e-tarded

http://www.pillreports.com/viewpill.php3?sub=1&area=1&id=1395 Thats the only thing I have heard on them, but these report is from boston. ------------------ ~*P*L*U*R*~ Four Simple Words To Live By....

Thanks everyone ! I just want to make sure that everyone gets the correct information when they are inquiring about certain drugs. Can't stop people from using so might as well edumacate them. ------------------ ~*P*L*U*R*~ Four Simple Words To Live By....

Yes they are Sominex, people have been selling for a while now as ecstasy. My advice don't buy them, and know your dealer ------------------ ~*P*L*U*R*~ Four Simple Words To Live By....

http://bbs.clubplanet.com/ubb/Forum19/HTML/000224.html This thread should answer most of your questions on 5-htp. Some people say that smoking a little pot on the comedown brings them right back up again. Other then that I really don't know of anything that would bring you back up. ------------------ ~*P*L*U*R*~ Four Simple Words To Live By.... [This message has been edited by e-tarded (edited 10-20-2000).] [This message has been edited by e-tarded (edited 10-20-2000).]

http://www.pillreports.com/test/main.html go there and click on the link at the left for the south west and then type JJ in the search, there were a couple of entries ------------------ ~*P*L*U*R*~ Four Simple Words To Live By....

The main drug of interest here is DMT. DMT causes intense visual hallucinations and other psychedelic phenomena. It has been mostly encountered in the technologically developed world as a pink (cool) crystalline powder, which was smoked or injected. This caused nearly instant, brief, and intense trips. Peaks occur immediately and last around 10 minutes, with another 30 or so minutes of mild effects. 5-Me-DMT is a close relative of DMT. 5-Me-DMT is reported to be about 4 times as potent as DMT and is often regarded as preferable to DMT. 5-Me-DMT has most of the psychedelic qualities as DMT but does not cause visual hallucinations. It follows the same time course. Bufotenine (5-OH-DMT) is another DMT relative. This compound is vaguely referred to as "noxious" by Jonathan Ott. Apparently 10mg of pure 5-OH-DMT injected is enough to cause "dramatic circulatory crises." There appears to be debate over the psychedelic qualities of bufotenine. However, McLeod & Sitaram, Shulgin, and Fabins & Hawkings all report the presence of psychotomimetic effects. Bufotenine causes anxiety, circulatory distress, skin flushing, and percieved color distortions. Injected doses of 16 mg (over 3 min. IV drip) have been reported. At this dose, the symptoms of mild skin flushing to extreme purple cast appear. Subjects also report a great deal of psychological distress and fear at this dose. Doses of 8 mg produce mild skin flushing and increased anxiety. Doses of 2-4 mg of bufotenine do not produce hallucinogenic effects. The above discussed negative side effects at 16 mg last for approximately 10 minutes. Other side effects reported are sweating, nausea, yellowed vision, and perception of colored spots. So it appears that bufotenine is a nasty drug to be avoided, Not only does it tend to induce panic, it also appears to have the potential for a fatal overdose, although no case studies to this effect have been found for humans. Other DMT relatives exist, but are not of great importance here. Some are, however, psychoactive. DMT in the past has only been used by smoking or injecting. Oral use was completely ineffective. It turns out that ancient tribal cultures solved that problem aeons ago, and have been dosing up the whole time. Now THAT'S technology. By combining plants that contained MAOIs (monoamine oxidase inhibitors) and other plants containing DMT, the DMT would become active orally. MAOIs block the destruction of DMT in the digestive track and in the brain. So, with MAOIs, DMT can be eaten and also becomes more potent. MAOIs also increase the potency of smoked DMT. The effect of the orally administered DMT with MOAI lengthens in time and decreases in intensity. Typical plateau period is 10-40 minutes, after a hour delay with low buzz for an hour after the plateau. Great for people who don't like the time investment of most psychedelics. MAOIs are reported to work for psilocybin ('shrooms) and mescaline. Subjective reports are that MAOIs double their potency. I hypothesize that it will also potentiate lysergic acid (woodrose and morning-glories). The effect of MAOIs on LSD appears debated in the literature. Some report no effect, others report significant potentiation. Some have very enthusiastically insisted that MAOIs double or triple the potency of LSD. The ancient solution mentioned above is the ayahuasca potion. This potion has been produced, in one form and name or another, throughout Central America and South America for quite some time. The most commonly referred to potion is made by combining ayahuasca, a jungle vine, and yopo, leaves from a small bush. The ayahuasca provides the MAOIs and the yopo provides DMT. Occasional, mescaline bearing cacti are added. The potion was usually used ceremonial for healing, divining, and teaching. Often there are reports of blue glows and jaguars, a holy animal in many endogenous South American cultures. I have been told that McKenna reports that eskimos given an ayahuasca type potion reported seeing large cats, which, of course, are not arctic animals. I however, have found (from admittedly little reading) McKenna's work to be questionable and less than scientific. However, his reports often do parallel others. MAOIs are a class of drugs that all do the same thing: prevent the destruction of monoamines (like DMT). One MAOI is harmaline. Harmaline is easily obtained. Syrian rue is an excellent source. Three grams of seed, extracted with the DMT or eaten alone should suffice. Harmaline containing plants can also be smoked for a more rapid onset. Doses over three grams do not add more potency. Caution should be used with MAOIs. Large doses are hallucinogenic in and of themselves. Large doses are unpleasant and sometimes fatal. The remainder of this section is information cited directly from "Legal Highs" by Twentieth Century Alchemists. They just did a better job than I could do. I have seen this posted around the net and is highly recommended. This information pertains to precautions for MAO inhibitors. READ THEM, KNOW THEM ! You will notice several discrepancies: Legal Highs says that MAOI and mescaline combinations are very dangerous, which contradicts Ott's later reports on the subject. Legal Highs suggests that 5- Me-DMT is a MAOI, which I cannot substantiate. This would render P. tuberosa psychoactive alone. I cannot substantiate this either. DANGEROUS COMBINATIONS READ THIS!! VERY IMPORTANT. IGNORING THIS COULD LEAD TO SERIOUS MEDICAL PROBLEMS (like death...) Unless one is very experienced in pharmacology it is unwise to experiment with combinations of drugs. Even when using a single drug, thought should be given to all substances, both food and drug, which have been taken recently. Most primitive people fast or at least abstain from certain substances for several days prior to taking a sacrament. Substances most universally avoided are alcohol, coffee, meat, fat and salt. Some drugs potentiate others. For example, atropine will increase the potency of mescaline, harmine, cannabis and opiates. Many of the substances discussed in this book are MAO inhibitors. MAO (monoamine oxidase) is an enzyme produced in the body which breaks down amines and renders them harmless and ineffective. A MAO inhibitors interfere with the protective enzyme and leaves the body vulnerable to these amines. A common substance such as tyramine, which is usually metabolized with little or no pharmacological effect, may become dangerous in the presence of an MAO inhibitor and cause headache, stiff neck, cardiovascular difficulties, and even death. MAO inhibitors may intensify and prolong the effects of other drugs (CNS depressants, narcotic analgesics, anticholinergics, dibenzazepine antidepressants, etc.) by interfering with their metabolism. In the presence of an MAO inhibitor many substances which are ordinarily non-active because of their swift metabolism may become potent psychoactive drugs. The phenomenon may create a new series of mind alterants. However, because of the complex and precarious variables involved, it is risky and foolish for anyone to experiment with these possibilities on the non-professional level. The most commonly used MAO inhibitors include hydrazines such as iproniazid, Marsilid, Marplan, Niamid, Nardil, Catron; also non-hydrazines such as propargylamines, cyclopropylamines, aminopyrazine derivatives, indolealkylamines, and carbolines. MAO-inhibiting materials discussed in this book include yohimbine, various tryptamines, especially 5-MeO-DMT and the methyltryptamines, and the various harmala alkaloids. The latter are especially potent inhibitors but, like yohimbine and the trytamines, are short)lasting in action (30 minutes to several hours). Some of the commercial MAO inhibitors listed above are effective for several days to several weeks. Among the materials which may be dangerous in combination with MAO inhibitors are sedatives, tranquilizers, antihistamines, narcotics and alcohol ) any of which can cause hypotensive crisis (severe blood pressure drop); and amphetamines (even diet pills), mescaline, asarone, nutmeg (active doses), macromerine, ephedrine, oils of dill, parsley or wild fennel, beer, wine, cocoa, aged cheese and other tyrosine)containing foods (tyrosine is converted into tyramine by bacteria in the bowel) ) any of which can cause hypertensive crises (severe blood pressure rise). SYRIAN RUE - Peganum harmala. Family Zygophyllaceae (Caltrop family.) Material: Seeds of woody perennial native to Middle East. (Roots also active but seldom used.) Usage: 1 oz. seeds are thoroughly chewed and swallowed. Most effective when combined with other psychotropic materials, especially those containing tropanes. Active Constituents: Harmine, harmaline and harmalol. Effects and Contraindications: Hallucinogen; see harmine. HARMINE - 7-methoxy-1-methyl-9H-pyrido (3,4- indole. Material: Indole-based alkaloid found in several plants including Banisteriopsis caapi (from which the South American hallucinogenic brew yage is prepared), Peganum harmala (Syrian rue), Zygophyllum fabago, and Passiflora incarnata (Passion flower). Usage: 25-750 mg harmine (see effects) is ingested on an empty stomach. In its hydrochloride form harmine may be snuffed (20-200 mg). Injection dosages are smaller: SC 40-70 mg; IV 10-30 mg. Absorbed poorly through stomach. Effects: Harmine and related alkaloids are serotonin antagonists, hallucinogens, CNS stimulants, and short-term MAO inhibitors (100 x MAO inhibition of iproniazid but lasting only several hours). Small doses (25-50 mg) act as mild and therapeutic cerebral stimulant, sometimes producing drowsy or dreamy state for 1-2 hours. Larger doses up to 750 mg may have hallucinogenic effects, the intensity of which varies widely with the individual. Doses of 25-250 mg taken with LSD or psilocybin alter the quality of the experience of the latter. Telepathic experience have been reported with this combination. Contraindications: Harmine is a brief MAO inhibitor. It should not be used with alcohol and certain foods and drugs (see list at end of file). When snuffed harmine may be slightly irritating to nasal passages. Large amounts may depress CNS. Since individual sensitivity varies this may occur with 250-750 mg. Notes on other harmala alkaloids: Different harmala alkaloids vary in potency. The equivalent of 100 mg harmine is 50 mg harmaline, 35 mg tetrahydraharman, 25 mg harmalol or harmol, 4 mg methoxyharmalan. Harmal alkaloids are synergistic (mutually potentiating) and are therefore most effective when combined in an appropriate balance. Tropines (belladonna alkaloids) also potentiate harmals. Harmol and harmalol (phenols) in overdoses can cause progressive CNS paralysis. THE PLANTS As reports show, there is a great variation in the alkaloid content of phalaris plants. Within phalaris tuberosa, one study found that total alkaloid levels ranged from 5 to 178 mg/ 100g dry plant matter. Thus 100g of phalaris tuberosa could contain anywhere from 1/10 of a trip to 4 trips. The trick is to find out (as I have) how to maximize the alkaloid levels. CAUTION: because alkaloid levels vary so drastically, you should always determine the potency of any product by starting with low doses. Most discussion so far on the internet has centered on Phalaris Arundinacae. However, P. tuberosa also has high alkaloid levels. Table one reports alkaloid levels of several plants. As you can see in the table, Phalaris Tuberosa does not have particularly high DMT levels, but it does have quite a bit of 5*Me-DMT. It appears that the alkaloid content of Phalaris Tuberosa is such that one dose of DMT also includes a dose of 5- Me-DMT. So Phalaris Tuberosa is actually just as strong as the other plants containing minimal 5-Me-DMT. The DMT in Phalaris Tuberosa should contribute visual hallucinations to the trip. The bad news for Phalaris Tuberosa is that it contains bufotenine. But even a large dose of Phalaris Tuberosa (100g containing 100mg DMT and 22mg 5-Me-DMT, a full dose of each) contains 5g of 5-OH-DMT, one half the dose given in the study cited in Ott. Most phalaris users report that they ingest or smoke the product. Such an administration route is less sudden and "shocking" than injection. Perhaps this will temper the effects of 5-OH-DMT. Caution should still be used with Phalaris Tuberosa. Phalaris arundinacae and desmanthus illinoesis, containing no 5-OH-DMT, appear to be safer, but lacking in 5- Me*DMT. The phalaris plants are tall grasses. They grow well in Australia, around the Mediterranean sea, and all over America. They grow in clumps up to 7 feet tall. Desmanthus Illinoisis is also called "Illinois Bundlweed." It's a bush that grows, obviously, in the Illinois area. Psychotria species are the yopo used in South American ayahuasca potions. Table 1 : ALKALOIDS REPORTED AS mg PER 100g RAW DRIED PLANT, AND AS PERCENT OF TOTAL PLANT SOURCE WEIGHT. P. Tuberosa: DMT 100 mg .100% 5-Me-DMT 22 mg .022% 5-OH-DMT 5 mg .005% P. Tuberosa (net gossip) DMT 170 mg .170% 5-Me-DMT 60 mg .060% P. Arundinacea (net gossip) DMT 60 mg .060% Desmanthus Illinoisis (root, from Ott) DMT 200 mg .200% Desmanthus Illinoisis (root bark only, from Ott) DMT 340 mg .340% Psychotria species (averaged, from Ott) DMT 200 mg .200% Unfortunately, sheep herders in Australian desired strains of low alkaloid phalaris plants. So now most commercially available phalaris are probably weak. Phalaris can be obtained through mail order herb companies, some of who advertise high alkaloid plants. Because I do not wish to associate these fine suppliers names' with an article on how to prepare a drug, I will not provide names or addresses. Just ask around on the net. SHEEP DEATH I put this as a separate section to highlight it's significance. Remember, if you try these drugs, you are using something that kills sheep. The toxic syndrome is called "phalaris staggers." It is manifested by apparent dizziness, staggering, and tremors, sometimes resulting in death. The syndrome affects sheep that have eaten high alkaloid phalaris. On autopsy, after naturally and experimentally induced phalaris staggers in sheep, portions of the lower brain are seen to be damaged and, oddly enough, tinted blue. The responsible agents are the alkaloids contained in the various phalaris species. There are whispered rumors that phalaris also contain beta carbolines, a type of MAOI. If so,it may be that sheep, in eating large quantities of phalaris, also obtain a dose of MAOI, making the already large dose (pounds of phalaris could easily be eaten by a sheep or cow in a day), of DMT active. However, MAOIs are not required for sheep death. Studies show that controlled injections of pure DMT, at human recreational doses, kill sheep. Why sheep and humans respond differently to DMT is still an open question here. It may be that it is not an important question, but the possibility of human death on phalaris still looms. DOSES There seems to be a variety of dosages (of pure drug) suggested in the literature. Table 2 lists some of the reported dosage levels. It should be noted that levels that are listed in table two are within the range reported to cause "phalaris staggers" in sheep and cause them to die. Table 2 REPORTED DOSES Jonathan Ott Net Lore Peter Gessner Bufotenine Literature DMT 1 mg / kg 60 mg --- --- 5-Me-DMT 0.25 mg / kg 5 mg 5-10 mg --- 5-OH-DMT None! --- --- 16 mg NOTE: These 'reported doses' are non-lethal dosages given to humans in the literature as referenced. THIS AUTHOR MAKES NO RECOMMENDATIONS! The "mg/kg" means one mg of drug for every kg of body weight. Using Ott's levels, approximately .5g of Phalaris Tuberosa per kilogram body weight should yield one dose of 50% DMT and 50% 5-Me-DMT. Using the net lore, 25g of Phalaris Tuberosa would yield 1 dose of 5-Me-DMT with less than 1/2 dose of DMT: still a fairly strong dose when totaled. These doses are based on plants that have not had their alkaloid levels boosted. Remember, there is WIDE variation of alkaloid levels. One week a plant may yield a minimal dose, the next week it may blow your mind away. BOOSTING ALKALOIDS The scientific literature, intended to solve the problem of "Phalaris staggers" in sheep has revealed the growth parameters that will optimize the alkaloid content of Phalaris Tuberosa It is not known if the information applies to other Phalaris plants. It is my own personal feeling that it will. The nutrient solutions suggested for phalaris resembles in some respects other formulas designed to boost tryptamine levels in morning glories, woodrose, and peyote. This discussion is based on the works of Oram & Williams, 1967; Baxtor & Slaytor, 1972; and Moore, Williams & Joice, 1967. The following factors have been shown to influence alkaloid levels in phalaris tuberosa: shading, nitrogen uptake, and temperature. It seems that shading causes increased (yes, increased) levels of alkaloids in Phalaris Tuberosa. The optimal amount of shading appears to be 15-25% the strength of full sunlight. Unfortunately, this also causes a significant decrease in growth. Enough plant mass is lost to almost make up for the alkaloid gains. However, careful growing, could maximize mass and alkaloids. Increasing temperatures to 21C for day and 16C for night not only caused an increase in the proportion of alkaloids per weight, but it also increased the growth rate of the plant. Temperature regimes of 9c/4c and 15c/10c resulted in much less weight and fewer alkaloids. The data suggest that even higher temperatures may be better. Increased nitrogen supply in the plant's nutrients increased the plant alkaloids. Nitrogen content of solutions were 0.05, 0.5, and 5.0 times the nitrogen levels of "Hoagland's nutrient solution (whatever that is). Just go with the principle "more is good." Day length does NOT influence alkaloid levels. Unfortunately, the data provided by the article do not specify how much the total increase in alkaloids were. However, examination of the data suggest the alkaloid content more than doubled as a result of the boosting treatments. Interestingly, the levels of 5-OH-DMT DID NOT INCREASE SIGNIFICANTLY!!!. Thus boosting the alkaloid levels appears to also decrease the relative concentration of this problematic alkaloid! Precursors to DMT, 5-Me-DMT, and 5-OH-DMT can be fed directly to the plants. No one precursor will boost one plant alkaloid level; all alkaloid levels rise regardless of the precursor. The precursors are: tryptophan (NH2-Co2), tryptamine (NH2), and MMT (NHMe). I am unable to translate exactly what the feeding levels were from this study, but again: "More is good." Unfortunately, I believe all of these substances are regulated. It has been whispered, in the dark and misty places in which people whisper these kinds of things, that maturity also influences that alkaloid levels of phalaris species. The maximum alkaloid levels were found during spring re-growth and in the seed shedding phase. At these times, alkaloids have been found to triple. Another factor influencing alkaloid levels is genetic strain. Again, low alkaloid phalaris plants have been developed through breeding. Great for the sheep, bad for trip seeking humans. The seed you'll find available commercially will be low grade. Try to obtain seed from herb companies that cater to the psychedelic community. INPLICATIONS FOR GROWING To make the most of the light intensity factor, one might grow the plant in full sunlight/growlight until a few weeks before harvest, then reduce the light or shade the plant. I see no reason why alkaloid levels would not peak during this time. However, this technique would provide more mature phalaris, rather than the potent young stuff. With this method, one would have a large quantity of moderately potent phalaris. If one could shade outside plants, with plastic or fabric for example, this would make a great outdoor technique. If one were going to perform a chemical extraction, this would probably make the effort worthwhile by maximizing overall yield. Perhaps the plant could be kept in a re-growth phase by frequent clipping, like a lawn. In this case, one might grow a patch of phalaris in a wide shallow pot under grow lights. It should be allowed to grow up healthy and fill the pot under light that will maximize growth. Reduce light and harvest by clipping the plant down. Allowing the plant to grow large and healthy ensures that a good root structure will be built and will maximize re-growth. Turn light intensity up and allow the plant to put on new growth. After a short period of regrowth, reduce light, then clip. Repeat as desired. Because day length does not seem to influence alkaloids, the light/dark schedule should be set to maximize growth. I have no idea what ratio is needed. Of course the plants should be watered with a strong nitrogen fertilizer. Remember, the research shows that the nitrogen, shading and temperature alkaloid boosts DO NOT increase 5-OH-DMT levels, resulting in a cleaner DMT / 5-Me-DMT experience! PREPARATION The simplest way to prepare phalaris is to use a wheat juice extractor. This device presses the juice out of the leaves and stalks. Of course dosage becomes harder to gauge. One report on the internet suggested 1 teaspoon as a good dose and 2 teaspoons as an extreme overdose, resulting in one freaky trip. It appears likely, and has been suggested in some reports, that alkaloid levels drop when the plant dries. By taking the fresh sap, alkaloid levels should be maximized. Extraction of alkaloids can be performed on dry plant materials (based on Dr. Jonathan Ott's reports). An acid is used to exact the alkaloids of both the DMT and the MAOI containing plants. A solution of 1/3 lemon juice and 2/3 water is used to quickly boil the plant material. Pour off and repeat two more times. The dose is easier to determine because it is based on dry plant material. Three grams of Syrian rue per dose of DMT provides the required MAOI. Again, increasing the dosage of Syrian rue beyond 3g does not increase the potency of the DMT significantly more than 3g. Important note: I have always seen references to staying away from aluminum for all sorts of chemical extractions and procedures. I believe that this is because aluminum bonds with a lot of contaminants that can then find their way into the brew (just think about having to clean calcium deposits off of your aluminum coffee maker with vinegar). Always use nice glass (pyrex is much less likely to break) or stainless steel. The liquid form can serve as an oral dose, or it can be evaporated GENTLY AND SLOWLY to a goo. This goo can then be smoked for a very intense dose of DMT. Or the goo can be saved for oral doses. I recommend refrigeration. I have no information as to how to best store phalaris products to prevent spoilage and loss of potency. There are a variety of chemical extraction techniques floating around on the net. I have little ability in evaluating the accuracy and safety of these techniques. I prefer to speak on subjects in which I have some faith in my knowledge. In any case, it does not seem likely that for small time experimenters, chemical reductions to pure alkaloids will be necessary. The above methods should work. Taken from www.erowid.org ------------------ ~*P*L*U*R*~ Four Simple Words To Live By....

Yeah crank is basically crystal. Its just another slang term that is used primarily in the midwest ------------------ ~*P*L*U*R*~ Four Simple Words To Live By....

Ez-Test is definitely the way to go, also checking out www.pillreports.com or www.dancesafe.org. However on a side note PMA doesn't cause a color change when doing a reagents testing of a pill. ------------------ ~*P*L*U*R*~ Four Simple Words To Live By....

Thanks ------------------ ~*P*L*U*R*~ Four Simple Words To Live By....

Since today. ------------------ ~*P*L*U*R*~ Four Simple Words To Live By....

yeah i agree with anthonyp on this one. ------------------ ~*P*L*U*R*~ Four Simple Words To Live By....

damn if i am not getting the pills, then I dont wanna be in your shoes ------------------ ~*P*L*U*R*~ Four Simple Words To Live By....

I would love to be in your shoes right now. mda and mdma make the perfect combo. I would drop the mdma pill first then the mda. There are no complications from mixing the two. ------------------ ~*P*L*U*R*~ Four Simple Words To Live By....

Well I talked to a few friends and they have tried them and said they were pretty good. They are all from the east coast area. Hopefully this helps a little. If you are worrying bout if they are real i would say buy an ez-test kit from dancesafe.org ------------------ ~*P*L*U*R*~ Four Simple Words To Live By....

A safe amount of water to drink while under the influences of mdma, is one 8oz bottle an hr. You woukd even be better off if you can drink a sports drink. Regarding your question, drinking a ton of water before dropping would not cause the drug to be flushed out of your system. ------------------ ~*P*L*U*R*~ Four Simple Words To Live By....

Substance Detection Time Amphetamines 2-5 days Barbituates (Short-Acting) 2 days Barbituates (Long-Acting) 3-4 weeks Benzodiazepines 7-10 days Cannabinoids (THC, Marijuana) 14-60 days Clenbuterol 4-6 days Cocaine 1-4 days Codeine 5-7 days Euphorics (Ecstacy, Shrooms) 5-7 days Ketamine (Special K) 5-7 days LSD 7-10 days Methadone 5-7 days Nicotine (Cigarettes) 4-10 days Opiates 5-7 days Peptide hormones undetectable Phencyclidine (PCP) 2-4 days Phenobarbital 10-20 days Propoxyphene 6 hours to 2 days Steroids (anabolic oral) 14-28 days Steroids (anabolic parenterally) 1-3 months ------------------ ~*P*L*U*R*~ Four Simple Words To Live By....

try www.pillreports.com ------------------ ~*P*L*U*R*~ Four Simple Words To Live By....

Neurotoxicity For an explicit definition of neurotixicity and its legal implications, refer to the site listed below. http://www.epa.gov/ncea/pdfs/nurotox.pdf To begin, animal studies show that, the list below, accurately defines the process in which neurotoxicity is allowed to manifest into a serious problem. (Credit to Deep) 1) MDMA amps up seratonin and dopamine levels 2) Seratonin runs out 3) Dopamine goes where seratonin normally would 4)Altered dopamine molocules cause damage to nerves. To begin, MAPS has done extensive research in the affects of neurotoxicity and their argument stands up to studies performed and released by the Journal of Neuroscience. "MAPS" MDMA is no exception to the rule that every drug has serious side effects in some users. Reports indicate that a small number of the millions of people who have taken MDMA over the last several decades have suffered negative consequences. Some people may be predisposed to react unfavorably to typical amounts of MDMA while heavy users may be placing themselves at special risk. MDMA increases blood pressure, posing a risk to people with preexisting heart conditions. MDMA can also increase body temperature which, in combination with hot environments, exhausting physical exercise (prolonged dancing) and lack of fluids has been linked in very rare cases to death from heat exhaustion. MDMA's psychological effects have been occasionally associated with acute anxiety, panic and depression and are substantially context-dependent. Several cases of longer-lasting effects have been identified. While no causal link has been established connecting serotonin reductions to any negative consequences, the potential risks as well as the benefits of MDMA must be carefully weighed before any decisions can be made concerning appropriate uses. We owe our gratitude to Dr. Ricaurte and associates for conducting this latest study and to the National Institute on Drug Abuse (NIDA) for funding it. Now that this new study is completed, each of us entitled to make our own risk assessment after a careful look at the data. Below is my risk assessment, made with what I hope is a healthy dose of common sense. The Latest Scientific Study In August 1995, the Journal of Neuroscience published a scientific study by Fischer et al. investigating the regrowth of rat and primate brain neurons previously exposed to extremely large doses of MDMA. The study was designed to determine whether there was long-term restoration of normal levels of serotonin in those brain regions in which serotonin levels were previously reduced as a result of exposure to very large amounts of MDMA. Also examined was whether the regrowth of serotonin nerve terminals (reinnervation) restored the original brain structures. The study concluded that "in some rats and most monkeys, there is a lasting reorganization of ascending 5-HT [serotonin] axon projections following severe MDMA injury. In particular, while some projections (e.g. those to the neocortex) fail to recover for up to 18 months after drug administration, others (e.g. projections to the basal forebrain) recover fully, sometimes in excess." The authors of the paper noted that the "aberrant serotonergic brain reinnervation" had no known functional consequences, but that "if 5-HT [serotonin] function declines with age, MDMA-exposed individuals could be at increased risk for developing age-related cognitive impairment."(2) The Media Coverage The results of the study were reported in newspapers all across the United States and Europe. The reports began with an article in the August 15, 1995 New York Times Science Section incorrectly stating that the animals were given "recreational doses of MDMA - the amounts taken by many young people." In terms of human use, Dr. Ricaurte was cited as stating that "people could probably take normal amounts of MDMA three or four times a year without noticing any neuropsychiatric problems but people who took seven or eight doses a night could be inviting problems." Published at the same time, but with a decidedly more alarming spin, was a report by the Associated Press (AP) wire service in which Dr. Ricaurte was quoted (he feels misquoted) as stating simplistically that "Results suggest that people who have used (Ecstasy) in the past have some kind of (brain) damage." To emphasize the point, the article quoted Dr. Robert Daroff, chief of staff at University Hospitals in Cleveland and editor-in-chief of the journal Neurology, as saying that "It makes you feel good, but you are going to probably get hurt." The only counterpoint to these reports that I'm aware of was a letter to the editor that I co-wrote with Neal Goldsmith, Ph.D., published in the August 24, 1995 New York Times. We pointed out that the doses used in Dr. Ricaurte's study were roughly 45 times larger than the typical human dose, and that MDMA had been used "in therapeutic, sacramental and recreational contexts for over 20 years by hundreds of thousands of people without evidence of harmful neurotoxic effects on appetite, sleep, mood, impulsiveness or other neurological functions." On August 31, 1995 another story about the study was published in the British New Scientist magazine, and the London branch of the Reuters News Service distributed a story that was widely disseminated on the Internet. In both these stories, Dr. Ricaurte was quoted as stating, "If there is a margin of safety, it is not a large margin." On September 2, 1995, yet another letter to the editor was published in the New York Times, this one by Richard A. Friedman, MD, Assistant Professor of Psychiatry, NY Hospital-Cornell Medical Center. He accused Dr. Goldsmith and me of entertaining ideas that were "dangerously naive and without scientific merit." He went on to assert that reports that MDMA had therapeutic benefits were pure speculation because "there are no long-term scientific studies of the effects of MDMA in humans," and that "lack of evidence of MDMA's possible dangers is by no means proof of its safety." Of course, Dr. Friedman was correct to assert that MDMA has not been proven safe; such a proposition can never be proven, only disproven. Furthermore, Dr. Friedman makes the valuable observation that drugs sold as MDMA "on the street" risk being contaminated. This risk of contamination complicates the question of "MDMA neurotoxicity." (The article then goes on to state more elaborately the arguments suggested, they came to this conclusion) Tentative Conclusion As with any substance, some people are likely to be particularly sensitive to relatively small amounts of MDMA. Other people take unusually large amounts, especially in recreational contexts. It would therefore not be surprising if some people took enough MDMA to cause long-term reductions in their levels of serotonin in some brain regions. What would be surprising is if these serotonin reductions are eventually shown to have significant harmful functional or behavioral effects. Such changes, if they do occur, could as easily be beneficial as harmful, especially considering the fact that many people report long-term benefits resulting from their use of MDMA. Over the last twenty years, millions of people have tried MDMA. This use of MDMA, though not conducted in the context of a scientifically controlled experiment, does provide an opportunity for a very large epidemiological study. Similarly, over fifty million people have tried a prescription drug called fenfluramine, a diet aid prescribed for daily use for months or years at a time that causes the same kind of neurotoxicity in animals as does MDMA.(9,10) The absence of a single confirmed case of functional or behavioral consequences related to serotonin neurotoxicity as a result of the use of fenfluramine(11) or MDMA does not mean that these drugs are without neurotoxic consequences. Appropriate epidemiological studies have not yet been conducted. Nevertheless, the lack of evidence of neurotoxic damage after such an enormous population of people has been exposed to these drugs certainly suggests that if any neurotoxicity-related problems have resulted, they are subtle and rare. It does seem possible that some physiological mechanism may partially explain the diminishing returns that many people report from continued use of MDMA. This is a negative consequence only to the extent that the MDMA experience is considered beneficial. After reviewing the new data reported by Fisher et al., I remain of the opinion that the risk of MDMA neurotoxicity is of no practical significance when typical or even somewhat larger doses of MDMA are used on an infrequent basis in therapeutic, sacramental or recreational contexts by people with normal brain function. Of course, I don't know this for sure, and neither does anyone else. I do know or have heard about many people who have used MDMA hundreds of times and seem unharmed and even helped by their use. As a result, I think that Dr. Ricaurte is being conservative when he states that "people could probably take normal amounts of MDMA three or four times a year without noticing any neuropsychiatric problems." While there is evidence that the neurotoxicity of MDMA can be blocked by the co-administration of Prozac or other selective-serotonin reuptake inhibitors (SSRIs) (12, 13) and that such drugs do not alter the MDMA experience in some people, (14) such protective measures do not seem to me to be necessary in normal use. Such measures might possibly be worth the trouble when exposure approaches seven or eight doses a night, a level which Dr. Ricaurte stated "could be inviting problems." Ironically, one could argue that MDMA neurotoxicity research in humans, with its spinal taps and injections of radioactive substances, is more dangerous than MDMA itself. Nevertheless, it is crucial that MDMA neurotoxicity research continue, and also research into the beneficial therapeutic uses of MDMA, so that the risks and benefits of MDMA can be accurately balanced. " -- Endnote Now, IMHO, the arguments on both sides were backed by personal beliefs. This is simply one report, I would not suggest using any less caution when using MDMA recreationally simply based on this knowledge. This is also an accurate depiction of how facts can be skewered and misinformation is doled out to the masses via media/news sources. The foremost thing to remember is that, while there has been no recognizable neurotoxic affects shown in this study, the pills that are sold in the street are most often not pure MDMA. A proper test will verify that your pills substance is pure. This article also states that Pre-Post loading is not necessary; However, the proper precursors to seratonin, namely 5HTP, in other studies, have proven quite affective as a deterrant. For a more in-depth look at this article, please visit the MAPS site below where this study was taken from. It further explains the arguments and conclusions listed above. http://www.maps.org/news-letters/v06n1/06108neu.html ------------------ ~*P*L*U*R*~ Four Simple Words To Live By....

try this site http://www.maps.org/news-letters/v07n3/07305tan.html ------------------ ~*P*L*U*R*~ Four Simple Words To Live By....

Those sites are all well and good, but you might also want to check out some pharmacology sites. I have tons of research papers on E usage and Serotonin depletion from school. Let me know if you want them. Endorphins "Endorphins are a group of substances formed within the body that naturally relieve pain. They have a similar chemical structure to morphine. In addition to their analgesic affect, endorphins are thought to be involved in controlling the body's response to stress, regulating contractions of the intestinal wall, and determining mood. They may also regulate the release of hormones from the pituitary gland, notably growth hormone and the gonadotropin hormones." ------------------ ~*P*L*U*R*~ Four Simple Words To Live By.... [This message has been edited by e-tarded (edited 10-09-2000).]

goto www.pillreports.com ------------------ ~*P*L*U*R*~ Four Simple Words To Live By....

goto www.rxlist.com and do a search. they def arent e ------------------ ~*P*L*U*R*~ Four Simple Words To Live By....

After finishing a synth of E, you have an oil left over that is then crystallized. I wont goto into specifics here, but if you would like to know further just pm me. ------------------ ~*P*L*U*R*~ Four Simple Words To Live By....

From everything I have read and studied on the effects of E there should be no reason to worry about it counter-acting your birth control. ------------------ ~*P*L*U*R*~ Four Simple Words To Live By....

Liquid E is usually GHB. Thats the name they give it, to sell it. If you were to actually get liquid E it would be an oil. Hope this helps ------------------ ~*P*L*U*R*~ Four Simple Words To Live By....