e-tarded

You need to do alot more research before you go posting. Neuro-transmitters is the word you were looking for possibly. Neurotoxicity MDMA is unambiguously neurotoxic in lab animals in high doses. Typical dose regimens which elicit neurotoxicity are 20mg/kg (rats) or 5mg/kg (primates) given twice daily for four days either i.m. (intramuscularly) or s.c. (subcutaneously). Humans typically use MDMA p.o (per oral) and at levels of about 2.5 mg/kg or less. Subcutaneous administration of MDMA tends to increase toxicity 2-3 times over p.o.[1] Extrapolation of animal studies to human use is difficult, since humans typically use a less toxic route of administration, take somewhat less per dose and take a smaller cumulative dose. One study of MDMA administered to primates most closely modelled human use and used doses of 2.5mg/kg given every 2 weeks for 4 months (2.5 mg/kg x 8) which found no evidence of neurotoxicity[2]. A single- dose study found a decrease in serotonin (5-HT) and it's major metabolite 5-hydroxyindoleacetic acid (5-HIAA) in rhesus monkeys at 5mg/kg but not 2.5mg/kg. Another study gave rhesus monkeys 2.5mg/kg twice daily for four days and found depletions of 5-HT and 5-HIAA, but without any evidence of neurotoxicity from [3H]paroxetine binding to the 5-HT reuptake transporter[3]. The finding that depletions of 5-HIAA could occur in the absense of 5-HT neurotoxicity creates problems in interpreting the results of CSF 5-HIAA reductions in human users, which remains the strongest evidence of putative MDMA neurotoxicity in humans[4]. Other results of human studies in MDMA users are at odds with the conclusion that MDMA is a human neurotoxin. McCann, et al. in the same study which analyzed CSF 5-HIAA, found that MDMA users tended to have better impulse control and lower hostility while lower serotonin levels are thought to be correlated with increased hostility. A study of sleep patterns of MDMA users found that MDMA users had normal sleep patterns, but with a statistically significant decrease in stage 2 sleep, leading to an overall improvement in sleep quality -- more importantly these results are not at all in accordance with studies on sleep patterns of humans given the 5-HT supressor para-chlorophenylalanine (PCPA) or with animals having lesioned 5-HT systems[5]. Prospective studies (giving users MDMA in a controlled environment with baseline testing and then checking for indications of neurotoxicity) rather than retrospective studies (after the fact with no baseline) are only just getting underway at the Harbor-UCLA medical center (other studies are starting in England, Switzerland and Germany[6]). Initial retrospective results of the UCLA study indicate that MDMA may increase cerebral blood flow [7]. This may be indicative of benficial rather than neurotoxic changes in the brain: We are aware of a variety of neuro-psychiatric disorders associated with measurements of low blood flow, including Alzheimer's Disease, HIV Dementia, Major Depressive Disorders and Chronic Cocaine Abuse. However, there are no known clinical disorders or drugs which induce long-term elevations of rates of cerebral blood flow. -- Charles S. Grob. There have been reports of adverse psychiatric effects in the literature particularly anxiety attacks, paranoia and depression. However, some cases present the onset of psychiatric symptoms after a single typical dose[8] which suggests a psychological rather than biological/neurotoxic mechanism. Also, some cases of paranoia reported appear to have occured after repeated daily abuse and probably represent a manifestation of amphetamine psychosis, possibly in part due to adulteration or substitution by amphetamines[9]. The diet drug d-fenfluramine (Redux) causes similar effects on the 5-HT system, and it has been suggested that the lack of adverse psychiatric effects to chronic ingestion of d-fenfluramine implies that MDMA is probably without adverse effects. However, it appears that the mechanism behind MDMA and d-fenfluramine neurotoxicity are not the same, and this may make extrapolation from one drug to the other problematic[10]. To summarize the clinical data, the available evidence tends to suggest that in human users a (probably reversable) decrease in 5-HT may occur (possibly via suppression of the enzyme tryptophan hydroxylase) but that 5-HT neurons remain functionally intact. However, neurotoxic levels in humans are probably "attainable" and the exact amount of MDMA required to elicit a neurotoxic response in humans is unknown. The exact mechanism of MDMA neurotoxicity in animals is not presently known [11], but it seems to require dopamine activity, oxidation, and access to the 5-HT transporter. Increasing dopamine activity via ingestion of methamphetamine, l-tyrosine, phenylalanine or l-dopa would tend to increase MDMA neurotoxicity. This is a concern since phenylalanine is in diet soft drinks and products sweeted with aspartame and is also in many "smart drinks" sold at raves and of course methamphetamine is a concern since MDMA is often cut with crystal. On the other hand ascorbate (vitamin C) and l-cystine which are anti-oxidants have been shown to prevent MDMA induced neurotoxicity in animals, as has the administration of a SSRI antidepressant (Prozac, Zoloft, Paxil, Luvox, etc.). Studies indicate that taking either an anti-oxidant or a SSRI up to 5 hours after taking MDMA will prevent neurotoxicity in animals[12]. It may be sensible irregardless of if MDMA is neurotoxic in humans for users to take an antioxidant (e.g. 2-4 g vitamin C, orange juice) along with some 5-HT precursors (l-trytophan or 5-hydroxytryptophan (5-HTP), bananas, milk). 1. Ricaurte, GA, DeLanney, LE, Irwin, I, Langston, JW. "Toxic Effects of MDMA on Central Serotonergic Neurons in the Primate: Importance of Route and Frequency of Drug Administration," Brain Research, Vol 446, P165-168, 1988. 2. Ricarute, GA, personal communication on the findings of an unpublished study. 3. Insel, TR, Battaglia, G, Johannessen, JN, Marra, S, DeSouza, EB, "3,4-Methylenedioxymethamphetamine (Ecstasy) Selectively Destroys Brain Serotonin Terminals in Rhesus Monkeys," Journal of Pharmacology and Experimental Therapeutics, Vol 249(1), P 713-720, 1989. 4. McCann, UD, Ridenour, A, Shaham, Y, Ricaurte, GA. "Serotonin neurotoxicity after (+/-) 3,4-methylenedioxy-methamphetamine (MDMA, Ecstasy): a controlled study in humans," Neuropsychopharmacology, Vol 10(2), P 129-138, 1994. 5. Allen, RP, McCann, UD, Ricaurte, GA, "Persistent effects of (+-) 3,4-methylenedioxymethamphetamine (MDMA, Ecstasy) on human sleep," Sleep, Vol 16(6), P 560-564. 6. MAPS Newslatter Vol 6, No 3, Summer 1996. http://www.maps.org/news-letters/v06n3/ 7. MAPS Newsletter Vol 5, No 4, Summer 1995. http://www.maps.org/news-letters/v05n4/05402mdm.html. Grob-C-S, Poland-R-E Chang-L, Ernst-T, "Psychobiologic effects of 3,4-methylenedioxymethamphetamine in humans: methodological considerations and preliminary observations," Behav. Brain Res., 1996 73(1-2), P 103-7. 8. McCann-U-D, Ricaurte-G-A, "MDMA ('ecstasy') and panic disorder: induction by a single dose," Biol. Psychiatry 1992 Nov 15 32(10):950-3. 9. McGuire-P-K, Cope-H, Fahy-T-A, "Diversity of psychopathology associated with use of 3,4-methylenedioxymethamphetamine ('Ecstasy')," Br. J. Psychiatry, 1994 Sep 165(3):391-5. 10. Colado-M-I, O'Shea-E, Granados-R, Murray-T-K, Green-A-R, "In vivo evidence for free radical involvement in the degeneration of rat brain 5-HT following administration of MDMA ('ecstasy') and p-chloroamphetamine but not the degeneration following fenfluramine," Br. J. Pharmacol., 1997 Jul 121(5):889-900. 11. Seiden-L-S, Sabol-K-E, "Methamphetamine and methylenedioxymethamphetamine neurotoxicity: possible mechanisms of cell destruction," NIDA Res. Monogr. 1996 163:251-76. 12. Gudelsky-G-A, "Effect of ascorbate and cysteine on the 3,4-methylenedioxymethamphetamine-induced depletion of brain serotonin," J. Neural Transm., 1996 103(12), P 1397-404. McCann-U-D, Ricaurte-G-A, "Reinforcing subjective effects of (+/-) 3,4-methylenedioxymethamphetamine ('ecstasy') may be separable from its neurotoxic actions: clinical evidence." J. Clin. Psychopharmacol. 1993 Jun 13(3):214-7. Schmidt-C-J, Kehne-J-H, "Neurotoxicity of MDMA: neurochemical effects.", Ann. N.Y. Acad. Sci. 1990 600:665-80. Steranka-L-R, Rhind-A-W, "Effect of cysteine on the persistent depletion of brain monoamines by amphetamine, p-chloroamphetamine and MPTP," Eur. J. Pharmacol. 1987 Jan 13 133(2):191-7. Battaglia-G, Yeh-S-Y, De-Souza-E-B, "MDMA-induced neurotoxicity: parameters of degeneration and recovery of brain serotonin neurons," Pharmacol. Biochem. Behav. 1988 Feb 29(2):269-74. ------------------ ~*P*L*U*R*~ Four Simple Words To Live By....

it maybe copy and paste, but at least it is correct information and not rumor or hearsay. ------------------ ~*P*L*U*R*~ Four Simple Words To Live By....

Also make sure you get the all natural stuff, there has been some discussion lately on some of the fillers involved with 5-HTP ------------------ ~*P*L*U*R*~ Four Simple Words To Live By....

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2C-B is highly dosage sensitive. Taking an amount just slightly above the recommended dose can produce an intense experience that most people find forced and unpleasant. With any substance there are a few people who will exhibit unusually high or low sensitivity. Therefore, in order to avoid an undesirably intense experience, many users start with a small dose of 2C-B, around 8 mg., and work their way up. INTENSITY: 2 to 7, varying with the dosage and the individual's sensitivity to this compound. MATERIAL: 2C-B (4-bromo-2,5-dimethoxyphenethylamine) is a psychedelic/empathogen developed by Alexander Shulgin. Shulgin has invented around 200 psychoactive compounds including DOM (a.k.a. STP), an ultra-potent psychedelic that appeared briefly on the street in the late Sixties. Recently a large amount of 2C-B has been distributed under the street name "Nexus." In the past 2C-B has also been distributed as "Eve" and "Venus. " DOSAGE and ADMINISTRATION: 2C-B should be ingested, preferably on an empty stomach. As mentioned above, 2C-B is extremely dosage sensitive, and the amount required is so small that a sophisticated scale is needed to accurately weigh a single dose. With "street" 2C-B it is hard to know exactly how much is in a capsule. This is likely to cause some unexpected heavy trips if 2C-B becomes a popular drug and dosage information and knowledge is not made available. People who have a quantity of 2C-B often dilute it in an inert powder before measuring individual doses to provide greater accuracy. In PIHKAL Shulgin lists the dosage range as 16 to 24 mg. Another writing on 2C-B lists the range as 12 to 30 mg. Shulgin's descriptions of the effects of different dosages can be summarized as follows: 16 mg. produces a "museum level" experience. One can go about in public with slightly enhanced perception, such as may be appropriate for going to a public museum, etc. 20 to 24 mg. will produce a more psychedelic experience with visuals and intensified feelings I've seen no literature on 2C-B which recommends a dose above 30 mg. Gracie and Zarkov, who are very experienced trippers, each took 40 mg. in error and had unpleasant experiences. Shulgin reports on overdoses up to 100 mg. that produced frightening experiences but caused no permanent damage. However, some people, like myself, have an unusually low sensitivity to 2C-B and other substances in the phenethylamine family. I find that I must consume 50 mg. to produce experiences that most people obtain with 25 to 35 mg. THE HIGH: My experiences with 2C-B have been quite varied. With a low, "museum level" dose, I experience what resembles a speedy acid high hardly worth discussing. It is when I take a somewhat larger dose that the unique aspects of this substance begin to manifest. It is definitely an "up" experience. There is lots of physical energy. The visual aspect can be extraordinary, with intense vivid colors and intricate patterning that is reminiscent of mescaline visuals and seems charged with electricity. In one experience the visuals appeared as complete chaos before becoming a portion of a vast cosmic order. On a good dose of 2C-B I'm content to just lay back for hours and trip on watching my mind. On some occasions 2C-B has given me visibility into what I will call the "assembly" or "machine" language of the mind. As an example, if you see the number 3, the typical response is to identify the symbol as the number 3, and think about its meaning within the context you are seeing it. On a finer scale, many thousands of neurons are connected in the brain's interpretation and identification of the symbol and linkage to the stored memory of 3. While on 2C-B, I've seen that only 80-90% of this mental "signal" comes back as 3, the remaining 10-20% having connected elsewhere in the mind or run into closed synapses, etc. I have found this awareness of the mind's "assembly" language to be simultaneously insightful, discombobulating, and humorous. 2C-B is considered an empathogen and many users have reported powerful and transformative empathogenic experiences from its use. I've only had strong empathogenic content in about 25% of my 2C-B experiences. However, I found this empathogenic quality to be very deep and transformative, much more meaningful than the comparatively shallow emotional bliss that I tend to experience on ecstasy. Where the feelings of ecstasy can be repetitive or predictable, 2C-B allows me to continually explore different types of feelings. On the negative side, the 2C-B experience has a tendency to feel "forced" in comparison with the more flowing nature of ecstasy or LSD. When taking a large dose of 2C-B, one's ability to accept whatever the mind presents, without trying to push away unwanted thoughts, will reduce the likelihood of an unpleasant experience. 2C-B also seems to produce a constant low-level agitation or interference in the mind. I notice this if I try to quiet my mind to meditate or listen to music. This slight "buzz' that is always present is quite distinct from the ocean of luxuriantly transparent silence that often surrounds one during an LSD trip. Like ecstasy, 2C-B can not match the depth, purity, or realism of the traditional psychedelics. However, it is much more psychedelic than ecstasy, and its unique attributes make it an interesting substance to explore. One of 2C-B's unique attributes is that it simultaneously strengthens certain aspects of the ego or identity while dissolving others. For myself and many friends who've used 2C-B this has resulted in a highly positive influence on our self-image, both during and after the experience, including the idea that the physical body is a sacred manifestation of the creative consciousness. Although I have yet to see this amongst the 2C-B users I know, I suspect that for less balanced or grounded individuals 2C-B could strengthen negative aspects of the ego, thereby producing the type of changes one often sees in amphetamine users. 2C-B is known for its ability to enhance sexual perception and performance, and I've found 2C-B to work excellently for this purpose. Whereas on ecstasy, although it is common to feel much love, emotional closeness, and empathy for your partner, it can be difficult to focus on sex or maintain an erection, and it's especially difficult to reach orgasm. With 2C-B, sexual feeling is greatly enhanced. I can remain in an excited state for hours and the experience of the sexual energy exchange is intense and electric. I've found that with any psychedelic it's best to begin sexual activity either early in the experience before awareness is too spread out, or shortly after the peak. I consider mescaline and LSD to be the best psychedelics for aphrodisiacs, although some people get too spaced out or emotionally involved to concentrate on sex. COMBINATIONS: Ecstasy - 2C-B is frequently combined with ecstasy. In therapeutic use the 2C-B is generally taken at the tail end of the ecstasy experience. Many people have found that 2C-B allows them to develop and retain the insights from the ecstasy experience which would otherwise have a tendency to slip away. I've also had excellent results taking a small amount of ecstasy (80 mg.) some 1 1/2 hours after the 2C-B. This produces a trip with an incredibly deep empathogenic content that I have never experienced on either of the substances alone. 2C-B combines quite remarkably with Ketamine. See the Multiple Combinations chapter. 2C-B may be significantly intensified and possibly dangerous if combined with MAO inhibitors. info courtesey of http://www.erowid.org ------------------ ~*P*L*U*R*~ Four Simple Words To Live By....

Well if havent rolled in a while there would be no reason for you too need 5-HTP since your serotonin wouldn't be depleted. If you still want to pre-load with 5-HTP take it about 5 hrs before you drop. 5-HTP (5-Hydroxytryptophan) 5-HTP is a metabolite of the amino acid tryptophan. it is the direct precursor of the inhibitory neurotransmitter serotoninl, the one associated with calmness; it soothes and comforts us from worry and stress. Stress causes the heightened release of serotonin, and if the stress lasts too long, it leads to serotonin depletion. Research strongly implies that boosted brain serotonin serves as a "stress immunizer." Serotonin seems to play the role of regulator to the ups and downs of mood disorders. Low serotonin levels are associated with irritability, aggression, impatience, and anxiety. Evidence suggests serotonin inhibits aggressive behavior in experimental animals and humans. Abundant laboratory research suggests there is a deficiency of serotonin or serotonin activity in the brains of most depressed persons., Suicidal patients show a significant decrease in serotonin levels. Most antidepressant drugs, including tricyclics, lithium, MAO inhibitors, and SSRI's (Prozac, Zoloft, Paxil, and Luvox), have this in common: they boost serotonin levels. 5-HTP differs from tryptophan in that it slightly increases the activity of an energizing neurotransmitter, norepinephrine, as well as the calming one, serotonin. in some clinical trials, 5-HTP outperformed tryptophan in treating mood disorders. it has also proved therapeutic for some who failed to respond to standard antidepressant drugs. The greater the agitation associated with depression, the more likely the response to 5-HTP. The usual dosage range of 5-HTP is 150-300 mg. per day in divided doses. A conservative starting dose is 50 mg., then boosting by 50 mg. every five days. A majority of responders notice a favorable mood effect within three days of beginning supplementation. in one study, of those who did respond, 80% did so within one week of therapy. Side effects are rare but may include mania, anxiety, and dermatitis. For some people, 5-HTP has a very narrow therapeutic window; the proper dosage may lie within a range as small as 10-25 mg. per day. if its antidepressant effects fade after a few weeks, it may be necessary to supplement 5-HTP at a different time of the day with a low dose of the complementary amino acid L-Tyrosine, to further raise the norepinephrine level or to eat more meat or other Tyrosine-rich foods. 5-HTP is able to pass the blood-brain barrier more easily than tryptophan, but to maximize its effectiveness it should not be taken along with protein food. one product manufacturer suggests taking it 45 minutes before or three hours after a protein meal. ------------------ ~*P*L*U*R*~ Four Simple Words To Live By....

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Yes, it works. Yes, it hits you quicker, and much harder. Yes, it's a little uncomfortable, burns slightly and feels 'weird' for usually around ten minutes. No, it doesn't hurt anything 'down there'. It works well because when you swallow it much of the MDMA gets filtered out. You make use of about 80%-90% of the chemical when you plug it, as opposed to 40%-60% swallowing and 70%-80% railing it. The further you push it up there, the less it will bother you. If you are a wuss about it and don't push it up far enough, it will burn like a sonuvabitch. If you crush it and put it in a capsule, it hurts less and hits quicker, but use a small capsule with a slippery surface. If you plug it whole, and you dance and move around, the sting is more intense but it breaks up quicker and will not bother you as long as it might if you sit still. You may very well feel the need to 'go' afterwards. Don't. Not for at least forty minutes to an hour, if you can help it. If you're peaking, go ahead, it's been dissolved by that point. If the roll is plugged, nausea is much less likely, and it doesn't matter if you've had a big meal before hand ------------------ ~*P*L*U*R*~ Four Simple Words To Live By.... [This message has been edited by e-tarded (edited 08-29-2000).]

5-HTP (5-Hydroxytryptophan) 5-HTP is a metabolite of the amino acid tryptophan. it is the direct precursor of the inhibitory neurotransmitter serotoninl, the one associated with calmness; it soothes and comforts us from worry and stress. Stress causes the heightened release of serotonin, and if the stress lasts too long, it leads to serotonin depletion. Research strongly implies that boosted brain serotonin serves as a "stress immunizer." Serotonin seems to play the role of regulator to the ups and downs of mood disorders. Low serotonin levels are associated with irritability, aggression, impatience, and anxiety. Evidence suggests serotonin inhibits aggressive behavior in experimental animals and humans. Abundant laboratory research suggests there is a deficiency of serotonin or serotonin activity in the brains of most depressed persons., Suicidal patients show a significant decrease in serotonin levels. Most antidepressant drugs, including tricyclics, lithium, MAO inhibitors, and SSRI's (Prozac, Zoloft, Paxil, and Luvox), have this in common: they boost serotonin levels. 5-HTP differs from tryptophan in that it slightly increases the activity of an energizing neurotransmitter, norepinephrine, as well as the calming one, serotonin. in some clinical trials, 5-HTP outperformed tryptophan in treating mood disorders. it has also proved therapeutic for some who failed to respond to standard antidepressant drugs. The greater the agitation associated with depression, the more likely the response to 5-HTP. The usual dosage range of 5-HTP is 150-300 mg. per day in divided doses. A conservative starting dose is 50 mg., then boosting by 50 mg. every five days. A majority of responders notice a favorable mood effect within three days of beginning supplementation. in one study, of those who did respond, 80% did so within one week of therapy. Side effects are rare but may include mania, anxiety, and dermatitis. For some people, 5-HTP has a very narrow therapeutic window; the proper dosage may lie within a range as small as 10-25 mg. per day. if its antidepressant effects fade after a few weeks, it may be necessary to supplement 5-HTP at a different time of the day with a low dose of the complementary amino acid L-Tyrosine, to further raise the norepinephrine level or to eat more meat or other Tyrosine-rich foods. 5-HTP is able to pass the blood-brain barrier more easily than tryptophan, but to maximize its effectiveness it should not be taken along with protein food. one product manufacturer suggests taking it 45 minutes before or three hours after a protein meal. ------------------ ~*P*L*U*R*~ Four Simple Words To Live By.... [This message has been edited by e-tarded (edited 08-29-2000).]

any word yet ? ------------------ ~*P*L*U*R*~ Four Simple Words To Live By....

i have to finish a lousy 3 credits, but i think i am skipping this semester. have fun in school ------------------ ~*P*L*U*R*~ Four Simple Words To Live By....

I saw Tony DeVit Spin with Seb Fontaine. Great fucking night ------------------ ~*P*L*U*R*~ Four Simple Words To Live By....

wish i could fall asleep ------------------ ~*P*L*U*R*~ Four Simple Words To Live By....

Wow some of the incredible rumors here regarding the usuage of E. I like parkinsons the best I think or pills laced with heroin. Not to offend anyone, but if you haven't done research on the effects please don't go posting rumors. Rumor #1: MDMA can cause Parkinson's disease False. MDMA does not cause Parkinson's disease. This rumor apparently got started when a sloppy journalist reported on an incident where some people took a contaminated synthetic opiate that caused neural damage similar to parkinson's disease. The contaminated opiate was MPTP, but the journalist mistakenly reported that it as MDMA. MPTP has no chemical relation to MDMA. What about fake pills? While some fake pills are dangerous, none have been known to cause Parkinson's disease. Rumor #2: MDMA drains your spinal fluid False. Some clinical studies on MDMA have been done by withdrawing some spinal fluid from laboratory animals (and occasionally humans) in order to measure the amount of serotonin metabolite present. This has led to the strange rumor that taking MDMA will drain your spinal fluid. We have spoken to a number of doctors who have assured us that the only way spinal fluid could drain out of one's spinal column is through some kind of hole, either from a spinal tap or some kind of physical injury. It is MDMA research, therefore, not MDMA, that can drain your spinal fluid! What about back-aches? People often dance for long periods of time while on MDMA. This can lead to muscle aches, especially in the back, as dancing utilizes back muscles which normally don't get much exercize. Rumor #3: Ecstasy pills often contain heroin False. Thousands of pills have been analysed in laboratories by law enforcement agencies as well as harm reduction programs, and no pill has ever contained heroin. Many other adulterants have been found in ecstasy tablets, like speed, ephedrine, ketamine, and others. But never heroin. This is because heroin is more expensive than MDMA, and it would not be profitable for manufacturers or dealers to put heroin into ecstasy pills. What about "mashy" pills? Some ecstasy pills contain adulterants like Ketamine or MDE, which can make you feel stoned and have less energy. Also, taking too many stimulants can lead to a crash that makes you feel extremely tired and spacey. This "mashed out" feeling is not because there was heroin in your pills. ------------------ ~*P*L*U*R*~ Four Simple Words To Live By....

Gamma-hydroxybutyric acid (GHB) is an intriguing, naturally-occurring, 4-carbon compound with a structure similar to gamma-aminobutyric acid (GABA). It is described as a neurotransmitter and as a regulator of energy metabolism. First synthesized in 1960, GHB initially was investigated as an anesthetic due to its rapid induction of deep coma with only minor cardiovascular and respiratory depressant effects. Its lack of analgesia and tendency to cause seizurelike activity soon dampened enthusiasm for its use. Purported to act as a fat-burner and growth hormone promoter, GHB enjoyed a resurgence in the late 1980s as a food supplement for body builders and dieters. The withdrawal of L-tryptophan from the market, a supplement with similar purported effects, spurred GHB use. Also used as a hallucinogenic, euphoric, and sleep aid, it was easily obtained at health food stores, gyms, and mail order outlets. This newfound popularity coincided with a rising tide of GHB-related morbidity that soon caught the attention of regional poison control centers. The FDA subsequently prohibited the sale and manufacture of GHB in 1990. Since then, GHB has continued to enjoy a more clandestine popularity as an illicit drug, particularly in the Southeast and Western US. It currently is prevalent in the dance music scene (at raves and nightclubs) as an alternative to Ecstasy and amphetamines and is often used in conjunction with alcohol. It has been implicated, with Rohipnol, as a "date rape" drug. GHB generally comes in pure powder form or mixed with water. Its highly-concentrated, street form is available as a liquid in small plastic bottles, the size and shape of hotel shampoo bottles. The bottles generally cost only $10 and usually contain about 10 "hits." GHB goes by many street names, including grievous bodily harm, scoop, liquid ecstasy, cherry meth, growth hormone booster, liquid x and Georgia homeboy. GHB is readily manufactured from its precursor, gamma-butyrolactone (also known as 2(3h)-furanose dihydro or GBL). GBL is a solvent found in floor cleaning products, nail polish, and super glue removers. Saponification of the lactone with sodium hydroxide in the form of lye results in nearly quantitative conversion. However, this method is not without its drawbacks. There are several case reports of caustic alkali ingestion from undissolved lye. GBL also undergoes conversion into GHB in-vivo (by an unknown mechanism) and, accordingly, is associated with many of the same symptoms. GBL presently is readily purchased over the Internet and at health food stores under several brand names, including Fire Water, Renewtrient, Revivarant or Revivarant G, Blue Nitro or Blue Nitro Vitality, GH Revitalizer, Gamma G, and Remforce. Several states have caught on to this practice and have banned these products. The FDA has issued a warning and notice requesting manufacturers to issue a recall of GBL-containing products on January 21, 1999. On January 28, 1999, the FDA issued a warning to consumers not to purchase or use GBL products. A ban of this product is imminent. In an effort to skirt FDA regulation, several manufacturers have begun marketing 1,4 butanediol (BD), a chemical structurally similar and in many cases clinically indistinguishable from GHB. The FDA has declared BD a Class I Health Hazard - a potentially life-threatening drug. GHB’s unique attributes do have some legitimate uses. In Europe it is still used as an anesthetic, for alcohol and opiate addiction therapy, and for narcolepsy therapy. Only this last indication is recognized by the U.S. FDA, which allows its use on an experimental basis in narcolepsy trials. Pathophysiology: GHB is found naturally in the CNS, with the highest concentrations in the basal ganglia. GHB binding sites are present in the cortex, midbrain, substantia nigra, basal ganglia and, most predominantly, in the hippocampus, where it appears to mediate intrinsic neurons. It also is found in the peripheral blood and readily crosses the blood-brain and placental barriers. It is rapidly absorbed after ingestion; it takes 20-30 minutes to reach a maximal plasma concentration after the ingestion of a 12.5 mg/kg dose and increases to 30-60 minutes with a dose of 50 mg/kg. The elimination half-life is 27 minutes and proceeds in a dose-dependent, saturable manner. Elimination is via expired carbon dioxide. The pharmacokinetics of GHB in alcoholics are similar to that of nonalcoholics, although the frequency of serious side effects are less in the alcoholics, suggesting a cross-tolerance between alcohol and GHB. Although readily detected in the urine and serum by gas chromatographic-mass spectrometric techniques,traditional hospital toxicology assays typically do not include GHB. CNS GHB has a myriad of neurological effects. It binds to GABA-B receptors in the brain, inhibits noradrenaline release in the hypothalamus and mediates the release of an opiatelike substance in the striatum. It produces a biphasic dopamine response, increasing release at high doses and inhibiting its release at lower doses. True to its body-building claims, it does show an increase in growth hormone in rats and in one small human study. However, no study has ever demonstrated weight loss or increased muscle growth. Although GHB traditionally has been considered a potent epileptogenic drug and has been noted to cause epileptiform electroencephalographs (EEGs) in animals, human studies have failed to demonstrate EEG changes associated with use. It is thought that a reemergence syndrome characterized by myoclonic jerks of the face and extremities may have been mistaken for evidence of seizures. CNS depression is the hallmark of GHB use. An oral dose of 10 mg/kg produces short-term amnesia and hypotonia and 20-30 mg/kg produces drowsiness and sleep. After the ingestion of approximately 50-70 mg/kg, profound hypnosis and then deep coma rapidly ensue. GHB rapidly initiates delta wave and REM sleep and produces moderate amnesia but does not produce analgesia or muscle relaxation. It decreases cerebral glucose metabolism and increases cerebral blood flow, yet reduces intracranial pressure. Myoclonic jerks and respiratory depression accompany the descent into anesthesia. A Glasgow Coma Score (GCS) of 3 is not uncommon. One peculiar characteristic of GHB toxicity, despite such profound CNS and respiratory depression, is that patients often demonstrate extreme combativeness and agitation. Several physicians have been surprised when the individual suddenly awakens during an intubation attempt. The coma usually lasts from 1-4 hours and spontaneously resolves. Those patients intubated for respiratory depression typically have a longer time to recovery, but extubation within 8-10 hours is common; extubation in the ED has been described. The resolution is characteristically rapid and usually accompanied by myoclonic jerks and agitation. Cardiovascular (CV) GHB has been noted to cause bradycardia, decreased systemic vascular resistance, and hypotension. Pain or atropine rapidly causes an increase in heart rate and blood pressure. Studies of GHB infusion in hypovolemic shock have demonstrated an increase in mean arterial pressure and cardiac output when compared to a normal saline infusion. GHB also has been noted to have antidysrhythmic properties. Other effects One particularly fascinating property of GHB is its ability to prevent cell damage. Several studies have shown a reduction in oxygen requirements and a subsequent reduction in hypoxic cell damage. The exact mechanism of this tissue protective effect is unknown; however, several effects have been noted, including reductions in lipid peroxidation, lipolysis, free radical production, and a dampening of the inflammatory response. It has also been shown to be protective in radiation exposure. Benefit has been noted in a wide range of organ systems and in dozens of conditions, including hemorrhagic shock, sepsis, CVA, mesenteric ischemia, organ transplant, and MI. It is this last entity that has received the greatest attention. GHB has been found consistently to improve outcomes, including mortality, in several animal MI trials. However, its benefit in human MI trials has not yet been confirmed. The combination of its cell-protective and anesthetic properties has made GHB a candidate in certain types of surgery. Predominantly European literature has described its use in emergency laparotomy for hemorrhagic shock, aortic surgery, operations involving heart bypass, cataract surgery, labor, and many others. Its shortcomings as an anesthetic have led to a decline in its use in favor of more effective anesthetics. CNS Neurologic effects can range from mild (eg, nystagmus, dizziness, ataxia) to severe (eg, coma, respiratory failure, apnea, death). Typically, the patient experiences a short period of euphoria followed by a rapid and profound decline in the level of consciousness. Seizurelike activity and myoclonus commonly are reported. Pulmonary Respiratory depression Decreased respiratory rate Apnea Gastrointestinal (GI) Nausea Vomiting Physical: CNS The typical GHB ingestion presents with a profoundly depressed level of consciousness. A recent study noted that two-thirds of patients present with a GCS of less than 9, with a full one-third presenting with a GCS of 3. One unique aspect of GHB-induced coma is sporadic violent agitation, usually accompanying stimuli such as intubation attempts. The coma typically resolves completely and rapidly after a period of 1-4 hours. Seizurelike movements and myoclonus are common, particularly when descending into unconsciousness or on reemergence. Cardiovascular (CV) Approximately 36% of ingestions are accompanied by bradycardia. The bradycardia appears to be related to the depressed level of consciousness and is easily reversed with atropine. Hypotension accompanies about 10% of GHB ingestions. This usually is associated with coingestion of GHB and alcohol or another drug and usually is mild. If not readily resolved by stimulation or atropine administration, another ingestion or coingestion must be considered. Pulmonary Respiratory depression, evidenced by bradypnea to frank apnea, often occurs. Decreased breath sounds and rales may indicate aspiration. Gastrointestinal (GI) Nausea and vomiting are common with GHB ingestion and often accompany reemergence from unconsciousness. Prehospital Care: Prehospital personnel can contribute a great deal to an accurate diagnosis by obtaining a history of ingestion from the patient, friends, and bystanders and securing evidence of potential GHB ingestion (small shampoo bottles). Prehospital care primarily is supportive. Attention should be paid first and foremost to airway management and breathing. Oxygen should be administered and a patent airway established. Aspiration and cervical spine precautions should be observed. IV access should be established if possible. Naloxone should be considered for all comatose patients with any respiratory compromise. This may not be beneficial for GHB ingestions but is not considered to be detrimental. Intubation in the field should be reserved for severe, refractory, respiratory compromise and attempted only by experienced personnel when the airway is at risk. Emergency Department Care: ED management of GHB overdose is primarily supportive. Airway patency and aspiration precautions are of paramount importance. Consideration should be given to gastric lavage and/or activated charcoal if coingestion is suspected. Cardiac monitoring is indicated, given the relative frequency with which arrhythmias and conduction deficits have been noted. These interventions are of a limited benefit in isolated GHB ingestions due to the small amounts usually ingested (from one-fourth of a teaspoon to 4 tablespoons) and because of the rapidity of absorption (usually 10-15 minutes). If gastric lavage is deemed appropriate, the patient should be intubated prior to lavage to prevent potential aspiration. Symptomatic bradycardia that is unresponsive to stimulation should be treated with atropine. Given the usually benign course and rapid recovery of uncomplicated GHB intoxications, a conservative approach to intubation has been suggested. However, certain conditions necessitate intubation. If the history of GHB ingestion is unreliable in the presence of severe respiratory depression, hypoxia, or in preparation for lavage, rapid-sequence intubation should be performed. A sedative usually is not required, but neuromuscular blockade is recommended to avert the paradoxical agitation common with GHB. The reversal of GHB-induced CNS depression is a controversial issue. Although physostigmine has been shown to reverse sedation in clinical trials, most experts presently believe that the risks of its use (eg, bradycardia, asystole, seizures) outweigh the benefits in most GHB ingestions and that it should be reserved for selected cases, if used at all. ------------------ ~*P*L*U*R*~ Four Simple Words To Live By....

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