for therapeutic intervention. Significant advances were made in clarifying the relationship between GABA(B) receptors and the receptors for gamma-hydroxybutyrate (GHB), a drug of abuse. Here we provide and update on the molecular composition, the physiology and the pharmacology of GABA(B) receptors and discuss to what extent our current knowledge influences ongoing and future drug discovery efforts.

Baclofen can cause side effects that may impair your thinking or reactions. Be careful if you drive or do anything that requires you to be awake and alert. Avoid drinking alcohol. It can increase some of the side effects of baclofen. Do not use baclofen at a time when muscle tone is needed to assure safe balance and movement for certain activities. In some situations, it may endanger your physical safety to be in a state of reduced muscle tone.

You may have withdrawal symptoms such as seizures or hallucinations, when you stop using baclofen after using it over a long period of time. Do not stop using this medication suddenly without first talking to your doctor. You may need to use less and less before you stop the medication completely.

 

 

 

 

 

HEROIN ABUSE

Alcohol. 2000 Apr;20(3):257-62.

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Gamma-hydroxybutyric acid in the treatment of alcohol and heroin dependence.

Gallimberti L, Spella MR, Soncini CA, Gessa GL.

Department of Medical and Surgical Sciences, Addictive Medicine Unit, University of Padua, Via Giustiniani 2, I-35100, Padua, Italy. l.gallimberti@libero.it

We briefly review two double-blind, placebo-controlled surveys conducted in this laboratory with the aim of evaluating the efficacy of gamma-hydroxybutyric acid in the treatment of alcohol withdrawal syndrome as well as alcohol craving and consumption in alcoholics. In the first study, acute administration of 50 mg/kg gamma-hydroxybutyric acid, a nonhypnotic dose in alcoholic patients, resulted in a rapid and significant reduction of the severity score of alcohol withdrawal signs and symptoms that lasted as long as 7 hours. In the second study, treatment with 50 mg/kg/day gamma-hydroxybutyric acid for 3 consecutive months (1) reduced the number of daily drinks by approximately 50%, (2) increased the days of abstinence approximately threefold, and (3) reduced the alcohol craving score by up to 60%. These results feature gamma-hydroxybutyric acid as an effective agent for the treatment of alcohol dependence. Data on the effect of gamma-hydroxybutyric acid on opiate withdrawal syndrome also are reviewed. Administration of 25 mg/kg induced a marked reduction of opiate withdrawal score in both heroin- and methadone-dependent subjects. Finally, we report the cases of adverse reactions to and abuse of gamma-hydroxybutyric acid revealed in a retrospective analysis of patients recruited in this laboratory over a 10-year period.
Alcohol. 2000 Apr;20(3):223-5.

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Safety and tolerability of gamma-hydroxybutyric acid in the treatment of alcohol-dependent patients.

Beghè F, Carpanini MT.

Clinical and Pharmacological Research Unit “Piertomaso Tessitore” and Pharmaco-surveillance Department, Laboratorio Farmaceutico C.T., Via Dante Alighieri 71, 18038, Sanremo, Italy.

Gamma-hydroxybutyric acid (GHB) has been in clinical use in Italy since 1991 for treatment of alcohol dependence. Results of phase III and phase IV studies have shown that the drug is effective and well tolerated in the treatment of alcohol withdrawal syndrome and in reducing alcohol consumption and alcohol craving. Pharmacosurveillance indicates that abuse of gamma-hydroxybutyric acid is a limited phenomenon in clinical settings when the drug is dispensed under strict medical surveillance and entrusted to a referring familiar member of the patient.

ALCOHOL ABUSE

 

Alcohol Clin Exp Res. 1999 Oct;23(10):1596-604.

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Gamma-hydroxybutyric acid (GHB) in the treatment of alcohol withdrawal syndrome: a randomized comparative study versus benzodiazepine.

Addolorato G, Balducci G, Capristo E, Attilia ML, Taggi F, Gasbarrini G, Ceccanti M.

Institute of Internal Medicine, Universita’ Cattolica del Sacro Cuore, Rome, Italy. ecapristo@pelagus.it

BACKGROUND: Benzodiazepine has been shown to be one of the most effective class of drugs in the management of alcohol withdrawal syndrome (AWS). Gamma-hydroxybutyric acid (GHB) has recently been introduced in the treatment of alcohol problems, including AWS. At present there are no comparative studies between benzodiazepines and GHB in AWS treatment. The aim of the present randomized, controlled, single-blind study was to evaluate the efficacy and safety of GHB compared with diazepam in the treatment of AWS. METHODS: Sixty alcoholics affected by AWS were enrolled in the study. Diazepam (0.5-0.75 mg/kg body weight for 6 days, tapering the dose 25% daily until day 10) was administered orally to 30 patients (25 males, 5 females; mean age 44.3 +/- 10.9 years); GHB (50 mg/kg body weight for 10 days) was administered orally to 30 patients (26 males,4 females; mean age 41.7 +/- 10.4 years).The Clinical Institute Withdrawal Assessment for Alcohol-revised scale (CIWA-Ar) was used to evaluate the AWS physical symptoms. The State Anxiety Inventory test for current anxiety assessment and the Zung self-rating Depression Scale for current depression assessment were performed. RESULTS: Eight patients (26.6%) in the diazepam group and 4 patients (13.3%) in the GHB group dropped out. Both treatments were effective in reducing AWS. No significant difference was found between the groups in CIWA-Ar total score at baseline and at the different times of observation. Considering the CIWA-Ar subscore and Zung scale, a significant reduction of anxiety on day 4 (p < 0.02), agitation on day 5 (p < 0.02) and time of recovery of depression on day 5 (p < 0.02) was observed in the GHB group with respect to the diazepam group. Drowsiness and vertigo developed after initial drug administration in the GHB (19.2%) and diazepam (36.4%) groups and quickly resolved in both groups. CONCLUSIONS: GHB is as effective in the management of AWS as benzodiazepine and it seems to be quicker in reducing anxiety, agitation, and depression. Both drugs are safe and well-tolerated in AWS management.

 

Life Sci. 1999;65(14):PL191-6.

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Long-term administration of GHB does not affect muscular mass in alcoholics.

Addolorato G, Capristo E, Gessa GL, Caputo F, Stefanini GF, Gasbarrini G.

Institute of Internal Medicine, Catholic University, Rome, Italy.

Gamma-hydroxybutyric acid (GHB) is a drug recently utilized for alcoholism management. It has been shown that GHB has anabolic effects since it can increase growth hormone (GH) release in healthy subjects. At present, there are no studies investigating body composition in alcoholics during long-term GHB treatment. In this study body composition and GH secretion in alcohol dependent subjects was evaluated during addiction and at different time of GHB administration and alcohol abstinence. A total of 45 male alcohol dependent patients (mean age 39.7+/-9.8 yrs, mean height: 171+/-6.8 cm, body mass index–BMI–22.1+/-1.6 kg/m(-2)) were consecutively enrolled. Body composition was assessed by anthropometry, bioimpedance analysis and tritiated water method. A 7-day food diary was collected. Plasma GH levels were determined by radioimmunoassay. A 6-month total abstinence was obtained in 22 patients, by means of psychological support counseling and self-help groups in 9 subjects and also by 50 mg/kg/day of GHB in 13 subjects. At 1, 2, 3 and 6 months of abstinence, the biochemical assessment and metabolic variables were re-examined. Fat-free mass (FFM) and basal GH secretion were similar at the different times of follow-up in both groups of patients. GHB treated patients and those receiving psychological support alone showed similar values in FFM and GH. Both groups of patients did not differ in FFM and plasma GH level from healthy controls at any of the times evaluated. Waist-to-hip ratio did not differ between patient groups, while higher values were shown in alcoholics with respect to control subjects. The present study shows that long-term administration of GHB did not affect muscular mass and did not determine an increase of GH release in chronic alcoholics. This findings could be due to an impairment of the hypothalamic-limbic system and of GABAergic neurotransmission in alcoholics’ brain.

 

Clin Neuropharmacol. 1999 Jan-Feb;22(1):60-2.

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A case of gamma-hydroxybutyric acid withdrawal syndrome during alcohol addiction treatment: utility of diazepam administration.

Addolorato G, Caputo F, Capristo E, Bernardi M, Stefanini GF, Gasbarrini G.

Institute of Internal Medicine, Universitá Cattolica, Rome, Italy.

Gamma-hydroxybutyric acid (GHB) is an emerging drug for alcoholism therapy. We present a case of GHB withdrawal syndrome secondary to GHB addiction during alcoholism treatment. A complete disappearance of drug withdrawal syndrome was achieved with oral diazepam and the symptoms resolved without sequelae. GHB has been used for alcoholism therapy for only a few years now, but the trend is increasing, and other cases similar to this one are foreseeable. This risk could be higher in some countries in which GHB use is increasing not for alcoholism therapy, but for its euphoric and anabolic effects. The present experience indicates that administration of benzodiazepines would seem to be sufficient to achieve total regression of the withdrawal syndrome in a short time, at least if recognized early.

 

Alcohol. 2000 Apr;20(3):271-6.

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Mechanism of the antialcohol effect of gamma-hydroxybutyric acid.

Gessa GL, Agabio R, Carai MA, Lobina C, Pani M, Reali R, Colombo G.

Bernard B. Brodie Department of Neuroscience, University of Cagliari, Cagliari, Italy.

Treatment with gamma-hydroxybutyric acid has been reported to effectively decrease alcohol craving and consumption as well as alcohol withdrawal symptoms in alcoholics. We describe the results of animal studies demonstrating the ability of gamma-hydroxybutyric acid to reduce (1) the severity of ethanol withdrawal signs in rats rendered physically dependent on ethanol and (2) voluntary ethanol intake in selectively bred Sardinian alcohol-preferring rats. Furthermore, we review experimental data suggesting that gamma-hydroxybutyric acid and ethanol have several pharmacological effects in common. Relevant similarities are: (1) stimulation of firing rate of dopaminergic neurons and dopamine release in specific rat brain areas; (2) development of cross-tolerance to the motor-impairing effects after repeated administration in rats; 3) abuse potential, as indicated by self-administration of pharmacologically relevant doses of gamma-hydroxybutyric acid in rats and mice; (4) induction of anxiolytic effects in rats; and (5) induction of similar discriminative stimulus effects, as evidenced by symmetrical generalization in a drug discrimination study in rats. These lines of evidence are discussed in relation to gamma-hydroxybutyric acid exerting its antialcohol effects by a substitution mechanism.

 

Alcohol Alcohol. 1989;24(5):447-51.

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Suppression by gamma-hydroxybutyric acid of ethanol withdrawal syndrome in rats.

Fadda F, Colombo G, Mosca E, Gessa GL.

Institute of Physiology, University of Cagliari, Italy.

The ability of gamma-hydroxybutyric acid to suppress ethanol withdrawal syndrome was tested in male rats rendered physically dependent on ethanol by several intragastric administrations of ethanol (9-15 g/kg daily for 7 days). Gamma-hydroxybutyrate (0.25, 0.50 and 1.00 g/kg i.p.), administered 8 hr after the last ethanol dose, produced a dose-dependent inhibition of withdrawal signs such as tremors and audiogenically-induced seizures; the highest dose tested suppressed all ethanol withdrawal symptoms.

Alcohol. 2000 Apr;20(3):285-91.

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Gamma-hydroxybutyric acid and alcohol-related syndromes.

Moncini M, Masini E, Gambassi F, Mannaioni PF.

Department of Preclinical and Clinical Pharmacology, Toxicological Unit, Florence University, Via G. Pieraccini 6, 50139, Florence, Italy.

We report on the effectiveness and safety of gamma-hydroxybutyric acid in the therapy of overt alcohol withdrawal syndromes, their prevention, and the prevention of relapses in formerly detoxified alcoholics. We studied 321 patients (236 men, 85 women), divided into two open-study groups for the treatment and prevention of alcohol withdrawal syndromes and one double-blind study group to evaluate the effects of gamma-hydroxybutyric acid versus placebo on alcoholic craving and relapses in detoxified patients. Gamma-hydroxybutyric acid treatment promptly reduced withdrawal symptoms in all patients and prevented alcohol withdrawal syndromes in 55% of cases. The attenuation of craving in detoxified patients was significantly greater in the gamma-hydroxybutyric acid-treated group in comparison with the placebo-treated group. The therapeutic use of gamma-hydroxybutyric acid was not accompanied by serious side effects. Gamma-hydroxybutyric acid diversion was poorly represented: gamma-hydroxybutyric acid-induced abuse was reported in 4 (1.1%) of 345 treated patients, and only 9 cases of gamma-hydroxybutyric acid acute poisoning were reported in the years 1992-1995. Our results suggest that gamma-hydroxybutyric acid, with a favorable risk/benefit ratio, is a clinically useful drug in the treatment of alcohol dependence.

Am J Addict. 2001 Summer;10(3):232-41.

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Gamma-hydroxybutyric acid: patterns of use, effects and withdrawal.

Miotto K, Darakjian J, Basch J, Murray S, Zogg J, Rawson R.

UCLA Dept. of Psychiatry and Biobehavioral Sciences, 760 Westwood Plaza, Los Angeles, CA 90024, USA. kmiotto@mednet.ucla.edu

Gamma-hydroxybutyric acid (GHB) is gaining popularity as a drug of abuse. Reports of toxicity and lethality associated with GHB use have increased. This survey study was designed to identify patterns of GHB use, its effects, and withdrawal syndrome. A survey inquiring about the effects of GHB was administered to 42 users. The results showed that GHB was used to increased feelings of euphoria, relaxation, and sexuality. Adverse effects occurred more frequently in daily users and polydrug users than in occasional GHB users. Loss of consciousness was reported by 66%, overdose by 28%, and amnesia by 13% of participants during GHB use and by 45% after GHB use. Three daily users developed a withdrawal syndrome that presented with anxiety, agitation, tremor, and delirium. Participants described GHB intoxication as having similarities to sedative-hypnotic or alcohol intoxication. Regular use has been shown to produce tolerance and dependence. Participants dependent on GHB reported using multiple daily doses around the clock. High frequency users appeared at the greatest risk for developing withdrawal delirium and psychosis after abrupt discontinuation of GHB use.

 

 

ABLE TO GO TO WORK
Eur J Clin Pharmacol. 1999 Jan;54(11):821-7.

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Effects of single dose of gamma-hydroxybutyric acid and lorazepam on psychomotor performance and subjective feelings in healthy volunteers.

Ferrara SD, Giorgetti R, Zancaner S, Orlando R, Tagliabracci A, Cavarzeran F, Palatini P.

Centre of Behavioural and Forensic Toxicology, Istituto di Medicina Legale, University of Padova, Italy.

OBJECTIVE: This study investigated the possible effects of gamma-hydroxybutyric acid (GHB) on human psychomotor performance and subjective feelings important for the safety of skilled performance. METHODS: Twelve healthy volunteers, six males and six females, aged 22-36 years, participated as subjects. Drugs and placebo were administered according to a single-dose, double-blind, balanced, four-way, crossover design. Treatments were separated by a wash-out period of 1 week and consisted of placebo, lorazepam 0.03 mg x kg(-1), GHB 12.5 mg x kg(-1) and GHB 25 mg x kg(-1). Subjects’ psychomotor performance was assessed at baseline and at 15, 60, 120 and 180 min after treatment. Mood was assessed using 16 visual analogue scales, before treatment and 120 min later. Psychomotor performance was measured using the following tests: Critical Flicker Fusion. Response Competition Test, Critical Tracking Task, Choice Reaction Time and Visual Vigilance Task. RESULTS: GHB at both doses had no effects on attention, vigilance, alertness, short-term memory or psychomotor co-ordination (delta-placebo, P > 0.05); calmness increased with the lower dose and contentedness decreased significantly at both doses (delta-baseline, P < 0.05); adverse effects were limited to slight subjective feelings of dizziness and dullness, which disappeared 30-60 min after administration of the dose. Lorazepam caused impairment of psychometric functions. CONCLUSION: After single therapeutic doses, GHB does not induce changes in psychomotor performance and therefore the drug does not influence the ability to drive or work. However, repeated reports of the abuse potential of GHB and its usefulness in treating ethyl alcohol addiction indicate that it may play an “agonist-like” role, which means that it should only used under close medical supervision.

 

Ann Emerg Med. 1998 Jun;31(6):729-36.

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Comment in:

·         Ann Emerg Med. 1999 Apr;33(4):475-6.

A tale of novel intoxication: a review of the effects of gamma-hydroxybutyric acid with recommendations for management.

Li J, Stokes SA, Woeckener A.

Department of Emergency Medicine, Mount Auburn Hospital, Cambridge, MA, USA.

gamma-Hydroxybutyric acid (GHB) is unfamiliar to many physicians in the United States but enjoys clinical use elsewhere for applications in resuscitation, anesthesia, and addiction therapy. Use within the United States is restricted to Food and Drug Administration-approved clinical trials for treatment of narcolepsy. Recently illicit use of GHB has emerged within the United States where it is distributed for purported euphoric and “fat-burning” metabolic effects. Clinical effects can be severe, progressing rapidly to respiratory arrest and death. We provide an updated comprehensive review of the literature with particular emphasis on toxicology, including GHB pharmacodynamics, clinical effects, and suggestions for overdose management. Recommended management of acute GHB intoxication includes prevention of aspiration, use of atropine for persistent symptomatic bradycardia, consideration of neostigmine as a reversal agent, and treatment for coingested substances. Emergency physicians are urged to become familiar with GHB because of its potential for severe morbidity as well as its potential use as a future resuscitative agent.

 

 

PARKINSON

 

Brain Res. 1991 Dec 6;566(1-2):208-11.

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Low doses of gamma-hydroxybutyric acid stimulate the firing rate of dopaminergic neurons in unanesthetized rats.

Diana M, Mereu G, Mura A, Fadda F, Passino N, Gessa G.

Dipartimento di Neuroscienze B.B. Brodie, Università di Cagliari, Italy.

In unanesthetized rats the intravenous (i.v.) administration of gamma-hydroxybutyric acid (GHB) at the doses of 50-400 mg/kg produced a dose-related stimulation (10-56%) of the firing rate of dopaminergic (DA) neurons in the pars compacta of the substantia nigra. Doses of 1000 and 1500 mg/kg inhibited the firing rate almost completely. In unanesthetized rats the intraperitoneal injection of GHB at the dose of 750 mg/kg produced a brief initial stimulation (23%) followed by a modest reduction in the firing rate (29%). On the other hand, in chloral hydrate-anesthetized rats the i.v. administration of GHB at cumulative doses of up to 200 mg/kg failed to modify the firing rate of DA neurons, while a cumulative dose of 400 mg/kg suppressed neuronal firing. The results indicate that sub-anesthetic doses of GHB stimulate the firing rate of DA neurons in unanesthetized rats.

 

Anasthesiol Intensivmed Notfallmed Schmerzther. 1995 Nov;30(7):393-402.

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[Gamma-hydroxybutyric acid–significance for anesthesia and intensive care medicine?]

[Article in German]

Kleinschmidt S, Mertzlufft F.

Klinik für Anaesthesiologie und Intensivmedizin, Universitätskliniken des Saarlandes, Homburg/Saar.

Gamma-hydroxybutyric acid (GHB) as a natural component of the mammalian brain was first introduced in clinical anaesthetic practice more than 30 years ago. Although GHB induced a reliable state of sedation and anaesthesia without depressing either respiratory or cardiocirculatory parameters or liver and kidney function, the drug was nearly displaced from clinical practice because of its prolonged duration of action. The results of recent clinical studies indicate a re-evaluation of GHB in emergency and critical care medicine. GHB is regarded as a natural neuronal transmitter with circuits which synthesise, accumulate and release GHB. Specific binding sites have also been demonstrated and identified. GHB is completely metabolized in the liver to the natural substrates carbon dioxide and water without accumulation in central or peripheral tissues. The reduction of energy metabolism and its possible properties as an “oxygen radical scavenger” may be of therapeutic benefit if tissues are exposed to hypoxia or reperfusion. Therefore, the application of GHB seems to be of advantage in states of traumatic brain injury with cerebral oedema or ischaemic lesions of brain or extraneural tissues. In hypovolaemic states or in patients with impaired cardiovascular function, the pressure effects of GHB may be beneficial for the prevention of tissue damage and may improve survival in the case of cardiocirculatory resuscitation. In the intensive care unit, GHB might be a favourable alternative to established sedative agents. Occurrence of side effects such as tolerance and withdrawal syndromes after the application of sedative drugs, an impaired metabolism with the accumulation of metabolites in the case of liver or kidney dysfunction as well as an insufficient regulation of natural sleep may be diminished by the application of GHB. The results of various clinical studies also suggest that GHB may be useful in the treatment of alcohol and opiate withdrawal syndrome. However, further studies are necessary to specify the proposed indications of GHB in anaesthesiology and critical care medicine.

 

 

CHILDHOOD FEBRILE SEIZURES
Epilepsia. 1988 Nov-Dec;29(6):738-42.

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Protection by GABA agonists, gamma-hydroxybutyric acid, and valproic acid against seizures evoked in epileptic chicks by hyperthermia.

Pedder SC, Wilcox R, Tuchek J, Johnson DD, Crawford RD.

Department of Pharmacology, University of Saskatchewan, Saskatoon, Canada.

With microwave diathermy, febrile seizures were produced in epileptic chicks aged 2-5 days. Drugs that enhance GABAergic activity (i.e., GABA, muscimol, and progabide), as well as valproic acid and gamma-hydroxybutyric acid, produced dose-dependent increases in latency to onset of seizures.

 

Neurochem Res. 1988 Jun;13(6):531-3.

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Effect of low doses of gamma-hydroxybutyric acid on serotonin, noradrenaline, and dopamine concentrations in rat brain areas.

Míguez I, Aldegunde M, Duran R, Veira JA.

Department of Physiology, Faculty of Pharmacy, University of Santiago de Compostela, Spain.

The effects of intraperitoneal administration of gamma-hydroxybutyric acid (GHB) on biogenic amine levels in hemispheres, hypothalamus, midbrain, and medulla-pons, and on tryptophan in serum and brain, were studied. One hour after GHB administration (50 and 100 mg/kg) significant increases of dopamine concentration were observed in the hemispheres with both doses and in the hypothalamus with the higher dose, but a significant decrease of noradrenaline in the hypothalamus. No significant changes of serotonin metabolism were observed. These results indicate that low doses of GHB selectively affect the catecholaminergic neuronal activity.

 

 

 

 

GHB in the prescription form of Sodium Oxybate  XYREM is carefully dispensed:

 

Drug Saf. 2004;27(5):293-306.

 

The Xyrem risk management program.

Fuller DE, Hornfeldt CS, Kelloway JS, Stahl PJ, Anderson TF.

Orphan Medical Inc., Minnetonka, Minnesota 55305, USA.

Sodium oxybate, also known as gamma-hydroxybutyric acid (GHB), was discovered in 1960 and has been described both as a therapeutic agent with high medical value and, more recently, a substance of abuse. The naturally occurring form of this drug is found in various body tissues but has been studied most extensively in the CNS where its possible function as a neurotransmitter continues to be studied. Sodium oxybate has been approved in different countries for such varied uses as general anaesthesia, the treatment of alcohol withdrawal and addiction, and, most recently, cataplexy associated with narcolepsy. During the 1980s, easy access to GHB-containing products led to various unapproved uses, including weight loss, bodybuilding and the treatment of sleeplessness, sometimes with serious long-term effects. The availability of these unapproved and unregulated forms of the drug led to GHB and its analogues being popularised as substances of abuse and subsequent notoriety as agents used in drug-facilitated sexual assault, or ‘date rape’, eventually leading to the prohibition of GHB sales in the US. Legal efforts to control the sale and distribution of GHB and its analogues nearly prevented the clinical development of sodium oxybate for narcolepsy in the US. However, following extensive discussions with a variety of interested parties, a satisfactory solution was devised, including legislative action and the development of the Xyrem Risk Management Program. Amendments to the US Controlled Substances Act made GHB a schedule I drug, but also contained provisions that allow US FDA-approved products to be placed under schedule III. This unique, bifurcated schedule for sodium oxybate/GHB allowed the clinical development of sodium oxybate to proceed and, in July 2002, it was approved by the FDA as an orphan drug for the treatment of cataplexy in patients with narcolepsy as Xyrem(sodium oxybate) oral solution. To promote the safe use of sodium oxybate, as well as alleviate concerns over possible diversion and abuse following product approval, a proprietary restricted drug distribution system was created, called the Xyrem Success Program. Components of the programme include a centralised distribution and dispensing system, a physician and patient registry, compulsory educational materials for patients and physicians, a specially trained pharmacy staff, a method for tracking prescription shipments, and an initial post-marketing surveillance programme. The system has created a unique opportunity to provide both physician and patient education and ongoing patient counselling, promoting greater drug safety and enhanced patient compliance.

 

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