 1 Datura
 2 DMT
 3 Dramamine
 4 Ecstacy
 5 Ecstasy, Herbal
 6 Ecstasy MDMA
 7 Hallucinogens
 8 Hemp
 9 Hemp last left over...

\1 Datura

A hallucinogen found in the poisonous Jimson weed plant. The active ingredients are the Belladonna alkaloids, atropine, scopolomine, and hyoscyamine. Users smoke the dried leaves. Datura is a useable drug, but if you don't know about it, it could very easily turn deadly. 1) THE PLANT 1a) General Description & Physical Appearance There is much confusion circling the Datura family of plants. There are many different species of the plant, which may or may not be the same. Probably the two most well-known species are: Datura inoxia (Devil's Weed)Datura strammonium(Jimson Weed or Thornapple)Datura brugmansia(Angel's Trumpets)(Erowid Note: I believe that Datura brugmansia has been reclassified to the Genus Brugmansia, often referred to as the "tree datura".) Other species may include: Datura meteloides •Datura fatuosa •Datura metel •Datura sanguinea •Datura tatula •Datura candida •Datura aurea •Datura dolichocarpa •Datura vulcanicola •Datura suaveolens •Datura arborea •Datura discolor •Datura indica •Datura willemsi •Datura ferox (Datura brugmansia may sometimes _incorrectly_ be referred to as "Brugmansia arborea" -- it is also not indiginous to the best of my knowledge. It is, however, sold in nurseries) All of the species of Datura are leafy green plants with bright pink to white flowers. The flowers are all fragrant, with D. Inoxia having a very distinct aroma, very hard to mistake with any other plant. Datura grows all over the world, it would seem. The seeds are found in small fruit which are completely covered with short, sharp, spines (hence the name "Thornapple"). The stalks are bristly, and somewhat thin in comparison to the rest of the plant. The leaves are flat, mostly featureless, and can either be multi-edged (with between 4 and 15 points) or basically ovoid. In southern Cllifornia, there appear to be two different species of Datura growing. However, Ive been a bit perplexed by this. First, since strammonium is not supposed to grow in southern california at all, it doesnt make sense that it grows here. However, a plant that looks VERY MUCH like strammonium is growing here. When it is not fully developed, the leaves look like depictions of inoxia, yet when it is fully developed, it looks like depictions of strammonium. Definitely something worth looking in to. However, I doubt that the two are misnamed (thus implying that they are instead one species). So until I actually resolve this, whenever I referr to "inoxia" in the FAQ, I may actually be mistakenly referring to strammonium. Keep that in mind. 1 a1) Fruit Upon bisection, the fruit apear to have a structure similar to that of a bell pepper. Many many seeds grow inside, and eventually the fruit breaks open and dries up, releasing the seeds on the ground (I have not heard of any animal that eats the plant, thus distributing the seeds through scat). The fruit is normally within .5" - 2" in diameter, and basically a sphere. There are spines covering the entire fruit, which are about .25" long. They do not appear to have toxins in them, and they are not sharp enough to pierce skin under normal conditions. Minus the seeds, there really isnt a whole lot of substance to the fruit. 1 a1a) Seeds When examing the seeds, one will notice that, they are fairly small as seeds go. They range in size, depending on maturity, from the miniscule to .25"x.25"x.05". When the seeds are still young (the fruit is still green, and the shell is intact) they are yellow or off-white. They have an unpleasant taste, midly bitter and somewhat spicy. It may be that the growth of the seeds causes the fruit to crack, but I doubt it.

1 a2) Leaves The leaves of the Datura Species vary a bit, and I havent ever had the priveledge of looking at a Tree Datura up close. I do know, however, how the strammonium and meteloides plants (which may in fact be inoxia!) look like. D. inoxia has small green ovoid leaves. The surface is not waxy or sticky. There is no fluid in them when broken. They are fairly plastic, and don't break unless one is trying to break them. They dry into a brownish color, and curl up. 1 a3) Stems & Stalk The stems and stalk of both D. Inoxia and D. Strammonium are fairly thing, but brittle. They break easily, and when broken, secrete a sticky milky white substance that is bitter in taste. They are covered with small bristles. I don'tkknow what the bristles are for as I havent ever seen any animals eat any part of this plant. 1 a4) Root I have not yet examined the roots of this plant. 1 a5) Flowers The flowers are, when closed, cylindrical, but twisted. They outer ends are vividly colored, from a light pink to a deep purple color. They bloom at night, usually around 4 or 5 pm. The rest of the flower is off-white to light yellow in color. The aroma of the flowers, it appears, in all species of the plant, is difficult to describe. The plant has a definite 'presence' in a room. >From reports, I have found that people have become intoxicated from the very aroma of the plants. Again, we are faced with two possibilities. Either this is a psychosomatic effect or the aroma is actually scopolamine-based (scopolaminic?). 1b) General Location(s) Datura seems to have a "strain" for every place in the world. Sufficed to say that wherever you are, you can look for the plant providing the following conditions are met. It seems to grow in a humid to somewhat dry environment (not very dry, i.e., you wouldnt find it in the desert, I don't think). It grows well in landfills. For this reason, the Native American Indians gave it the name "White Mans Weed." It also grows well in rainforests, with several species growing in south american jungles (the validity of each specie is unknown; there is a lot of confusion circling this plant). In the United States, it grows from Florida to California, almost everwhere. It can grow in very poor soil, and is generally regarded as a pest. 2) HISTORICAL USAGE OF DATURA 1676 a group of soldiers go insane in jamestown upon ingestion of cooked Datura plants. 1968 Datura over-the-counter remedies for athsmatic difficulties are banned after people begin using them recreationally. 2b) General Overview of Historical Usage Datura has been used for a very long time. Originally, it seems it was used as a shamanistic tool, one that could help a shaman gain entrance to "other worlds of existance." It also contains several chemicals that are helpful to the body in certain conditions. Atropine, a chemical derived from plants in the Solanaceae, is used in hospitals and generally a trusted drug. As such, one can imagine that it is fairly safe when used within the suggested dosages. It would seem that people discovered its medicinal properties through shamans, or "Medicine Men." Often shamanism is used to cure ilness, and certainly Datura would be a very good cure for some diseases. 2c) Medicinal Uses Atropine, Scopolamine, Hyoscine, and Hyosciamine have all been used mainly two ways: Opthamologically and Systemically. I will not cover opthalmic use very much for two reasons. One, it is fairly well documented, and I'm sure your optometrist would be happy to explain how the yellow drops they put in your eyes actually work. Two, it has no psychedelic effect whatsoever.

Systemic use is also well-documented, but there is very little information at all on anticholinergenic poisoning (i.e., delerium-inducing doses). Thats mainly what the FAQ is for. 2 c2) Atropine Brand Names For what it's worth, the name "Atropine" comes from the greek goddess, Atropis, "she who cuts the thread of life." Also, Atropine was used by "dark age assassins and sorcerors to poison their enemies." Comments: It would seem that when tropane alkaloids are used in a medicinal preparation, something like belladonna extract is used in the preparation of it instead of just isolating the relevant chemicals. I have difficulty believing that atropine, scopolamine and hyoscyamine all have the same effect. I have been unable to find a boiling point for any of the alkaloids, so it may just be that they are difficult to separate from belladonna extracts. I cant imagine .0065mg of scopolamine doing anyone any harm. 2 c3) Treatment of the Urinary Tract Atropine is not used to treat the urinary tract, per se, but to treat the discomfort associated with urinary infections and the like. It is often prescribed in one of the above brand names, with a relatively low dosage to prevent delerium, cyclopegia, hyperpyrexia, and other effects associated with high (recreational) doses. 2 c4) Treatment of Heart Ailments Its ironic that modern medicine often uses atropine for treatment of heart problems when in fact, at higer doses, atropine actually CAUSES heart problems. For the most part, atropine is used to stimulate the heart rate in patients who have an abnormally slow beat. 2 c5) Treatment of Premenstrual Syndrome The sedative effects of phenobarbital and scopolamine are well known, and are thus often prescribed for many conditions. PMS is one of these conditions, but surely not the only one. Treatment of PMS is sometimes carried out with a regular dosage of several tropane alkaloids including atropine and scopolamine, in combination with phenobarbital. Phenobarbital is a CNS depressant. Usually, the dose of the tropanes is VERY MUCH smaller than that of the phenobarbital. I am unaware as to why one would prescribe two depressants and a stimulant in the same medication. WARNING: The Kinsey Institute for Research in Sex, Gender and Reproduction at Indiana University in Bloomington conducted a recent study on the intelligence of children (all male for some reason) that seems to indicate that children exposed to phenobarbital in the womb are likely to have an average 7 points lower intelligence than those not exposed. 2 c6) Treatment of Cholinergenic Overdose Much like physostigmine is used to treat anticholinergenic syndrome, atropine is used to treat the opposite effect. If there is a high concentration of acetylcholine in the brain and the neuromuscular junction (causing seizures) atropine and other tropanes are prescribed. As of yet, I do not know anything that would cause this condition.

2 c7) Side Effects Usually the worst part of any drug. Datura is no exception. Datura is a vasodilator. This means that your veins enlarge and have heightened bloodflow. This alone can cause dizziness (and may contribute to the delerient effects). Datura dries up the mucous memranes tremendously. The eyes, mouth, anus, and other mucous surfaces (presumably, also, the vagina) in the body become uncomfortably dry. The best cures for a dry mouth include chewing sugarless gum, hard candy (not "rock candy"), or sucking on an ice cube. It is especially unpleasant. Datura can cause hyperpyrexia. Hyperpyrexia is an uncomfortable heating of the body which can be treated either by lying in a cold water-filled bathtub, or a cold shower. Also, a cool cloth on the forehead seems to work as well. Datura also causes an increased heart rate (tachycardia). It is reasonable to assume that a heart attack or irregular heartbeat could result if someone who had a weak heart (or previous heart attacks) used the drug. Datura is said to cause the following conditions in the elderly: Confusion and/or Memory loss •Constipation •Mania •Agitation •Drowsiness Datura causes eye pain in glaucoma sufferers. Dizziness results from low-dose atropine use, and is usually gone either after the body adjusts to frequent doses, or the full effects set in (the full effects being total delerium). To reduce dizziness, one should try to increase circulation (temporarily or otherwise). This can be done by flexing the muscles in the leg repeatedly for a minute or so. Take caution with this step, however, as recreational atropine use causes a heightened pulse, thus making excersize possibly dangerous. Datura also makes you sensitive to light in the days after a recreational dose because of the pupil dilation. Unlike "redeye," simple eye drops wont work. Sunglasses are recommended. 2d) Folk Uses Folk uses of Datura is a tricky subject. First, since Datura grows all over the world, every culture has its own opinion of the plant's best use. Second, almost every field guide you will ever encounter will tell you of the dangers of Datura. A few will even tell you of "thrillseekers" that become ill looking for hallucinations. Only a very rare guide will actually tell you of non-poisonous doses, and use of Datura as a dietary supplement. The rest I have procured from various sources. Here are a few Folk Uses I unearthed: Powdered Herb Topical Salve: Dry herb Tincture 1:10, 60% Alcohol 3-12 drops up to 5x daily Smoking Preparation for Lung Ailments (especially bronchial spasms) Crushed leaves mixed with Western Coltsfoot Topical poultice for a local analgesic "Almost no other plant has such a history of crime. In the Middle Ages, especially in Italy, professional poisoners woulc concoct a brew of Datura that would be almost painlessly fatal. That Quality of deadening the senses before death, or during the perpetration of a crime, made it of the greatest value to criminals. So well known was this ability that Christoval Acosta, who was in India in 1578, wrote that Hindu whores gave it to their patrons because 'these mundane ladies are such mistresses and adepts in the use of the seed that they gave it in doses corresponding to as many hours as they wish their poor victims to be unconscious or transported.' Still worse was the use of Datura Strammonium by the nefarious white slavers. Virgins who may not have wanted to become prostitutes were given a pleasant-tasting but diabolical brew containing an aphrodisiac and Datura. Under the combined influence of these drugs, the actively contributed to the loss of their virginity, but upon subsequent awakening had no memory of their actions." (Plant Drugs That Changed The World) Dammerschlaf - translated almost literally to "twilight sleep." A mixture of morphine and scopolamine (from henbane, most likely) was used during childbirth to both prevent pain and to suppress memory of the incident. It is a sound assumption that it could serve as a mild pain-reliever (even without morphine) were one in serious need of one. Opiates, such as the California Poppy, could be combined with henbane or Scopola in small amounts to lower the pain from a hiking accident. I've also heard that the FBI (bless their hearts) had experimented with scopolamine as a suggestive drug in interrogations. I suppose this would have a chance of achieving the desired effect, but I also think there would be better chemicals to use. Scopolamine is still an anticholinergenic and could cause delerium (thus making it somewhat useless as an interrogation drug). Notes: Western coltsfoot has been used as an antispasmodic for the lungs. Why someone would mix Datura with something that works is beyond me. It would seem that Datura would elevate the heart rate, and do more harm than good. As for analgesic properties: well that's one that is _very_ questionable. The author of the above uses also went as far to add the following comment, "Nasty stuff!" I wouldn't recommend any of the salve, smoking mix, or analgesic. Regarding the "whore story" and deflowering virgins: it seems unlikely that a small amount of the drug could have such a drastic effect, and a large amount would either be fatal or extremely delerient (thus making sexual intercourse and/or favors near impossible). Poisons would be extremely deadly with Datura, but would have to be mixed with a sleep ingredient; without that, the unfortunate victim would have full knowledge they were under the influence of _something_. Of the above, I think the only sound use would be as a pain reliever. The trouble in that would of course be making sure that only scopolamine was present. Although hyosciamine is less potent than atropine, its tachycardial effects could be dangerous (especially in a less-than-ideal situation). 2e) Shamanic Uses Datura has been used shamanical for centuries, if not longer. It is used very widely as a psychotropic drug for shamanistic rituals, and more recently as as recreational hallucinogen. 3)BIOACTIVE CHEMICALS PRESENT 3a) Merck Manual Descriptions of Chemicals ATROPINE Atropine (dl-hyosciamine) a plant alkaloid, is the prototype drug of the group, and when used systematically in adequate doses, it provides all of the affects described above for the group as a whole. In most cases, it produces and initial transitory central vagal stimulant action before the blocking effect is manifested. The CNS is stimulated by atropine; restlessness, mental excitement, mania, delerium, and hallucinations occurr with large doses. Large doses also cause hyperpyrexia because of a combination of central and peripheral effects (decreased sweating). Atropine is well absorbed when given orally, and is rapidly eliminated from the body. About equal amounts of unchanged atropine and inactive metabolites are excreted in the urine; excretion is nearly complete in 24 h. Usually, 3 or 4 doses/day are needed to sustain pharmacologic effects, but cycloplegia and mydriasis may persist for days after a single dose, especially if given topically. The usual dose of atropine sulfate is 0.4 to 3mg/day orally or parentally (s.c., IM, or IV). Above 3mg, mental status and behavior usually change. The dose and maximum tolerated daily dose is usually given orally in 3 or 4 divided doses. Its use in the treatment of sinus bradycardia and incomplete atrioventricular block is described under CARDIAC ARRYTHMIAS in Ch. 25. In opthamology, it is used topically as a mydriatic and cycloplegic drug (for cycloplegia, 1 drop t.i.d. for 3 days prior to examination and 1 drop on day of examination; for iritis, solution or ointment b.i.d. or t.i.d.). Atropine can also be given orally as tincture of belladonna (0.03% solution, 0.3 to 3ml daily) or belladonna extract (15 to 60mg daily). Poisoning with atropine is best treated with physostigmine salicylate (see above), which antagonizes atropine effects both in the CNS and the priphery. SCOPOLAMINE Scopolamine (hyoscine) differs from atropine chiefly in being a CNS depressant instead of a stimulant. It is used mainly in obstetrics (where its sedative and amnesic properties are useful), as an antiemetic, and to prevent motion sickness. The usual dose is 0.3 to 3mg. Many hypnotics sold without a prescription contain scopolamine in combinations with a mildly sedative antihistamine; the hypnotic efficacy of these preparations is minimal. Note: hysocyamine, a chemical in Datura species, does not seem to be in the merck manual. Also, doses indicated are not given in mg/kg ratios. Doses almost certainly may be different for someone who weighs 120kg than for someone who weighs 60kg. 3 a1) Author Summary of Above I do not know, chemically, what the difference is, or how they actually affect the body differently. It would appear that scopolamine would be more the delerient (actually referred to as a "hypnotic" more than seditive and/or delerient, however) than atropine. Maybe the increased bloodflow cause by atropine has an effect with the scopolamine which increases the effects of the scopolamine. (I will consult with a doctor about this) VERY IMPORTANT: Know what is needed to cure you if you get too high a dosage. Physostigmine salicylate. Those should stop the effects of the delerium, and also decrease the effects of the atropine. I recommend you have a pre-prepared piece of paper indicating what you are using, (see section nine in addendum) how much you used, what chemicals are in the plant, and what the suggested chemicals are for treatment. It is my guess that it works fairly quickly. Both chemicals are available in various preparations to the public. 3b) Psychoactive Chemicals _Psychedelic Shamanism_ states that "It has been proved that the smoke from a strammonium cigarette, containing 0.25 grams of strammonium leaves contains as much as 0.5 milligrams of atropine. The leaves may be made up into cigarettes or smoked in a pipe, either alone, or with a mixture of cubebs, sage, belladonna and other drugs. Dryness of the throat and mouth are indications that too large a quantity is being taken." I have learned to take everything said about this plant "with a grain of salt." If we are to believe that the above is true, then the leaves of the plant contain .2% atropine. The plant, as well as other plants in this family, contain tropane alkaloids. Some of these alkaloids are (as far as they pertain to the FAQ, inoxia, and strammonium): Hyosciamine Hyoscine Scopolamine Atropine Both atropine and scopolamine interface directly with the CNS. The effects don't seem to vary between recreational dosages. All the effects of atropine are evident at recreational levels (though I don't know if anyone with heart problems has used Datura recreationally). 3c) Other Chemicals Currently I don't know of any other bioactive chemicals in Datura. I continue to research, but there simply may not be. --------------------------------------------------------- --------------- 5) AUTHOR'S WARNING Never believe everything you read. I have tried my absolute hardest to make this the most accurate piece of information on recreational anticholinergenics. I took information from literally dozens of sources, some less credible than others. Nobody can know everything about something, and to think that after reading this, you are safe, is sheer folly. I recommend you read all of this, and think VERY HARD about the decisions floating about in your head. Take everything with a grain of salt. You have been warned. The centers for disease and poison control state that 89% of all Datura usage results in poisoning. Whether they meant that the person hallucinated or became ill, I don't know. It would seem, however, that Datura is a VERY dangerous plant. Plants vary. It is important to understand that. Just as there are more potent varieties of marijuana, some Datura plants may contain more atropine than others. don't ever take a heroic dose all at once (or at all!). I specifically discourage anyone from using Datura recreationally. It may or may not be illegal (there are plenty of laws regarding use of psychotropic plants, and probably more will be passed -- hopefully I will be able to cover this in a future version), and it is definitely unhealthy. I recommend, also, a complete psychiatric evaluation BEFORE embarking on anything as complex as atropine. People who are mentally unstable (emotionally or otherwise) may not even know it. Hallucinogens often bring those effects out (especially DMT and LSD/LAA!). Im not sure of a way to do that, some health insurance companies would welcome the oppurtunity were you to ask, and some employers routinely test their employees. NEVER DRIVE UNDER THE INFLUENCE OF ANY DRUG. Datura's pupil-dilating effect lasts for weeks. This impairs vision somewhat, and I would recommend not driving for at least TWO DAYS after ingestion (thats 48 hours, not two lighted intervals). --------------------------------------------------------- --------------- 6) EFFECTS OF RECREATIONAL AND SHAMANISTIC USAGE 6a) Ingestion 6 a1) Smoking My experience with smoking the leaves of Datura was, at best, "inconclusive." On two occasions, I smoked Datura leaves. On one occasion, I smoked a flower. The first time, I smoked three leaves. The leaves were about two inches long, and one inch wide. Datura Inoxia was used in this case. They produced no effects, including no pupil dilation. The second time I smoked no more than the first, although I got a stomache ache. This may or may not have been because of the nervousness. The third time I smoked three leaves, the same size as the previous ones, and I smoked an entire flower. The flower was about 6 inches long. No effects whatsoever resulted. _Psychedelic Shamanism_ states that "no more than 2 grams should be smoked per week" Im pretty sure I smoked more than that, (in two days) with no effects. The taste of Datura smoke is unpleasant. It has a vague "dirty" taste to it. It was smoked out of a water pipe about 8 inches long (the actual chamber was around 5-5.5"). 6 a2) Tea My experience with tea is also inconclusive. The first time I made a tea with boiling water, and seeds in a coffee filter. I used about 45 seeds, that were not quite mature (still rather small and somewhat yellow). The tea was very bright yellow and was not particularly pleasant tasting, with a mild spicy taste (like jalapeno) to it. The effects came on in about half an hour, with a mild stupor. Basically it was difficult to walk (I felt almost drunk) and thought was somehwat impaired. This didn't last very long at all, probably about 3 hours. Note: This stuporous effect could have come from the blocking of anticholinergenic receptors. Drugs that produce acetylcholine have long been called "smart drugs" (Nootropics) for the way they make a user feel intelligent (and they actually perform better intellectually) and stimulated. Some have even been dubbed healthy coffee substitutes. Perhaps atropine is a "dumb drug?" My second experience was with more seeds, perhaps 60, but this time I ran the tea through the seeds 5 times. I added a very big (proportionally) amount of Grenadine and I also put a bag of Celestial Seasoning's 'Red Zinger' into the mix. The taste was mainly sugary, and the taste of the Datura was almost non-existant. The effects lasted about as long. The second dose was taken 2 days after the first, so it is important to note that they may have had a combined effect. After the second dose, I went to sleep, and had incredibly vivid dreams. I remember being in a room talking to friends of mine. It seemed proper to speak out loud (I was aware that I was speaking out loud as well as in the dream), and was overall a very pleasant experience (the dream). This is probably delerium, along with interference in the brain stem. My third experience was just the same as the first, and dreaming was no different than "normal." 6 a3) Uncooked Ingestion I have only one report of this method. However, I did read in a field guide that uncooked ingestion can kill you. I would recommend against this. Acetylcholine, a chemical that atropine blocks, has been known to stop one from dreaming. As a result of this, a person might be more difficult to rouse from REM sleep, and their dreams may be more intense. Delerium in general may result from the body entering a pseudo-dream-state even when awake. This would explain not only the hallucinations, but some of the effects that occur when one is asleep. Hyperpyrexia "So how does overheating kill someone? Our body temperature (like that of other mammals) has to be controlled very precisely for us to function, which is why we use a thermometer to indicate when we are ill. If we get too hot, above 42 degrees C (108 degrees F), our blood starts to form tiny clots that stick to the artery walls. This is not usually a problem in itself, but the process uses up the clotting agent in the blood, so that there is nothing to prevent bleeding. There are always tiny cuts and scratches inside the body and brain which are due to the body constantly replacing worn out tissue with new cells, and normally these leaks are blocked by the clotting of blood so that you don't even notice them. But above 42 degrees bleeding is unfettered, and this is made worse by high blood pressure due to the speedy effect of MDMA and exercise. People can bleed to death in this way, and if bleeding occurs in the brain it can cause a stroke. When someone is bleeding internally, blood may run out of their mouth or anus." (E is for Ecstasy, Ch 6) When hyperpyrexia results from atropine usage, it is usually a compound effect. The main reason is most likely the stoppage of secretion from the body. One simply doesnt sweat. Circulation is increased, thus warming the extremities uncomfortably, especially with the lack of sweat. One, as a result of the hyperpyrexia, becomes dehydrated which also adds to the effect. This is not dangerous unless the person is outside, or away from water, or unable to cool off in any way. It could lead to a heat stroke, which requires IMMEDIATE medical attention.

Synonyms: angel's trumpet, devil's apple, devil's weed, stinkweed, thorn apple.


\2 DMT

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 rept to be about 4 times as potent as DMT and is often as prefer- able to DMT. 5-Me-DMT has most of the psychedelic quali- ties 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. 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 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.

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.

DOSES

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.

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, 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.

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. 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.

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.
 Message-ID: <035301Z24111994@anon.penet.fi> Newsgroups: alt.drugs From: an135054@anon.penet.fi Date: Thu, 24 Nov 1994 03:51:21 UTC Subject:PALARIS FAQ (1/1) work damnit!

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)


\3 Dramamine

anticholinergics/antihistamines such as diphenhydramine hydrochloride, dimenhydrinate, cyclizine hydrochloride, and meclizine hydrochloride. These drugs are available over-the-counter in the USA and other parts of the world. They're commonly used as allergy medicines, sleep aids, and motion sickness medication. Some medications which contain these anticholinergics are Dramamine, Dramamine II, Benadryl Allergy, and Marizene, along with a wide assortment of others. Weirdly enough, the bizarre truth about these OTC medicines is that they are very powerful psychoactive drugs when taken in sufficient quantities.
 The problem with their use is that the "high" is very uncomfortable and longterm use may cause internal damage. While nausea may be rare, there are a number of other unpleasant side-effects and, when taken under the wrong circumstances, an excruciatingly bad trip may result.
 It is not my intention to get people to use anticholin- ergics and cause a lot of unhappy trips. It is my intention, however, for people to know the truth so they don't make bad decisions for lack of knowledge. Anticho- linergics are not safe or harmless; hardly anything is. I do believe that people will make better decisions when there is sufficient info avail, however, and that is my intention here. And with any drug, please use your head when taking this stuff!
 One final note; the FAQ will mention Dramamine II (meclizine HCl) as a viable source, however meclizene HCl trips are not as intense as the other drugs mentioned therein, and should be avoided; you will barely see any effects from meclizine, so if you read later on in the FAQ how it is in the same class as diphenhydramine HCl, it is; however, it will not produce the desired effect which you want, regardless of not causing any drowsy effects.
 1. Preliminary This text covers the recreational and medical uses of diphenhydramine, dimenhydrinate, cyclizine hydrochloride and meclizine hydrochloride, drugs known as anticholin- ergics/ antihistamines and found in many over-the-counter (non-prescription) allergy, motion sickness, and sleep medicines. This is version 1.1.
 How to Reach the Author - Gravol: Hiya325@aol.com 

1.2 Why a Dramamine FAQ? It is not my intention to cover just Dramamine, as there are many other medicines that have much the same effects. However, if I named this the Anticholinergic/Antihistamine FAQ, people would pretty much ignore it (perhaps not knowing what it means) and/or expect other anticholinergic/antihistamine sources to be discussed, such as plants, etc.
 The drugs mentioned in this FAQ are Dramamine, Dramamine II, Benadryl Allergy, Marezene, and a few others. When referring to Dramamine, I am also referring to these other drugs as well. It's just a lot easier to refer to these drugs as just "Dramamine" than "diphenhydramine, dimenhydrinate, cyclizine HCl, and meclizine HCl."
 Also, this FAQ is to set up to provide answers to the FAQs regarding Dramamine use and present several experiences of peoples' Dramamine trips.
 After searching the Internet and NOT finding a Dramamine FAQ (I could only find reports of experiences) I decided to write this and close the book once and for all on any speculation regarding the use of Dramamine. If you find any part of this FAQ incomplete or in any way wrong let me know via e-mail and I will do my best at correcting the info and acknowledging your help. Thanks.
 2 General Information 2.1 What's the difference between all these drugs? The effects of diphenhydramine HCl and dimenhydrinate are virtually the same. However, diphenhydramine HCl produces a more marked, rapid effect. Dimenhydrinate was developed to avoid those effects, but still have the H2 effects.
 Dimenhydrinate is the 8-chlorotheophyllinate salt of diphenhydramine HCl. You don't have to worry too much about what that means! [if you wanna know: it means there's an additional bunch of atoms attached to each of the diphenhydramine molecules. This bunch of atoms is stripped off when it dissolves in water, so that the effect of the drug is not changed. However, it adds to the weight of the molecule, which means that the drug is less potent.] 

The only important difference is potency: 50mg of dimenhydrinate and cyclizine HCl is equivalent to 25mg of diphenhydramine HCl and meclizine HCl. It's basically the same drug. Of course, these drugs are more expensive as a sleep aid than as an allergy medicine, though it is the same formulation. Be sure to keep your eyes open if you want the best deal. Meclizine hydrochloride is much like dimenhydrinate, except that it produces less sleepiness and has a weaker effect.
 2.2 What are these drugs generally used for? Diphenhy- dramine HCl can be used for the treatment of everything from allergies to anxiety disorders, and even the treat- ment of Parkinson's disease. Dimenhydrinate can be used as a sleep aid, and as an anti-nausea motion-sickness medication. However, quite paradoxically, in higher doses it can cause nausea.
 2.3 What are some brand name medicines containing these drugs? Some brand names of dimenhydrinate include: Calm-X, Dimetabs, Dramamine, Marmine, Nico-Vert, Tega- Vert, and Triptone. Some brand names of diphenhydramine HCl include: Aller Max, Banophen, Belix, Benadryl, Benylin Cough, Bydramine, Compoz, Diphen Cough, Dormarex-2, Genahist, Hydramine, Hydramyn, Nervine Nighttime Sleep-Aid, Nidryl, Nordryl, Nytol, Phendry, Sleep-Eze 3, Sominex 2, Tusstat, and Twilite.
 Other variations may include Marezene (containing cyclizine hydrochloride 50mg per tablet) and Dramamine II (containing meclizine hydrochloride 25mg per tablet). Note that some of the above brand names are not over-the-counter medications. Dramamine is also avail in the form of Gravol in Canada and other countries.
 2.4 How does diphenhydramine Hcl and dimenhydrinate work? Antihistamines generally, and Diphenydramine Hcl specifically, act by antagonizing histamine at the site of the H1 histamine receptor. Antihistamines dry up the secretion of the nose, throat, and eyes. They relieve itch and will help you go to sleep.
 Dimenhydrinate depresses the middle-ear function, but the way in which it actually prevents nausea, vomiting, or dizziness is not known.
 However, these drugs are not just antihistamines. They have a significant amount of anticholinergic activity. What does this mean? There's a chemical in the nervous system called acetylcholine, which is one of a set of substances called neurotransmitters. These chemicals transmit signals from one neuron to another. Acetylcholine is present in many different parts of the brain. Notably, it's present in areas thought to be associated with memory, and is the primary transmitter of the motor pathways leading off from the spinal cord. It plays a role in just about every system, however.
 Dramamine et al work to prevent acetylcholine from trans- mitting its signals. The importance of acetyhholine to memory may explain the amnesia people usually have for the events during a high-dose Dramamine trip. The heavi- ness that people often report is most likely a result of the blocking of signals to muscles: the brain has to send a much stronger signal to overcome the opposition pro- duced by diphenhydramine, and this is interpreted as a sensation of greater effort by the brain.
 2.5 Cautions and Warnings - People with a prostate condi- tion, some types of stomach ulcers, bladder problems, difficulty urinating, glaucoma, asthma, or abnormal heart rhythms should not use dimenhydrinate. Because it reduces nausea and vomiting, dimenhydrinate can hide symptoms of overdose of other medicines or the symptoms of appendi- citis. Your doctor may have difficulty reaching an accurate diagnosis in these conditions unless he or she knows you are taking dimenhydrinate.
 Diphenhydramine HCl should not be used if you are allergic to this drug. (That's another reason that it's a good idea to start off with really small doses.) It should be avoided or used with extreme care if you have narrow-angle glaucoma (pressure in the eye), stomach ulcer or other stomach problems, enlarged prostate, or problems passing urine. It should not be used by people who have deep-breathing problems such as asthma. Use with extra care - if at all - if you have a history of thyroid disease, heart disease, high blood pressure, or diabetes.

The same cautions/warnings should be used while taking similar drugs such as cyclizine HCl and meclizine HCl. Also, do not drive while on these medications as they can be quite sedating. (not to mention the hallucinations!)
 2.6 Possible side effects - The most common side effect of dimenhydrinate is dizziness. Other, less frequent, side effects are blurred vision, difficult or painful urination, increased sensitivity to the sun, loss of appetite, nightmares, rash, ringing or buzzing in the ears, and dry mouth, nose, or throat. Similar effects persist with the use of diphenhydramine HCl since it is basically the same drug.
 2.7 Drug Interactions - Taking dimenhydrinate together with alcoholic beverages, other antihistamines, tranqui- lizers, or other nervous-system depressants can result in excessive dizziness, drowsiness, or other signs of nervoussystem depression.
 Diphenhydramine HCl should not be taken with monoamine oxidase (MAO) inhibitors. Interaction with tranquilizers, sedatives, and sleeping medication will increase the effects of these drugs. Again, be extremely cautious when drinking alcohol while taking diphenhydramine HCl, which will enhance the intoxicating effect of the alcohol. Alcohol also has a sedative effect.
 2.8 Food Interactions - Take this medicine with food or milk if it upsets your stomach.
 2.9 What is the lethal dose of Diphenhydramine Hcl? The LD50 of Diphenhydramine in rats is 500mg/kg. For humans it is not known, so be careful! Lethal doses in humans are almost always far less than lethal doses in rats (allowing for body weight differences), so don't try to take the rat LD50 and apply it to yourself. Also, note that the LD50 is the dose at which 50% of the subjects will die. A lower dose will still kill a smaller proportion of the subjects - i.e. it may be that the LD10 (i.e. 10% mortality) for rats is just 100 mg/kg.
 3 The Trip 3.1 How many pills should I take for my first trip? It's difficult to say. Some people seem to have a much higher sensitivity to this drug than others. For most people, a dose of 8-12 pills is about right. HOWEVER, keep in mind that you may be one of the more sensitive people, or that you may have an allergy to this stuff. 

To use this drug safely, start with a low dose (just 1-2 pills) and work up from there. Remember, you can always work up from a dose that doesn't do anything at all, but it's damm hard to come down from a lethal dose. It's not much fun being in the hosp and explaining to people why you were taking a whole packet of pills, if you wake up.
 3.2 How long does the trip last? Usually the trip can last anywhere from 8-12 hrs. Sometimes less, rarely longer... your mileage may vary. Note that some people experience a hangover that lasts most of the next day.
 3.3 Precautions - Be prepared. Familiarize yourself with the reports in this FAQ and don't make the mistakes some of those people made. Make sure you're physically healthy and reasonably psychologically well-balanced. Absolutely do not take if you have asthma/heart problems. You should also be in a comfortable/safe environment.

If you're doing it for the first time, don't leave home. It's also good (read: almost essential) to have a sober person with you to help in case you need it. It's possible for people using Dramamine to respond to hallucinations and delusions *as if they were real*, so it's sensible to have someone there to make sure you don't do a second stupid thing.
 If you should wander away from home, do not drive a car; you might fall asleep or hallucinate, possibly causing a fatal accident. To avoid the nausea, most people say to take on an empty stomach, while other pharmacology and medicine sources say to take the drug with food or milk. You can see what works best for you.
 3.4 What is a Dramamine trip like? A Dramamine trip can be very much like a dream... what you may see can be totally fantastical; however it seems very much like reality. Also, you may forget a large majority of what happened (which may be for the better).
 Things appear to happen that are totally irrational, yet seem perfectly normal at the time. You got to be careful, as you may find yourself doing things you wouldn't normally try in reality (eg. jumping out of a window to escape a "monster") and it's best to use it while your parents or anybody else that might find you is not near.
 People tend to get a "heavy" feeling, one of being "pulled down" a lot while using Dramamine/Benadryl. It may also be hard to stay awake. Taking Dramamine II (meclizine HCl) may help; it was developed to reduce the sleep-inducing effects of Dramamine.
 Dramamine is an non-social, experimental drug. It can't really be used for recreational purposes, since it usually isn't much fun. Great care must be taken in preparing for the trip before you actually dose on it.
 The most common hallucinations of Dramamine are auditory; you frequently hear voices, sounds, and sometimes your name being called by an unknown person/thing. The auditory hallucinations can be enjoyable: listening to music, you may find yourself hearing melodies and even lyrics that just aren't there. Often, these changes are improvements!
 Some users say olfactory (smell) hallucinations may be present,such as smelling food, etc. The visual hallucinations that are experienced are usually full-blown. You may find yourself talking to a person or being that is not really there. You will find yourself believing - at least temporarily - that they ARE there, and this may result in problems. Usually (not always) by touching the object/ hallucination it will vapourize and disappear. Try not to do anything you wouldn't normally do in real life. If something strange happens, think "Wait a minute... is this physically possible?"
 These hallucinations can become downright scary and lead to an extremely bad trip. Just remember that they aren't truly there, and nothing can hurt you... only you yourself can. That is why it is not recommended that you take more than 12 tablets for your first trip.
 Once again, your mileage may vary. Some people experience more bad effects than others; some don't get any halluci- nations at all, though possibly you will hallucinate.
 The "high" you experience is not really a high. It is quite uncomfortable and can cause nausea or a severe case of "cotton-mouth." That is why people usually do this drug very infrequently (e.g. once or twice a year) along with other reasons such as possible long-term damage to the body.
 If you have an experience on Dramamine or any similar drug for that matter, don't be shy..post it on alt.drugs. psychedelics or any other appropriate newsgroup or mail me a copy of it. We can only learn from others' mistakes.
 3.5 Any long-term effects? Rumors persist of brain/ stomach damage resulting from frequent use of dipheny- dramine HCl and similar drugs. Chronic users seem to be depressed most of the time, but they seem to recover when they stop doing the drug. Also there is a risk of liver/kidney damage. Since it is not addictive, you don't really run a risk of frequent use; however, exercise control when taking it and don't take it too freq... the results may be devastating.
 3.6 Are there any published reports of abuse of this drug? Yes, in the journal of Canadian Psychiatry 1993 (38:113-116) is a section on dimenhydrinate abuse among adolescents.
 To summarize, several cases are described where teens typically took 5-15 tabs (250-750 mg) at a time habitu- ally for a year or more. The patients were described as chronically depressed and amotivated. Symptoms "remitted with successful treatment of dimenhydrinate abuse". Based on this paper abusing this OTC antihistamine appears remarkably safe. However, don't be fooled into thinking the abuse of this drug is anything NEAR safe.
 There is also a case on record where a suspected Gravol-abuser was kicked out of a taxi on a rural highway in northern Saskatchewan due to her behavior, and froze to death, but since I cannot properly cite the reference, this may just as well be regarded as rumor.
 3.7 Are there any reports of human fatalities from an overdose? Yes, one interesting and somewhat ominous thing I ran across was the story of Daniel Berrey, a Missouri University student who apparently died one October from an overdose of Benadryl. Any decent search engine will turn up his name, but essentially, authorities were stymied, at least officially, as to the cause of death at first. 

Descriptions in newspaper articles and on his sister's home page paint a picture of the stereotypical "college student next door", and for a while, the speculation was that he took Benadryl as medication, and suffered an allergic reaction. Eventually, though, the autopsy revealed that there was a substantial (but unspecified) amount in Daniel's system, and the newspaper article about that finding reports puzzlement at how the Benadryl was ingested or for what reason. There's no reference at all to the notion that Daniel might have tried to use Benadryl recreationally. Nor, unfortunately, would the coroner publicly say how much was found in his system.
 Did Daniel Berrey die from eating a box of Benadryl? Or did he indeed have an allergic reaction which was accelerated by a recreational dose? The real answer may never be known.
 3.8 What can I take with Dramamine to stay awake/rid the bad effects? Some users take ephedrine tabs (Mini-thins) to help breathe easy and to rid some of the bad effects. Usually the dose of 25mg per 250mg of diphenhydramine HCl or 500mg of dimenhydrinate. The ephedrine also helps keep the trip clear and easy to remember. Other users report that caffeine (Vivarin, NoDoz) will help keep them awake during the trip. Note that the cheapest way of keeping awake is probably to drink some coffee.
 3.9 Can Dramamine be taken in combination with DXM? Recent rise in the use of dextromethorphan (DXM), aka cough syrup, has caused speculation whether it is safe to take Dramamine in combination with DXM. The answer is surprisingly (for the most part) yes; however, if you have not taken DXM before, it is not advisable to combine it with something else, since you don't know how your body will react to it.
 Usually when taking them in combination, the trip may become a little more comfortable and more like a typical DXM trip, with a few bad side effects (such as nausea or a dry mouth), and more intense visuals. The DXM causes an increase in CEV's (Closed Eye Visuals) and the Dramamine causes an increase in OEV's (Open Eye Visuals), along with auditory hallucinations so this would make for a very interesting trip to say the least (Check out the experiences listed in the DXM FAQ; you'll find a few relating to combined DXM and Dramamine use).
 Also, it is rumoured that DXM enhances the effect of Dramamine and related medicines... so if you are taking Dramamine for the first time but have tripped on DXM before, it is advisable to try a lower dose of Dramamine the first time. Don't forget, you have very little mental control on a Dramamine trip and very little physical control on a high-dosage DXM trip!
 3.10 What is Marezene? Marezene use in the last couple of years has become almost as popular as Dramamine and Benadryl use.
 Marezine is an over-the-counter motion sickness medicine, similar to Dramamine. The active ingredient is cyclizine hydrochloride, an anticholinergic that is used because it relaxes the smooth muscles in the stomach. If you take a lot of Marezine pills, you will become delirious and experience strong hallucinations. It is fairly intense, but it makes one feel quite physically uncomfortable, leaves a nasty hangover, and in high enough doses can space you out so much that you forget you are tripping.
 3.11 What are some other anticholinergics? First, some background on anticholinergic deleriants: These drugs are not usually regarded as psychedelic, although they have a great deal in common historically, culturally, and pharmacologically with other drugs taken for their mind-altering powers. They are called anticholinergic because they block the action of acetylcholine, a nerve transmitter substance that controls the contraction of skeletal muscles and also plays an important role in the chemistry of the brain. They are called deleriants because their effects at high doses include incoherent speech, disorientation, delusions, and hallucinations, often followed by depression and amnesia for the period of intoxication. 

The classical anticholinergic delirients are the belladonna alkaloids: These tropane derivatives, the most powerful and important of which is scopolamine, are found in differing concentrations in various plants of the nightshade Family or Solanaceae, among them deadly nightshade (Atropa Belladona), mandrake (Mandragora Officinarum), black henbane (Hyoscyamus Niger), jimsonweed (Datura Stramonium), and over twenty other species of henbane and datura. Of all psychoactive drugs, only alcohol has been in use for so long over such a large part of the world. For thousands of years on all inhabited continents the belladonna alkaloids have been a tool of shamans and sorcerers, who take advantage of the sensations they evoke to leave their bodies, soar through the air, or change into an animal in their imagination. They also produce toxic organic symptoms like headache, dry throat, loss of motor control, blurred vision, and greatly increased heart rate and and body temperature; death from paralysis and respiratory may occur.
 The belladonna alkaloids are so terrifying and incapacitating - the physical effects often so unpleasant, and the loss of contact with ordinary reality so complete - that they are used only with great caution and rarely for pleasure. For the same reasons, ironically, they are not regarded as a drug abuse problem and can be bought in small doses on prescription or in over-the-counter sedatives and pills for asthma, colds, and motion sickness.
 If you want info on Anticholinergics or Anticholinergic Psychosis see: vh.radiology.uiowa.edu/Providers/Lectures/ Conferences/CPS/22Psychosis.html
 "Anticholinergic neuropyschiatric effects may occur secondary to standard or excessive doses of these compounds. This handout will discuss the presentation and management of these reactions as the result of intentional (e.g., abuse) or nonintentional ingestion."
 4 Dramamine/Benadryl/Marezene Experiences: All of the following stories are left the way the author typed them; I did not take time to fix spelling and grammatical errors since a few of the experiences were typed while under the influence of these drugs, and I wanted you to see what the context looked like.
 All of the following stories remain anonymous. I did not take any names mentioned in the following text out, but I did remove the e-mail adrses and names of the authors. Keep in mind, the stories may or may not be true, and the experiences should not be duplicated in any way, shape, or form! Illegal use of any drug, prescription or OTC.
 4.2 Dramamine Experiences - The following are all Dramamine experiences. I took out the redundant stories and included the most unique experiences.
 Gravol (Dramamine), which I HAVE tried. I for one would class it more as a deleriant than a hallucinogen. The trip started with a nice stoned feeling, but quickly changed. When staring at any white object (ceilings, and even cups or cupped hands) I noticed a strange clear gellatin-like substance that seemed to jiggle and spread towards me (looked a lot like the alien in the Predator movies). While doing LSD or psilocybin, I have always been able to tell reality from hallucinations. 

This is not the case with Dramamine. Several times I carried on conversations with individuals before discovering they were non- existant. I saw people and objects that were not there as well. Perhaps the worst aspect of the trip was the auditory part. I constantly heard my name being called, and sound is magnified to a very uncomfortable level. Speech (even from myself) was not only loud and difficult, but VERY slurred. 

Communication was difficult due to the fact that I would forget what I was talk- ing about in mid-sentence, and would finish most sentences off by saying "Uh, nevermind...I forgot." The amount of paranoia that prevailed throughout the trip was unbearable: especially after I saw my brother rise out of a pile of clothes in the floor to tell me that my father (who happens to be the head of a drug task force) was calling me. Maybe all of this was due to the fact that I was alone for the majority of this experience (nightmare). 

Definitley a one time experience for me. Not recomended for the weak of heart or mind. Especially at that dosage: 24 tablets!


\4 Ecstacy

Aug 2000 Heavy Ecstasy use linked to brain damage ALEX LO

The dangers of the rave party drug Ecstasy need to be more widely publicised, experts say, after a new study found habitual abusers could suffer serious depletion of an important brain chemical.

A team from the Centre for Addiction and Mental Health in Toronto, found the levels of serotonin and a related chem were 50-80% lower than normal in the brain of a 26 yr old man who died after using the drug heavily since he was 17. Serotonin is linked to feelings of well-being, and Ecstasy, an amphetamine derivative, is known to trigger a surge in the chemical, creating a feeling of intimacy with other people. Users often report feeling depressed or lethargic after the drug wears off. 

The Canadian team compared the levels of the chem from 11 people who never used Ecstasy with those in the brain of the dead man. The results were published in the latest issue of the intl science jrnl Neurology. The study is the first to demonstrate serotonin depletion in humans, although animal studies have shown a similar effect.

"The depletion effect is very serious. It shows this so-called soft drug is not soft at all," said Dr Dominic Lee Tak-shing, an addiction expert and assoc prof in the Chinese Univ's psychiatry dept. He said the drug damaged brain cells which produced the mood-altering chemical, and called for education starting in primary schools. "When they are young, they are open-minded, like a blank sheet of paper and that's when we should target them for drug education," he said.

Police seizure figures on Ecstasy have rocketed from 282 tablets in 1998 to 369,252 in the first six months of this year. The Narcotics Division of the Security Bureau said the reported number of drug abusers under 21 rose to 1,057 in the first three months of this year from 765 in the last quarter of 1999. Nearly half were Ecstasy-users compared with 25% in the previous quarter. Police have stepped up raids on rave parties, and the Narc Div will stage a seminar with party organisers later this month to discuss ways to stamp out the drug.

Mya Kirwan, executive director of the Kely Support Group, a youth counselling service, said the effects of Ecstasy may be compounded because it is usually taken with other illegal drugs. "Ecstasy is a popular drug of choice for young people at dance parties, although it is seldom taken in isolation and is often taken with other drugs," she said. "Ecstasy is considered by many young people to be one of the less harmful drugs. The attraction of using Ecstasy is about how it makes a person feel more sociable and less inhibited in social situations."

--------------------------------------------------------- Feb 19 2001 Ecstasy's Dividend. Has a Parkinson's disease sufferer, who can only find relief—albeit temporarily—in an illegal drug, accidentally discovered a reliable treatment? BY JONATHAN MARGOLIS 

British film stuntman Tim Lawrence was only 34 when he was diagnosed with the debilitating neurological cond Parkinson's disease six years ago. It meant a swift end not just to his parts in movies like Braveheart, Split- ting Heirs and Frankenstein, but also to an active life- style that included acrobatics, martial arts and sky- diving. With his body alternating between rigidity and uncontrollable spasms, almost the only physical recre- ation left for Lawrence was going out with friends to London clubs. 

Under the strobe lights his thrashing movements could be mistaken for enthusiastic dancing. So clubs became the one place he didn't feel self-conscious. 

It was at such a club three years ago that Lawrence took the illegal drug ecstasy. What happened next is promising to turn established theories about Parkinson's disease on their head. While experts still warn strongly against Parkinson's sufferers taking ecstasy, Lawrence may have stumbled accidentally on the nearest thing yet to a reliable treatment for the disease, which afflicts an estimated 4 million people worldwide. Within half an hour of taking ecstasy, Lawrence felt more than just the sense of elation users of the drug experience.

For the first time in years, he regained control of his body, and he retained it until the next morning. "It was like a Road to Damascus," he told Time. "I was suddenly looking down at my body aware that the twitching had gone, and I had this incredible fluidity. I was completely normal." 

At first, Lawrence regarded the episode as a freak occurrence. The symptoms of Parkinson's are notoriously unpredictable, and it seemed like just another of the disease's erratic turns. But then he tried ecstasy again, and once more he was able for hours at a time to regain something close to the athletic grace he once possessed. Yet when he mentioned the experience to his doctors, they dismissed it as a result of the street drug's known amphetamine qualities.

So Lawrence thought little more about it, other than to make the most of ecstasy's unexpected side effect the couple of times a month he went clubbing. He also kept quiet about his chance discovery, since, in Britain as in many countries, taking the drug is a criminal offense as serious as using heroin or crack cocaine. 

Now, however, Lawrence's discovery is being hailed as the beginning of a medical breakthrough. After seeing footage from a forthcoming bbc television documentary, two leading Parkinson's researchers have begun full-time investigation into why ecstasy has such a dramatic effect on his condition. The documentary, to be aired this week, shows Lawrence in a gym doing forward rolls, somersaults, backflips and swallow dives despite his debilitating condition.

The researchers, Prof Alan R. Crossman and Dr Jonathan M. Brotchie of the Univ of Manchester, are trying to find a component of the banned substance that might be developed into a safe drug to mimic ecstasy's good effects while suppressing the bad, which include memory loss, brain cell death and depression. And they think such a safe drug could be available for testing within a year. 

Parkinson's is an incurable disorder of the central nervous system usually associated with the elderly but now increasingly affecting younger people. Sufferers include Muhammad Ali, Billy Graham, Janet Reno and, according to some reports, the Pope. But research into Parkinson's remained underfunded and under-publicized until actor Michael J. Fox announced he had the disease in 1998, having developed it a decade ago at age 30. 

Parkinson's is caused by a breakdown of the brain's production of the neurotransmitter dopamine, which relays the electrical impulses involved in muscular movement. The last great breakthrough in treatment was in the late 1960s, when the "miracle" drug levadopa, or L-dopa—the chemical precursor of dopamine—was discovered to "unfreeze" patients who for decades had been practically rigid, unable even to produce facial expressions. Though it remains the standard treatment for Parkinson's, there is a serious downside to L-dopa.

After a couple of years, during which patients seem to be cured, they start developing the jerky, uncontrolled twitching and tremors that most people today associate with Parkinson's. 

In a healthy person, natural dopamine is released in tune with the body's needs, but using L-dopa is the equivalent of running a car's turbocharger in traffic. The result for Parkinson's patients is that their condition oscillates between hyperactivity while they are on L-dopa and immobility when they are not. Pharmacologists have been searching for 30 years for a drug to combine effectively with L-dopa and mute the turbocharger effect, but none has emerged. 

Ecstasy is an amphetamine-like drug that affects emotions by boosting levels of another neurotransmitter, serotonin, which is normally connected with feeling happy. Serotonin has rarely been associated with muscular movement. Confusingly for the researchers, scans of Lawrence's brain show that ecstasy has a beneficial effect on his Parkinson's even when he takes it on its own, without L-dopa. 

Researchers around the world, including Crossman and Brotchie, have suspected that serotonin may have some connection with Parkinson's and have been searching for a serotonin-stimulating drug to combine with L-dopa. They have had little success, though, and the news that the missing link may be ecstasy, or at least something in it, has cheered the Manchester duo.

"The reason we're excited by Tim's case is that we've spent between us the best part of 50 years trying to understand movement disorders, and the effect we see in him with mdma [ecstasy's scientific name] is the biggest we've ever seen," says Brotchie. "Ecstasy on its own isn't going to be a useful treatment. But the potential may now be there to develop completely new drugs for Parkinson's." 

Brotchie's enthusiasm is shared by Dr. Thomas N. Chase, a neurologist who heads the experimental therapeutics branch of the National Institutes of Health in Bethesda, Maryland. "We don't work with street drugs, but we are not averse to taking clues from all sources," Chase says. "Parkinson's is a condition for which there is no adequate therapy, so if this observation with ecstasy is reliable, it could lead to a line of research which could benefit many, many people with this disease. And my guess is that this observation will pay off." 

It was by chance that Lawrence's case came to the notice of researchers at all. Doc director Jemima Harrison of Carlton TV, which produced the BBC doc, was making what looked like a routine report on Parkinson's research. A friend of hers had recommended Lawrence as an especially articulate sufferer. "We were talking about filming him trying a new surgical technique in Spain," says Harrison. "Then one day I asked him out of curiosity if cannabis helped him at all. He said no, and I nosily asked if he'd tried any other drugs. He said, Well, I occasionally take ecstasy, and it renders me completely normal for several hours.' So I started looking up the science, and it seemed impossible for ecstasy to have that effect. That's where it started getting interesting." 

Lawrence is uneasy about his impending celebrity: the former British soldier's views on drug use are far from libertarian. "Other people take ecstasy because they want to be in an impassive state, have a different perception listening to music and to dance all night. I do it to experience normality. But I also feel the heightened sensory perception, and I wouldn't want to be experien- cing that on a daily basis because you wouldn't get anything else done. So if there is an outcry over my using ecstasy, if I was investigated and if people were really anti, I'd have to be a bit more careful." Yet if the research Lawrence has inspired somehow does pay off, nobody is likely to fault him simply for wanting to dance. 


\5 Ecstasy, Herbal

Herbal ecstasy is a term used to describe a combination of herbs which are legal, inexpensive, and marketed as a "natural high." It can be purchased over the counter in drug stores, music stores, and shops around the country at a cost of approx $3.00 per pill. The recommended dose for the "natural high" is approx 4 pills.
 The packaging on these products, including brand names "Herbal Ecstacy" (sic), "Cloud 9" and "Ultimate Xphoria," promises "increased energy," "inner visions," "sexual sensations," and "cosmic consciousness." Users report feeling relaxed, tingly, and energetic. These sensations are caused primarily by caffeine and ephedra (ma huang), which is the key ingredient in herbal ecstasy. Ephedra is an herb that has been used in China for 2000 years to treat respiratory problems. The active chemical of the herb ephedra is ephedrine, a chemical used pharmaceuti- cally in decongestant and asthma medications. 

The FDA has recently received hundreds of reports of adverse reactions, including liver failure, elevated blood pressure, strokes, and deaths. The FDA is currently deciding whether a safe level of ephedrine in food supplements exists, or whether sales of some ephedrine-based substances should be stopped altogether. Meanwhile many states have banned the sale of herbal ecstasy following the reports of deaths of users. 

----------------------------- Wesley Hsu Nightlife -- Ecstasy

Mind-altering substances are at least as old as written history. Entire books have been written about how brewing mead and ale directly contributed to the conversion of ancient societies from hunter-gatherer to agrarian modalities. Government attempts to prohibit, regulate, or at least profitably tax people's chemical pleasures have a long history as well, from the Chinese Opium Wars through American Prohibition to the currently commonplace government monopolies on tobacco. 

For civil libertarians there is an inherent hypocrisy, or at least a rational inconsistency, in most governments' distinction between drugs which are legal and illegal. While advocating the decriminalization of all hard drugs remains an extremist position, the possibility of legalizing some drugs which are demonstrably less destructive than certain legal substances has become a popular, almost mainstream idea in some countries. In recent years much attention has been focused on marijuana, which has demonstrable therapeutic and medicinal uses and is less addictive than either alcohol or tobacco. Accusations have been made that the resistance to the loosening of marijuana laws is a conspiracy by social reactionaries and corporations who fear loss of market share from the development of hemp fiber, a natural textile which has been used for centuries. 

Meanwhile a drug of a very different nature has gained both popularity and viability as a candidate for de-criminalization. Popularly known as ecstasy or E, the drug methylenedioxymethamphetamine (MDMA) has become a favorite not just among the late-night urban ravers who brought it onto the scene in the 1980s, but also among adults seeking a controlled recreational high and terminally ill patients who suffer from chronic pain or depression. Along with its increased popularity has come increased production, government scrutiny, and in many cases harsher crackdowns on its trafficking and distribution. 

Bangkok has seen a major resurgence in ecstasy usage, especially among those who frequent dance clubs. This is no surprise given E's unique effects, which users describe as a tremendous feeling of joy, well-being, and empathy. Sensations are heightened, music sounds incredibly good, all textures are wonderful to the touch, and animosity between people is eliminated to the point where large groups are engaged in a seemingly unbounded mass-love in. This effect has been touted as one of E's benefits, in that unlike alcohol, speed, or cocaine it almost never results in assaults, abusive behavior, or date rape. Its nickname "The Love Drug" is apparently well-earned. 

Its lack of side effects such as paranoia, hallucinations, or paralysis have led psychiatrists and counselors to experiment with it--legally and illegally--as a tool for therapy. A recent cover article in TIME magazine outlined several cases where E's relaxation and mood effects were used successfully to help overcome grief, denial, and psychological trauma. Such preliminary results have put E's advocates on the offensive to have the drug studied further for medicinal applications. Its detractors have been put on the defensive, insisting that E's popularity should be treated as a call to arms, just as the surge in crack cocaine usage in the US resulted in increases in federal sentencing laws. A major crackdown on E in Bangkok several years ago, which included the arrest of a major dealer, almost removed it completely from the nightlife scene. Should its return be viewed as a need for another crackdown, or a re-examination of E's place in urban life? Opinions are deeply divided. 

The truth almost certainly lies somewhere between the extremes, but lack of large-scale long-term studies makes it difficult for either side to back up its claims with much hard science. MDMA is in fact a much older drug than most think. It was created by the German company E. Merck in 1914, not as a product in itself but as an intermediary stage of another drug. Its properties weren't studied in detail until 1953, during a US government funded project which studied mind-altering substances for potential use as weapons against the Communists (if you can imagine the effect of the entire Soviet Bloc on E, perhaps it wasn't such a crazy idea…) In 1974 a biochemist named Alexander Shulgin published a paper documenting E's wide range of therapeutic effects, which led to its experimentation as a medication as well as its recreational use at parties. The party ended in 1984, when the DEA placed it on its Schedule 1 list of controlled substances. -------- As with all drugs, turning it illegal drove production and distribution underground, raised the prices, and made the purity of any given dosage questionable. In fact, most experts agree that the greatest danger from E is not MDMA itself but what else might be mixed in by a less-than-honest manufacturer. Additives range from harmless rip-offs such as caffeine to a potentially fatal dose of dextromethorphan, a hallucinogenic found in some cough syrups. Contrary to urban legend heroin and LSD are uncommon, since they aren't cost effective to the manufacturer. Many pills are mixed with versions of speed (crystal methamphetamine, ya ba) to give an "energy boost" to the MDMA high, a cocktail disdained by purists. Apparently speed violates the spirit of E. 

The other documented danger of E is dehydration and overheating. MDMA in large doses can raise a person's body temperature several degrees above what is normal, which can cause brain damage if sustained for a long time. Such temperature extremes are unusual, however, and can be alleviated by drinking plenty of water. Ecstasy's high tends to cause a feeling of thirst, so most users are inclined to drink as much water as they need--more, in fact. 

Chemically, MDMA targets the brain cells which store seratonin, the hormone responsible for mood regulation. Unlike Prozac, which boosts happiness by preventing naturally-secreted seratonin from being re-absorbed by the brain, MDMA actually forces seratonin out of its storage. It's sort of like the difference between collecting rainwater and blowing up the dam. This flood of seratonin is what causes the rush. The 1953 study concluded, among other things, that it would take about 14 pills ingested at once to cause a fatal seratonin overload. Short of that, the long term dangers of moderate or occasional MDMA usage is speculative. Some evidence indicates that seratonin levels, once depleted, may never return. Other evidence shows that the seratonin-releasing cells can be permanently damaged by their forced disgorging of their cargo. But these studies are not conclusive, and are countered by other studies which show no significant loss of function even in those who take it regularly over years. 

Perhaps the best warnings about E come from the anecdotal evidence provided by its advocates rather than its detractors. The coming down from such a high is necessarily a bit of a disappointment, and the seratonin withdrawal apparently can create a day or two of moderate depression, sort of a complimentary swing of the mood pendulum. Some users speculate that overuse can deaden the sensibilities, and that being ecstatic all the time destroys the natural dynamism of life. There is also a very rapid development of tolerance among most users, who have to increase dosage to retain the same effect. The informal recommendations are to proceed in moderation, and to not let the joy of E become a replacement for the other pleasures in life. Of course the same could be said about alcohol, heroin, or football. 

The difference, of course, is that football won't kill you (unless you're an English fan in Turkey) and that heroin will almost certainly kill you eventually. Equating E with the either healthiness of sport or the destruction of heroin is equally myopic, and for the time being it's no surprise that the government is erring on the side of safety and classifying E as a dangerous drug. In time, research, social change, and open discussion may place ecstasy in a better public light, legal and safe and used in moderation. In the meantime, regardless of one's opinion of ecstasy's benefits its legal liabilities remain beyond speculation. 

--------------------------------------------------------- Here's the latest on it's legality. It's previous classification as a Schedule 1 drug has been struck down. I don't understand where that leaves it now; I'm sure it's still controlled, but this may open the way for further research, as well as legal progress.
 Here's the text from High Times, Jan 1988:
 COURT VOIDS "ECSTASY" PROHIBITION. In a landmark ruling, a US Court of Appeals judge struck down the classifi- cation of MDMA ("Ecstasy") as a Schedule 1 drug under the Ctrl Substances Act in a decree issued this past Sep.
 There are five classifications for drugs under the CSA. A substance may be classified as Schedule 1 if it is found to have: a high potential for abuse; no accepted medical use; no way to safely supervise its medical use. Marijuana and heroin are currently classified as Schedule 1 substances, for which the CSA mandates the most severe controls and penalties.
 The DEA had initially classified MDMA as a Schedule 1 substance in 1984. The ruling was challenged but the scheduling was subsequently upheld in a 1985 decision. However, the ruling was challenged again, this time by Dr Lester Grinspoon, an associate professor of psychiatry at Harvard Med School. Dr Grinspoon contended that his research on the therapeutic uses of MDMA would be elimin- ated by its Schedule 1 classification. He cited four reasons for the classification to be voided, challenging the DEA's assertion that the drug has a high potential for abuse and contending that the ruling was based "upon incomplete and arbitrary recommendations from the Secretary of Health and Human Services."
 Dr. Grinspoon further contended that the DEA had applied the wrong legal standards in making its assessment and in classifying MDMA as a Schedule 1 substance. Grinspoon's arguments were eventually upheld and the ruling was vacated and remanded back to the administrator of the DEA "for further proceedings consistent with this opinion." The DEA may decide to reclassify, or sharpen its legal argument and continue to press for Schedule 1 classifi- cation. So stay tuned: a battle has been won, but the war continues.
 In article , shawn@laidbak.UUCP (Shawn McKay) writes: > I know I spelled that wrong, but I don't remember seeing a proper name for it, if memory serves, this was recently made illegal in CA, anyone ever have any experience with it? Know what its effect is/was or where it comes from?Thanks.-- Shawn
 XTC is one of the more common names for a drug named MDMA. MDMA is one of many metamphetamines like MDA, Crystal Meth, and others. MDMA is one of the least toxic of these, although it still does some damage to your liver. But then, alcohol in reasonable quantities does a lot more damage to your liver.

MDA is the worst. The effects of MDMA as I experienced an unspecified time ago last about half as long as those of MDA, only 4 to 6 hrs. It is taken in crystal form, in caplets or just solved in water. The effects are quite pleasant (trust me). The stuff does something to your nerves. Feeling and touching things becomes the most awesome experience. Soft objects (especially cats!) feel very different. It is hard to describe. Other people are also a nice ecxperience. You feel like hugging them all the time (this is the reason people call it XTC/ecstacy or just the love drug.

I'm not a chemist, so I can't tell what it actually does, but I know that it drains water from your spine or something like that. That's why drinking liquids like water or juices is absolutely necessary when on MDMA. The chemists here might even be able to explain to me why it is very harmful to drink alcoholic beverages, to eat/drink dairy products or to eat chocolate. Prices for MDMA are not really high, but since availbility varies, it is hard for me to jut give a price. I paid around $5 per hit. I expect that most prices are somewhere between $4 and $10. -Mike
 .............................. Not completely on subject, but I would like to comment on the ingestion of MDMA analogs. Not long ago I would have warned everyone off it and its analogs because shortly after the appearance of "X" and its rapid growth as a psuedo-legal drug, scientific reports started to surface stating that permanent damage was caused to dopamine receptors in certain parts of the brain. 

Now 2 and 3 years after those reports very similar tests have been done by various groups and they show that the results of the government sponsored original trials are not reproducable. Clearly these too are to some extent goverment sponsored, but seem to lack the bias the previous experiments had (I'm trusting a biologist on this, I don't claim to be able to analyze neurobiological techniqe). 

In any case everyone should be aware that the effective doses for MDA and its analogs are quite close to the LD50. And finaly,does anyone know anything about the effects of "euphoria", its chemical structure or relation to other newly developed psychedelics. Maybe my feeling of outrage is silly after watching the responce so far of the war on drugs, but asking scientists to fake reports sets a really bad precident. May be this should have just been posted to alt.conspiricy. 

If you would like the references to the papers above please send e-mail they should be available in full at your local large sized collage library.


\6 Ecstasy MDMA

Three ways that MDMA can be dangerous: Brain damage, psycological damage, medical effects (increased heart rate and blood pressure) heat stroke. MDMA was patented in 1912 by Merck. MDMA ;(extacy) (XTC); metheylenedimethoxymethamphetamine. Is an analog of MDA (methylenedimethoxyamphetamine). MDA Was first synthesized in 1917 by Parke-Davis company as an appetite suppressant drug. The drug, in addition to suppressing appetite, produced what is now termed as an "entacto-effect" in the test subjects. Because of the adverse side effects, Parke-Davis did not market the drug and let the patent expire. The drug resurfaced in the 1960's along with the advent of many other psychoactive substance. Known negative side effects are around a 40% reduction of serotonergic synapses in the rat brain with a 5mg/kg dosage (no data is available for neurotoxicity in humans). Cerebral spinal fluid of admitted users has been shown to have a marked decrease in 5-HT levels. More on the pharmacology later.... When DOM (2,5-dimethoxy-4-methylphenylisopropylamine) first hit the streets of San Francisco in the late sixties, it was distributed in tablets of 10 or 20 mg. Threshold effects begin at 1 mg (you get muscle tremors, facial flushing, and minor sensory amplification) and the more you do, the longer and more intense the trip. Obviously, if people took two or three tablets, they'd be in for a long trip. So, the stories of DOM trips lasting for days are just the result of people not knowing the ED. It is really a nice psychedlic at 5 mgs or so, no worse than LSD. As for the stories of antipsychotics not helping or worsening a DOM trip, such stories are nonsense from a pharmacological standpoint. There is nothing really unusual about DOM as a psychedelic, if anything it is a cleaner 5-HT2 agonist than LSD. This rumor was studied using 50-200 m g chlorpromazine to counteract large DOM doses. While the effects of DOM w eren't completely reversed, the chlorpromazine did calm the people down. Check out Snyder et al (1968) in Amer. J. Psychiat. 125: 357-364 and Hollister et al (1969) in Psychopharmacologia 14: 62-73 for studies on humans with low and high doses respectively.

MDMA has been shown to be toxic to serotonergic neurons in rats and primates >at doses only slightly higher than the typical recreational dose in humans >(on a mg/kg basis.) This should be tempered by the observation that there >have been no observable long-term behavioral effects in people who have >taken MDMA, but it is unfashionable to decapitate humans and examine their >brains' serotonergic neurons directly. Additionally, many drugs (meth- >amphetamine, fenfluramine) have similar effects in animal models, but they >are still used without any ill effects. I think the jury is still out, myself. >Steve Dyer >dyer@ursa-major.spdcc.com aka {ima,harvard,rayssd,linus,m2c}!spdcc!dyer >dyer@arktouros.mit.edu > I agree with that conclusion, but would also like to point to a couple of related facts. First, people will show symptoms of Parkinson's disease only after about 80 % of their dopaminergic neurons are destroyed. Second, patients will notice a loss of memory only after tests show their short term memory has been impaired by 85% Which means that half your serotonergic receptors could be destroyed and you would probably not notice any difference. The brain is a wonderful organ with a lot of redundancy built in it! The problem is that you might feel this loss of receptors later in life as some of your brain cells die due to normal aging and there are not enough "backup" receptors. Of course, no data exist on MDMA users who have been using it for 50 years. Since MDMA has been shown to be toxic to some animals, no research is likely to be done on humans for ethical reasons. I have used MDMA (when it was legal) and enjoyed it, but now I would be scared to do it even assuming it was still legal. This is of course a personal opinion. Has there been some more recent info on this serotonergic receptor stuff in the litterature?

Pierre St-HilaireMIT Media Laboratory Subject: Re: long term dangers of MDMA In article MASSOUD@auvm.auvm.edu (NADIM MASSOUD) writes: >Hi, could any knowledgeble person tell me about the possible dangers >of occasional MDMA use? I have read lots of articles on the subject, >but no study offered convincing evidence as to the negative effects >on humans.... All answers are greatly appreciated.. Thanks.. Well, that's because there ISN'T evidence of any observable deleterious behavioral or neuropsychological effects in humans, but what is observed in animal models (histological and neurochemical) probably should be interpreted conservatively. Matt F. mentions that there are some upcoming studies of HIAA levels in spinal fluid in MDMA users, a test which may be a marker for evidence of neurotoxicity. On the other hand, Ricaurte's other human studies have not been without criticism. We'll have to see. I have no reason to beat the drum for MDMA, but the thing that makes me somewhat suspicious and uneasy about the facileness of these studies purporting to point to MDMA's neurotoxicity (and thus support the conclusion that the drug should be banned), is that drugs which are far more neurotoxic in the same models are used quite routinely without harm. Fenfluramine, a serotonergic appetite suppressant is three times more potent than MDMA in producing the same experimental lesions in animals. It has been marketed and sold for more than 25 years, and millions of doses have been administered to people, usually chronically, without any particular side effects which would point to a lasting neurological lesion. In fact, one of its two isomers, d-fenfluramine, is in the middle of clinical trials for FDA approval as an appetite suppressant which lacks some of the side-effects of the racemic drug. Methamphetamine also appears to be neurotoxic in the same models, but even though it is a very abusable drug, no one would say that it produces obvious neurological deficits when used in the treatment of narcolepsy or attention- deficit disorder. The lack of evidence of side effects in people who have used MDMA, even in those who have used it more than a few times, taken together with the evidence of the safe use of other drugs which would otherwise be thought to be dangerous according to this model, suggests that the neurotoxicity of MDMA in humans might very well have been exaggerated. Now, you have to balance that rather cool assessment with the question "Well, just what IS going on?" (especially if the studies in humans become better refined.) Maybe there is a lot of redundancy in the areas where MDMA (and other drugs) ostensibly exert their serotonergic neurotoxicity, such that any deficit remains subclinical. What might it take to unmask that damage in the future? Who knows? It depends on how conservative you want to be. -- Steve Dyer dyer@ursa-major.spdcc.com aka {ima,harvard,rayssd,linus,m2c}!spdcc!dyer dyer@arktouros.mit.edu, dyer@hstbme.mit.edu

Subject: Re: MDMA/Ecstasy Summary: MDMA, MDA are neurotoxic to serotonergic neurons

In article honig@ics.uci.edu (David Honig) writes: >I don't believe the neurotoxicity reports are relevent to human use; I know >of people who've taken several times the usual dose with no adverse effects >other than tiredness afterwards, and slight visuals during. >David A. Honig Yes, and I have a few friends who shoot MPTP and they haven't had any problems either. While I generally find your opinions to be thoughtful and well-informed, I have a difficult time understanding your reasoning here, David. Are you saying that, since you and people you know have noticed no obvious behavioral (or introspective) correlates to MDMA's neurotoxicty, that neurotoxicity is irrelevant? If so, this seems to be a very premature judgement to me. After all, although we don't generally see any effects of dopamine depletion in humans until they've lost 80 or more percent (at which point they develop parkinson's syndrome), it isn't really advisable to shoot MPTP. Why weaken the reliability of your system unless there are significant benefits to the medication (as may be true in MDMA's use in psychotherapy)? Furthermore, it may be that our tests just aren't sensitive enough to detect the behavioral changes associated with the damage. There's been some recent success in detecting damage to the dopaminergic system using reactions. While I don't think this has yet been replicated in humans, researchers (Spirduso et all, I think) have found that rats with dopamine losses of approx. 45% and more have slightly impaired reaction times. Basically, it seems to me that uncontrolled, anecdotal data shouldn't be relied on. I realize that the serotonergic system is very different from the dopamine one and that NO behavioral changes have been found for MDMA-induced seroton- ergic depletion, still judging the neurotoxicity as "irrelevant" seems to me to be very premature. It seems to me that the benefits would have to be better than a good trip in order to out weight the cost. Neurotoxic effects of MDMA have been found at 3-4 times the effective dose (IP injected) in rats and monkeys are even more susceptable. Admittedly, the "effective dose" is probably on the high end (since one can't ask a rat if it feels good, but must give enough to alter its behavior measurably), but even if we couldn't pick up the neurotoxicity until 6-8 times the ED, that's still wouldn't be a very safe window (given the variables and unknown doses involved and the likely- hood of better tests revealing neurotoxicity at lower doses). For those interested in reading primary sources on this subject, I recommend the work by George Ricaurte, who's done a great deal of MDMA research (including studies involving oral doses in squirrel monkeys). G. Battaglia's also active in this field. I recall a paper in Pharmacol-Biochem-Behav. (journal) in the Feb. 88 issue on the parameters of the neurotoxicity. In any case, one would want to look up the latest articles by these two and read the abstracts, intros, and discussions. People interested in the importance of serotonin (5-hydroxytryptamine, 5-HT) should find the target article in Behavioral and Brain Sciences (BBS, an excellent, readable journal with important articles and extensive peer reviews). Serotonin is believed to be related to aggression, sexual behavior, and sleep, to name a few things. Oh, and it's also important in the activity of hallucinogens. --Matt Funkchick. den0@quads.uchicago.edu Subject: mdma neurotoxocity

Yesterday, I posted info on MDMA, working from memory. Today, I brought the June '91 High Times article on the Bridge Conference, held at Stanford (!) February 2-3. Here are some excerpts from the article regarding MDMA:

... Bruce Eisner eloquently characterized MDMA ("ecstasy") as a substance which reveals "the inner nature of human beings, that we all have a core of love and beauty that we can tap into". The question on everyone else's minds seemed to be whether this miraculous chemical also causes brain damage in humans.

In several presentations, audience questions about this issue were addressed by Debby Harlow and Jerome Beck, authors of a sociological study of MDMA funded by the National Institute on Drug Abuse; Dennis McKenna, who has been associated with some of the major MDMA neurotoxicity researchers; and David Nichols, whose 20 years of research on the effects of psychedelics on rats at the Pharmacology Department of Purdue University has also been funded by the NIDA. They did their best to dispel several myths about MDMA toxicity, and to set the record straight on what is known about MDMA neurotoxicity in humans.

The first myth put to rest was that MDMA causes Parkinson's disease or a Parkinson's-like syndrome. This rumor was apparently caused by confusion of MDMA with MPTP, an impurity present in a designer analog of heroin, long-term use of which has caused at least one case of this kind of effect. The second misapprehension concerned the fact that MDMA causes some sort of drainage of spinal fluid. This misconception somehow resulted from a misunderstanding of research into the effects of MDMA on levels of the neurotransmitter serotonin, which are accessed through spinal taps. It's the spinal taps that drain the fluid, NOT the MDMA.

Research into possible MDMA-caused damage to serotonin neurons has spawned a great deal of anxiety and misinterpretation. (Some of the problem results from the fact that MDMA research has been frequently confused with MDA research). Huge, repeated doses of MDMA administered to rats DO cause selective damage to serotonin- receptor sites. (Mice are apparently less sensitive). A similar effect has been observed in primates at dosages above, but approximating, human levels. Recovery from this damage seems to occur in about four months, followed mysteriously by a reappearance of deterioration.

David Nichols offered the most detailed and cogent explanation of what happens in this process. The temporary decrease in serotonin levels following an MDMA trip, which initiates a massive release of serotonin, causes the absorption into serotonin neurons of another neurotransmitter, dopamine, in place of serotonin. Dopamine does not belong in these serotonin-receptor sites, and it is likely that a toxic metabolite created by the enzyme-induced breakdown of dopamine causes the observed damage. This deterioration is "axodentritic", which means that it occurs in the terminals of the nerve cell, not in its main body.

A number of other relevant facts were noted. Nichols pointed out that for over 20 years, large doses of fenfluoramine -- an FDA- approved, MDMA-related chemical prescribed as an appetite suppressant -- have been taken by one and a half to two million people in the US. This drug is twice as toxic as MDMA and is ingested on a daily basis. However, no aberrations have been observed.

Furthermore, Harlow remarked that there are no "behavioral correlates" to MDMA neurotoxicity in any mammals, including humans. This means that no cognitive, emotional, or physiological dysfunctions have been observed to occur as a result of this nerve damage. Harlow asked how, without such correlates, "can we know that this is a negative thing ? What the neurotoxicity researchers are calling brain DAMAGE is really brain CHANGE". Dennis McKenna agreed: "There is no rational reason to assume that this is negative, given the well-known plasticity of the brain".

One psychopharmacologist, who has asked not to be quoted by name, takes this issue even further. "Who knows ? Maybe the trimming back of serotonin receptors has the effect of pruning the psyche!"

For those still concerned about brain damage from MDMA, Nichols referred to a study involving MDMA and the popular antidepressant Prozac. The latter drug blocks the "reuptake" or reabsorption of serotonin into serotonin nerve cells, and has been shown to counteract as well the absorption of the culprit neurotransmitter dopamine into these same cells after administration of MDMA in rats. The conclusion is that a single therapeutic dose of Prozac taken three hours after MDMA would block any possible neuro- toxicity in humans, and one dose three-to-six-hours after MDMA should significantly decrease such damage.

In spite of all the controversy, there is still no positive indication that the animal studies have any bearing on humans. Nichols flatly summed up the situation: "There is no evidence of MDMA neurotoxicity in humans".

In article geraldb@tau-ceti.isc-br.com (Gerald Bryan (Denver)) writes: >Here's what I've read about MDMA's effects: > > o In the average person, given the right set and setting, there are no > long lasting psychological effects that would generally be considered > deleterious. > > o One of the arguments used by the DEA to schedule MDMA was that tests > done with MDA (note, not the same as MDMA) on rats showed some damage > at nerve cell receptor sites. > o After being scheduled, similar tests were done with MDMA, also showing > similar "neurotoxocity", though not as bad as that with MDA. > o Further tests revealed that the nerve cell receptor site damage goes > away after a period of abstinence (I believe the period of time was > 1 month). Also, the amounts of MDMA needed to produce the neurotoxicity > were significantly higher than human dosages (I think based on body > weight). You get the quote unquote neurotoxic effect in squirrel monkeys at about 2-3 times the human ED orally (based on body weight). > o There is at least one commonly prescribed drug, called something like > Fleurotin (help me on this one, netters), that fails the neurotoxicity > test worse than MDMA, yet no one seems concerned about it when > prescribing the drug. Fenfluramine. Used for weight loss.One difference between MDMA and Fenfluramine is that MDMA is used recreationally. The comparison is a good one given that Fenfluramine has been prescribed for many years with no noticable problems. My inclination would be to hold off on it for a few years. It's good for weight loss but there are other drugs. Given MDMA's very probable efficacy in therapy (as Lester Grinspoon has argued), there is no way that it should be Schedule I. At worst, it should be categorized with its cousins, amp and MA, in Schedule II where researchers can get to it more easily. As has been previously posted here (by, I think, Tim Basher) there is a good chance that the neurotoxic effects of MDMA can be prevented, without effecting its psychactive effects. The neurotoxic effects of MDMA happen AFTER the psychoactive ones. A 5-HT reuptake blocker administered at this point can prevent the 5-HT neurotoxicty. I've all but seen it done in real time with microdialysis (with fenfluramine and fluoxetine) in rats. > o The neuro-toxicity has never been observed in humans (but, I've > always wondered, how would they know ?) 5-HIAA levels in the spinal fluid have been found to be lowered in human users, suggesting that the neurotoxicity exists as well. > o There is some disagreement about what the perceived (and temporary) > neuro-toxicity means, if anything. It's more than just a > disagreement -- I don't think anyone has ventured to guess what it > implies. Not saying that I agree with this, but I once heard > Andrew Weil venture that the supposed neurotoxicity might even be > beneficial brain pruning, much like that that occurs normally > in infants. The only successful experiments I've seen were with dopamine neurotoxicity from MA. This was a poster at Neuroscience which found that DA loss of about 50% was correlated with the number of times a rat slipped when walking across a thin beam. Weil's 'beneficial brain pruning' seems intuitively implausible to me, but that's just my inclination. > o According to Dr. David Nichols (within the last several months), > MDMA has not been proven to cause any damage (he may have qualified > this with the word "permanent" -- see the HT article mentioned below). > Dr. David Nichols, by the way, is probably the number 2 psychedelic > chemist in the world today, right after Alexander Shulgin. Dr. Nichols is correct. And Gerald is correct that Nichols knows what he's talking about. >Sources: "Ecstasy: The MDMA Story" by Bruce Eisner. > This month's High Times coverage of the psychedelics conference > held in Santa Cruz, San Francisco, or some place like that. >-- >gerald Bryan | "I don't like myself sober," confided Alan Watts to a > |friend of mine, "so I spend much of my time drunk." > |-- Robert S. deRopp


From: Chemical & Engineering News. September 9, 1985.

"3,4-methylenedioxymethamphetamine (MDMA)....
 HH To a number of psychiatrists scattered across \ / the country, MDMA is a useful therapeutic tool. CThose psychiatrists have been using MDMA quietly /\ since the mid-1970's in counseling sessions as O O an adjunct to psychotherapy. They report that, \ /when used under controlled conditions, MDMA has ----- few negative side effects and can act to ease // \\ psychic trauma and break down barriers to '< >` communication. \ / ===== The National Institute on Drug Abuse (NIDA) \maintains that MDMA is a 'nationwide problem /as well as a serious health threat.' According H C--< to a NIDA publication, MDMA users experience problems 3 \similar to those associated with use of amphetamines NHCH and cocaine. The publication cites specifically 3 'psychological difficulties, including confusion, depression, sleep problems, drug craving, severe anxiety, and paranoia - during and sometimes weeks after taking MDMA.'

MDMA was first synthesized and patented by E. Merck & Co., Germany, in 1914 as an appetite suppressant. The compound was never marketed, however, and the patent on it has long since expired.

It is currently accepted CHEMICAL ABSTRACTS designation is N, alpha-dimethyl-1,3-benzodioxole-5-ethanamine. On the street, it is sold as MDMA, MDM, Adam, Ecstasy, or XTC.

Chemically, MDMA is related both to methamphetamine and 3,4-methylenedioxyamphetamine (MDA). According to a number of research workers, however, it bears little pharmacological relationsh\ ip to those drugs. 'It stands out as unique in its constellation of properties,' says one.

Unlike MDA, MDMA appears to have almost no hallucinogenic properties. Nor is its effects primarily that of a stimulant such as methamphetamine. Instead, MDMA seems to break down barriers to communication between people, ease psychic trauma, and allow individuals access to repressed psychological information.

George Greer, a psychiatrist in private practice in Santa Fe, N.M., ...concluded that 'the single best use of MDMA is to facilitate more direct communication between people involved in a significant emotional relationship....'

The psychiatrists who have used MDMA in therapy also believe that it has relatively low abuse potential because its beneficial or pleasant side effects diminish rapidly with regular use.

...DEA proposed in July, 1984 that MDMA be classified as a Schedule I controlled substance.

...DEA's Frank Sapienza...defends DEA's action on the grounds that research conducted at the University of Chicago demonstrated that MDA is selectively neurotoxic to seratonergic neurons in the brain. Although MDMA's mechanism of action remains unknown, research has shown that its action involves seratonergic neurons. By extrapolatio\ n, MDMA also might be neurotoxic to such neurons.

Such a classification, however, creates a catch-22 situation for the proponents of MDMA as a useful therapeutic drug. The laws applying to Schedule I controlled substances make it quite difficult to obtain approval to conduct clinical trials of a drug. Because it is impossible to obtain patent protection on MDMA, it is unlikely that a pharmaceutical firm will undertake the costly effort to obtain FDA approval for its use. " *** END QUOTE If anyone is interested I would be willing to find out if there has been any further research on MDMA and report any results of the research. A few people have written to me, asking for more information on the possible neurotoxic effects of MDMA. So off I went, once more, to the library in search of... "The Journal of Phamacology and Experimental Therapeutics", 1987, 240(1), 1-7. _Neurotoxicity of the Psychedelic Amphetamine, Methylenedioxymethamphetamine_ by Christopher Joseph Schmidt
 [Ed. note - All emphasis mine] "The neurochemical effects of the unique psychedelic agent, methylenedioxymethamphetamine (MDMA), inidicate it may be a seratonergic neurotoxin related to agents such as p-chloro- amphetamine (PCA)."

"The results clearly demonstrate that MDMA has two distinct influences on the serotonergic system of the rat brain, both of which are manifested by a significant decrease in the concentration of 5-HT (serotonin). Whereas the first effect of MDMA appears to produce a REVERSIBLE depletion of 5-HT, the second is due to a NEUROTOXIC effect of the drug on serotonergic neurons or nerve terminals."

"As demonstrated by the results of the experiments...these two effects can be separated temporally into an early and a later phase."

"This early phase of depletion was REVERSIBLE because cortical serotonin concentrations had recovered to control levels by 24 hours."

"The depletion observed at 3 hr is due almost completely to the acute effect of the drug inasmuch as it is reversed completely by 24 hr...."

"However, transmitter concentrations were reduced significantly 1 week later, indicating a second phase of depletion. The latter phase of depletion was associated with a decrease in synaptosomal serotonin uptake due to a loss in the number of uptake sites with no change in the affinity of the carrier for serotonin."

"The similarities between the neurochemical effects of MDMA and those reported for PCA led us to suggest that the long-term depletions of 5-HT produced by MDMA and PCA occurred though similar mechanisms, i.e., a selective degeneration of seratonergic neurons or nerve terminals."

"... The results from the uptake studies here present [the confirming] biochemical evidence of TERMINAL DAMAGE." Okay, folks. That is the bottom line. Ecstasy does have a neurotoxic effect. I will quote some more on the author's views on what this means to humans.

"Although it is difficult to extrapolate from animal studies to the human situation, some comment about the risk to human MDMA users seems appropriate ...."

"It is first important to point out that the parenteral doses used in this study are approximately 4 to 8 times the human oral dose. There is also evidence to suggest that drugs such as MDMA and MDA may be subject to significant first pass metabolism .... This would mean that the does used in this study may be even further from those to which a user taking the drug p.o. is normally exposed. However, all effects described in this study were produced with a SINGLE ADMINISTRATION of MDMA; consequently, the possible cumulative effects of multiple MDMA exposures remain to be evaluated. Finally ... the possibility that humans might ... be more sensitive to MDMA-induced neurotoxicity must not be overlooked." Well that's the bad news. The good news is ...

"Coadministration of the selective seratonin uptake inhibitor, fluoxetine, completely blocked the reduction in cortical serotonin concentrations 1 week after MDMA. Administration of fluoxetine at various times after MDMA revealed that the long-term effects of the drug developed independently of the acute depletion of serotonin."

"...[The] inhibition of the uptake system by 3 hr postMDMA can still completely protect the serotonergic neurons from the later effects of MDMA." But the good news gets worse ... "At 6 hr after MDMA the irreversible effects of the drug have progress to the extent that the administration of the fluoxetine at this point blocks only an approximate 50% of the depletion." "By 12 hr the steps required for the drug's irreversible effects ... have been completed." However, more good news is..."The two phases of 5-HT depletion are also differ- entiated by their stereoselectivity ... The long term or persis- tent effect of MDMA on serotonergic neurons is ... a property of [only] the (+)-stereoisomer." The bad news is...According to Christopher (in a telcon), it is this (+)-stereoisomer which is PROBABLY responsible for most of MDMA's interesting effects (this info is from other peoples' behaviorial studies). And also that by blocking the acute effect you PROBABLY block its interesting effects also. He said it was not his area of expertise but was his impression from his reading. This article is very well written. It includes method- ology, results, and a nice bibliography. You should be able to find the journal in a good hospital or medical school library. If you cannot locate it, reprints can be requested by writing:

Christopher J. Schmidt Merrill Dow Research Inst 2110 E. Galbraith Road Cincinnati, OH 45215 Please, do not say I sent you :-) I already called him once. 

Once again I will offer to find out more, if there is something you need to know. If you want to try to locate info yourself here is the data you might need. Try Chemical Abstracts. Look under C H NO. 11 15 2. Then look under 1,3-Benzodioxole-5-ethanamine -alpha, alpha- dimethyl


\7 Hallucinogens

BOTANY: Lysergic compounds appear in ergot, a fungal parasite of cereal grains; morning glory and hawaiian baby wood rose seeds; psychedelic tryptamines also occur in psilocybe mushrooms, in some south american trees and the poison glands of the cane toad. (Mescaline is not in this chemical family).
  --------------------------------------------------------- "Indole Alkaloids In Plant Hallucinogens" Richard Evans Schultes, PhD. Journal of Psychedelic Drugs Vol.8(No.1) Jan-Mar 1976
  "The main constituent of the seeds of Rivea corymbosa is ergine or d-lysergic acid amide. Minor alkaloids present are the related d-isolysergic acid amide (isoergine), chanoclavine, elymoclavine and lysergol. The seeds of Ipomoea violacea have a similar composition, but instead of lysergol, they have ergometrine (ergonovine). Later, very minor amounts of two alkaloids ergometrinine and penniclavine - were found in I. violacea by chromatography. the total alkaloid content of the seeds of Ipomoea viloacea is approximately five times as great as that of the seeds of Rivea corymbosa: 0.06% in the former; 0.012% in the latter. This difference in the alkaloid content explains why Indians employ smaller doses of seeds of the Ipomoea than of the Rivea.
  "Ethnopharmacology and Taxonomy of Mexican Psychodysleptic Plants" Jose Luis Diaz M.D. Journal of Psychedelic Drugs Vol. 11(1-2) Jan-Jun 1979
  Seeds of various Morning Glories contain Ergolines: ergine,isoergine,ergonovine Glucosides: turbicoryn [apparently in Rivea corymbosa only]
  called Tlitlitzen (Aztec word for "The Divine Black One") to the Aztecs, Black is a "hot" color, a property of psychotropics associated with light
  --------------------------------------------------------- "The Botanical and Chemical Distribution of Hallucinogens"Richard Evans Schultes, PhD. Journal of Psychedelic Drugs Vol.9(No.3) Jul-Sep 1977
  "I. violacea, often referred to by it's synonyms I. rubro-caerulea and I. tricolor, is represented in horticulture by a number of "varieties," such as: Heavenly Blue, Pearly Gates, Flying Saucers, Wedding Bells, Summer Skies, and Blue Stars - all of which contain the hallucinogenic ergot alkaloids."
  >In the Journal of Psychoactive Drugs, 1980, there is an article >on an ergot derivative used in obstetrics which is an hallucinogen. >Although the dose required is ten times the ED50 (.2 mg) no >significant ill effects were reported. >I believe the name of this drug is methyl ergovine(?) The drug >without the methyl group is supposed to be more effective. It >was (is?) a Sandoz drug, for those with a PDR.
  Ergonovine and methylergonovine are both oxytocic agents: they increase uterine tone and are used (rarely) to assist in delivery and (more frequently) to stop post-partum uterine hemorrhage. Less frequently, they can be used to abort a migraine headache. If they have any hallucinogenic effects, it is certainly a well-kept secret.
  I would be quite concerned about taking 10x the therapeutic dose of a drug like ergonovine, since it can cause arterial spasm and precordial distress even in healthy persons, and intense vasoconstriction and gangrene can follow from an overdose. These are not drugs to fool around with.
  Another related drug, 1-methyl-methylergonovine, or methysergide (Sansert), is used in migraine prophylaxis, and is claimed to have LSD-like actions when high doses are taken. The methyl group on the indole nitrogen reduces the drug's vasoconstrictive actions. Chronic, uninterrupted use of the drug causes a fibrosis of the heart valves and the lungs.
  --------------------------------------------------------- IPOMOEA PURPUREA: A NATURALLY OCCURRING PSYCHEDELIC
  Charles Savage, Willis W. Harman and James Fadiman >From "Altered States of Consciousness, A Book of Readings"edited by Charles Tart BF311.T28
  Of the naturally occurring plant alkaloids used in ancient and modern religious rites and divination one of the least studied is ololiuqui. The earliest known description of its use is by Hernandez, the King of Spain's personal physician, who spent a number of years in Mexico studying the medicinal plants of the Indians and "accurately illustrated ololiuqui as a morning glory in his work which was not published until 1651" (Schultes, 1960). In his words, "When a person takes ololiuqui, in a short time he loses clear reasoning because of the strength of the seed, and he believes he is in communion with the devil" (Alacon, 1945). Schultes (1941) and Wasson (1961) have reported in detail on the religious and divinatory use of two kinds of morning-glory seeds, Rivea corymbosa and Ipomoea violacea, among the Mazatec and Zapotec indians. The first of these is assumed to be the ololiuqui of the ancient Aztecs.
  In 1955 Osmond described personal experiments with Rivea corymbosa seeds and reported that the effects were similar to those of d-lysergic acid diethylamide (LSD-25). He suggested (1957) that the word psychedelic (meaning mind-manifesting) be used as a generic term for this class of substances to refer to their consciousness-expanding and psychotherapeutic function as contrasted with the hallucinogenic aspect. In 1960 Hoffman reported that he had isolated d-lysergic acid amide (LA) and d-isolysergic acid amide from the seed of both Rivea corymbosa and Ipomoea violacea. LA is very similar to LSD in its psychological and physiological manifestations but is reported to have about one twentieth the psychological effectiveness of LSD (Cerletti & Doepfner, 1958).
  The work of these investigators led us to a preliminary study of the psychedelic properties of species of Ipomoea which are commonly found within the continental United States. The seeds of Ipomoea purpurea, the common climbing morning glory, resemble the seeds of Ipomoea violacea and have been found to have similar psychedelic properties. Recent analysis by Taber et al. (1963) has verified that LA is present in the varieties used and is probably the primary active agent.
  The effects of the seeds of Ipomoea purpurea (varieties Heavenly Blue and Pearly Gates) in a total of 45 cases are summarized below. The subjects are all normally functioning adults and the majority had previous experience with LSD. The onset of effects is about half an hour after the seeds have been chewed and swallowed and they last from five to eight hours.
  Low Dose, 20-50 Seeds (11 Subjects)
  This dosage rarely produces any visual distortions, although with eyes closed there may be beginning imagery. Restlessness, evidenced by alternating periods of pacing about and lying down, may be present. There tends to be a heightened awareness of objects and of nature, and enhanced rapport with other persons. A feeling of emotional clarity and of relaxation is likely to persist for several hours after other effects are no longer noticeable.
  Medium Dose, 100-150 Seeds (22 Subjects)
  In this range the effects resemble those reported for medium-dose (75-150 micrograms) LSD experiences, including spatial distortions, visual and auditory hallucinations, intense imagery with eyes closed, synaesthesia and mood elevation. These effects, which occur mainly during the period of 1 to 4 hours after ingestion, are typically followed by a period of alert calmness which may last until the subject goes to sleep.
  High Dose, 200-500 Seeds (12 Subjects)
  In this range the first few hours may resemble the medium dose effects described above. However, there is usually a period during which the subjective states are of a sort not describable in terms of images or distortions, states characterized by loss of ego boundaries coupled with feelings of euphoria and philosophical insight. These seem to parallel the published descriptions of exper- iences with high doses (200-500 micrograms) of LSD given in a supportive, therapeutic setting as reported by Sherwood et al. (1962).
  All the subjects who had previous experience with LSD claimed the effects of the seeds were similar to those of LSD. Transient nausea was the most commonly reported side effect, beginning about one half hour after ingestion and lasting a few minutes to several hours. Other reported side effects not commonly found with LSD were a drowsiness or torpor (possibly due to a glucoside also present in the seeds) and a coldness in the extremities suggesting that the ergine content of the seeds may be causing some vascular constriction. (If this is the case, there may be some danger of ergot poisoning resulting from excessive dosages of the seeds.) The only untoward psychic effect was a prolonged (eight hours) disassociative reaction which was terminate with chlorpromazine [Thorazine]. The possibility of prolonged adverse reactions to the psychological effects of the seeds is essentially the same as with LSD, and the same precautions should be observed (Cohen & Ditman, 1963).
  --------------------------------------------------------- IPOMOEA 7-MAY-90Additional Notes: Ipomoea purpurea is sold as the "Heavenly Blue" variety of morning glory. "Ipomoea tricolor" is the trade name used for that variety. It is identical with the species of morning glory described above.
  The seeds must be chewed or ground in order to be effective. Soaking the ground seeds in water for several hours, filtering out the grounds, and then drinking only the water portion of the mixture can reduce some of the stomach-upset symptoms if such occur.
  Unpleasant LSD and morning glory trips can be smoothed out or even stopped by taking niacin (in the form of nicotinic acid, vitamin B-3 or "niacin"). Vitamin C has been shown to reduce the incidence of paranoia and prevent depletion of the vitamin from the adrenal glands during LSD trips.
  There have been reports that commercially available packets of morning glory seeds from some distributors are coated with fungicides or other chemicals to increase shelf life or discourage the practice of eating them. Seeds from plants grown in one's own garden will be safe as long as you do not spray them with insecticides.
  The last few notes about Niacin and Vitamin C are based on a paperback edition of Hoffer & Osmonds "The Psychedelics"
  It's pretty clear that the latin names of this plant are somewhat confused (which is typical). Ipomoea purpurea, Ipomoea tricolor, Ipomoea violacea and Ipomoea rubro-caerulea are all the same plant.
  The other variety of morning glory, "Ololiuhqui" has at least two Latin names as well: Rivea corymbosa, and Turbina corymbosa.
  "Recreational use of Ergoline Alkaloids from Argyreia Nervosa" William E. Shawcross Journal of Psychedelic Drugs Vol. 15(4) Oct-Dec 1983
  --------------------------------------------------------- Ergot is a product of the fungus Claviceps purpurea. The bio-active ingredients of ergot are all derivatives of lysergic acid. LSD is a semisynthetic derivative of lysergic acid. Thus LSD is an "ergot"-like substance. --------------------------------------------------------- CHEMISTRY AND EFFECT OF THE SEEDS The Hawaiian baby woodrose entered the drug scene in 1965 with the publication of a paper in "Science" entitled "Ergoline Alkaloids in Tropical Wood Roses" by Hylin and Watson. The wide circulation of this journal assured thorough dissemination of the information they presented. They wrote, "The possible health and legal problems associated with the presence of similar compounds in commercially cultivated plants led us to examine the ornamental wood roses, Ipomoea tuberosa and Argyreia nervosa, both common Hawaiian crops that have assumed commerical importance as components of [the] dried tropical flower industry." Comparing the seeds of these two plants with those of the morning glory varieties Pearly Gates and Heavenly Blue, they found the following yield of alkaloids (mg of alkaloid/g of seed material):
  Heavenly Blue 0.813 Pearly Gates 0.423 I. tuberosa [None] A. nervosa 3.050
  The seed of A. nervosa is the best plant source of ergoline alkaloids discovered; it contains approximately 3 mg of alkaloidal material per gram of seed. Approximately one-eighth of this is lysergamide.
  Hylin and Watson found the major alkaloidal constituents in A. nervosa seeds to be ergine (780 mcg/g of fresh seed) and isoergine and penniclavine (555 mcg).
  [Note: Argyreia nervosa has NO history of shamanic use as a hallucinogen]
  This is an excerpt from the article cited : There's no record of Argyreia being used as an hallucinogen in India, but it was used externally as some kind of skin medicine. There's been speculation that Argyreia might have been a component of "Soma", but there's no evidence for that, apparently. Because there's not a long history of human usage of Argyreia, it may be that there are glycosides not mentioned here that take effect at higher doses or might cause stomach upset, tachycardia etc. The article mentioned intestinal complaints in one or two cases at higher experimental doses.
  --------------------------------------------------------- MECHANISM OF ACTION: (Note: the mechanism of action of LSD and other psychedelics is uncertain.)
  From a chapter titled Hallucinogens and Other Psychotomimetics: Biological Mechanisms by S.J.Watson
  "The current thesis of the effect of indole hallucinogens on 5-hydroxytrypamine might be stated as follows: LSD acts to preferentially inhibit serotonergic cell firing and seems to spare postsynaptic serotnergic receptors. This preference is shared by other simillar hallucinogens but in a limited fashion. Nonhallucinogenic analogs of LSD show no preference. These results suggest that there are two different steric conformation of serotonergic receptors, one of which has higher affinity for LSD than the other. In general, 5-ht is an inhibitory transmitter; thus, when its activity is decreased, the next neuron in the chain is freed from inhibition and becomes more active. Since serotnergic systems appear to be intimately involved int eh control of sensation, sleep, attention, and mood, it may be possible to explain the actions of LSD and other hallucinogens by their disinhibition of these critical systems.
  There is also evidence for interaction with dopaminergic systems.
  --------------------------------------------------------- LSD acts as a 5HT autoreceptor agonist in the raphe nucleus. These autoreceptors are typically considered to be 5HT1As. It also acts as a 5HT2 agonist, which is thought to be the main site of hallucinogenic activity. It's probably best called a a mixed 5HT2/5HT1 receptor partial agonist.
  I don't know of its effects on dopamine. Wouldn't be surprised if it has 'em; the systems aren't really functionally separable. The DA effects wouldn't be necessary for hallucinogenic activity, I'd bet.
  --------------------------------------------------------- (From Snyder, "Drugs and the Brain", 1986, Sci Am Books Inc., Reprinted w/o permission, blah, blah, blah... )
  In more recent studies, Aghajanian has focuses not on the serotonin neu rons of the raphe nuclei but on the norepinephrine neurons of the locus coeruleus. As we saw in Chapter 6, the locus coeruleus cell bodies give rise to axons that ramify all over the brain and provide the majority of the norepinephrine neuronal input in most brain regions. Amphetamine releases norepinephrine from these nerve terminals by diplacing the norepinephrine from the neurotransmitter storage vesicles. Presumably, the overall influence of amphetamine on brain function is therefore somewhat different than what occurs when the locus coeruleus fires rapidly. The amphetamine-induced seepage of norepinephrine out of nerve terminals probably elicts a milder type of activation than does the repetitive and presumably more robust ejection of norepinephrine that occurs with rapid firing of the locus coeruleus. Drug-induced changes in animal behavior support this conceptual model. Amphetamine elicits behavioral activation, represented by the rats or mice running about the cage. In contrast, electrical stimulation of the locus coeruleus produces a more dramatic startle response. It is difficult to observe a rat and make inferences about what the animal is feeling, but rats in whom the locus coeruleus has been stimulated seem to go into a state of panic. They stare about, hyper-responsive to all stimuli in the enviornment, whether visual, auditory, or tactile.
  Rats show the same hyper-responsiveness to environmental-stimuli--jumping abruptly at the sound of fingers snapping or in response to a puff of air in the face--when they have been treated with a psychedelic drug. And as you will recall, hyper-responsiveness to sensory stimuli of all modalities is just what one observes in humans under the influence of psychedelic drugs. At- tracted by the similarity between the behavior of rats on LSD and their reac- tion to stimulation of the locus coeruleus, Aghajanian embarked in 1980 upon a series of studies to evaluate how psychedelic drugs affect the locus coeruleus. He showed that any kind of sensory stimulation--sight, sound, smell, taste, or tactile sensation--speeds up the firing of locus coeruleus neurons in rats, and that the accelerated firing is greatly enhanced by treating the animals with LSD or mescaline. In contrast, nonpsychedelic drugs, such as amphetamines and antidepressants, fail to exert this effect. Moreover, the LSD analogue methysergide, which has no psychedelic effects in humans, is correspondingly ineffective in enhancing the reactivity of locus coeruleus neurons to sensory stimulation. Although psychedelic drugs increase the response of locus coeruleus cells to sensory stimulation, they do not cause the neurons to fire spontaneously in the absence of such stimulation. Moreover, directly applying LSD or mescaline to locus coeruleus neurons does not enhance the neurons' reponse to sensory stimulation. We must therefore conclude that the effect of psychedelic drugs on sensory stimulation is indirect--the drugs presumably interact with a different set of neurons that in turn make direct contact with the locus coeruleus. What is particularly fascinating about Aghajanian's findings is how nicely they correspond to what we know about the effects of psychedelic drugs in humans, and how readily they explain the way psychedelic drugs accentuate all our sensory perceptions. The locus coeruleus is a funneling mechanism that integrates all sensory input. Viewed in this way, the observations of Aghajanian can explain synesthesia. If the locus coeruleus lumps all types of sensory messages--from sights, sounds, tactile pressures, smells, tastes--into a generalized excitation system within the brain, one can readily appreciate that stimulation of the locus coeruleus will cause the drug user to feel that sensations are crossing the boundaries between different modalities.
  Aghajanian's research may also illuminate how LSD influences the user's sence of self. The greatly accelerated firing of the locus coeruleus presumably provokes a powerful, patterned release of norepinephrine from nerve terminals throughout the brain. As we discussed earlier, the consequent alerting action would be much more pronounced than what occurs with the far more gradual leaking out of norepinephrine produced when amphetamine displaces the transmitter from the storage vesicles. This extremely enhanced level of alert- ness might possibly account for the "transendent" mental state produced by psychedelic drugs. In other words, in a state of such heightened awareness, the drug user may become conscious of an "inner self" to which he or she is normally oblivious.
  Did that answer any of your questions? Probably not, but I thought it was interesting.
  P.S. Snyder has tripped before =)
  --------------------------------------------------------- Lysergic-acid diethylamide. When ingested into the human body, LSD act as 5-HT (Serotonin) autoreceptor inhibitor, thus it is a 5-HT agonist. LSD increases the level of active 5-HT molecules by disaffecting their autoreceptors (a safeguard type feature in the brain which reduces levels of certain neurotransmitter and the like).
  That "thus" in the first sentence should be an "and." I'm not certain what "disaffecting" should be (autoreceptors' only true loyalty is to the laws of chemistry & physics) for the second sentence to be true.
  The autoreceptors in question are 5-HT1As. 5-HT2s, which are not autoreceptors and which hallucinogens agonize, seem to be the more important ones for hallucinogenic activity. Hallucinogens need not affect 1As directly (some definitely don't). However, 5-HT2 receptor activation seems to facilitate presynaptic 1A function (such that, for example, hallucinogen use produces rapid 5-HT2 downregulation which, in turn, decreases 5-HT1A function). So hallucinogens would inhibit autorecetpor activity, but not necessarily directly.
  LSD also has effects on 5-HT1C receptors, and its not entirely sure what the specific receptor mechanism is -- there's also the question of why the psychological effects seem to last much longer than the presence of the LSD molecule. One thing that is fairly sure is that LSD shuts down the firing of the seratonin neurons in the raphe, though.
  It is difficult to separate 1Cs from 2s because of their great similarity. However, hallucinogens seem to be all 2 & 1C agonists. Molecules which (like LSD) are partial 2 agonists, and which (unlike LSD) are 1c antagonists are not hallucinogenic.
  I believe that the effects of DOI (and probably LSD) on firing in the raphe nucleus are not blocked by 5-HT2 antagonists (like ketanserin), implying that these effects are not mediated by 5-HT2 receptors. Oddly enough, ritanserin (which antagonizes 2 and 1C) doesn't block 'em either. That's kind of mysterious to me.
  5-HT has been implicated in certain behaviors, notably dreaming and sleep, which explains the hallucinatory >>effect. We are in effect dreaming while completely awake and aware. >Actually, a better explanation is the increased firing of the locus coereleus by its disinhibition due to the neurons in the raphe slowing down (since you are inhibiting an inhibitory neuron the result is excitation). The l.c. has been associated with being a "sensory highway" in the brain, and has also been associated with feelings of anxiety, and theorized that its invovled with depression. My guess is that the hallucinations and stimulatory effects of LSD come from potentiating the l.c., while the effect on the 5-HT neurons in the raphe is responsible for its entheogenic effect on the mind.
  This isn't the full story since this decrease in firing (in the raphe) is still produced by hallucinogens even after chronic treatment with hallucinogens. Since tolerance does develop to hallucinogens, we would have expected to see it in the firing. Of course, rate of firing and amount of 5-HT released _are_ two different things. Besides, tolerance may occur via another route.
  [Reminder: FYI only, consult your shamans & attorneys etc., you are self-responsible, regardless of what anyone asserts.]


\8 Hemp

INTRODUCTION: This doc contains straight ans to tough questions about hemp and marijuana. Every effort has been made to ensure their accuracy, and sources, if not provided, are available by request. BE WARNED -- this text has changed minds. The author and contributers do not take responsibility for any change in outlook, new ideas, or re-evaluation of one's relationship with current political parties which may result from allowing photons to travel into your eyeballs, even when said photons originate from a cathode ray tube, backlit LCD screen, microfiche reader or illuminated sheet of paper on which this document is being displayed. Unless of course you feel like showering us with fan mail and candy-grams. In that case we'll take the blame.
  The following persons have contributed to this document at some point in it's evolution: Laura Kriho (orig list of questions) Marc Anderson (fact finding), Paul L. Allen (LaTeX formatting), plus some others who haven't said they want their name put in.
  This material is maintained and written by Brian S. Julin, with help from other. It is copyrighted material. The copyright is only there to prevent anyone from editing or selling this material. Feel free to pass it around in any form as long as it is unaltered in content, and no credit or money is taken for the contents. Questions, contributions or ideas should be mailed to verdant@twain.ucs.umass.edu or c/o Brian S. Julin at UMACRC, S.A.O. box #2, Student Union Bldg, UMASS, 01003
  More info on doc at the end -- wouldn't want to bore you... So without further ado:

--------------------------------------------------------- PART I: WHAT'S ALL THIS FUSS ABOUT HEMP?
  1) What is hemp? For our purposes, hemp is the plant called `cannabis sativa.' There are other plants that are called hemp, but cannabis hemp is the most useful of these plants. In fact, `cannabis sativa' means `useful (sativa) hemp (cannabis)'.
  `Hemp' is any durable plant that has been used since pre-history for many purposes. Fiber is the most well known product, and the word `hemp' can mean the rope or twine which is made from the hemp plant, as well as just the stalk of the plant which produced it.
  2) What is cannabis? Cannabis is the most durable of the hemp plants, and it produces the toughest cloth, called `canvass.' (Canvass was widely used as sails in the early shipping industry, as it was the only cloth which would not rot on contact with sea spray.) The cannabis plant also produces three other very important products which the other hemp plants do not (in usable form, that is): seed, pulp, and medicine.
  The pulp is used as fuel, and to make paper. The seed is suitable for both human and animal foods. The oil from the seed can be used in as a base for paints and varnishes. The medicine is a tincture or admixture of the sticky resin in the blossoms and leaves of the hemp plant, and is used for a variety of purposes.
  3) Where did the word `marijuana' come from? The word `marijuana' is a Mexican slang term which became popular in the late 1930's, during a series of media and govt pgms which we now refer to as the `Reefer Madness Movement.' It refers specifically to the medicine part of cannabis, which Mexican soldiers used to smoke.
  Today in the U.S., hemp (meaning the roots, stalk, and stems of the cannabis plant) is legal to possess. No one can arrest you for wearing a hemp shirt, or using hemp paper. Marijuana (The flowers, buds, or leaves of the cannabis plant) is not legal to possess, and there are stiff fines and possible jail terms for having any marijuana in your possession. The seeds are legal to possess and eat, but only if they are sterilized (will not grow to maturity.)
  Since it is not possible to grow the hemp plant without being in possession of marijuana, the United States does not produce any industrial hemp products, and must import them or, more often, substitute others. (There is a way to grow hemp legally, but it involves filing an application with the Drug Enforcement Administration and the DEA very rarely ever gives its permission.) This does not seem to have stopped people from producing and using marijuana, though. In many of the United States, marijuana is the number one cash crop, mostly because it fetches a very high price on the black market.
  4) How can hemp be used as a food? Hemp seed is a highly nutritious source of protein and essential fatty oils. Many populations have grown hemp for its seed -- most of them eat it as `gruel' which is a lot like oatmeal. The leaves can be used as roughage, but not without slight psycho-active side-effects. Hemp seeds do not contain any marijuana and they do not get you `high.'
  Hemp seed protein closely resembles protein as it is found in the human blood. It is fantastically easy to digest, and many patients who have trouble digesting food are given hemp seed by their doctors. Hemp seed was once called `edestine' and was used by scientists as the model for vegetable protein.
  Hemp seed oil provides the human body with essential fatty acids. Hemp seed is the only seed which contains these oils with almost no saturated fat. As a supplement to the diet, these oils can reduce the risk of heart disease. It is because of these oils that birds will live much longer if they eat hemp seed.
  With hemp seed, a vegan or vegetarian can survive and eat virtually no saturated fats. One handful of hemp seed per day will supply adequate protein and essential oils for an adult.
  5) What are the benefits of hemp compared to other food crops?Hemp requires little fertilizer, and grows well almost everywhere. It also resists pests, so it uses little pesticides. Hemp puts down deep roots, which is good for the soil, and when the leaves drop off the hemp plant, minerals and nitrogen are returned to the soil. Hemp has been grown on the same soil for twenty years in a row without any noticeable depletion of the soil.
  Using less fertilizer and agricultural chemicals is good for two reasons. First, it costs less and requires less effort. Second, many agricultural chemicals are dangerous and contaminate the environment -- the less we have to use, the better.
  6) How about soy? Is hemp competitive as a world source of protein? Hemp does not produce quite as much protein as soy, but hemp seed protein is of a higher quality than soy. Agricultural considerations may make hemp the food crop of the future. In addition to the fact that hemp is an easy crop to grow, it also resists UV-B light, which is a kind of sunlight blocked by the ozone layer. Soy beans do not take UV-B light very well. If the ozone layer were to deplete by 16%, which by some estimates is very possible, soy production would fall by 25-30%.
  We may have to grow hemp or starve, and it won't be the first time that this has happened. Hemp has been used to `bail out' many populations in time of famine. Unfortunately, because of various political factors, starving people in today's underdeveloped countries are not taking advantage of this crop. In some places, this is because government officials would call it `marijuana' and pull up the crop. In other countries, it is because the farmers are busy growing coca and poppies to produce cocaine and heroin for the local Drug Lord. This is truly a sad state of affairs. Hopefully someday the Peace Corps will be able to teach modern hemp seed farming techniques and end the world's protein shortage.
  7) How can hemp be used for cloth? The stalk of the hemp plant has two parts, called the bast and the hurd. The fiber (bast) of the hemp plant can be woven into almost any kind of cloth. It is very durable. In fact, the first Levi's blue jeans were made out of hemp for just this reason. Compared to all the other natural fibers available, hemp is more suitable for a large number of applications.
  Here is how hemp is harvested for fiber: A field of closely spaced hemp is allowed to grow until the leaves fall off. The hemp is then cut down and it lies in the field for some time washed by the rain. It is turned over once to expose both sides of the stalk evenly. During this time, the hurd softens up and many minerals are returned to the soil. This is called `retting,' and after this step is complete, the stalks are brought to a machine which separates the bast and the hurd. We are lucky to have machines today -- men used to do this last part by hand with hours of back-breaking labor.
  8) Why is it better than cotton? The cloth that hemp makes may be a little less soft than cotton, (though there are also special kinds of hemp, or ways to grow or treat hemp, that can produce a soft cloth) but it is much stronger and longer lasting. (It does not stretch out.) Environmentally, hemp is a better crop to grow than cotton, especially the way cotton is grown nowadays. In the United States, the cotton crop uses half of the total pesticides. (Yes, you heard right, one half of the pesticides used in the entire U.S. are used on cotton.) Cotton is a soil damaging crop and needs a lot of fertilizer.
  9) How can hemp be used to make paper? Both the fiber (bast) and pulp (hurd) of the hemp plant can be used to make paper. Fiber paper was the first kind of paper, and the first batch was made out of hemp in ancient China. Fiber paper is thin, tough, brittle, and a bit rough. Pulp paper is not as strong as fiber paper, but it is easier to make, softer, thicker, and preferable for most everyday purposes. The paper we use most today is a `chemical pulp' paper made from trees. Hemp pulp paper can be made without chemicals from the hemp hurd. Most hemp paper made today uses the entire hemp stalk, bast and hurd. High-strength fiber paper can be made from the hemp baste, also without chemicals.
  The problem with today's paper is that so many chemicals are used to make it. High strength acids are needed to make quality (smooth, strong, and white) paper out of trees. These acids produce chemicals which are very dangerous to the environment. Paper companies do their best to clean these chemicals up (we hope.) Hemp offers us an opportunity to make affordable and environmentally safe paper for all of our needs, since it does not need much chemical treatment. It is up to consumers, though, to make the right choice -- these dangerous chemicals can also be used on hemp to make a slightly more attractive product. Instead of buying the whiter, brighter role of toilet paper, we will need to think about what we are doing to the planet.
  Because of the chemicals in today's paper, it will turn yellow and fall apart as acids eat away at the pulp. This takes several decades, but because of this publishers, libraries and archives have to order specially processed acid free paper, which is much more expensive, in order to keep records. Paper made naturally from hemp is acid free and will last for centuries.
  10) Why can't we just keep using trees? The chemicals used to make wood chemical pulp paper today could cause us a lot of trouble tomorrow. Environmentalists have long been concerned about the effects of dioxin and other compounds on wildlife and even people. Beyond the chemical pollution, there are agricultural reasons why we should use cannabis hemp instead. When trees are harvested, minerals are taken with them. Hemp is much less damaging to the land where it is grown because it leaves these minerals behind.
  A simpler answer to the above question is: Because we are running out! It was once said that a squirrel could climb from New England to the banks of the Mississippi River without touching the ground once. The European settler's appetite for firewood and farmland put an end to this. When the first wood paper became a huge industry, the United States Department of Agriculture began to worry about the `tree supply.' That is why they went in search of plant pulp to replace wood. Today some `conservatives' argue that there are more forests now than there ever were. This is neither true, realistic nor conservative: these statistics do not reflect the real world. Once trees have been removed from a plot of land, it takes many decades before biological diversity and natural cycles return to the forest, and commercial tree farms simply do not count as forest -- they are farm land.
  As just mentioned, many plant fibers were investigated by the USDA -- some, like kenaf, were even better suited than cannabis hemp for making some qualities of paper, but hemp had one huge advantage: robust vitality. Hemp generates immense amounts of plant matter in a three month growing season. When it came down to producing the deluge of paper used by Americans, only hemp could compete with trees. In fact, according to the 1916 calculations of the USDA, one acre of hemp would replace an entire four acres of forest. And, at the same time, this acre would be producing textiles and rope.
  Today, only 4% of America's old-growth forest remains standing -- and there is talk about building roads into that for logging purposes! Will our policy makers realize in time how easy it would be to save them?
  11) How can hemp be used as a fuel? The pulp (hurd) of the hemp plant can be burned as is or processed into charcoal, methanol, methane, or gasoline. The process for doing this is called destructive distillation, or `pyrolysis.' Fuels made out of plants like this are called `biomass' fuels. This charcoal may be burned in today's coal-powered electric generators. Methanol makes a good automobile fuel, in fact it is used in prof auto races. It may someday replace gasoline.
  Hemp may also be used to produce ethanol (grain alcohol) The US govt has developed a way to make this auto fuel additive from cellulosic biomass. Hemp is an excellent source of high quality cellulosic biomass. One other way to use hemp as fuel is to use the oil from the hemp seed - some diesel engines can run on pure pressed hemp seed oil. However, the oil is more useful for other purposes, even if we could produce and press enough hemp seed to power many millions of cars.
  12) Why is it better than petroleum? Biomass fuels are clean and virtually free from metals and sulfur, so they do not cause nearly as much air pollution as fossil fuels. Even more importantly, burning biomass fuels does not increase the total amount of carbon dioxide in the Earth's atmosphere. When petroleum products are burned, carbon that has been stored underground for millions of years is added to the air; this may contribute to global warming through the `Greenhouse Effect', (a popular theory which says that certain gases will act like a wool blanket over the entire Earth, preventing heat from escaping into space.) In order to make biomass fuels, this carbon dioxide has to be taken out of the air to begin with -- when they are burned it is just being put back where it started.
  Another advantage over fossil fuels is that biomass fuels can be made right here in the United States, instead of buying them from other countries. Instead of paying oil drillers, super-tanker captains, and soldiers to get our fuel to us, we could pay local farmers and delivery drivers instead. Of course, it is possible to chop down trees and use them as biomass. This would not be as beneficial to the environment as using hemp, especially since trees that are cut down for burning are `whole tree harvested.' This means the entire tree is ripped up and burned, not just the wood. Since most of the minerals which trees use are in the leaves, this practice could ruin the soil where the trees are grown. In several places in the United States, power companies are starting to do this -- burning the trees in order to produce electricity, because that is cheaper than using coal. They should be using hemp, like researchers in Australia started doing a few years ago. (Besides, hemp provides a higher quality and quantity of biomass than trees do.)
  13) How can hemp be used as a medicine? Marijuana has thousands of possible uses in medicine. Marijuana (actually cannabis extract) was available as a medicine legally in this country until 1937, and was sold as a nerve tonic -- but mankind has been using cannabis medicines much longer than that. Marijuana appears in almost every known book of medicine written by ancient scholars and wise men. It is usually ranked among the top medicines, called `panaceas', a word which means `cure-all'. The list of diseases which cannabis can be used for includes: multiple sclerosis, cancer treatment, AIDS (treatment), glaucoma, depression, epilepsy, migraine headaches, asthma, pruritis, sclerodoma, severe pain, and dystonia. This list does not even consider the other medicines which can be made out of marijuana -- these are just some of the illnesses for which people smoke or eat whole marijuana today.
  There are over 60 chemicals in marijuana which may have medical uses. It is relatively easy to extract these into food or beverage, or into some sort of lotion, using butter, fat, oil, or alcohol. One chemical, cannabinol, may be useful to help people who cannot sleep. Another is taken from premature buds and is called cannabidiolic acid. It is a powerful disinfectant. Marijuana dissolved in rubbing alcohol helps people with the skin disease herpes control their sores, and a salve like this was one of the earliest medical uses for cannabis. The leaves were once used in bandages and a relaxing non-psycho active herbal tea can be made from small cannabis stems.
  The most well known use of marijuana today is to control nausea and vomiting. One of the most important things when treating cancer with chemotherapy or when treating AIDS with AZT or Foscavir, being able to eat well, makes the difference between life or death. Patients have found marijuana to be extremely effective in fighting nausea; in fact so many patients use it for this purpose even though it is illegal that they have formed `buyers clubs' to help them find a steady supply. In California, some city governments have decided to look the other way and allow these clubs to operate openly.
  Marijuana is also useful for fighting two other very serious and wide-spread disabilities. Glaucoma is the second leading cause of blindness, caused by uncontrollable eye pressure. Marijuana can control the eye pressure and keep glaucoma from causing blindness. Multiple Sclerosis is a disease where the body's immune system attacks nerve cells. Spasms and many other problems result from this. Marijuana not only helps stop these spasms, but it may also keep multiple sclerosis from getting worse.
  14) What's wrong with all the prescription drugs we have? They cost money and are hard to make. In many cases, they do not work as well, either. Some prescription drugs which marijuana can replace have very bad, even downright dangerous, side-effects. Cannabis medicines are cheap, safe, and easy to make.
  Many people think that the drug dronabinol should be used instead of marijuana. Dronabinol is an exact imitation of one of the chemicals found in marijuana, and it may actually work on a lot of the above diseases, but there are some big problems with dronabinol, and most patients who have used both dronabinol and marijuana say that marijuana works better.
  The first problem with Dronabinol is that it is even harder to get than marijuana. Many doctors do not like to prescribe dronabinol, and many drug stores do not want to supply it, because a lot of paperwork has to be filed with the Drug Enforcement Administration. Secondly, dronabinol comes in pills which are virtually useless to anyone who is throwing up, and it is hard to take just the right amount of dronabinol since it cannot be smoked. Finally, because dronabinol is only one of the many chemicals in cannabis, it just does not work for some diseases. Many patients do not like the effects of dronabinol because it does not contain some of the more calming chemicals which are present in marijuana.
  15) What other uses for hemp are there? One of the newest uses of hemp is in construction materials. Hemp can be used in the manufacture of `press board' or `composite board.' This involves gluing fibrous hemp stalks together under pressure to produce a board which is many times more elastic and durable than hardwood. Because hemp produces a long, tough fiber it is the perfect source for press-board. Another interesting application of hemp in industry is making plastic. Many plastics can be made from the high-cellulose hemp hurd. Hemp seed oil has a multitude of uses in products such as varnishes and lubricants.
  Using hemp to build is by no means a new idea. French archeologists have discovered bridges built with a process that mineralizes hemp stalks into a long-lasting cement. The process involves no synthetic chemicals and produces a material which works as a filler in building construction. Called Isochanvre, it is gaining popularity in France. Isochanvre can be used as drywall, insulates against heat and noise, and is very long lasting.
  `Bio-plastics' are not a new idea, either, way back in the 30's Henry Ford had already made a whole car body out of them, but the processes for making them do need more research and development. Bio-plastics can be made w/o much pollution. Unfortunately, companies are not likely to explore bio-plastics if they have to either import the raw materials or break the law. (Not to mention compete with the already est petrochemical prods.)
  --------------------------------------------------------- Part II: WELL WHY AREN'T WE USING HEMP, THEN?
  1) How and why was hemp made illegal? Tough question! In order to explain why hemp, the most useful plant known to mankind, became illegal, we have to understand the reasons why marijuana, the drug, became illegal. In fact, it helps to go way back to the beginning of the century and talk about two other drugs, opium (the grandfather of heroin) and cocaine.
  Opium, a very addictive drug (but relatively harmless by today's standards) was once widely used by the Chinese. The reasons for this are a whole other story, but suffice to say that when Chinese started to immigrate to the United States, they brought opium with them. Chinese workers used opium to induce a trance-like state which helped make boring, repetitive tasks more interesting. It also numbs the mind to pain and exhaustion. By using opium, the Chinese were able to pull very long hours in the sweat shops of the Industrial Revolution. During this period of time, there was no such thing as fair wages, and the only way a worker could make a living was to produce as much as humanly possible.
  Since they were such good workers, the Chinese held a lot of jobs in the highly competitive industrial work-place. Even before the Great Depression, when millions of jobs disappeared overnight, the White Americans began to resent this, and Chinese became hated among the White working class. Even more than today, White Americans had a very big political advantage over the Chinese -- they spoke English and had a few relatives in the government, so it was easy for them to come up with a plan to force Chinese immigrants to leave the country (or at least keep them from inviting all their relatives to come and live in America.) This plan depended on stirring up racist feelings, and one of the easiest things to focus these feelings on was the foreign and mysterious practice of using opium.
  We can see this pattern again with cocaine, except with cocaine it was Black Americans who were the target. Cocaine probably was not especially useful in the work-place, but the strategy against Chinese immigrants (picking on their drug of choice) had been so successful that it was used again. In the case of Blacks, though, the racist feelings ran deeper, and the main thrust of the propaganda campaign was to control the Black community and keep Blacks from becoming successful. Articles appeared in newspapers which blamed cocaine for violent crime by Blacks. Black Americans were painted as savage, uncontrollable beasts when under the influence of cocaine -- it was said to make a single Black man as strong as four or five police officers. (sound familiar?) By capitalizing on racist sentiments, a powerful political lobby banned opium and then cocaine.
  Marijuana was next. It was well known that the Mexican soldiers who fought America during the war with Spain smoked marijuana. Poncho Villa, A Mexican general, was considered a nemesis for the behavior of his troops, who were known to be especially rowdy. They were also known to be heavy marijuana smokers, as the original lyrics to the song `la cucaracha' show. (The song was originally about a Mexican soldier who refused to march until he was provided with some marijuana.)
  After the war had ended and Mexicans had begun to immigrate into the South Eastern United States, there were relatively few race problems. There were plenty of jobs in agriculture and industry and Mexicans were willing to work cheap. Once the depression hit and jobs became scarce, however, Mexicans suddenly became a public nuisance. It was said by politicians (who were trying to please the White working class) that Mexicans were responsible for a violent crime wave. Police statistics showed nothing of the sort -- in fact Mexicans were involved in less crime than Whites. Marijuana, of course, got the blame for this phony outbreak of crime and health problems, and so many of these states made laws against using cannabis. (In the Northern states, marijuana was also associated with Black jazz musicians.)
  Here is where things start to get complicated. Put aside, for a moment, all the above, because there are a few other things involved in this twisted tale. At the beginning of the Great Depression, there was a very popular movement called Prohibition, which made alcohol illegal. This was motivated mainly by a Puritan religious ethic left over from the first European settlers. Today we have movies and television shows such as the "Untouchables" which tell us what it was like to live during this period. Since it is perhaps the world's most popular drug, alcohol prohibition spawned a huge `black market' where illegal alcohol was smuggled and traded at extremely high prices. Crime got out-of-hand as criminals fought with each other over who could sell alcohol where. Organized crime became an American institution, and hard liquor, which was easy to smuggle, took the place of beer and wine.
  In order to combat the crime wave, a large police force was formed. The number of police grew rapidly until the end of Prohibition when the government decided that the best way to deal with the situation was to just give up and allow people to use alcohol legally. Under Prohibition the American government had essentially (and unwittingly) provided the military back-up for the take-over of the alcohol business by armed thugs. Even today, the Mob still controls liquor sales in many areas. After Prohibition the United States was left with nothing to show but a decade of political turmoil -- and a lot of unemployed police officers.
  During Prohibition, being a police officer was a very nice thing -- you got a relatively decent salary, respect, partial immunity to the law, and the opportunity to take bribes (if you were that sort of person.) Many of these officers were not about to let this life-style slip away. Incidentally, it was about this time when the Federal Bureau of Narcotics and Dangerous Drugs was reformed, and a man named Harry J. Anslinger was appointed as its head. (Anslinger was appointed by his uncle-in-law, Andrew Mellon, who was the Secretary of the United States Treasury.) Anslinger campaigned tirelessly for funding in order to hire a large force of narcotics officers. After retiring, Anslinger once mused that the FBNDD was a place where young men were given a license to steal and rape.
  The FBNDD is the organization which preceded what we now call the DEA, and was responsible for enforcing the new Federal drug laws against heroin, opium, and cocaine. One of Anslinger's biggest concerns as head of the FBNDD was getting uniform drug laws passed in all States and the Federal legislature. (Anslinger also had a personal dislike of jazz music and the Black musicians who made it. He hated them so much that he spent years tracking each of them and dreamed of arresting them all in one huge, cross-country sweep.) Anslinger frequented parent's and teacher's meetings giving scary speeches about the dangers of marijuana, and this period of time became known as Reefer Madness. (The name comes from the title of a silly movie produced by a public health group.)
  2) OK, so what the heck does all this other stuff have to do with hemp? To make a long story short, during the first decades of this century, opium was made illegal to kick out the Chinese immigrants who had flooded the work-force. Cocaine was made illegal to repress and control the Black community. And, marijuana was made illegal in order to control Mexicans in the Southeast (and Blacks.) All these laws were based mainly on emotional racism, without much else to back them up -- you can easily tell this by reading the hearings held in state legislatures. Also at this time, the end of Prohibition left us with a large force of unemployed police officers, who looked for work enforcing the new drug laws. Consequently, these same police officers needed to convince the country that their jobs were important. They did so by scaring parents about the dangers of drugs. All this set the stage for a law passed in the Federal legislature which put a prohibitive tax on marijuana. This is what killed the hemp industry in 1937, since it made business in hemp impossible.
  Before the 1937 Marijuana Tax Act, the state of Kentucky was the center of a relatively large American hemp industry which produced cloth and tow (rope for use in shipping.) The industry would have been larger, but hemp had one major disadvantage: processing it required a lot of work. Men had to `brake' hemp stalks in order to separate the fiber from the woody core. This was done on a small machine called a hand-brake, and it was a job fit for Hercules. It was not until the 1930's that machines to do this became widely available.
  Today we use paper made by a process called `chemical pulping'. Before this, trees were processed by `mechanical pulping' instead, which was much more expensive. At about the same time as machines to brake hemp appeared, the idea of using hemp hurds for making paper and plastic was proposed. Hemp hurds were normally considered to be a worthless waste product that was thrown away after it was stripped of fiber. New research showed that these hurds could be used instead of wood in mechanical pulping, and that this would drastically reduce the cost of making paper. Popular Mechanics Magazine predicted that hemp would rise to become the number one crop in America. In fact, the 1937 Marijuana Tax Act was so unexpected that Popular Mechanics had already gone to press with a cover story about hemp, published in 1938 just two months after the Tax Act took effect.

3) Doesn't Marijuana cause brain damage? The short answer: No.
  The long answer: The reason why you ask this is because you probably heard or read somewhere that marijuana damages brain cells, or makes you stupid. These claims are untrue.
  The first one -- marijuana kills brain cells -- is based on research done during the second Reefer Madness Movement. A study attempted to show that marijuana smoking damaged brain structures in monkeys. However, the study was poorly performed and it was severely criticized by a medical review board. Studies done afterwards failed to show any brain damage, in fact a very recent study on Rhesus monkeys used technology so sensitive that scientists could actually see the effect of learning on brain cells, and it found no damage.
  But this was Reefer Madness II, and the prohibitionists were looking around for anything they could find to keep the marijuana legalization movement in check, so this study was widely used in anti-marijuana propaganda. It was recanted later.
  (To this day, the radical anti-drug groups, like P.R.I.D.E. and Dr. Gabriel Nahas, still use it -- In fact, America's most popular drug education program, Drug Abuse Resistance Education, claims that marijuana ``can impair memory perception & judgement by destroying brain cells.'' When police and teachers read this and believe it, our job gets really tough, since it takes a long time to explain to children how Ms. Jones and Officer Bob were wrong.)
  The truth is, no study has ever demonstrated cellular damage, stupidity, mental impairment, or insanity brought on specifically by marijuana use -- even heavy marijuana use. This is not to say that it cannot be abused, however.
  4) If it doesn't kill brain cells, how does it get you `high'?
  Killing brain cells is not a pre-requisite for getting `high.' Marijuana contains a chemical which substitutes for a natural brain chemical, with a few differences. This chemical touches special `buttons' on brain cells called `receptors.' Essentially, marijuana `tickles' brain cells. The legal drug alcohol also tickles brain cells, but it will damage and kill them by producing toxins (poisons) and sometimes mini-seizures. Also, some drugs will wear out the buttons which they push, but marijuana does not.
  5) Don't people die from smoking pot? Nobody has ever overdosed. For any given substance, there are bound to be some people who have allergic reactions. With marijuana this is extremely rare, but it could happen with anything from apples to pop-tarts. Not one death has ever been directly linked to marijuana itself. In contrast, many legal drugs cause hundreds to hundreds of thousands of deaths per year, foremost among them are alcohol, nicotine, valium, aspirin, and caffiene. The biggest danger with marijuana is that it is illegal, and someone may mix it with another drug like PCP.
  Marijuana is so safe that it would be almost impossible to overdose on it. Doctors determine how safe a drug is by measuring how much it takes to kill a person (they call this the LD50) and comparing it to the amount of the drug which is usually taken (ED50). This makes marijuana hundreds of times safer than alcohol, tobacco, or caffiene. According to a DEA Judge ``marijuana is the safest therapeutically active substance known to mankind.''
  6) I forgot, does marijuana cause short-term memory impairment?
 F:effect of marijuana on memory is its most dramatic and the easiest to notice. Many inexperienced marijuana users find that they have very strange, sudden and unexpected memory lapses. These usually take the form of completely forgetting what you were talking about when you were right in the middle of saying something important. However, these symptoms only occur while a person is `high'. They do not carry over or become permanent, and examinations of extremely heavy users has not shown any memory or thinking problems. More experienced marijuana users seem to be able to remember about as well as they do when they are not `high.'
  Studies which have claimed to show short-term memory impairment have not stood up to scrutiny and have not been duplicated. Newer studies show that marijuana does not impair simple, real-world memory processes. Marijuana does slow reaction time slightly, and this effect has sometimes been misconstrued as a memory problem. To put things in perspective, one group of researchers made a control group hold their breath, like marijuana smokers do. Marijuana itself only produced about twice as many effects on test scores as breath holding. Many people use marijuana to study. Other people cannot, for some reason, use marijuana and do anything that involves deep thought. Nobody knows what makes the difference.
 
  7) Is marijuana going to make my boyfriend go psycho? Marijuana does not `cause' psychosis. Psychotic people can smoke marijuana and have an episode, but there is nothing in marijuana that actually initiates or increases these episodes. Of course, if any mentally ill person is given marijuana for the first time or without their knowledge, they might get scared and `freak.' Persons who suffer from severe psychological disorders often use marijuana as a way of coping. Because of this, some researchers have assumed that marijuana is the cause of these problems, when it is actually a symptom. If you have heard that marijuana makes people go crazy, this is probably why.
  8) Don't users of marijuana withdraw from society? To some extent, yes. That's probably just because they are afraid of being arrested, though. The same situation exists with socially maladjusted persons as does with the mentally ill. Emotionally troubled individuals find marijuana to be soothing, and so they tend to use it more than your average person. Treatment specialists see this, and assume that the marijuana is causing the problem. This is a mistake which hurts the patient, because their doctors will pay less attention to their actual needs, and concentrate on ending their drug habit. Sometimes the cannabis is even helping them to recover. Cannabis can be abused, and it can make these situations worse, but psychologists should approach marijuana use with an open mind or they risk hurting their patient.
  Marijuana itself does not make normal people anti-social. In fact, a large psychological study of teenagers found that casual marijuana users are more well adjusted than `drug free' people. This would be very amusing, but it is a serious problem. There are children who have emotional problems which keep them from participating in healthy, explorative behavior. They need psychological help but instead they are skipped over. Marijuana users who do not need help are having treatment forced on them, and in the mean-time marijuana takes the blame for the personality characteristics and problems of the people who like to use it improperly.
  9) Is it true that marijuana makes you lazy and unmotivated? Not if you are a responsible adult, it doesn't. Ask the U.S. Army. They did a study and showed no effect. If this were true, why would many Eastern cultures, and Jamaicans, use marijuana to help them work harder? `Amotivational syndrome' started as a media myth based on the racial stereotype of a lazy Mexican borracho. The prohibitionists claimed that marijuana made people worthless and sluggish. Since then, however, it has been scientifically researched, and a symptom resembling amotivational syndrome has actually been found. However, it only occurs in adolescent teenagers -- adults are not affected.
  When a person reaches adolescence, their willingness to work usually increases, but this does not happen for teenagers using marijuana regularly -- even just on the weekends. The actual studies involved monkeys, not humans, and the results are not verified, but older studies which tried to show `amotivational syndrome' usually only suceeded when they studied adolescents. Adults are not effected.
  The symptoms are not permanent, and motivation returns to normal levels several months after marijuana smoking stops. However, a small number of people may be unusually sensitive to this effect. One of the monkeys in the experiment was severely amotivated and did not recover. Doctors will need to study this more before they know why.
  10) Isn't marijuana a gateway drug? Doesn't it lead to use of harder drugs? This is totally untrue. In fact, researchers are looking into using marijuana to help crack addicts to quit. There are 40 million people in this country (U.S.) who have smoked marijuana for a period of their lives -- why aren't there tens of millions of heroin users, then? In Amsterdam, both marijuana use and heroin use went *down* after marijuana was decriminalized -- even though there was a short rise in cannabis use right after decriminalization. Unlike addictive drugs, marijuana causes almost no tolerance. Some people even report a reverse tolerance. That is, the longer they have used the less marijuana they need to get `high.' So users of marijuana do not usually get bored and `look for something more powerful'. If anything, marijuana keeps people from doing harder drugs.
  The idea that using marijuana will lead you to use heroin or speed is called the `gateway theory' or the `stepping stone hypothesis.' It has been a favorite trick of the anti-drug propaganda artists, because it casts marijuana as something insidious with hidden dangers and pitfalls. There have never been any real statistics to back this idea up, but somehow it was the single biggest thing which the newspapers yelled about during Reefer Madness II. (Perhaps this was because the CIA was looking for someone to blame for the increase in heroin use after Viet Nam.)
  The gateway theory of drug use is no longer generally accepted by the medical community. Prohibitionists used to point at numbers which showed that a large percentage of the hard drug users `started with marijuana.' They had it backwards -- many hard drug users also use marijuana. There are two reasons for this. One is that marijuana can be used to `take the edge off' the effects of some hard drugs. The other is a recently discovered fact of adolescent psychology -- there is a personality type which uses drugs, basically because drugs are exciting and dangerous, a thrill.
  On sociological grounds, another sort of gateway theory has been argued which claims that marijuana is the source of the drug subculture and leads to other drugs through that culture. By the same token this is untrue -- marijuana does not create the drug subculture, the drug subculture uses marijuana. There are many marijuana users who are not a part of the subculture.
  This brings up another example of how marijuana legalization could actually reduce the use of illicit drugs. Even though there is no magical `stepping stone' effect, people who choose to buy marijuana often buy from dealers who deal in many different illegal drugs. This means that they have access to illegal drugs, and might decide to try them out. In this case it is the laws which lead to hard drug use. If marijuana were legal, the drug markets would be separated, and less people would start using the illegal drugs. Maybe this is why emergency room admissions for hard drugs have gone down in the states that decriminalized marijuana during the 70's.
  11) I don't want children (minors) to be able to smoke marijuana. How can I stop this?
  Legalize it. They can smoke it now; it is about as easy to get as alcohol. There would be less marijuana being sold in schools, playgrounds, and street corners, though, if it was sold legally through pharmacies -- because the dealers would not be able to compete with the prices. If you are a parent, the choice is really up to you: Do you want your children to sneak off with their friends and use marijuana which they bought off the street, or do you want to talk to them calmly and explain to them why they should wait until they are older? Your children are not going to walk up to you and tell you that they use an illegal drug, but if it was not such a big deal they might give you a chance to explain your feelings. Besides, would you rather children use speed, cocaine, and alcohol?
  Consider, also, that children have a natural urge to do things that they aren't supposed to. It is called curiosity. By making such a fuss over marijuana, you make it interesting (some call it the `forbidden fruit' factor.) This is made worse when children are lied to about drugs by teachers and police -- they lose respect for the school and the government. In a lot of ways, it is the hysteria about drugs which causes the most harm. When marijuana users do none of the horrible things they are supposed to, children may think that other more harmful drugs are OK, too. Your children will not respect you unless you are calm and give good reasons for your rules. The first step is for you, the parent, to learn the facts about drugs.
  12) Won't children be able to steal marijuana plants that people are growing?
  Well, if you are worried about them stealing the hemp plants from the paper-pulp farm down the road, you should know that the commercial grades of hemp do not contain much THC (the stuff that gets you high.) If they were to smoke it, they would probably just get a headache. Otherwise, it should be the responsibility of the grower to take measures to prevent this. Most ``home-grown'' marijuana is cultivated indoors anyway. If the children in your town have nothing better to do than go around stealing marijuana to smoke, your town needs to buy a library or something.
  13) Hey, don't you know that marijuana drops testosterone levels in teenage boys causing [various physical and developmental problems]?
  Marijuana does not turn young healthy boys into lanky, girlish looking wimps, no. This scare tactic (call it homo-phobic if you will) was a common device used in early anti-drug literature. It attempts to scare boys away from marijuana by telling them, essentially, that it will turn them into a girl. Young men probably should not use marijuana heavily (see the section on amotivational syndrome), but the risks are not horrendous.
  Anti-marijuana pamphlets used this claim often during Reefer Madness II, but the studies which are cited are mostly faulty or misinterpreted. This is not to say that marijuana use does not affect childhood development at all, just that the effects are not as drastic as some people would like them to sound. In fact they are pretty much unknown.
  14) Doesn't heavy marijuana use lower the sperm count in males?
  Not by much, (if at all) and this can be a good thing. It does not make you impotent or sterile. (If it did -- there would be no Rastafarians left!) Give those testicles a rest, already! Marijuana is certainly _not_ birth control, please don't let your lover tell you it is.
  Many people think that marijuana enhances their sex lives. It is not an aphrodisiac, that is, it does not make people want to have sex. What it does do for some people is make everything more sensual -- it makes food taste better and feelings and emotions more vivid.
  15) I heard marijuana use by teenage girls may impair hormone production, menstrual cycles, and fertility. Is this true?
  Also unproven and unfounded, but there is no data available to tell either way, (and it won't be coming from the U.S. -- current U.S. laws prohibit research on women.) This is the female version of the boy's ``It'll turn you into a sissy'' tactic. As far as anyone knows, it is only a scare tactic.
  16) I forgot, does marijuana cause short-term memory impairment? Go away.
  17) Isn't smoking marijuana worse for you than smoking cigarettes? There are many reasons why it is not. You may have heard that ``one joint is equal to ten cigarrettes'' but this is exagerrated and misleading. Marijuana does contain more tar than tobacco -- but low tar cigarettes cause just as much cancer, so what is that supposed to mean? Scientists have shown that smoking any plant is bad for your lungs, because it increases the number of `lesions' in your small airways. This usually does not threaten your life, but there is a chance it will lead to infections. Marijuana users who are worried about this can find less harmful ways of taking marijuana like eating or vaporizing. (Be careful -- marijuana is safe to eat -- but tobacco is not, you might overdose!) Marijuana does not seem to cause cancer the way tobacco does, though.
  Here is a list of interesting facts about marijuana smoking and tobacco smoking:
  Marijuana smokers generally don't chain smoke, and so they smoke less. (Marijuana is not physically addictive like tobacco.) The more potent marijuana is, the less a smoker will use at a time. •Tobacco contains nicotine, and marijuana doesn't. Nicotine may harden the arteries and may be responsible for much of the heart disease caused by tobacco. New research has found that it may also cause a lot of the cancer in tobacco smokers and people who live or work where tobacco is smoked. This is because it breaks down into a cancer causing chemical called `N Nitrosamine' when it is burned (and maybe even while it is inside the body as well.) •Marijuana contains THC. THC is a bronchial dilator, which means it works like a cough drop and opens up your lungs, which aids clearance of smoke and dirt. Nicotine does just the opposite; it makes your lungs bunch up and makes it harder to cough anything up. •There are benefits from marijuana (besides bronchial dilation) that you don't get from tobacco. Mainly, marijuana makes you relax, which improves your health and well-being. •Scientists do not really know what it is that causes malignant lung cancer in tobacco. Many think it may be a substance known as Lead 210. Of course, there are many other theories as to what does cause cancer, but if this is true, it is easy to see why NO CASE OF LUNG CANCER RESULTING FROM MARIJUANA USE ALONE HAS EVER BEEN DOCUMENTED, because tobacco contains much more of this substance than marijuana. •Marijuana laws make it harder to use marijuana without damaging your body. Water-pipes are illegal in many states. Filtered cigarettes, vaporizers, and inhalers have to be mass produced, which is hard to arrange `underground.' People don't eat marijuana often because you need more to get as high that way, and it isn't cheap or easy to get (which is the reason why some people will stoop to smoking leaves.) This may sound funny to you -- but the more legal marijuana gets, the safer it is.
  It is pretty obvious to users that marijuana prohibition laws are not ``for their own good.'' In addition to the above, legal marijuana would be clean and free from adulturants. Some people add other drugs to marijuana before they sell it. Some people spray room freshener on it or soak in in chemicals like formaldehyde! A lot of the marijuana is grown outdoors, where it may be sprayed with pesticides or contaminated with dangerous fungi. If the government really cared about our health, they would form an agency which would make sure only quality marijuana was sold. This would be cheaper than keeping it illegal, and it would keep people from getting hurt and going to the emergency room.
  18) Don't children born to pot-smoking mothers suffer from ``Fetal Marijuana Syndrome?''
  If a fetal cannabis syndrome exists, cases are so rare that it cannot be demonstrated. Many mothers use marijuana during pregnancy -- it controls the nausea called `morning sickness' and many say it actually increases the appetite and reduces stress. This is especially important in less developed countries, where modern medical care is not as easily available, but even so, the benefits of responsible marijuana use may outweigh the risks even under modern medicine.
  Studies conducted in Jamiaca have shown that mothers who smoke marijuana have healthier children, but this may be due to the extra income generated by marijuana dealing and other factors. It has been a common ploy in the War on Drugs to claim that marijuana, and especially cocaine, causes birth defects or behavior problems like alcohol does. This scares caring mothers into thinking drugs are `evil.' The claims are not based on valid scientific research -- many of them do not even consider the life-style or living conditions of the mothers before pointing at drugs with the blame.
  Obviously, pregnant mothers should not smoke as much pot as they possibly can. If marijuana is abused, it may hurt the health of both mother and child. Delta-9-THC does cross the placenta and enter the fetus. Oddly, though, the marijuana metabolite, 11-nor-9-carboxy-delta-9-THC does not, and the fetus does not break delta-9-THC down into 11-nor like the mother's body does, so unborn children are not exposed to 11-nor. The third trimester is the time when the child is most vulnerable. Parents should bear these facts in mind when they make decisions about using cannabis.
  19) Doesn't marijuana cause a lot of automobile accidents? Not really. The marijuana using public has the same or lower rate of automobile accidents as the general public. Studies of marijuana smoking while driving showed that it does affect reaction time, but not nearly as much as alcohol. Also, those who drive `stoned' have been shown to be less foolish on the road (they demonstrate `increased risk aversion'.) Recent studies have emphasized that alcohol is the major problem on our highways, and that illicit drugs do not even come close to being as dangerous.
  As funny as it may seem, you may be safer driving `stoned', as long as you aren't `totally blasted' and seeing things -- but few users are irresponsible enough to drive in this state of mind, anyway. Still, many people have reported making mistakes while driving because they were stoned.
  There are those who think that marijuana is a major problem on the streets, because of a newspaper article or news story which they have seen which said a large number of people who were killed in driving accidents tested postive for marijuana use. For various reasons, these studies are not reliable:
  Some studies use drug tests which can only tell whether a person has used marijuana in the last month. •Some studies were done near colleges or other areas where drinking, marijuana use, and accidents are all very high, and they did not correct for age or alcohol use. •In many of the studies there were more stoned drivers killed -- but it was not their fault, and when the police ``culpability scores'' were factored in marijuana was not to blame for the accidents.
  20) Aren't you afraid everyone will get hooked? Marijuana produces no withdrawal symptoms no matter how heavy it is used. It is habit forming (psychologically addictive), but not physically addictive. The majority of people who quit marijuana don't even have to think twice about it. Comparing marijuana to addictive drugs is really quite silly.
  For a drug to be physically addictive, it must be reinforcing, produce withdrawal symptoms, and produce tolerance. Marijuana is reinforcing, because it feels good, but it does not do the other two things. Caffeine, nicotine and alcohol are all physically addictive.
  21) Is urine testing for marijuana use as a terms of employment a good idea? I want to make sure my business is run safely.
  No! Some of your most brilliant, hard working, and reliable employees are marijuana users. When you drug test, you put all marijuana users in the same place as the abusers -- the unemployment line. Drug testing is bad for business. (Not to mention it is an invasion of privacy.) If a worker has a drug problem, you can tell by testing how well he does his job. Firing *all* the drug users who work for you will hurt your business, costs money, and will get people very mad at you -- and for what? There isn't even any hard evidence that marijuana users have more accidents or health problems.
  Your employees will probably resent being drug tested; drug testing allows an employer to govern the actions of an employee in his off time -- even when these actions do not effect his job performance. (As told above, marijuana drug tests do not test whether a person is `high'. They test whether or not they have used in the last few weeks.) Asking employees to urinate in a plastic cup every month is not a good way to make them feel like part of the business, or make friends, either. There is growing concern about drug tests, sometimes because they misfire and accuse the wrong person, but mostly because they might be used to find out other confidential information about an employee. Legal professionals are beginning to question whether they are even constitutional.
  22) Isn't all this worth the trouble, though, in order to reduce accident risks and health care costs?
  Everyone knows that marijuana users are bad employees, right? Wrong -- or at least someone forgot to tell the millions of hard working marijuana smokers that. Drug testing companies will hand you piles of statistics which they say prove marijuana use costs you money. The truth is there are just as many studies which show that marijuana users are more successful, use less health care, and produce more than non-users. Before you buy into workplace drug testing, make sure you get the other side of the story.
  In the 1980's, the Bush administration went to great lengths to promote drug testing. In fact, George Bush estimated the cost of drug use at over 60 billion dollars a year, based on a study which supposedly showed that persons who had used marijuana at some time during their life were less successful. The very same study could be used to show that current, heavy users of marijuana and other illegal drugs were actually more successful. Something is a bit fishy here, and when you add to that the fact that several former heads of the DEA and former Drug Czars now own or work in the urinalysis industry, this whole scene begins to smell a bit funny.
  23) Wouldn't it be best to just lock the users all up?
  How do you plan to pay for that? Already, well over five percent of the people in this country (U.S) are in custody (including probation, parole, bail, etc.) Murderers and rapists are being let out of our penatentiaries right now to make room for a few more `deadheads' -- there are about 2,500 Grateful Dead fans in our federal prisons. Imprisoning one person for one year costs about $20,000. The United States leads the world in imprisonment -- at any one time, 425 people out of every 100,000 are behind bars. In the Federal Prison System, one fifth of the prisoners are drug offenders who have done nothing violent. State laws are usually less strict, but state mandatory minumum sentences for drugs are getting more popular.
  Our prisons and our courtrooms are so crowded that the American Bar Association's annual report on the state of the Justice System is basically one long plea for an end to drug laws that imprison users. Even the Clinton Administration recognizes that locking people up is not the solution. This is especially true for the people who actually have drug abuse problems -- they need treatment, not mistreatment. The Drug War put mandatory minimum jail sentences for drug crimes on the lawbooks. If we do not take those laws (at least) back off, we will be in sorry shape come the end of the century. A retroactive policy of marijuana legalization or decriminalization would go a long way in helping to solve this crisis.
  Also consider this -- Once a person gets put in jail, he becomes angry with the world. He will probably be victimized while he is there, and most likely will learn criminal behaviors from hard-core violent offenders. There is also a very good chance that he will have caught AIDS or tuberculosis by the time he gets let back out. By locking up drug users, you are digging yourself a very big trench to fall in -- is it worth it?
  Besides, lots of these people don't deserve to be in jail. Why should they serve time just because they like to get `high' on marijuana? Especially when someone can drink alcohol without being arrested... what kind of law is that? You have to think about what kind of a world you are making for yourself before you act. How are the police of the future going to treat the people? How far are you willing to let the government go to get the drug users? How many of your own rights will you sacrifice by trying to jail `the druggies'?
  24) I heard that there are over 400 chemicals in marijuana... Wellllll...?
  True, but so what? There are also over 400 chemicals in many foods, (including coffee, which contains over 800 chemicals and many rat carcinogens) and we don't see police arresting people in McDonald's, or giving Driving while Eating citations. Only THC is very psycho-active; a few other chemicals also have very small degrees of psycho-activity. People who use marijuana do not get sick more, or die earlier, or lose their jobs (except to drug tests), or have mutant kids... so what's your point?
  The fact that there are over 60 unique chemicals in cannabis, called `cannabinoids,' is something that scientists find very interesting. Many of these cannabinoids may have valuable effects as medicine. For example, `cannabinol' is a cannabinoid which can help people with insomnia. Doctors think that this chemical is why most patients prefer to use marijuana rather than pure Delta-9-THC pills (called dronabinol) -- the cannabinol takes the edge off being `high' and calms the nerves. Another cannabinoid, `cannabidiolic acid', is a very effective anti-biotic, like pennicillin. Many of these chemicals can be extracted from marijuana without any fancy laboratory equipment.
  25) Doesn't that stuff mess up your immune system and make it easier for you catch colds?
  Marijuana (Delta-nine-THC) does have an `immunosuppressive effect.' It acts on certain cells in the liver, called macrophages, in much the same way that it acts on brain cells. Instead of stimulating the cells, though, it shuts them off. This effect is temporary (just like the `high') and goes away quickly; people who suffer from multiple sclerosis may actually find this effect useful in fighting the disease.
  Recent research has also found that marijuana metabolites are left over in the lungs for up to seven months after the smoking has stopped. While they are there, the immune system of the lungs may be affected (but the macrophages do not get ``turned off'' like in the liver.) The effects of smoking itself are probably worse than the effects of the THC, and last just as long.
  All this said, doctors still have not decided whether marijuana users are at risk for colds or not. With the possible exception of bronchitis, there are no numbers which suggest that marijuana users catch more colds, but... this did not stop Carlton Turner, a United States Drug Czar, from saying many times in his public addresses that marijuana caused AIDS and homosexuality. His claims were so ridiculus that the Washington Post and Newsweek Magazine made fun of him, and he was forced to resign.
  Today, AIDS patients use marijuana to treat their symptoms without any aparrent problems. Some studies suggest that marijuana may actually stimulate certain forms of immunity. Researchers have tried to show major effects on the healthy human's immune system, but if marijuana does have any substantial effects, good or bad, they are either too subtle or too small to notice.


\9 Hemp last left over...

m, and he was forced to resign.
  Today, AIDS patients use marijuana to treat their symptoms without any aparrent problems. Some studies suggest that marijuana may actually stimulate certain forms of immunity. Researchers have tried to show major effects on the healthy human's immune system, but if marijuana does have any substantial effects, good or bad, they are either too subtle or too small to notice.
  --------------------------------------------------------- --------------- Part IV: WHY IS IT STILL ILLEGAL?
  1) Why is it STILL illegal?: The official answer: Because you shouldn't use it. You can't use it because it is illegal, and it is illegal so you can't use it. You should not use it. It is illegal. It is illegal so you should not use it.
  The manic-depressive answer: It'll never happen. People are too unorganized/stupid/disempowered. It's just futility. Try, but don't expect to get anywhere. I won't get my hopes up.
  The paranoid-schizophrenic answer: Don't you SEE?!?!? The guys at the top have it SEWN!! They own everything. They'll never let it happen. I shouldn't even be talking to you, but let me give you some advice!! listen... you shouldn't mess with THEM, THEY know everything. THEY are practically psychic, see? And the only way to get it to happen is to become one of THEM. You'd better watch it, or THEY will come and take you away -- THEY do that, you know. It's all a CONSPIRACY!!!
  The neurotic answer: Marijuana? Eeek! Don't you know that stuff is dangerous? People don't make laws for no good reason, you know! Where did you hear about marijuana? Wait! Don't tell me, I don't want to know. If anybody even knew you thought it should be legal -- well -- they'd never talk to you again! Don't you know that marijuana this... marijuana that... ... ... ...
  THE REAL ANSWER: Marijuana is still illegal because enough people have not yet stood up together and said:
  `` THIS IS STUPID!!
 I WANT CANNABIS HEMP LEGAL!!!
 FOR PRODUCTS; FOR MEDICINE;
 FOR FOOD;
 FOR FUN;
 FOR GOODNESS'S SAKE! ISN'T THAT WHAT LIFE'S ALL ABOUT ?!''
  Future Versions: The text of the FAQ is now pretty much stable. New questions may be added and any mistakes corrected. Work on the text will concentrate on fleshing out the resource and sources section, providing more cites, especially pointers to on-line textfiles and information.
  ÄÄÄÄÄÄÄÄÄÄÄÄÄÄÄÄÄ Plants of the Gods ÄÄÄÄÄÄÄÄÄÄÄÄÄÄÄÄÄÄÄÄ Their Sacred, Healing and Hallucinogenic Powers
  Tradition in India maintains that the gods sent man the Hemp plant so that
 he might attain delight, courage, and have heightened sexual desires. When nectar or Amrita dropped down from heaven, Cannabis sprouted from it.
  Another story tells how, when the gods, helped by demons, churned the milk ocean to obtain Amrita, one of the resulting nectars was Cannabis. It was consecrated to Shiva and was [the godess] Indra’s favourite drink. After the churning of the ocean, demons attempted to gain control of Amrita, but
 the gods were able to prevent this seizure, giving Cannabis the name Vijaya (victory) to commemorate their success. Ever since, this plant of
 the gods has been held in India to bestow supernatural powers on its users.
 
 The partnership of Cannabis and man has existed now probably for ten thousand years – since the discovery of agriculture in the Old World. One of our oldest cultivars, Cannabis has been a five- purpose plant: as a
 source of hempen fibres; for its oil; for its akenes or seeds, consumed
 by man for food; for its narcotic properties; and therapeutically to treat a wide spectrum of ills in folk medicine and in modern pharmacopoeias.
 
 Mainly because of its various uses, Cannabis has been taken to many regions around the world. Unusual things happen to plants after long association with man and agriculture. They are grown in new and strange environments and often have opportunities to hybridize that are not offered in their native habitats. They escape from cultivation and frequently become aggressive weeds. They may be changed through human selection for characteristics associated with a specific use. Many cultivated plants are so changed from their ancestral typed that it is not possible to unravel their evolutionary history. Such is not the case, however, with Cannabis. Yet, despite its long history as a major crop plant, Cannabis is still characterised more by what is not known about its biology than what is known.
 
 The botanical classification of Cannabis has long been uncertain. Botanists have not agreed on the family to which Cannabis belongs; early investigators put it in the Nettle family (Urticaceae); later it was accommodated in the Fig family (Moraceae); the general trend today is to assign it to a special family, Cannabaceae, in which only Cannabis and
 Humulus, the genus of Hops, are members. There has even been disagreement as to how many species of Cannabis exist: whether the genus comprises one highly variable species or several distinct species. Evidence now strongly indicates that three species can be recognised: C. indica, C. ruderalia, and C. sativa. These species are distinguished by different growth habits, characters of the akenes, and especially by major differences in structure of the wood. Although all species possess cannabinols, there may possible be significant chemical differences, but the evidence is not yet available.
 
 We cannot known now which of the several uses of Cannabis was
 earliest. Since plant uses normally proceed from the simpler to the more
 complex, one might presume that its useful fibers first attracted man’s attention. Indeed remains of hempen fibers have been found in the earliest
 archaeological sites in the cradles of Asiatic civilisation: evidence of fiber in China dating from 4000 B.C. and hempen rope and thread from Turkestan from 3000 B.C.. Stone beaters for pounding hemp fiber and
 impressions of hempen cord bakery into pottery have been found in ancient sites in Taiwan. Hempen fabrics have been found in Turkish sites of the
 late eighth century B.C., and there is a questionable specimen of Hemp in an Egyptian tomb dated between three and four thousand years ago.
 The Indian vadas sang of Cannabis as one of the divine nectars, able to give man anything from good health and long life to visions of the gods. The Zend-Avesta of 600 B.C. mentions an intoxicating resin, and the
 Assyrians used Cannabis as an incense as early as the ninth century B.C..
  Inscriptions from the Chou dynasty in China, dated 700-500 B.C., have a negative connotation that accompanies the ancient character for Cannabis, Ma, implying its stupefying properties. Since this idea obviously predated writing, the Pen Tsao Ching, written in A.D. 100 but going back to a legendary emperor, Shen-Nung, 2000 B.C., may be taken as evidence that the hallucinogenic properties at very early dates. It was said that Ma-fen (“Hemp fruit”) “if taken to excess, will produce hallucinations [literally, ‘seeing devils’]. If taken over a long term, it makes one communicate with spirits and lightens one’s body.” A Taoist priest wrote in the fifth century B.C. that Cannabis was employed by
 necromancers, in combination with Ginseng, to set forward time and reveal future events. In these early periods, use of Cannabis as an hallucinogen was undoubtedly associated with Chinese shamanism, but by the time of
 European contact 1500 years later, shamanism had fallen into decline, and the use of the plant for inebriation seems to have ceased and had been forgotten. Its value in China then was primarily as a fiber source. There was, however, a continuous record of Hemp cultivation in China from Neolithic times, and it has been suggested that Cannabis may have originated in China, not in central Asia.

 About 500 B.C. the Greek writer Herodotus described a marvelous bath of the Scythians, aggressive horsemen who swept out of the Transcaucasus eastward and westward. He reported that “they make a booth by fixing in the ground three sticks inclined toward one another, and stretching around them woollen plets which they arrange so as to fit as close as possible: inside the booth a dish is place upon the ground into which they put a number of red hot stones and then add some Hemp seed … immediately it smokes and gives out such a vapour as no Grecian vapour bath can exceed; the Scyths, delighted, shout for joy….

 Only recently, archaeologists have excavated frozen Scythian tombs in central Asia, dated between 500 and 300 B.C., and have found tripods and pelts, braziers and charcoal with remains of Cannabis leaves and fruit. It has generally been accepted that Cannabis originated in central Asia and that it was the Scythians who spread it westward to Europe.
  While the Greeks and Romans may not generally have taken Cannabis for inebriation, there are indications that they were aware of the psychoactive effects of the drug. Democritus reported that it was occasionally drunk with wine and myrrh to produce visionary states, and Galen, about A.D. 200, wrote that it was sometimes customary to give Hemp to guests to promote hilarity and enjoyment.

 Cannabis arrived in Europe from the north. In classical Greece and Rome, it was not cultivated as a fiber plant. Filter for ropes and sails, however, was available to the Romans from Gaul as early as the third century B.C.. The Roman writer Lucilius mentioned it in 120 B.C.. Pliny the Elder outlined the preparation and grades of hempen fibers in the first century A.D., and hempen rope was found in a Roman site in England dated A.D. 140-180. Whether the Vikings used Hemp rope or not is not known, but palynological evidence indicates that Hemp cultivation had a tremendous increment in England from the early Anglo-Saxon period to late Saxon and Norman times – from 400 to 1100. Henry VIII fostered the cultivation of Hemp in England. The maritime supremacy of England during Elizabethan times greatly increased the demand. Hemp cultivation began in the British colonies in the New World: first in Canada in 1606, then in Virginia in 1611; the Pilgrims took the crop to New England in 1632. In pre-Revolutionary North America, Hemp was employed even for making work clothes. Hemp was introduced quite independently into Spanish colonies in America: Chile, 1545; Peru, 1554. 
 There is no doubt that hempen fiber production represents an early use of Cannabis, but perhaps consumption of its edible akenes as food predated the discovery of the useful fiber. These akenes are very nutritious, and it is difficult to imagine that early man, constantly searching for food, would have missed this opportunity. Archaeological finds of Hemp akenes in Germany, dated with reservation at 500 B.C., indicate the nutritional use of these plant products. From early times to the present, Hemp akenes have been used as food in eastern Europe, and in the United States as a major ingredient of bird food.
 
 The folk-medicinal value of Hemp – frequently indistinguishable from its hallucinogenic properties – may even be its earliest role as an economic plant. The earliest record of the medicinal use of the plant is that of the Chinese emperor herbalist Shen Nung who, five thousand years ago, recommended Cannabis for malaria, beri-beri, constipation, rheumatic pains, absent-mindedness, and female disorders. Hoa-Glio, another ancient Chinese herbalist, recommended a mixture of Hemp resin and wine as an analgesic during surgery.
 
 It was in ancient India that this “gift of the gods” founded excessive use in folk medicine. It was believed to quicken the mind, prolong life, improve judgement, lower fevers, induce sleep, cure dysentery. Because of its psychoactive properties it was more highly valued than medicines with only physical activity. Several systems of Indian medicine esteemed Cannabis. The medical work Sushruta claimed that it cured leprosy. The Bharaprakasha of about A.D. 1600 described it as antiphlegmatic, digestive, bile affecting, pungent, and astringent, prescribing it to stimulate the appetite, improve digestion, and better the voice. The spectrum of medicinal uses in India covered control of dandruff and relief of headache, mania, insomnia, venereal disease, whooping cough, earaches, and tuberculosis!
 
 The fame of Cannabis as a medicine spread with the plant. In parts of Africa, it was valued in treating dysentery, malaria, anthrax, and fevers. Even today the Hottentots and Mfengu claim its efficacy in treating snake bites, and Sotho women induce partial stupefaction by smoking Hemp before childbirth.
 
 Although Cannabis seems not to have been employed in medieval Europe as an hallucinogen, it was highly valued in medicine and its therapeutic uses can be traced back to early classical physicians such as
 Diosco-rides and Galen. Medieval herbalists distinguished “manured hempe (cultivated) from “bastard hempe” (weedy), recommending the latter against nodes and wennes and other hard tumors,” the former for a host of uses from curing cough to jaundice. They cautioned, however, that in excess it might cause sterility, that “it drieth up… the seeds of generation” in men “and the milke of women’s breasts.” An interesting use in the sixteenth century – source of the name Angler’s Weed in England – was locally important: “poured into the holes of earthwormes [it] will draw them forth and… fishermen and anglers have used this feate to baite their hooks.

The value of Cannabis in folk medicine has clearly been closely tied with its euphoric and hallucinogenic properties, knowledge of which may be as old as its use as a source of fibre. Primitive man, trying all sorts of plant materials as food, must have known the ecstatic hallucinatory effects of Hemp, and intoxication introducing him to an other-worldly plane leading to religious beliefs. Thus the plant early was viewed as a special gift of the gods, a sacred medium for communion with the spirit world. Although Cannabis today is the most widely employed of the hallucinogens, its use purely as a narcotic, except in Asia, appears not to be ancient. In classical times it euphoric properties were, however, recognised. In Thebes, Hemp was made into a drink said to have opium-like properties.
  Galen reported that cakes with Hemp, if eaten to excess, were intoxicating. The use as an inebriant seems to have been spread east and west by barbarian hordes of central Asia, especially the Scythians, who had a profound cultural influence on early Greece and eastern Europe. And knowledge of the intoxicating effects of Hemp goes far back in Indian history, as indicated by the deep mythological and spiritual beliefs about the plant. One preparation, Bhang, was so sacred that it was thought to deter evil, bring luck, and cleanse man of sin. Those treading upon the leaves of this holy plant would suffer harm or disaster, and sacred oaths were sealed over Hemp. The favourite drink of Indra, god of the firmament, was made from Cannabis, and the Hindu god Shiva commanded that the word Bhangi must be chanted repeatedly during sowing, weeding, and harvesting of the holy plant. Knowledge and use of the intoxicating properties eventually spread to Asia Minor. Hemp was employed as an incense in Assyria in the first millennium B.C., suggesting its use as an inebriant.
  While there is no direct mention of Hemp in the Bible, several obscure passages may refer tangentially to the effects of Cannabis resin or Hashish.
 
 It is perhaps in the Himalayas of India and the Tibetan plateau that Cannabis preparations assumed their greatest hallucinogenic importance in religious contexts. Bhang is a mild preparation: dried leaves or flowering shoots are pounded with spices into a paste and consumed as candy – known as maajun – or in tea form. Ganja is made from the resin-rich dried pistillate flowering tops of cultivated plants which are pressed into a compacted mass and kept under pressure for several days to induce chemical changes; most Ganja is smoked, often with Tobacco. Charas consists of the resin itself, a brownish mass which is employed generally in smoking mixtures.
 
 The Tibetans considered Cannabis sacred. A Mahayana Buddhist tradition maintains that during the six steps of asceticism leading to his enlightenment, Buddha lived on one Hemp seed a day. He is often depicted with Soma leaves in his begging bowl and the mysterious god-narcotic Soma has occasionally been identified with Hemp. In Tantric Buddhism of the Himalayas of Tibet, Cannabis plays a very significant role in the meditative ritual used to facilitate deep meditation and heighten awareness. Both medicinal and recreational secular use of Hemp is likewise so common now in this region that the plant is taken for granted as an everyday necessity.
  Folklore maintians that the use of Hemp was introduced to Persia during the reign of Khursu (A.D. 531-579), but it is known that the Assyrians used Hemp as an incense during the first millennium B.C..

Although at first prohibited among islamic peoples, Hashish spread widely west throughout Asia Minor. In 1378, authorities tried to extirpate Hemp from Arabian territory by the imposition of harsh punishments. As early as 1271, the eating of Hemp was so well known that Marco Polo described its consumption in the secret order of Hashishins, who used the narcotic to experience the rewards in store for them in the afterlife. Cannabis extended early and widely from Asia Minor into Africa, partly under the pressure of Islamic influence, but the use of Hemp transcends Mohammedan use. It is widely believed that Hemp was introduced also with slaves from Malaya. Commonly known in Africa as Kif or Dagga, the plant has entered into primitive native cultures in social and religious contexts. The Hottentots, Bushmen, and Kaffirs used Hemp for centuries as a medicine and as an intoxicant. 

In an ancient tribal ceremony in the Zambesi Valley, participants inhaled vapours from a pile of smouldering Hemp; later, reed tubes and pipes were employed, and the plant material was burned on an altar. The Kasai tribes of the Congo have revived an old Riamba cult in which Hemp, replacing ancient fetishes and symbols, was elev- ated to a god – a protector against physical and spiri- tual harm. Treaties are sealed with puffs of smoke from calabash pipes. Hemp-smoking and Hashish-snuffing cults exist in many parts of east Africa, especially near Lake Victoria. Hemp has spread to many areas of the New World, but with few exceptions the plant has not penetrated significantly into many native American religious beliefs and ceremo- nies. There are, however, exceptions such as its use under the name Rosa Maria, by the Tepecano Indians of NW Mexico who occasionally employ Hemp when Peyote is not avail. It has recently been learned that Indians in the Mexican states of Veracruz, Hidalgo, and Puebla practice a communal curing ceremony with a plant called Santa Rosa, identified as Cannabis sativa, which is considered both a plant and a sacred intercessor with the Virgin. 

Although the ceremony is based mainly on Christian elements, the plant is worshipped as an earth deity and is thought to be alive and to represent a part of the heart of God. The participants in this cult believe that the plant can be dangerous and that it can assume the form of a man’s soul, make him ill, enrage him, and even cause death.
  Sixty years ago, when Mexican peons intro the smoking of Marihuana to the US, it spread across the south, and by the 1920s, its use was established in New Orleans, confined primarily among the poor and minority groups. The continued spread of the custom in the US and Europe has resulted in a still unresolved controversy.
  Cannabis sativa was officially in the US Pharmacopoeia until 1937, recommended for a wide variety of disorders, especially as a mild sedative. It is no longer an official drug, altho research in the med potential of some of the cannabinolic constituents or their semi- synthetic analogues is at present very active, particul- arly in relation to the side-effects of cancer therapy.
  The psychoactive effects of Cannabis preparations vary widely, depending on dosage, the preparation and the type of plant used, the method of admin, personality of the user, and social and cultural background. Perhaps the most frequent characteristic is a dreamy state. Long forgotten events are often recalled and thoughts occur in unrelated sequences. Perception of time, and occasionally of space, is altered.

Visual and auditory hallucinations follow the use of large doses. Euphoria, excitement, inner happiness often with hilarity and laughter are typical. In some cases, a final mood of depression may be experienced. While behaviour is sometimes impulsive, violence or aggression is seldom induced.
  In relatively recent years, the use of Cannabis as an intoxicant has spread widely in Western society especi- ally in the US and Europe and has caused apprehension in law-making and law- enforcing circles and has created social and health problems. There is still little, if any, agreement on the magnitude of these problems or on their solution. 

Opinion appears to be pulled in two directions: that the use of Cannabis is an extreme social, moral, and health danger that must be stamped out, or that it is an innocuous, pleasant pastime that should be legalised. It may be some time before all of the truths concerning the use in our times and society of this ancient drug are fully known. Since an understanding of the history and attitudes of peoples who have long used the plant may play a part in furthering our handling of the situation in modern society, it behooves us to consider the role of Cannabis in man’s past and to learn what lessons it can teach us: whether to maintain wise restraint in our urbanised, industrialised life or to free it for general use. For it appears that Cannabis may be with us for a long time.

by Richard Evans Schultes and Albert Hoffman Healing Arts Press (Vermont) 1992