This article was in last month's issue of Urb magazine (#26) - is this a late April Fool's joke or something real? All I can say is I haven't heard it mentioned here or among anyone I know.... I checked PIHKAL, and the only thing I could find was GAMMA, which is related to MDA. This drug below sounds a little like MDA I guess. I make no apologies as to the grammar and content of the article, I just want to know what this stuff is. A lot of his references sound pretty bogus... LIQUID X What is GHB? In the past few months GHB (Gamma Hydroxy Butyrate) has become a staple drug in the underground scene. All but replacing Ecstasy (MDMA), it's now on the forefront of what seems like a new drug revolution. It has even been dubbed "liquid ecstasy." It's highly concentrated street form is available as a liquid in small plastic bottles, about the size and shape of a hotel shampoo bottle. One dosage is usually a capful. There are approximately 9 hits per bottle, and at $10 a bottle, not only is this drug potent, it's very cheap as well. GHB's relation to MDMA is uncanny, but some say its effects are more like a hybrid of acid and ecstasy. Despite its relatedness though, it's chemical composition is a far cry from that of X. Ecstasy is in the chemical family of amphetamines, GHB is not. The analogy between the two probably stems from the physical effects the drug has on the user. Both enhance the sense of touch greatly, causing the user the desire to touch and feel. The sedative effects of the drug are also worth mentioning, as it can be very strong. Quite often, with a sufficient dose, the user can nod off completely and go to sleep or find themselves in a state of unmovable [sic] helplessness. To some, this is unpleasant because the brain is functioning quite rapidly but they don't have much control over what they can do physically. Several ephedrine or a rail of amphetamines have been used to counteract this effect with much success, causing a very happy and ecstatic high. This combination of GHB and speed are for many the only way they will take the drug. The history of GHB is very interesting. Developed almost a decade ago, it's [sic] initial purpose was an alternative anaesthetic to be used for surgery and medical operations. Due to the unpredicatable qualities of the drug and its obvious side effects, it was soon discarded by the medical community at large. Later, other doctors realized that it was a very strong growth hormone stimulate and was then promoted for muscle growth, weight loss and dieting. This caught on very big in the body building community and before long every health food store had a good supply of it. During the late '80s, it's [sic] overwhelming popularity among body builders incited increased medical testing to further study the effects of the drug. During these tests, they found that it was a very powerful neurotransmitter, increasing the dopamine level in the central nervous system. This caused an upset, and in 1991 the FDA had it classified as _Narcotics_1_, restricting its use to licensed researchers only and made it a misdemeanor to possess or sell it. The negative effects of GHB are documented, although I have little knowlege of any of these things happening. _Epileptic_Grand_Mal_Seizures_ sometimes occur under high dosages of the drug. Coma has also been known to occur. The addictive qualities are unknown, but I have yet to meet any "GHB Junkies." A few weeks ago at a club in L.A., a girl died while on GHB and several other drugs. Because of the mix of drugs, it's hard to attribute it to any one thing. GHB may have played a part in her death. Another thing to consider with this drug is it's [sic] unpredictability with certain individuals. A half hit to one person may seem like 5 or 6 hits to another. Because of this, great caution and care should be taken while experimenting with this drug. Don't overdo it! The fact that GHB was made illegal is not surprising. But it serves as further evidence that consciousness-expanding practices are not tolerated and [are] seen as a direct threat to the establishment. Yet the establishment will not look deeper to find the benefits or revelance such drugs can have. The ban on drugs like GHB exhibits the lack of control we have over our own bodies and minds. _Remember,_drug_use_is_a_personal_choice_. You choose. Food for thought. --- Cohry O. ============================================================================= In a previous article (Brian Behlendorf (Vitamin B)) has written: > This article was in last month's issue of Urb magazine (#26) - is this >a late April Fool's joke or something real? All I can say is I haven't heard >it mentioned here or among anyone I know.... I just poked Medline for the following info. Apparently the name is exactly correct and it DOES have abuse potential. As far as it being an MDMA substitute- I doubt this material has that potential, especially with respect to therapeutic applications. Joseph A Tucker poet@uclink.berkeley.edu ************************************************************************* MED-> f kw gamma hydroxy butyrate Search request: F KW GAMMA HYDROXY BUTYRATE Search result: 5 citations in the Medline database Type D to display; D LOC to see locations; HELP for more detail. MED-> d short ab Search request: F KW GAMMA HYDROXY BUTYRATE Search result: 5 citations in the Medline database Type HELP for other display options. 1. Lane RB. Gamma hydroxy butyrate (GHB) [letter; comment]. Jama, 1991 Jun 12, 265(22):2959. (UI: 91237970) Pub type: Comment; Letter. 2. Gamma hydroxy butyrate poisoning. Medical Letter on Drugs and Therapeutics, 1991 Jan 25, 33(836):8. (UI: 91094712) 3. From the Centers for Disease Control. Multistate outbreak of poisonings associated with illicit use of gamma hydroxy butyrate [see comments]. Jama, 1991 Jan 23-30, 265(4):447-8. (UI: 91087349) 4. Multistate outbreak of poisonings associated with illicit use of gamma hydroxy butyrate. Mmwr. Morbidity and Mortality Weekly Report, 1990 Nov 30, 39(47):861-3. (UI: 91042306) 5. Fisher RS. Animal models of the epilepsies. Brain Research. Brain Research Reviews, 1989 Jul-Sep, 14(3):245-78. (UI: 90029159) Pub type: Journal Article; Review; Review, Academic. Abstract: The study of mechanisms of the epilepsies requires employment of animal models. Choice of a model system depends upon several factors, including the question to be studied, the type of epilepsy to be modelled, familiarity and convenience. Over 50 models are reviewed. Major categories of models are those for simple partial seizures: topical convulsants, acute electrical stimulation, cortically implanted metals, cryogenic injury; for complex partial seizures: kainic acid, tetanus toxin, injections into area tempesta, kindling, rodent hippocampal slice, isolated cell preparations, human neurosurgical tissue; for generalized tonic-clonic seizures: genetically seizure-prone strains of mouse, rat, gerbil, fruitfly and baboon, maximal electroshock seizures, systemic chemical convulsants, metabolic derangements; and for generalized absence seizures: thalamic stimulation, bilateral cortical foci, systemic penicillin, gamma-hydroxy-butyrate, intraventricular opiates, genetic rat models. The lithium-pilocarpine, homocysteine and rapid repetitive stimulation models are most useful in studies of status epilepticus. Key findings learned from each of the models, the model's strengths and weaknesses are detailed. Interpretation of findings from each of these models can be difficult. Do results pertain to the epilepsies or to the particular model under study? How important are species differences? Which clinical seizure type is really being modelled? In a model are behavior or EEG findings only similar superficially to epilepsy, or are the mechanisms comparable? The wealth of preparations available to model the epilepsies underscores the need for unifying themes, and for better understanding of basic mechanisms of the epilepsies. There are no more records to display. Type PS to see previous screen. MED-> MED-> fuck off Thanks for using the MELVYL Online Catalog. Type LOGOFF and press RETURN to terminate your TELNET session. Press RETURN for the MELVYL catalog. -> logoff ELAPSED TIME = 0:00:49 END OF SESSION Connection closed by foreign host. % exit ============================================================================= From: dk104@cleveland.Freenet.Edu (Herb Greene) Newsgroups: alt.psychoactives Subject: G H B Date: 28 May 1993 18:29:21 GMT Message-ID: <1u5lm1$548@usenet.INS.CWRU.Edu> Posted anonymously for my friend Frank. I will forward all replies. -------------------------------------------------------------------- Sorry for being anonymous but I wish to be too frank. I have been doing some self experimentation with GHB that I would like to report. GHB is gamma-hydroxy-butyrate (I think I spelled it right.) It is a waxy and very hygroscopic solid. The literature shows results in experiments using it as treatment for several things but the one that caught my eye was its use with alcoholics. I am an alcoholic with a perpetual fight to keep control. I do not abstain. I have a desire or need to alter my conciousness in the evenings mostly that I don't wish to speculate about. For the purpose of this discussion, for whatever reason, that is a given. The research results relate to its use in alcoholics as a treatment for the effects of alcohol poisoning. A detox helper as it were. It seems to aleviate many of the symptoms such as trembling and sweating. I tried it out of curiousity and found the psychoactive effect to be extremely pleasant. For me it satisfies virtually every reason that I drink alcohol. The subjective experience is similar in a few regards. Dizziness and disruption of motor control are equivalent to or worse than alcohol for the equivalent buzz. That is about the only down side. An astonishing thing for me though is that one is much less likely to be foolish enough to attempt to drive or operate machinery than one would with an equivalent motor disruption from alcohol. It lacks the agressive quality that seems to make one feel capable with alcohol. This lack of agressive content is a very distinguishing difference between it and alcohol in general. I tend to get nasty or fight easily when on alcohol as do many and I think my own observation is likely to be a general effect. One tends to get silly. One can become as intoxicated as one wishes but I find I tend to modulate it much better than alcohol which has a runaway effect with me. It definitely acts as a disinhibitor similarly to alcohol. Talking is facilitated but one retains a coherence that makes it a good deal more meaningful than talk similarly facilitated with alcohol. I am also a very good listner when high on GHB. It has an empathogenic quality. Not nearly as profound as MDMA for example but in the same vein. I feel it actually does facilitate communication that is more normal than what alcohol provides. I am fairly buzzed at the moment and I will let you judge my coherence. I, as many alcoholics, turn to aclcohol particularly heavily when in emotional pain due to loss, rejection and the like. I have found though that it does not help a whit as much as we treat ourselves with it for that pain. In fact alcohol causes depression and a deeper slide into self pity and sorrow. GHB on the other hand does relieve such pain to a remarkable degree. To a degree that I have found lasting. I am saying that it may well be therapeutic for people in such a state. I have two personal experiences with this effect. Physiologically, and speaking only subjectively, it is much kinder than alcohol. There does not appear to be any toxicity. No shaking, no sweating, no weak knees or any of the symptoms we alcoholics have come to know and love. And most miraculously, no hangover. On the contrary I and others that I know who have experimented with it all agree that one awakes feeling more rested than normal and in a far better mood the morning after a GHB evening than an evening without. I know of no toxicity studies at the dosages I take however and wish one of y'all would take that on. The dosage I take recreationally is about a half teaspoon. I haven't weighed it. It comes on pretty fast, under a half an hour, and I will usually take another half teaspoon within an hour and no more then for several. It is long lasting, four to six hours of motor impairment. It also makes one pee for some reason in the middle of the night which I rarely do normally. One takes it mixed in a glass of warm to hot water. It takes a few minutes to disolve and is sort of fun to watch since it seriously messes with the index of refraction of water as it disolves. It is fairly soporific and highly relaxing with a time dilating effect similar to mushrooms but less profound. It is not at all psychedelic or entactogenic. It is easy to go to sleep at any time after the effects come on. It is sexually arousing in a very relaxed sort of way but I find it difficult to climax. I can enjoy sex however for prolonged periods. A friend of mine has an occasional incidence of falling asleep during sex however. It doesn't bother him but it does not thrill his wife. :-) I would definitely clasify it as a mild aphrodesiac especially with its disinhibiting effect. I have not "tried it out" on the unwary, however, to see if it would entice the reluctant. I suspect, however, that it would and might even be useful for sexual dysfunction brought on by stress or by anxiety about the act itself in many of the myriad ways that can be caused. To me its most profound effect is how it has changed my relationship to alcohol. I struggle nightly with the desire to drink. I lose all too frequently. I have controlled it for several years with antabuse when I get a hangover two days in a row. If I have GHB available I have *no* desire for alcohol. I would much rather use it for whatever it is I use alcohol for. I have been using it regularly this round for about two weeks and in that time have used alcohol to excess twice. Each time I stopped short of going where I usually do with distinct feelings of dysphoria. Like, why on earth did I do that and how long do I have to wait for the effects of the alcohol to wear off? This is a new experience for me with regard to alcohol. I am out of it as of tonight with no chance for resupply for a while and I am interested to see if this effect lasts. This is my third or fourth round with it, this being the longest. I have not experienced any sort of withdrawal symptoms when my supply is removed. There is no excess craving or nervousness. It is much like being cut off from marijuana. You miss it but so what. For me, however, the effects are positive enough that I probably would use it regularly if regularly available. I have used it in several small groups without it being seriously noticed and the next time it is available I wish to try it out in a bar or club setting. It should *not* be mixed with alcohol. They each enhance the other and one feels very inebriated very fast. It mixes well with pot. I am now feeling near full effects of about a level teasoon. It is sufficient. A friend uses much larger dosages. He had an experience combining a fiarly large dose of GHB, probably three or four times my dosage, and an amphetamine like stimulant. He lost all motor control, couldn't even hold a glass. He scared the hell out of his wife who thought he was lost to the world but internally he was having a thouroughly delightful time bouncing between the stimulated state and the soporific state. I have decided that the next time I am able to obtain a signifignat quantity I am going to give it to a very close woman friend that is also struggling and losing with alcohol. I have told her all about it so I am not talking dosing any one. I am not very comfortable with the ethics of doing this since so damned little research has been done on long term use but I see her life slipping away and I really think this will help. She knows it is experimental and I have summarized the research I have done and made the synopses of the papers available for her to read herself. I would like feedback on this. Please keep your flamethrowers on standby for a bit though and consider the alternatives first. This person is not a candidate for any treatment program or help group. Just out of the question for many reasons. As far as treatment for alcoholism it first must be shown that it is safe and then one must deal with the thorny issue of whether or not it is ok to substitute one mind altering substance for another as therapy. I know that the established alcohol treatment infrastructure will not like that idea much at all. Well, that's about it. I wish someone of you would do some kind of controled research on this stuff. There seem to me to be many areas that could be explored. BTW The last half or so of this post was written while in a fairly delightful state of mild alteration from GHB and it still has a bit to come on yet. ============================================================================= Newsgroups: alt.psychoactives From: brians@unislc.slc.unisys.com (Brian Sassone) Subject: Re: G H B Message-ID: <1993Jun18.220537.5595@unislc.slc.unisys.com> Date: Fri, 18 Jun 1993 22:05:37 GMT In article <24.296.2252.0NB291CA@pcohio.com> rick.myers@pcohio.com (Rick Myers) writes: >A friend of mine in Florida is doing a newspaper article on the >rave scene, and he called me to ask if I'd ever heard of GHB... >I hadn't... It's supposedly a big deal in LA, Vegas and NYC... >All I know is it comes as a liquid, it's supposedly a hallucenogen, >and there are allegedly no 'after effects'... Anyone tried this?? A friend of mine (in SF) accidently ingested a high dose (2-3 hits?) of this that was in someone's beer. She said it was *very* intense. It only lasted a few hours and as she came down, she started crying uncontrollably. (However, she *had* just broken up with her boyfriend, so was already emotionally disraught.) She likened the effects similar to MDMA as far as empathy goes. She also said she lost partial motor-control as she kept dropping things. She didn't have any significant lingering effects after only 5-6 hours. She was concerned the following week that it may have had some more subtle lasting effects. She noticed seeing herself in the mirror as 'different'; like she had never seen herself that way before. However, she had also just quit a long caffeine addiction (with high octane coffee) so this may also have been a contributing factor. It's been a couple of weeks since then, and she has ad no furhter evidence of any lasting effects. I've looked through various archives and have found no mention of this drug. We would still like to find out exactly what it is and any other information about it. -----------------------===<>===------------------------------------------ -bS "A happy face, brians@ios.convergent.com a funkin' bass, A lowly raver without a glowstick. for a loving race." ------------------------------------------===<>===----------------------- ============================================================================= From: brians@unislc.slc.unisys.com (Brian Sassone) Message-Id: <9311050703.AA28884@unislc.slc.unisys.com> Subject: GHB References [long] To: sfraves@techno.Stanford.EDU (Bay Area Ravers) Date: Fri, 5 Nov 1993 00:03:25 -0700 (MST) Just so everybody knows some of the facts about this stuff, here is a list of references w/ abstracts culled from a medline search awhile back. Sorry for the long post, but I think it's important if your entertaining ideas of possible experimentation. I also have a fairly long post of a person who has done some experimentation with GHB to offset alcohol cravings. If anybody is interested, let me know. 1 AN MJJA-338363. 91034. OC 91034. TI Gamma Hydroxy Butyrate Poisoning. SO The Medical Letter on Drugs and Therapeutics. 1991 Jan 25. 33(836). p 8. PU The Medical Letter, Inc. Copyright 1991 by The Medical Letter, Inc. PD 910125. PT Article (ART). IS 0025-732X. TX 1 OF 5. Gamma hydroxy butyrate (GHB) sold in health food stores has recently caused outbreaks of gastrointestinal illness, central-nervous-system (CNS) depression, and seizures (Morbid Mortal Weekly Rep, 39:861, Nov 30, 1990). THE DRUG - GHB is an endogenous substance produced by the metabolism of the neurotransmitter gamma-aminobutyric acid. The metabolite is itself neuroactive, increasing dopamine levels in the brain and acting on the endogenous opioid system (M Mamelak, Neurosci Biobehav Rev, 13:187, 1989). 3 OF 5. SOURCES - GHB has been used experimentally in the USA for treatment of narcolepsy because it can induce a normal pattern of rapid-eye-movement (REM) and non-REM sleep. GHB is sold in health food stoes in the USA, usually as the sodium salt in tablets or as a powder, with instructions to take 1 tablet or 1/2 tablet to three teaspoons of the powder dissolved in water at bedtime. The amount of GHB contained in these preparations is not known. Names for the drug have included Sodium Oxybate, Sodium Oxybutyrate, Gamma Hydroxybutyrate Sodium, Gamm-OH, 4-Hydroxy Butyrate, Gamma Hydrate, and Somatomax PM. It is promoted (illegally) for sleep, weight control, and for euphoric and anabolic effects. GHB has been sold particularly to bodybuilders with the claim that stimulates growth hormone release. 4 OF 5. CLINICAL EFFECTS - An oral dose of 10 mg/kg can cause amnesia and hypotonia; 20 to 30 mg/kg of GHB can produce somnolence within 15 minutes. Taking more than 50 mg/kg can result in abrupt unconsciousness and coma. Patients who have taken 1/2 to 3 teaspoons have had symptoms varying from nausea, vomiting, dizziness, confusion, and drowsiness to depressed respiration and seizure-like activity. Some patients have developed bradycardia and hypotension. No deaths have been reported. Signs and symptoms subsided spontaneously within eight hours in most patients, although some complained of dizziness for as long as two weeks. GHB apparently acts synergistically with alcohol to produce CNS and respiratory depression. Naloxone (Narcan; and others) has not been effective as an antidote. 5 OF 5. CONCLUSION - Gamma hydroxy butyrate (GHB) sold in health food stores as an aid to sleep and bodybuilding has caused severe illness, including seizures and coma. No specific treatment is available, but all patients so far have recovered spontaneously. *LINK CCML SCREEN 1 OF 11* 1 AN MJBB-394706. 91074. OC 91074. TI Epidemiologic Notes and Reports: Multistate Outbreak of Poisonings Associated with Illicit Use of Gamma Hydroxy Butyrate. SO Morbidity and Mortality Weekly Report (MMWR). 1990 Nov 30. 39(47). pp 861-863. PU Printed and distributed by the Massachusetts Medical Society; Information provided by the Centers for Disease Control. PD 901130. PT Article (ART). IS 0149-2195. TX 1 OF 12. On August 7, 1990, the San Francisco Bay Area Regional Poison Control Center notified the regional office of the Food and Drug Administration (FDA) and the California Department of Health Services of acute poisonings attributed to ingestion of gamma hydroxy butyrate (GHB), which recently has been illicitly marketed nationwide. Manifestations included gastrointestinal symptoms, central nervous system (CNS) and respiratory depression, and uncontrolled movements. Subsequent surveillance, based on contacts among poison-control centers, led to the recognition that similar poisonings had been independently identified in several states. This report summarizes findings from the preliminary investigation of this problem. 2 OF 12. From June 4 through November 28, 1990, at least 57 cases of illness attributed to GHB exposure have been reported from California (25 cases, 17 from the San Francisco area); Georgia (15, all from the greater Atlanta area); Florida (seven, six from the greater Tampa area); South Carolina (three); Minnesota (two); Arizona (two); and Ohio, Texas, and Virginia (one each). Patients have presented with histories of ingesting 1/2 -3 teaspoons of GHB dissolved in water; ingestion is followed within 15-60 minutes by onset of one or more of the following: vomiting, drowsiness, hypnagogic state, hypotonia, and/or vertigo. Loss of consciousness, irregular and depressed respiration, tremors, or myoclonus may follow. Seizure-like activity, bradycardia, hypotension, and/or respiratory arrest have also been reported. Spontaneous resolution occurs in 2-96 hours. The severity and duration of symptoms appear to depend on the dose of GHB and/or the presence of other CNS depressants, most frequently ethanol. In 11 of 12 Georgia patients, four of five Florida patients, and three of four California patients for whom concurrent drug status was known, other psychoactive drugs--including ethanol, benzodiazepines, cannabis, and amphetamines--also had been used. 3 OF 12. Although no deaths have been reported, most patients have required emergency room care; at least 11 were hospitalized, and nine required ventilator support or other intensive care. Therapeutic efforts consisted of nonspecific supportive care. 4 OF 12. On November 8, FDA issued an advisory warning that GHB use outside of FDA-approved physician-supervised protocols was unsafe and illicit and should stop *RF 1 *. Persons who have used GHB and have symptoms should consult a physician. Ill persons, physicians, and emergency room staff are encouraged to report suspected cases of GHB-related illness to their regional poison-control centers and state health departments. FDA's investigation into the source(s) of this illicit distribution is ongoing. Sale of GHB was banned by California on November 8 and by Florida on November 9. 5 OF 12. Reported by: JE Dyer, PharmD, San Francisco Bay Area Regional Poison Control Center; R Kreutzer, MD, A Quattrone, PhD, KW Kizer, MD, California Dept of Health Svcs. RJ Geller, MD, Georgia Poison Control Center; JD Smith, Georgia Dept of Human Resources. SA Normann, PharmD, Florida Poison Information Center; AJ Hill, RA Calder, MD, State Epidemiologist, Florida Dept of Health and Rehabilitative Svcs. T Litovitz, MD, American Association of Poison Control Centers. Food and Drug Administration. Div of Environmental Hazards and Health Effects, Center for Environmental Health and Injury Control, CDC. 6 OF 12. Editorial Note: In the United States, the only legal use of GHB (HOOC-CH sub 2 -CH sub 2 -CH sub 2 OH) has been under specific FDA exemptions for investigational research protocols (e.g., treatment of narcolepsy). In Europe, GHB has also been used as an anesthetic adjunct and experimentally to treat posthypoxic cerebral edema and ethanol withdrawal. During controlled clinical use, the same dose of GHB sometimes caused different responses in different patients and different responses in the same person at different times (M. Mamelak, personal communication, 1990). GHB has been illegally marketed under a variety of names, including Gamma Hydroxybutyric Acid, Sodium Oxybate, Sodium Oxybutyrate, Gamma Hydroxybutyrate Sodium, Gamma-OH, 4-Hydroxy Butyrate, Gamma Hydrate, and Somatomax PM. It is distributed as the sodium salt in powder or tablet form and is commonly dissolved in water. 8 OF 12. GHB has been marketed illicitly to body builders since at least May 1990; it also has been promoted illicitly for weight control and as a sleep aid. In addition, GHB has been illicitly touted as a "replacement" for L-tryptophan, which had been marketed as a food supplement but was recalled in November 1989 when the epidemic of eosinophilia-myalgia syndrome was recognized *RF 2 *. 9 OF 12. GHB allegedly produces a "high," which has led to its further use as an illicit drug. Although the concurrent use of other drugs with similar toxicities may confuse the clinical, toxicologic, and epidemiologic presentation of this problem, the reported symptoms of GHB toxicity are the same as the known pharmacologic effects of the drug. A causal association between use of GHB and these poisonings is also supported by the rapid onset of symptoms after ingestion of GHB, more severe and prolonged symptoms associated with larger doses of GHB, and occurrence of illness in persons who have not used other drugs. 10 OF 12. GHB is produced by the body as a normal metabolite and is not a nutritional requirement. In the brain, GHB increases dopamine levels, has effects through the endogenous opioid system, and probably has effects through other independent receptor-dependent mechanisms. GHB is present in many peripheral sites, including the kidney, heart, skeletal muscle, and brown fat. GHB is well absorbed orally, readily crosses the blood-brain barrier, and is subsequently metabolized to carbon dioxide and water without active metabolites *RF 3,4 *. Effects include amnesia and hypotonia from doses as low as 10 mg/kg, a normal sequence of REM and non-REM sleep from 20-30 mg/kg doses (1-3 g per dose were used in U. S. narcolepsy studies *RF 5 *), and anesthesia from doses of approximately 50 mg/kg. In doses greater than 50 mg/kg, GHB decreases cardiac output and subsequently produces increasingly severe respiratory depression, seizure-like activity, and/or coma *RF 4,5 *. Other effects suggest that, during hypoxia and other energy-limiting conditions, GHB may play a role in reducing energy-substrate demand and consumption and in preventing the production of free radicals *RF 4 *. 11 OF 12. GHB acts synergistically with ethanol to produce CNS and respiratory depression; ethanol also increases the endogenous levels of GHB *RF 4 *. GHB may potentiate the effects of narcotic analgesics and skeletal muscle relaxants and may be potentiated by the actions of benzodiazepines and neuroleptics *RF 5 *. Although antagonism may occur with d-amphetamine, naloxone, haloperidol, and drugs used for absence seizures *RF 4 *, these experimental antagonists have not been assessed as possible treatments for GHB overdose. Anecdotally, naloxone has not been effective in treating a limited number of GHB-related poisonings. 12 OF 12. The focus of public education efforts should be that products such as GHB that are promoted for physiologic effects act on the body as drugs. In this context, advertising terms such as "natural," "organic," or "supplement" do not imply safety or legality. RF 1 OF 5. REFERENCES 1. Food and Drug Administration. Gamma hydroxybutyric acid (Press release). Rockville, Maryland: Food and Drug Administration, November 8, 1990. 2 OF 5. 2. Swygert LA, Maes EF, Sewell LE, Miller L, Falk H, Kilbourne EM. Eosinophilia-myalgia syndrome: results of national surveillance. JAMA 1990;264:1698-703. 3 OF 5. 3. Vayer P, Mandel P, Maitre M. Minireview: gamma-hydroxybutyrate, a possible neurotransmitter. Life Sci 1987;41:1547-57. 4 OF 5. 4. Mamelak M. Gammhydroxybutyrate: an endogenous regulator of energy metabolism. Neurosci Biobehav Rev 1989;13:187-98. 5 OF 5. 5. United States Pharmaceutical Convention, Inc. USP dispensing information. Vol IB. Drug information for the health care professional, 1990:2914. 1 RF 3 OF 5. 3. Vayer P, Mandel P, Maitre M. Minireview: gamma-hydroxybutyrate, a possible neurotransmitter. Life Sci 1987;41:1547-57. -END OF DISPLAY REQUEST- November 8, 1990. 2 OF 5. 2. Swygert LA, Maes EF, Sewell LE, Miller L, Falk H, Kilbourne EM. Eosinophilia-myalgia syndrome: results of national surveillance. JAMA 1990;264:1698-703. 3 OF 5. 3. Vayer P, Mandel P, Maitre M. Minireview: gamma-hydroxybutyrate, a possible neurotransmitter. Life Sci 1987;41:1547-57. 4 OF 5. 4. Mamelak M. Gammhydroxybutyrate: an endogenous regulator of energy metabolism. Neurosci Biobehav Rev 1989;13:187-98. 5 OF 5. 5. United States Pharmaceutical Convention, Inc. USP dispensing information. Vol IB. Drug information for the health care professional, 1990:2914. 1 AN 91237970. 91000. AU Lane-R-B. TI Gamma hydroxy butyrate (GHB) [letter; comment]. CM Comment on: JAMA 1991 Jan 23-30;265(4):447-8. SO JAMA. 1991 Jun 12. 265(22). P 2959. JT JAMA. PT COMMENT (COM). LETTER (LET). LG English (EN). MJ HYDROXYBUTYRATES: poisoning (po). MN ADULT. ANESTHESIA. CHILD. CHILD-PRESCHOOL. HUMAN. RN 0 -- Hydroxybutyrates. SB Abridged Index Medicus Journals (A). Priority Journals (M). Cancer Journals (X). YR 1991. IS 0098-7484. KFR. CP UNITED-STATES (Z1.107.567.875). IM 9108. ND ENTRY DATE: 910627. LAST REVISION DATE: 910912. CLASS UPDATE: 91. 2 The full text of this document is available using the link command LK. AN 91094712. 91000. TI Gamma hydroxy butyrate poisoning. SO Med-Lett-Drugs-Ther. 1991 Jan 25. 33(836). P 8. JT MEDICAL LETTER ON DRUGS AND THERAPEUTICS. PT JOURNAL-ARTICLE (ART). LG English (EN). MJ CENTRAL-NERVOUS-SYSTEM-DISEASES: chemically-induced (ci). GASTROINTESTINAL-DISEASES: chemically-induced (ci). SEIZURES: chemically-induced (ci). SODIUM-OXYBATE: poisoning (po). MN HUMAN. QUACKERY. RN 502-85-2 -- Sodium-Oxybate. SB Abridged Index Medicus Journals (A). Priority Journals (M). YR 1991. IS 0025-732X. M52. CP UNITED-STATES (Z1.107.567.875). IM 9104. ND ENTRY DATE: 910213. 3 AN 91087349. 91000. TI From the Centers for Disease Control. Multistate outbreak of poisonings associated with illicit use of gamma hydroxy butyrate [see comments]. CM Comment in: JAMA 1991 Jun 12;265(22):2959. SO JAMA. 1991 Jan 23-30. 265(4). P 447-8. JT JAMA. PT JOURNAL-ARTICLE (ART). LG English (EN). MJ DISEASE-OUTBREAKS. SODIUM-OXYBATE: poisoning (po). MN EMERGENCIES. HUMAN. POISONING: epidemiology (ep). POPULATION-SURVEILLANCE. UNITED-STATES: epidemiology (ep). RN 502-85-2 -- Sodium-Oxybate. SB Abridged Index Medicus Journals (A). Priority Journals (M). Cancer Journals (X). YR 1991. IS 0098-7484. KFR. CP UNITED-STATES (Z1.107.567.875). IM 9104. ND ENTRY DATE: 910207. LAST REVISION DATE: 910912. 4 The full text of this document is available using the link command LK. AN 91042306. 91000. TI Multistate outbreak of poisonings associated with illicit use of gamma hydroxy butyrate. SO MMWR-Morb-Mortal-Wkly-Rep. 1990 Nov 30. 39(47). P 861-3. JT MMWR. MORBIDITY AND MORTALITY WEEKLY REPORT. PT JOURNAL-ARTICLE (ART). LG English (EN). MJ DISEASE-OUTBREAKS. SODIUM-OXYBATE: poisoning (po). MN EMERGENCIES. HUMAN. POISONING: epidemiology (ep). POPULATION-SURVEILLANCE. UNITED-STATES: epidemiology (ep). RN 502-85-2 -- Sodium-Oxybate. SB Priority Journals (M). YR 1990. IS 0149-2195. NE8. CP UNITED-STATES (Z1.107.567.875). IM 9102. ND ENTRY DATE: 901219. CLASS UPDATE: 91. 5 AN 90029159. 90000. AU Fisher-R-S. IN Department of Neurology, Johns Hopkins University School of Medicine, Baltimore, MD 21205. TI Animal models of the epilepsies. SO Brain-Res-Brain-Res-Rev. 1989 Jul-Sep. 14(3). P 245-78. JT BRAIN RESEARCH. BRAIN RESEARCH REVIEWS. PT JOURNAL-ARTICLE (ART). REVIEW (REV). REVIEW-ACADEMIC (RAC). LG English (EN). AB The study of mechanisms of the epilepsies requires employment of animal models. Choice of a model system depends upon several factors, including the question to be studied, the type of epilepsy to be modelled, familiarity and convenience. Over 50 models are reviewed. Major categories of models are those for simple partial seizures: topical convulsants, acute electrical stimulation, cortically implanted metals, cryogenic injury; for complex partial seizures: kainic acid, tetanus toxin, injections into area tempesta, kindling, rodent hippocampal slice, isolated cell preparations, human neurosurgical tissue; for generalized tonic-clonic seizures: genetically seizure-prone strains of mouse, rat, gerbil, fruitfly and baboon, maximal electroshock seizures, systemic chemical convulsants, metabolic derangements; and for generalized absence seizures: thalamic stimulation, bilateral cortical foci, systemic penicillin, gamma-hydroxy-butyrate, intraventricular opiates, genetic rat models. The lithium-pilocarpine, homocysteine and rapid repetitive stimulation models are most useful in studies of status epilepticus. Key findings learned from each of the models, the model's strengths and weaknesses are detailed. Interpretation of findings from each of these models can be difficult. Do results pertain to the epilepsies or to the particular model under study? How important are species differences? Which clinical seizure type is really being modelled? In a model are behavior or EEG findings only similar superficially to epilepsy, or are the mechanisms comparable? The wealth of preparations available to model the epilepsies underscores the need for unifying themes, and for better understanding of basic mechanisms of the epilepsies. Author-abstract. 332 Refs. MJ CONVULSANTS: pharmacology (pd). DISEASE-MODELS-ANIMAL. EPILEPSY: physiopathology (pp). KINDLING-NEUROLOGY. MN ANIMAL. EPILEPSY: chemically-induced (ci). SUPPORT-NON-U-S-GOVT. SUPPORT-U-S-GOVT-P-H-S. RN 0 -- Convulsants. SB Priority Journals (M). YR 1989. IS 0165-0173. BRS. CP NETHERLANDS (Z1.542.651). IM 9002. ND ENTRY DATE: 891220. CLASS UPDATE: 92. NO RO1NS2512802. PO1NS0722618. 6 AN 81230352. 81000. AU Hoang-P-T. Pourriat-J-L. Rathat-C. Cupa-M. IN Departement D'Anesthesie-Reanimation, Bobigny-Bondy, Hopital Avicenne, Bobigny. TI [Status asthmaticus. Mechanical ventilation with association sodium gamma hydroxy-butyrate and pancuronium bromide (author's transl)]. TT L'etat de mal asthmatique. Ventilation assistee a l'aide de l'association gamma-hydroxy-butyrate de sodium-bromure de pancuronium. SO Anesth-Analg (Paris). 1981. 38(1-2). P 43-6. JT ANESTHESIE, ANALGESIE, REANIMATION. PT JOURNAL-ARTICLE (ART). LG French (FR). AB The authors have added to the usual therapy (corticoids, antibiotics, bronchodilatators) of 13 cases of status asthmaticus the following association: sodic gamma hydroxybutyrate and pancuronium bromid so they have noted in every case of quick decrease of bronchospasm allowing the stopping of the mechanical ventilation. Author-abstract. MJ ASTHMA: therapy (th). HYDROXYBUTYRATES: therapeutic-use (tu). PANCURONIUM: therapeutic-use (tu). RESPIRATION-ARTIFICIAL. SODIUM-OXYBATE: therapeutic-use (tu). MN ADULT. DRUG-THERAPY-COMBINATION. ENGLISH-ABSTRACT. FEMALE. HUMAN. MALE. MIDDLE-AGE. RN 0 -- Hydroxybutyrates. 15500-66-0 -- Pancuronium. 502-85-2 -- Sodium-Oxybate. SB Priority Journals (M). YR 1981. IS 0003-3014. 4RU. CP FRANCE (Z1.542.286). IM 8110. ND ENTRY DATE: 810810. CLASS UPDATE: 91. 7 AN 81107525. 81000. AU Defossez-M. Le-Bec-G. Sancier-A. Manelfe-C. Espagno-M-T. Bouzat-A. Sevely-A. TI [Neuro-sedation and cranial C.-T. scan in infants and children (author's transl)]. TT Neuro-sedation et examens tomodensitometriques chez le nourrisson et l'enfant. SO Anesth-Analg (Paris). 1979. 36(11-12). P 525-9. JT ANESTHESIE, ANALGESIE, REANIMATION. PT JOURNAL-ARTICLE (ART). LG French (FR). AB Sixty-four infants and children under 14 years of age had a neuro-sedation, for a cranial C.-T. Scan. This entirely painless procedure requires complete immobility of the patient. We used two sorts of methods: for infants under eight months of age, a premedication followed by a feeding-bottle is sufficient. For children over eight months of age, intravenous administration of gamma-hydroxy-butyrate at 30 to 50 mg/kg induces light but sufficient sleep in obtaining a useful scan. Within the group of 24 infants we obtained 14 good results, 8 mild ones and 2 failures. Within the 40 children over eight months of age, 28 procedures were good, 10 children had to undergo more anesthesia during the examination and twice the exploration was impossible. Author-abstract. MJ BRAIN: radiography (ra). HYPNOTICS-AND-SEDATIVES: administration-and-dosage (ad). TOMOGRAPHY-X-RAY-COMPUTED. MN ADOLESCENCE. CHILD. CHILD-PRESCHOOL. ENGLISH-ABSTRACT. HUMAN. HYDROXYBUTYRATES: administration-and-dosage (ad). INFANT. RN 0 -- Hydroxybutyrates. 0 -- Hypnotics-and-Sedatives. 502-85-2 -- Sodium-Oxybate. SB Priority Journals (M). YR 1979. IS 0003-3014. 4RU. CP FRANCE (Z1.542.286). IM 8105. ND ENTRY DATE: 810327. CLASS UPDATE: 91. 8 AN 75035869. 75000. AU Puca-F-M. Genco-S. Masi-G. Federico-F. Di-Lauro-L. TI [Vestibulo-oculomotor reflexes in relation to the level of vigilance. III. The vestibulo-oculomotor reflexes during central depression caused by sodium gamma-hydroxy-butyrate]. TT I riflessi vestibolo-oculomotori in rapporto al livello di vigi lanza. III. I riflessi vestibolo-oculomotori in corso di defres sione centrale da gamma-idrossibutirrato di sodio. SO Boll-Soc-Ital-Biol-Sper. 1973 Sep 15. 49(17). P 1001-6. JT BOLLETTINO - SOCIETA ITALIANA BIOLOGIA SPERIMENTALE. PT JOURNAL-ARTICLE (ART). LG Italian (IT). MJ BRAIN: drug-effects (de). EYE-MOVEMENTS. HYDROXYBUTYRATES: pharmacology (pd). REFLEX. VESTIBULAR-NERVE: physiopathology (pp). MN ADULT. ATTENTION. HUMAN. MALE. NYSTAGMUS. SLEEP. SB Priority Journals (M). YR 1973. IS 0037-8771. ALS. CP ITALY (Z1.542.489). IM 7503. ND ENTRY DATE: 750122. nd age. SO Mech-Ageing-Dev. 1989 Mar. 47(3). P 229-39. JT MECHANISMS OF AGEING AND DEVELOPMENT. ============================================================================= From: rich@weeds.xs4all.nl (Richard v.d. Horst) Newsgroups: alt.drugs Subject: GHB Information Message-ID: <120694220054Rnf0.77b8@weeds.xs4all.nl> Date: Tue, 06 Dec 1994 22:00:00 PST Here the promised GHB information, straight off the Smart-P list... --Richard =*=*=*=*=*=*=*=*=*=*=*=*=*=*=*=*=*=*=*=*=*=*=*=*=*=*=*==*=*=*=*=*=*=*=*=*=*=*= * S M A R T - P M A I L I N G L I S T * =*=*=*=*=*=*=*=*=*=*=*=*=*=*=*=*=*=*=*=*=*=*=*=*=*=*=*==*=*=*=*=*=*=*=*=*=*=*= =*=*=*=*=*=*=*=*=*=*=*=*=*=*=*=*=*=*=*=*=*=*=*=*=*=*=*==*=*=*=*=*=*=*=*=*=*=*= * L I F E E N H A N C E M E N T N E W S * Issue #001 - November 7, 1994 =*=*=*=*=*=*=*=*=*=*=*=*=*=*=*=*=*=*=*=*=*=*=*=*=*=*=*==*=*=*=*=*=*=*=*=*=*=*= < Smart@andronix.org > John Morgenthaler, Ward Dean, MD, & Steven Wm. Fowkes To subscribe, email Smart@andronix.org with "subscribe your@email.address". =*=*=*=*=*=*=*=*=*=*=*=*=*=*=*=*=*=*=*=*=*=*=*=*=*=*=*==*=*=*=*=*=*=*=*=*=*=*= ***** "Life Enhancement News" is (C) Copyright 1994 by John Morganthaler ***** =*=*=*=*=*=*=*=*=*=*=*=*=*=*=*=*=*=*=*=*=*=*=*=*=*=*=*==*=*=*=*=*=*=*=*=*=*=*= -=-=-=-=-=-=-=-=-=-=-=-=-=-=-=-=-=-=-=-=-=-=-=-=-=-=-=-=-=-=-=-=-=-=-=-=-=-=-= 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. This difference allows GHB to cross the blood brain barrier where some of it is metabolized into GABA [Vickers, 1969]. As it turned out, Laborit found that GHB exhibited a range of effects beyond those expected from GABA. Over the intervening years, numerous researchers have extensively studied GHB's effects. It is has come to be used in Europe as a general anesthetic, a treatment for insomnia and narcolepsy (a daytime sleeping disorder), an aid to childbirth (increasing strength of contractions, decreasing pain, and increasing dilation of the cervix), a treatment for alcoholism and alcohol withdrawal syndrome, and for many other uses. During the 1980s, GHB was widely available over-the-counter in health-food stores, purchased largely by body-builders for its ability to stimulate growth hormone release which aids in fat reduction and muscle building. In the last few years it has been gaining popularity as a "recreational" drug offering a pleasant, alcohol-like, hangover-free "high" with potent prosexual effects. --- Scientific Reports on GHB --- For the thirty years prior to 1990, the scientific papers on GHB were unanimous in reporting numerous beneficial physiological effects and the absence of long-term negative effects. In 1964, Laborit listed "very low toxicity" as one of the "principle elements" of the compound's pharmacology. In a 1969 report on GHB's anesthetic uses, Vickers referred to GHB as "a truly nontoxic hypnotic" and repeatedly emphasized its "lack of toxicity." Vickers cited evidence that GHB demonstrates "no toxic effects on the liver and kidney." In 1972, Laborit described the body's metabolism of GHB and stressed "the absence of any need of detoxification by the organism." As recently as 1989, this scientific consensus on GHB's benign nature remained unchanged. Gallimberti's study from that year on its uses in treating alcohol withdrawal in humans notes that "GHB's action ...seems to be without serious side effects." His almost off-hand reference to the "safety of GHB" shows how well-established this property of the nutrient had become. Then, on November 8th, 1990, the FDA banned the over-the-counter sale of GHB in the United States. In 1991, two scientists from the California Department of Health Services wrote a report on ten "poisonings" associated with GHB. The authors, Chin and Kreutzer, warned of GHB's "tremendous potential for abuse." They observed that "all interviewed patients reported a pleasurable sensation or a `high.' Several of them...continued taking [GHB] because it made them `feel good'." Apparently, the authors construed feeling good in and of itself as a potential threat to public health. Despite such dire language, the report acknowledged that "there are no documented reports of long-term [detrimental] effects. Nor is there any evidence for physiologic addiction." Of the ten "poisonings" reported, four involved "unknown doses," four featured the "coingestion" of other drugs, (usually alcohol), one involved unmedicated epilepsy, and another a history of grand mal seizures. Since alcohol and other central nervous system (CNS) depressants are not recommended with GHB, and because GHB is contraindicated for epileptics, such cases are not unexpected. Chin and Kreutzer acknowledge that the "more severe reactions...generally occurred when patients took an unmeasured dose, a particularly large dose, or several doses within a short period of time." Such problems are easily avoided by following the directions for GHB's use. Although the specific clinical details of these ten cases are too lengthy to go into here, one point needs addressing--the use of the terms "coma" and "seizures" in descriptions of these cases. At a sufficiently high dose, GHB can cause CLONUS, a rapid, rhythmic contraction and relaxation of muscles which would be better described as muscle spasm or uncontrollable twitching than a seizure. GHB can also cause intense drowsiness, abrupt sedation, and deep sleep which is probably better described as unarrousability or deep sedation than coma. Vickers [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." --- Why Was GHB Banned? --- It seems likely, then, that at least some of the motives behind the 1990 FDA ban of GHB were other than those of public safety. Such a ban constitutes the only means of Federal control of a substance neither scheduled by the DEA nor approved by the FDA as a drug. In the absence of a genuine public-health concern, such control might have been motivated by a desire to protect the pharmaceutical industry (with which the FDA is closely intertwined) from competition from a safer, more effective and less expensive alternative to sleeping pills. Is it a coincidence that the FDA has also banned L-tryptophan, another nutrient that functions as a safe and effective sleep aid? --- What Are the Real Concerns? --- As with most substances, unpleasant and possibly dangerous side effects can be associated with excessive doses of GHB. A dose usually only about twice the amount required for relaxation or a prosexual effect can, as one user put it, "knock you out but fast." In this respect, GHB is probably comparable to alcohol: if you drink twice as much as you normally would, you probably wouldn't function very well. Despite its general safety and lack of toxicity, the safe use of GHB requires information, preparation, caution, and good judgment. In other words, follow the usage guidelines! --- How Does It Feel? --- Most users find that GHB induces a pleasant state of relaxation and tranquility. Frequent effects are placidity, sensuality, mild euphoria, and a tendency to verbalize. Anxieties and inhibitions tend to dissolve into a feeling of emotional warmth, wellbeing, and pleasant drowsiness. The "morning after" effects of GHB lack the unpleasant or debilitating characteristics associated with alcohol and other relaxation-oriented drugs. In fact, many users report feeling particularly refreshed, even energized, the next day. The effects of GHB can generally be felt within five to twenty minutes after ingestion. They usually last no more than one and a half to three hours, although they can be indefinitely prolonged through repeated dosing. The effects of GHB are very dose-dependent. SMALL INCREASES IN THE AMOUNT INGESTED LEAD TO SIGNIFICANT INTENSIFICATION OF THE EFFECT. Higher levels feature greater giddiness, silliness, and interference with mobility and verbal coherence, and maybe even dizziness. Even higher doses usually induce sleep. --- The Actions of GHB in the Body --- GHB temporarily inhibits the release of dopamine in the brain. This may cause increased dopamine storage, and later increased dopamine release when the GHB influence wears off [Chin and Kreutzer, 1992]. This effect could account for the middle-of-the-night wakings common with use of higher GHB doses, and the general feelings of increased well-being, alertness and arousal the next day. GHB also stimulates pituitary growth hormone (GH) release. One methodologically rigorous Japanese study reported nine-fold and sixteen-fold increases in growth hormone 30 and 60 minutes respectively after intravenous administration of 2.5 grams of GHB in six healthy men between the ages of twenty-five and forty [Takahara, 1977]. GH levels were still seven-fold higher at 120 minutes. The mechanism by which GHB stimulates growth-hormone release is not known. Dopamine activity in the hypothalamus is known to stimulate pituitary release of growth hormone, but GHB inhibits dopamine release at the same time that it stimulates GH release. This suggests that GHB's GH-releasing effect takes place through an entirely different mechanism [Takahara, 1977]. At the same time GH is being released, prolactin levels also rise. Serum prolactin levels increase in a similar time-dependent manner as GH, peaking at five-fold above baseline at 60 minutes [Takahara, 1977]. This effect, unlike the release of GH, is entirely consistent with GHB's inhibition of dopamine. Other compounds which lessen dopamine activity in the brain (such as the neuroleptic Thorazine) have been shown to result in prolactin release. Although prolactin tends to counteract many of the beneficial effects of GH, the sixteen-fold increases in GH probably overwhelm the five-fold increases in prolactin. GHB induces "remarkable hypotonia" (muscle relaxation) [Vickers, 1969]. It is now gaining popularity in France and Italy as an aid to childbirth. GHB causes "spectacular action on the dilation of the cervix," decreased anxiety, greater intensity and frequency of uterine contractions, increased sensitivity to oxytocic drugs (used to induce contractions), preservation of reflexes, a lack of respiratory depression in the fetus, and protection against fetal cardiac anoxia (especially in cases where the umbilical cord wraps around the fetus' neck) [Vickers, 1969; Laborit, 1964]. GHB is completely metabolized into carbon dioxide and water, leaving absolutely no residue of toxic metabolites [Vickers, 1969; Laborit, 1972]. Metabolism is so efficient that GHB can no longer be detected in urine four to five hours after it is taken by injection [Laborit, 1964]. GHB activates a metabolic process known as the "pentose pathway" which plays an important role in the synthesis of protein within the body [Laborit, 1972]. It also causes a "protein sparing" effect [Laborit, 1964] which reduces the rate at which the body breaks down its own proteins. These properties, along with GHB's effect on growth hormone, underlie its common use as an aid to muscle-building and fat loss. Anesthetic (large) doses of GHB are accompanied by a small increase in blood sugar levels, and a significant decrease in cholesterol. Respiration becomes slower and deeper. Blood pressure may rise or fall slightly, or remain stable, but a moderate bradycardia (slowing of the heart) is consistent [Vickers, 1969; Laborit, 1964]. A slight drop in body temperature also occurs [Laborit, 1964]. GHB also stimulates the release of acetylcholine in the brain [Gallimberti, 1989]. --- GHB and Sleep --- GHB has been called "almost an ideal sleep inducing substance" [SMART DRUGS II, p245]. Small doses produce relaxation, tranquility and drowsiness which make it extremely easy to fall asleep naturally. Higher doses increase the drowsiness effect and decrease the time it takes to fall asleep. A sufficiently large dose of GHB will induce sudden sleep within five to ten minutes [Laborit, 1964]. Many other hypnotics interfere with various stages of the sleep cycle thus preventing the body from achieving a complete and balanced session of rest and recuperation. The most remarkable facet of GHB-induced sleep is its physiological resemblance to normal sleep. For instance, GHB sleep is characterized by increased levels of carbon dioxide in the arteries, as in normal sleep [Vickers, 1969]. During normal and GHB sleep, the CNS continues to be responsive to "noxious stimuli" (pain and other irritations), a factor which sets limits on GHB's uses in anesthesia [Vickers, 1969]. GHB facilitates both REM (rapid eye movement) sleep, and "slow-wave" (non-REM) sleep, the stage of sleep featuring increased release of growth hormone [Laborit, 1972]. And unlike the unconsciousness induced by other anesthetics, that triggered by GHB does not feature a systemic decrease in oxygen consumption [Laborit, 1964]. The primary disadvantage to GHB's use as a sleep aid is it's short-term influence--about three hours. During GHB's influence, sleep is deeper and more restful, but after the GHB has worn off, people have a tendency to wake up. The higher the dose, the greater is this tendency. Some have called this pattern the "dawn effect" and have speculated that it is related to the release of stored-up dopamine. Some people minimize this effect by taking minimal doses of GHB. Others take advantage of this effect by getting a couple of hours of work done in the middle of the night. Still others choose to take a second dose of GHB to sleep for another three hours. It should be noted that not everyone can be put to sleep by GHB. We have spoken to three men who have never achieved sleep even with the doses normally used for such purposes. In addition, Takahara [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. --- GHB, Alcohol and Alcoholism --- GHB shows great promise in the treatment of alcoholism. In Europe, one of its primary uses is to relieve withdrawal symptoms, cravings, and anxiety among alcoholics. In laboratory rats addicted to alcohol, withdrawal symptoms closely resemble those exhibited by humans, including tremors, convulsions, and hypersensitivity to sound. All of these symptoms were blocked by sufficiently high doses of GHB [Fadda, 1989]. Administration of GHB has also been found to prevent alcohol consumption among rats that voluntarily ingest alcohol [Fadda, 1989; Gallimberti, 1989]. In a rigorous, double-blind, placebo-controlled study conducted of human alcoholics, "nearly all withdrawal symptoms disappeared within two to seven hours" after administration of GHB. On a severe-moderate-mild-or-none scale, withdrawal symptoms remained below moderate during the entire period. The only side effect observed was slight, occasional, and transient dizziness. The researchers concluded, "the results clearly indicated that GHB is effective for the suppression of withdrawal symptoms in alcoholics" [Gallimberti, 1989]. --- Other Uses of GHB --- GHB has a decades long track record of use as a general anesthetic. Administered intravenously, an anesthetic dose of GHB is in the range of 4-5 grams for a 150-pound person [Vickers, 1969]. Its advantages as an anesthetic include low toxicity, relatively few contraindications, slowing of the heart rate without loss of blood pressure, the absence of irritation to the veins with intravenous administration, muscle relaxation, absence of respiratory depression (usually), reduction of body temperature (hypothermia), and various protective and anti-shock actions [Laborit, 1964]. However, GHB can almost never be used in anesthesia without the additional administration of other drugs [Vickers, 1969] because it does not produce complete surgical anesthesia except in children [Laborit, 1964]. The autonomic nervous system remains active during GHB-induced anesthetic coma, and thus the body continues to respond to surgical stimuli through increases in heart rate, blood pressure, and cardiac output, as well as through sweating, peripheral vasoconstriction, vocalization, and reflex muscle action [Vickers, 1969]. Local anesthetics or other drugs which suppress these responses must therefore also be used, like the way a dentist or orthodontic surgeon might use Novocaine to kill pain along with nitrous oxide to render a patient unconscious. It is suspected that part of GHB's protective function involves a slowing of the metabolism of brain cells, thus reducing their requirements for oxygen and glucose [Chin and Kreutzer, 1992; Artru, 1980]. Another factor in GHB's anti-shock capability may be the marked vasodilation induced in the liver and kidney, thus increasing blood flow to those vital organs. GHB's efficacy for treating anxiety has been positively demonstrated in tests involving schizophrenic subjects [Laborit, 1964]. Its sedative properties have earned it a role as a psychotherapeutic adjunct [Vickers, 1969]. It has also been used to assist the process of "abreaction," or the release (usually through verbalization) of repressed emotion [Vickers, 1969]. Unlike other "anxiolytic" (or anti-anxiety) drugs, GHB's effect is non-toxic. Furthermore, GHB's reduction of inhibitions, its tendency to encourage verbalization, and the typical lack of fear during the GHB experience would seem to provide an ideal context for the verbal exploration of difficult emotional territory during therapy. --- GHB and Sex --- Scientists and doctors have traditionally been reluctant to ascribe aphrodisiac properties to any substance, although this tendency may have abated somewhat in recent years. It is a testament, then, to the power the GHB's sexual effects that they were clearly acknowledged in the scientific literature by 1972. Dr. Laborit wrote: "A last point should still be mentioned: the [GHB] action on Man which could be called 'aphrodisiac.' We cannot present any animal experiments on this subject. However, the oral form has now been sufficiently used so that, as generally agreed, no doubt can subsist as to its existence." We have identified four main prosexual properties: 1) disinhibition, 2) heightening of the sense of touch (tactility), 3) enhancement of male erectile capacity, and 4) increased intensity of orgasm. Perhaps the foremost prosexual property of GHB is disinhibition. Some users suggest that GHB's other sexual benefits are secondary effects, made possible (or at least amplified) by this loosening of psychosomatic constraint. A number of people have commented that this disinhibition is particularly marked among women. Women often report that GHB makes their orgasms longer and more intense, as well as more difficult or time-consuming to achieve, especially at higher doses. As with its other effects, GHB's impact on female orgasm seems highly sensitive to small adjustments in dosage. --- Legal Status and Availability --- GHB is not approved in the US and has been banned from over-the-counter sale by the FDA. GHB has not yet been "scheduled" as a "controlled substance" by the DEA, and therefore simple possession is not illegal. GHB continues to be sold to legitimate laboratories and scientists for research purposes, but selling it specifically for human consumption, especially while making claims about its health benefits, is a violation of current FDA regulations and policy. In some European countries, GHB is an approved drug available by prescription. Local doctors, pharmacists and government bureaucrats should be able to provide country-by-country specifics. GHB is growing in popularity and seems to be widely available in the underground "gray market." Since most of the GHB available through such channels is of the "bootleg" variety, manufactured by nonprofessional "kitchen" chemists, concerns about quality and purity should be kept in mind. Caveat emptor (buyer beware)! --- Safety Issues --- As has been emphasized, the overall safety of GHB is well-established, and no deaths attributable to GHB have been reported over the thirty year period that this compound has been in use [Vickers, 1969; Chin and Kreutzer, 1992]. In fact, as of 1990, only forty-six adverse reactions had been reported in the United States surely constituting only an infinitesimal fraction of actual usage, all followed by rapid and complete recovery [Chin and Kreutzer, 1992]. Unlike a large proportion of other drugs including alcohol and even Tylenol, GHB has no toxic effects on the liver, kidney or other organs [Vickers, 1969; Chin and Kreutzer, 1992]. One program of sleep therapy using six to eight grams daily for a period of eight to ten days produced no side effects. Vickers [1969] even reports that doses as high as twenty to thirty grams per twenty-four hour period have been used for several days without negative consequences (don't do this at home kids!). In the Canadian studies of narcolepsy mentioned earlier, the nightly use of two to six teaspoons (one teaspoon equaling roughly 2.5 grams) for several years resulted in no reports of long-term adverse effects, or problems with issues of addiction or dependence. In one of these studies, one patient inadvertently ingested fifteen teaspoons without adverse consequence "other than deep sedation and headache the next day" [Chin and Kreutzer, 1992]. And in France, sub-anesthetic oral doses were used by "a large number of patients for about six years" without untoward effect [Laborit, 1972]. --- Side Effects --- According to Dr. Gallimberti [1989], the action of GHB is "without serious side effects." Some research programs have reported no side effects at all. Nonetheless, it's clear that some minor side effects can occur. Those most commonly experienced are drowsiness, dizziness, nausea, and sometimes vomiting. As a sedative-hypnotic, GHB's effects bear some similarity to those of alcohol and tranquilizers. GHB not only "may cause drowsiness" like these other drugs, IT WILL ALMOST INVARIABLY DO SO. Ataxia, or incoordination, can also be a side effect of GHB. DO NOT DRIVE A VEHICLE OR OPERATE DANGEROUS MACHINERY WHILE UNDER THE INFLUENCE OF GHB. As mentioned, clonic movements (muscle contractions or "seizures") have been observed during the onset of GHB-induced sleep. Headache is sometimes reported. A moderate slowing of the heart rate is a consistent effect, and small changes in blood pressure can take place. Likewise, orthostatic hypotension (a sudden drop in blood pressure caused by standing up quickly) has also been reported. Sometimes this is experienced as brief dizziness, and rarely people can briefly lose consciousness. At very high doses, cardiac and respiratory depression can occur. Sufficiently large doses of GHB can cause sudden sedation and loss of consciousness. Do not take such doses except when reclining on a bed or sofa. It is also a bad idea to take such doses in the presence of people who don't know anything about GHB. You may alarm your family or friends and wake up in an emergency room (with a large medical bill). More unusual and extreme reactions have included diarrhea, lack of bladder control, temporary amnesia, and sleepwalking. Whatever side effects may be noted, they are often much more severe when GHB is combined with other central nervous system depressants [Chin and Kreutzer, 1992, Gallimberti, 1989; Takahara, 1977; Vickers, 1969]. --- Contraindications --- Although contraindications for GHB have been described as "remarkably few" [Vickers, 1969], those who suffer from any of the following conditions should not use GHB: severe illness of any kind, epilepsy, eclampsia (convulsions), bradycardia (slowed heart-beat) due to conduction problems [left-bundle-branch-block is an example of conduction difficulty], Cushing's syndrome, severe cardiovascular disease, hyperprolactinemia, and severe hypertension [Gallimberti, 1989; Vickers, 1969]. Severe alcoholism is sometimes mentioned as a contraindication for GHB [SMART DRUGS II, p244] even though GHB has been used quite successfully in the treatment of withdrawal symptoms. The explanation for this seeming contradiction probably lies in the likelihood that severe alcoholics may combine GHB with alcohol. GHB should not be used with benzodiazepines ("minor tranquilizers" such as Valium and Xanax), phenothiazines ("major tranquilizers" like Thorazine and Stellazine), various painkillers (barbiturates and opiates), alcohol, anticonvulsants (Dilantin and phenobarbital) and even many over-the-counter allergy and sleep remedies--without direct medical supervision. --- Dosage --- Determining the ideal dose is probably the trickiest aspect of working with GHB. The amount required for a given level of effect will vary from person to person, and the dose-response curve is fairly steep. Overestimating the dose can have consequences ranging in seriousness from ruining your plans for the evening to waking up in the emergency ward as a result of panic on the part of concerned-but-uninformed friends or relatives. Once you have found the levels that give you the effects you desire, they will remain consistent. Tolerance to GHB does not develop. However, recent (not current) alcohol consumption may decrease the effect of a given dose of GHB [Fadda, 1989]. Most people find that a dose in the range of 0.75-1.5 grams is suitable for prosexual purposes, and that a quantity in the range of 2.5 grams is sufficient to force sleep. Some people think that GHB might lower potassium levels and should therefore be taken with potassium supplementation. Some research papers have identified such an effect, others have not. If you want to play it safe, take a potassium supplement equal to 10% of the GHB dose. --- Notes: --- Note 1: This article is excerpted and adapted from a 40-page special report on GHB written by the authors and available from: Smart Publications Post Office Box 4667 Petaluma, California, 94955 To order send a check for $22.95 ($19.95 for the report and $3 for shipping). We do not accept credit cards. (*) Note 2: This article was originally published in SMART DRUG NEWS [3(6): p1] and is copyright (c) 1994 by the Cognitive Enhancement Research Institute and the authors. For free information about CERI and SMART DRUG NEWS, telephone (415) 321-CERI or (415) 323-3864 FAX or e-mail to CERI's Executive Director Steven Wm. Fowkes at 71702.760@compuserve.com. A small sidebar to this article written by Steven Wm. Fowkes and entitled "The Demonization of GHB" is also available for downloading from this directory. Note 3: John Morgenthaler and Steven Wm. Fowkes (along with Ward Dean, M.D.) are coauthors of the book SMART DRUGS II: THE NEXT GENERATION (Smart Publications, 1993). This book is available from CERI and your local bookstores. It is a supplement to the first smart-drug book SMART DRUGS & NUTRIENTS, authored by Dr. Ward Dean and John Morgenthaler in 1990. The two books provide a comprehensive summary of smart drugs. --- References Cited in this Article --- Artru AA, Steen PA and Michenfelder JD. Gamma-Hydroxybutyrate: Cerebral metabolic, vascular, and protective effects. J NEUROCHEMISTRY 35(5): 1114-9, November 1980. Chin MY, Kreutzer RA and Dyer JE. Acute poisoning from gamma-hydroxybutyrate in California. WEST J MED (United States). 156(4): 380-4, April 1992. Fadda F, Colombo G, Mosca E and Gessa GL. Suppression by gamma-hydroxybutyric acid of ethanol withdrawal syndrome in rats. ALCOHOL AND ALCOHOLISM (Great Britain). 24(5): 447-51, 1989. Gallimberti L, Gentile N, Cibin M, Fadda F, Canton G, Ferri M, Ferrara SD and Gessa GL. Gamma-hydroxybutyric acid for treatment of alcohol withdrawal syndrome. THE LANCET, 787-9, 30 September 1989. Kleimenova NN, Ostrovskaya RU and Arefolov VA. Effect of sodium hydroxybutyrate on the ultrastructure of the cross-striated muscle tissue myocytes during physical exercise. BYULL EKSP BIOL MED 88(9): 358-61, 1979. Laborit H. Correlations between protein and serotonin synthesis during various activities of the central nervous system (slow and desynchronized sleep, learning and memory, sexual activity, morphine tolerance, aggressiveness, and pharmacological action of sodium gamma-hydroxybutyrate). RESEARCH COMMUNICATIONS IN CHEMICAL PATHOLOGY AND PHARMACOLOGY 3(1): January 1972. Laborit H. Sodium 4-Hydroxybutyrate. INT J NEUROPHARMACOLOGY (Great Britain). 3: 433-52, 1964. Ostrovskaya RU, Kleimenova NN, Kamisheva V, Molodavkin GM, Yavorskii AN and Boikko SS. Effect of sodium hydroxybutyrate on functional biochemical and morphological indexes of physical working ability. FARMAKOL REGUL PROTSESSOV UTOMLENIYA [Moscow, USSR] 39-56: 112-17, 1982. Takahara J, Yunoki S, Yakushiji W, Yamauchi J, Yamane J and Ofuji T. Stimulatory effects of gamma-hydroxybutyric acid on growth hormone and prolactin release in humans. J CLIN ENDOCRINAL METAB 44: 1014, 1977. Vickers MD. Gamma-hydroxybutyric Acid. INT ANAESTHESIA CLINIC 7: 75-89, 1969. -=-=-=-=-=-=-=-=-=-=-=-=-=-=-=-=-=-=-=-=-=-=-=-=-=-=-=-=-=-=-=-=-=-=-=-=-=-=-= The Demonization of GHB* --- by Steven Wm. Fowkes -=-=-=-=-=-=-=-=-=-=-=-=-=-=-=-=-=-=-=-=-=-=-=-=-=-=-=-=-=-=-=-=-=-=-=-=-=-=-= Many Americans first heard of GHB through a widespread rumor that actor River Phoenix's death was caused by a GHB overdose. This rumor was started by club-goers, exaggerated by reporters, confused by DEA agents, and rejected by the subsequent coroner's report. NEWSWEEK called GHB "an obscure and dangerous steroid substitute," but perhaps the most egregious purveyors of misinformation were DEA field agents who informed reporters that GHB's slang name was "Great Bodily Harm," a designer drug with a less-than-benign reputation on the streets of Los Angeles. The press took it hook, line and sinker, failing even to recognize that the three-letter acronym G-B-H was a scrambled version of G-H-B. The DEA's attempt at misinformation was a brilliant attempt to scare the American people and support the FDA's questionable ban of GHB. Although it worked on the mass media, it boomeranged in the clubs. Said one New York nightclub patron, "I'd never heard of GHB before. No one in New York had. This month it's the only drug" [Rogers, 1993]. Rogers P and Katel P. The New View From On High. NEWSWEEK, 6 December 1993. * This brief note on GHB was originally published as a sidebar in SMART DRUG NEWS, the newsletter of the CERI. Copyright (c) 1994 by CERI. Cognitive Enhancement Research Institute Post Office Box 4029 Menlo Park, California, 94026 (415) 321-CERI (415) 323-3864 FAX Internet: smart@crl.com CompuServe: 71702,760 =*=*=*=*=*=*=*=*=*=*=*=*=*=*=*=*=*=*=*=*=*=*=*=*=*=*=*==*=*=*=*=*=*=*=*=*=*=*= ***** "Life Enhancement News" is (C) Copyright 1994 by John Morganthaler ***** =*=*=*=*=*=*=*=*=*=*=*=*=*=*=*=*=*=*=*=*=*=*=*=*=*=*=*==*=*=*=*=*=*=*=*=*=*=*= < Smart@andronix.org > John Morgenthaler, Ward Dean, MD, & Steven Wm. 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