Newsgroups: alt.drugs From: [an 135054] at [anon.penet.fi] Date: Thu, 24 Nov 1994 03:51:21 UTC Subject: PALARIS FAQ (1/1) work damnit! Hope this post attempt works. Thanx for the help and feedback! XXXXXXXXX INITIAL NOTES XXXXXXXXXXX This author assumes absolutely no responsibility for anything you do, as a result of reading this material, or for any other reason. I make no claims as to accuracy. Always assume your own responsibility for research and for your actions. Read all the warnings. Read the articles. Decide what you may be willing and unwilling to put in your head. The following alkaloids are discussed and abbreviated as indicated: N,N-dimethyltryptamine (DMT), 5-Hydroxy-N,N- Dimethyltryptamine (5-Me-DMT) and 5-Hydroxy-N,N- Dimethyltryptamine (5-OH-DMT or bufotenine). XXXXXXXXXX THE DRUGS IN QUESTION XXXXXXXXXX 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 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. 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." Other DMT relatives exist, but are not of great importance here. 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. 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). LSD does not interact with MAOIs. 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. 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. 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. ><><><><><><><><><><><><><><><><><><><><><><><><><><><><><><><><> !!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-b) 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. ><><><><><><><><><><><><><><><><><><><><><><><><><><><><><><><><> XXXXXXXXXX THE PLANTS XXXXXXXXXX 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 Arundinacea. 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. 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. Arundinacea DMT ? ? Desmanthus Illinoisis (root) DMT 200 .200% Desmanthus Illinoisis (root bark only) DMT 340 mg .340% Psychotria species (averaged) 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. XXXXXXXXXX DOSES XXXXXXXXXX There seems to be a variety of dosages 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 Jonathan Net Peter REPORTED DOSES Ott Lore Gessner **************************************************************** DMT 1mg/kg 60mg --- 5-Me-DMT .25mg/kg 5mg 5-10 mg 5-OH-DMT NONE! ? --- **************************************************************** NOTE: These 'reported doses' are non-lethal dosages given to humans in the literature and 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, .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. XXXXXXXXXX BOOSTING ALKALOIDS XXXXXXXXXXX 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, 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. 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. XXXXXXXXXXX PREPARATION XXXXXXXXXX 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. 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. 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. XXXXXXXXXX IN CLOSING XXXXXXXXXX This article, as noted in opening, is probably not totally accurate or complete. If new or more accurate information arises, or if a topic has been missed, I would appreciate it if new chapters are written, and notes are made. Please type in the text "(See note ##)" and add your note to the END of the text. Stick new chapters where appropriate. I consider this a public work. XXXXXXXXXX UNANSWERED QUESTIONS XXXXXXXXXX Why are human recreational doses of DMT fatal to sheep? Just what exactly happens at what doses of 5-OH-DMT? What is the alkaloid level of PA? XXXXXXXXXXXXXXXXXXXXXXXXXXXXXXXXXXXXXXXXXXXXXXXXXXXXXXXXXXXXXXXXX Baxtor, C. & Slaytor, M. (1972). Phytochemisty, 11, pp.2767-73. Gessner, P K. In D. H. Efron (editor) Psychotomimetic Drugs. 1970. Raven Press. Moore, R. M., Williams, J. D., Chia, J. (1967). Australian Journal of Biological Science, 20, 1131-40. Oram, R. N., Williams, J. D. (1967). Nature, March 4, pp.946-7. Ott, J. Ayahuasca Analogues: Panthaen Ethnogens. 1994. Natural Products Co.  ------------------------------------------------------------------------- To find out more about the anon service, send mail to [h--p] at [anon.penet.fi.] Due to the double-blind, any mail replies to this message will be anonymized, and an anonymous id will be allocated automatically. You have been warned. Please report any problems, inappropriate use etc. to [a--m--n] at [anon.penet.fi.]