1 What is Heroin? 2 Heroin, Poppy to the Street 3 Heroin, smack, horse 4 Heroin, SW Asian 5 Heroin process 6 Heroin - Chasing the dragon 7 Ibogaine 8 Ketamine (special K) 9 Kung-Sa 10 Laws 11 Methcathinone 12 Methcathinone questions 13 Mushroom toxins incl.PEYOTE 14 Hallucinogenic mushrooms have been part of human history 15 Opium 16 FAQ \1 What is Heroin? Heroin, a very powerful narcotic, is one of the most addictive drugs on earth, both physically and psychologically. It is classified as a depressant (as opposed to a stimulant) meaning that the user apprears tired, drowsy, or drunk rather than energetic or hyperactive (as one might act when under the influence of a stimulant such as cocaine or speed.) Heroin may be smoked when in pure powder form, "snorted" into the nose through a straw or rolled up dollar bill, "skin popped" (injected just under the skin), or "mainlined" (injecting directly into the vein). Heroin most commonly comes in three forms: black-tar, brown powder, or white powder. Black-tar heroin appears just as its name implees - a black ball of tar. Addicts place a small amount (for beginners this would be about half the size of a pea or less) of the heroin in a spoon (which is bent so as to sit level without spilling when placed on a table) with a small amount of water which is then. heated over a flame. Once the heroin has melted it is drawn up into a syringe and injected. Heroin is also produced in a form that looks similar to cocaine - a white powder. And today this form is much more pure and potent than than it has been in the past. While many addicts still inject this form of heroin, because of its purity, many others are able to smoke it through a glass pipe, similar to the way cocaine and speed are smoked. This makes the use of heroin more acceptable to middle and upperclass students and business folk who would other wise shun the stigma of sticking a needle in their arm like a "common junkie" (not to mention the risk of becoming infected with the AIDS virus through the use of dirty needles.) For an alarming report on the increased use of heroin by students and professionals see our excerpts from a recent LA Times article called Heroin Use is on the Increase. Some of the long term physical conditions that accompany heroin addiction include reduced energy level, reduced sex drive, and an overall lethargy and lack of motivation when it comes to involvement with any activities other than those associated with obatining their next "fix" (the next dose and subsequent injection.) Those "associated activities" include burglery, robbery, prostitution, etc. to get money for their next fix. Being on heroin is exactly the same (albeit more powerful) as being on pain pills like Vicodin, Percodan, MS-Contin, etc. It gives a pleasant feeling of well-being just like being high on pain pills: warm, drowsy, a tiny bit itchy. The only way to get anywhere near one's money's worth is to shoot it (unless one comes across snortable stuff like China White, almost-pure powder heroin). Smoking it is a terrible waste which, by the way, isn't done by putting on top of buds and hitting it with a direct flame. It's done by "Chasing the Dragon": it's put on aluminum foil and heated from the bottom and allowed to run down the foil if possible while inhaling the smoke. From personal experience, the user can be on heroin for a few days straight ( a quarter-gram or so per day ) and stop cold- turkey with no symptoms of physical withdrawl whatsoever. Staying on it for periods longer than this is playing with fire. What is a good dosage of heroin for a beginner to start with? Purity of street drugs can vary so much that it would be dangerous to give an estimate. The first time the user tries it he or she should start out with a teeny, tiny bit and go up from there until the user gets an idea of what a good dose is. Personally, it's a good idea to always inject half of the dose and wait a minute ( leaving the needle in ) to see how it feels and then inject the rest. This info is only for people who are mature enough to respect the dangers involved with injecting heroin. These dangers include physical and mental addiction and the possibility of contracting a terrible disease like AIDS or hepatitis if the user doesn't take the time to be as sanitary as possible and NOT SHARE NEEDLES. -Alcohol swabs are available in a box of about 100 for $2 at Safeway. -A commonly used syringe is the U-100. It is 1CC which is divided into 100 "units". -The bottom of a soda pop can is commonly used as a "spoon" to dissolve the heroin in because it is curved inward like a spoon. The bottom is torn off of a can as close to the bottom as possible. Procedure: The "spoon" is thoroughly cleaned with an alcohol swab. In this example black tar heroin is used. In my area a $15 chunk is about the size of 2 tic-tac candies side-by-side and works just fine. It has no smell exept for a faint smell of vinegar. It comes wrapped in plastic inside a tiny balloon. A chunk is placed in the spoon. The syringe is used to suck up about 50-75 units of water and squirt it into the spoon. The spoon is then heated from the bottom with a lighter to make it dissolve better. The plunger can be pulled out of the syringe and used to stir the heroin solution. The end of the plunger should be clean before putting it back in the syringe. A piece of cotton is rolled into a ball a little bigger than a tic-tac. It is a good idea to clean one's fingers with an alcohol swab before rolling the cotton. The cotton is dropped into the heroin and it puffs up like a sponge. The tip of the syringe is pushed into the center of the cotton and the plunger is slowly pulled back until all of the heroin is sucked in. This cotton is necessary to filter out any particles and such in the heroin solution. The area on the body chosen for injection is thoroughly cleaned with an alcohol swab. I think the spot on the bend of the arm is so commonly used because it's so darned easy to get the needle into the vein properly. The needle is placed almost flat on the skin so it doesn't get wiggled around too much. The needle is inserted so it goes down the length of the vein and not across it. Going across it just makes it way too easy to accidentally poke through the other side or pull out. Holding the syringe almost flat against the skin after the user feels the needle is deep enough in keeps the syringe from accidentally being jostled around and the needle being pulled out or pushed through the side of the vein. Now for the tricky part. The user has to make sure that the needle is in the vein before injecting. If the heroin is injected when the needle isn't in the vein the heroin will just form a big heroin blister which takes hours and hours to get absorbed by the body. Usually it will burn while it's being injected if it's not going in the vein. This is one way to tell if it's not going in the vein. The user should also keep a close eye to see if a blister isfforming. When the needle is inserted the plunger is pulled slowly a tiny bit to see if blood comes in. This shows that it's in the vein. Sometimes when the plunger is pulled, only a slow trickle of blood comes in and the rest is air. With practice it's easier to tell if this trickle indicates a good enough insertion into the vein. Injecting a tiny bit of air ( about an eighth-inch ) with the heroin is harmless but if the user is nervous about this the syringe could be tilted so the air floats to the other end. From personal experience a quarter- inch (about 10 units) of air being injected with heroin is harmless but there's no need to make a habit of injecting air. With a little practice the user can be pretty sure the heroin is going in the vein without first checking for blood but still checking for a burning feeling where it's being injected or a blister forming. When trying heroin for the first time the user, of course, starts out with a tiny bit to see how his or her body reacts to it. As with pain pills sometimes the stomach gets queasy when the body isn't used to it. In the case of an overdose the only thing I know to do is to keep the person up and walking around to keep the heart going. If medical attention is needed I'm pretty sure the paramedics use a drug called "narcan" which blocks the effects of opiate narcotics like heroin. Right im not going to put any returns in here because it's causing great problems, the document I would like to request that the document 'How to Shoot' that can be found in the opiates section on Hyperreal.com be ammended so that in the part about sharing needles it also says about sharing water, the water that sits in the 'spoon' that the needle is cleaned in. Even if you use different needles if you use the same water the AIDS virus can still be transfered from needle to needle. I point this out only because the point of this article is obviouly as an informative piece intended for people who want to shoot up (safely) if it is merely intended for casual interest I really dont know if it's waranted, but that is up to you I suppose, well I hope this letter arrives in one piece, \2 Heroin, Poppy to the Street Heroin's long journey to America's streets begins with the planting of the seed of an opium poppy. The flower's botanical name is papaver somniferum. The Sumerians called it Hul Gil, the 'flower of joy.' The flower is grown mainly by impoverished farmers on small plots in remote regions of the world. It flourishes in dry, warm climates and the vast majority of opium poppies are grown in a narrow, 4500 mile stretch of mts extending across southern Asia from Turkey through Pakistan and Laos. Heroin is also increasingly becoming an export from Latin America, notably Colombia. About three months after the poppy seeds are planted, brightly colored flowers bloom at the tips of greenish, tubular stems. As the petals fall away, they expose an egg-shaped seed pod. Inside the pod is an opaque, milky sap. This is opium in its crudest form. The sap is extracted by slitting the pod vertically in parallel strokes with a special curved knife. As the sap oozes out, it turns darker and thicker, forming a brownish-black gum. A farmer collects the gum with a scraping knife, bundles it into bricks, cakes or balls and wraps them in a simple material such as plastic or leaves. Then the opium enters the black market. A merchant or broker buys the packages for transport to a morphine refinery. "Most traffickers do their morphine refining close to the poppy fields, since compact morphine bricks are much easier to smuggle than bundles of pungent, jelly-like opium," writes Alfred W. McCoy in The Politics of Heroin. At the refinery, which may be little more than a rickety laboratory equipped with oil drums and shrouded in a jungle thicket, the opium is mixed with lime in boiling water. A precipitate of organic waste sinks to the bottom. On the surface a white band of morphine forms. This is drawn off, reheated with ammonia, filtered and boiled again until it is reduced to a brown paste. Poured into molds and dried in the sun, it is now morphine base, which has the consistency of dense modeling clay. Morphine base is smokable in a pipe - a practice introduced by the Dutch in the 17th century - or ready for further processing into heroin. The first to process heroin was C.R. Wright, an English researcher who unwittingly synthesized heroin (diacetylmorphine) in 1874 when he boiled morphine and a common chemical, acetic anhydride, over a stove for several hours. The modern technique entails a complicated series of steps in a good laboratory. In his book, Opium A History, Martin Booth describes the process: "First, equal quantities of morphine and acetic anhydride are heated in a glass or enamel-lined container for six hours at 85ÉC. The morphine and the acid combine to form impure diacetylmorphine. Second, water and chloroform are added to the solution to precipitate impurities. The solution is drained and sodium carbonate added to make the heroin solidify and sink. Third, the heroin is filtered out of the sodium carbonate solution with activated charcoal and purified with alcohol. [Fourth,] this solution is gently heated to evaporate the alcohol and leave heroin, which may be purified further ..." Purification in the fourth stage, involving ether and hydrochloric acid, is notoriously risky. "In the hands of a careless chemist the volatile ether gas may ignite and produce a violent explosion that can level a clandestine laboratory," writes McCoy. The final product is a fluffy, white powder known in the trade as number four heroin. When the heroin emerges from laboratories in places such as Bangkok or Hong Kong, it enters a multi-layered chain of distribution. Top brokers usually deal in bulk shipments of 20 to 100 kilos. A broker in New York might divide a bulk shipment into wholesale lots of 1 to 10 kilos for sale to underlings. A kilo of Southeast Asian heroin in 1997 costs $100,000 to $120,000, according to the Drug Enforcement Administration. Oddly, for a shadowy commerce, the one-kilo bricks are brightly packaged and imprinted with brands worthy of Madison Avenue. Heroin originating in Burma's Shan State, for example, sports a red-lettered logo, "Double UO Globe Brand", framed by a pair of lions. By the time heroin is peddled on city streets in small "bags" at $5 to $100, its value has ballooned more than ten- fold since its arrival in the United States. Not many years ago virtually all the heroin sold on America's streets was so heavily diluted that it was rarely more than 10 percent pure. Purity has risen sharply in the mid-'90's - routinely hitting 50 to 60 percent - as dealers have tried to expand their market beyond those addicts who inject heroin into their veins with hypodermic needles. Higher purity means "you can inhale it, you can smoke it, you can get high without the threat of AIDS or those nasty intravenous needles." says DEA administrator Thomas Constantine, in a recent Washington Post story. Greater purity also reflects a relatively high level of worldwide production. Last year the illicit output of raw opium amounted to a record 4,300 tons, an increase of almost 1000 tons since 1992, according to U.S. estimates. Burma's 1996 share of more than 2500 tons made it, far and away, the world leader. By an age-old rule of thumb, every 10 tons of raw opium reduces to one ton of heroin. In other words, the worldwide opium output in 1996 translates into 430 tons of heroin. About half of that is destined for the United States. PBS and WGBH/Frontline \3 Heroin, smack, horse Heroin, an Old Nemesis, Makes an Encore Jan 9 2001 Single-Page Format By EVELYN NIEVES SAN FRANCISCO, Jan. 8 — At 5 a.m. in San Francisco's seedy Tenderloin area, the drug addicts are just about the only ones out. A young woman with matted blond hair stumbles down the street with her eyes closed; a man in a red spandex dress and silver pumps nods out against the door of a single-room- occupancy hotel; small clusters of hollow-eyed men and women hover on corners. It is no wonder the polcce call this strip of the Tenderloin the heroin corridor. Everyone on the street looks either high or hung over. Later in the day, Matt Dodman, a blond, angelic-looking 26-year-old, is sitting in a cafe in another, hipper neighborhood, the Mission. A heroin user for three years, he avoids the Tenderloin drug scene. "I'm not part of a hard- core drug clique," he said, taking a sip of mineral water. But down the block, a dozen of his friends and acquaintances — all heroin addicts in their teens and 20's, and all disheveled and homeless, as he is — sit on the sidewalk outside a community center and wait to be tested for hepatitis C. More than half will test positive, as do the larger population of San Francisco heroin users who have been taking the drug at least five years. Heroin was supposed to be over, yesterday's drug. But almost 20 years after AIDS made injecting it deadlier than it had ever been, it is as common in some neighborhoods here as Starbucks. A draw for drug experimenters since the heyday of Haight-Ashbury, the city remains a place where "old" heroin addicts — those who have been using the narcotic for 20 or 25 years — feed their habit. But more and more young people as well are using it. And not just here. Hospitals and treatment centers in other large cities, especially in the West, are seeing record numbers of heroin cases. Chicago officials attribute a surge in life- threatening cases of asthma to increased use of heroin among the young. And while H.I.V. and AIDS are down among users, needles used to inject heroin are responsible for an increase in hepatitis C, which can cause liver failure. In fact, hepatitis C is growing across the United States and in Vancouver, British Columbia, a major trafficking point for a drug pipeline that extends from Canada to California. The estimated number of heroin users in the United States has risen to 980,000 from 600,000 at the beginning of the 1990's, while cocaine use has decreased 70 percent, according to the White House Office of National Drug Control Policy. The agency attributes the resurgence in heroin use to new forms of the drug, smokable and snortable alike; to a prevailing myth among the young that heroin is safer when not injected; and to the "heroin chic" look of models in the early 90's. Washington State, Oregon and California have the highest incidence of heroin abuse in the West. Elsewhere, New York, New Jersey, Michigan, Massachusetts and Delaware also have big problems with it, according to the Substance Abuse and Mental Health Services Administration, an agency of the Department of Health and Human Services. Dr. H. Westley Clark, the agency's director, says its household surveys show that from 1996 to 1998, an estimated 471,000 people used heroin for the first time, with a quarter of the new users under 18 and 47 percent age 18 to 25. Heroin is not only cheaper than it once was, "it's cleaner, purer," said Joseph A. Califano Jr., who was secretary of health, education and welfare in the Carter administration and now directs the Center for Addiction and Substance Abuse at Columbia University. "And too many young people think they can snort it and they won't get hooked." Eventually, Mr. Califano added, they do get hooked, and turn to needles to achieve a more potent high. "The next drug czar, in the Bush administration, is going to have to deal with heroin in a big way," he said. Public health experts see the big increase in heroin use as further evidence that the nation's 20-year-old war on drugs, with its emphasis on punishment rather than addict treatment, needs a new approach. Here in San Francisco, heroin users, like homeless people (many are both), are part of the landscape. The city draws young people with troubled backgrounds from all over the country, even as it tries coping with inveterate users who have lived on the streets for years. The new people, like Matt Dodman, from Michigan, arrive with no money and no plans. Often they end up in loose-knit communities of homeless drug users, scorned by the rest of the city and consumed with a need to get their fixes. People cross the street to avoid them. "They look at us like dogs," Mr. Dodman said. To support his habit, which costs him $20 to $30 a day, Mr. Dodman steals. Or he "boosts" — steals an item from a store, then returns it for cash. He has panhandled, but says he does not "have the patience for it." Dr. David E. Smith, founder and president of the Haight-Ashbury Free Clinics, drug treatment centers here, has described the city's young addict population as people looking for "geographical cheer" — hope that life is going to be better in San Francisco than it was in Des Moines, say. Instead, they become alienated. The same is true of neighborhoods that attract young transients in Seattle and Portland. Officials in both cities consider heroin use at epidemic levels. In 1999, Portland had the nation's highest rate of death from heroin overdose. "You look back into the early 90's, and the heroin deaths are one to two dozen per year, and then in 1999 it was 111," said Gary Oxman, director of the Multnomah County Health Department in Portland. The department expects the final number for last year to drop to the low to middle 70's, he said, in part because of aggressive education programs. San Francisco has stepped up efforts in recent years to divert drug users to treatment. Such programs are making the city a model for California now that a statewide voter initiative, to take effect on July 1, makes first-time drug offenders eligible for treatment rather than jail. But more people keep coming to San Francisco than the city can help. Matt Dodman was one of several addicts, young and old alike, who said in interviews on the streets that they could not find a program that would accept them. Another was R. J., who said he had been using heroin for 40 of his 49 years and could not find a space in the city's detoxification centers. R. J., who would identify himself only by his initials, saying he wanted to spare his four children, is a walking sign of what heroin can cost. He has overdosed five times. He has been stabbed and raped while selling himself to support his habit. He has done time behind bars, almost nine years in all. And his inner forearms have so many needle tracks that they look striped. By selling his body, R. J. earns enough money to pay for his heroin, if nothing else. "When I see young people, I tell them, `Don't end up like me,' " he said. "I tell them, `Look at me.' " Gloria Clay, like R. J. a Tenderloin regular, is a little luckier. At 35, she is in a detoxification program and says she is on her way to kicking a heroin habit she picked up two years ago, after being addicted to crack. Her scars keep her motivated. While on drugs, she was kicked by her drug-addicted boyfriend, a beating that cost her an eye and permanently damaged her spine. Although infected sores in heroin addicts are the leading cause of admissions at San Francisco General Hospital, and while San Francisco consistently ranks among the worst metropolitan areas for emergency-room visits related to heroin, health officials here are more worried about the drug's long-term effects. Experts compare heroin users to smokers, in that risk accumulates over time. Many people infected with the hepatitis C virus, for example, do not exhibit symptoms for many years, said Dr. Andrew Moss, professor in residence of epidemiology and biostatistics at the University of California at San Francisco. But, Dr. Moss said, a segment of those afflicted will develop liver disease, cancer or cirrhosis, and hepatitis C is very infectious. In San Francisco, where young users as well as old overdose routinely, the young are very difficult to reach, because their problems transcend drug use, Dr. Moss said. "They're America's damaged children," he said. Matt Dodman is not worried. He is sure he will not overdose, and certain he will remain free of disease. Why? "Because," he said, "I know so." Heroin (invented by Bayer Co) is a white or brown powder synthesized from morphine in 1898. It was thought to be non addictive, a better analgesic, and a cure for morphine, but it is ten times more potent. Pure heroin must be diluted (milk sugar/quinine) about 9 to 1 before injection into a vein. Today it has no medical use. A pain relieving narcotic derived from morphine that depresses the CNS. Developed in Germany 1898, controled by the Harrison Act in 1914, and prohibited in 1924. Street Brands: Double UO Globe, Crouching Lion Lucky Strike, Panda, Dragon \4 Heroin, SW Asian From the Golden Cresent (Middle East from Iran to Pakistan). Turkey was a big source. BISHKEK, Kyrgyzstan, Oct 15 2000. Sveta stretched across the couch in the cramped apartment with lace curtains, tilted her head back and slowly massaged her bare neck. With the tenderness of a lover and the expertise of a long-time practitioner, Aleksandr located the vein, slipped the needle into her neck and sent the heroin on its way. The drug turned Sveta's eyes bright and her slightly crooked smile was pretty. Aleksandr took her place on the couch, tugging his right sleeve up to expose his under arm. Sveta thumped hard on his skin found a reluctant vein and injected the heroin. A third person, Yuri, sat in a chair, silent and staring, transported to his own world by the drug they had just mixed in a small pink plastic bowl. Pulling back a curtain, Sveta dropped the needles and syringes into two separate plastic containers. In a few days, they would be taken to a clinic and traded for new ones, courtesy of a groundbreaking — and possibly lifesaving — needle exchange program in the capital of this small, remote country. Bishkek, capital of Kyrgyzstan, seems an unlikely spot for heroin addicts, let alone something as reformist as a needle exchange. This country of 4.5 million is largely mountainous, and through decades of Soviet domination retained many of its nomadic traditions and tightly knit communities. But heroin addiction has arrived all across Central Asia, the sad if predictable byproduct of the transformation — after the end of more rigid Communist control — of the ancient Great Silk Road into a major conduit for drug traffickers. UN experts estimate that 80 percent of Europe's heroin originates in Afghanistan and Pakistan. The principal route to market winds through the mountains and steppes of three former Soviet republics, Kazakhstan, Kyrgyzstan and Tajikistan. The influx of drug trafficking has strained the limited resources of the police, increased corruption and helped finance Islamic militants trying to destabilize the region. The new availability of heroin also expanded the number of addicts. Heroin is cheap, plentiful and powerful. An average dose, about a tenth of a gram, costs $2 in Bishkek, half that in Osh, the major city in southern Kyrgyzstan where the supply is greater, and 50 cents in Tajikistan. In those poor Soviet republics, where average income rarely tops $600 a year, it has replaced its weaker cousin, opium, as the drug of choice. And it is far more addictive. "Five years ago, we didn't see heroin," said Col. Zhanybek S. Bakiyev, the top drug enforcement officer with the Kyrgyzstan Ministry of Internal Affairs. "Now we are concerned that our people consume heroin in greater quantities." The number of intravenous drug users in Kyrgyzstan has increased fourfold in the last decade. Yet police and drug experts believe that the number is still small enough to avoid an epidemic. Tough enforcement is one means. But the police are also supporting an attempt to reduce the harm to addicts through needle-exchange programs. "This is the moment when we should act," said Yuri Misnikov, an official with the United Nations Development Program in Bishkek. The first needle exchanges opened last February in Bishkek and Osh. They are financed by the United Nations program and the Open Society Institute, part of the New York-based Soros Foundation. They were the first needle-exchange programs in Central Asia, though the Soros group has since opened two centers in Kazakhstan and plans one in Tajikistan soon. The idea is simple and common in Europe and the United States. Addicts swap used needles and syringes for as many new ones as they need, usually five or six a day. Discarding used needles and not sharing them reduces the spread of the AIDS virus and diseases like hepatitis. At the exchanges, the addicts also get free medical care and blood tests. Estebesova Batma, a psychiatrist who coordinates the program, said she expected 10 or 15 new clients a month when the two exchange offices opened here. Within weeks, more than 500 addicts were taking part and new clients were turned away because the program was running out of needles. About 180 people show up monthly at the Osh center. The need was demonstrated by a survey of 100 clients in March. Ninety-six said they shared needles and 35 reported using the same syringe more than 20 times. One addict exchanged a syringe that had dangled from his belt on a key chain. Others turned in syringes used so often that the gauge marks had worn off and been replaced with notches to determine how much heroin to load in. One in five used tap water to wash needles and syringes before the next use and half did not know they could be infected by a needle. The number of drug-related AIDS cases is surprisingly low. When the police announced two weeks ago that a heroin user who had been jailed had tested positive for AIDS, it was the first publicized case of a drug user contracting the disease in Bishkek, a city of about 650,000 residents, though experts say there are several others. In addition, a study by the United Nations and the Soros Foundation found that between 11 percent and 18 percent of intravenous drug users in Bishkek are infected with H.I.V. and between 32 percent and 49 percent in Osh, where there are fewer education programs. The news of the first drug-related AIDS case sent a chill through the drug-addict population. Two dozen friends of the jailed addict showed up the next day at Dr. Batma's two offices, asking for blood tests. Among them were Sveta, Aleksandr and Yuri. All three are longtime drug users who switched from opium to heroin within the last three years. They agreed to be interviewed and photographed in Aleksandr's apartment as long as their last names were not used. The apartment was on the second floor of a rundown building on the outskirts of Bishkek. Inside the paint was peeling and plumbing was exposed, but Aleksandr's wife, Olga, does not use drugs and tries to keep the place neat and clean for the sake of their two children. Sveta, 35, said she started using drugs when she was 17. She said she stopped four times while using opium, once for three months. But she cannot stop using heroin. "We are scared to quit because we know that this withdrawal is waiting for us," she said, gesturing to her friends, too. "I would like to quit. I'm trying to reduce my use." Aleksandr, who once made a good living as a driver despite his opium habit, has been unable to work since becoming addicted to heroin three years ago. He said he wants desperately to quit and emigrate to Germany with his family to start a new life, but he cannot leave his heroin. Despite the expressed desires to quit, the apartment crackled with anticipation as drug paraphernalia and a foil-wrapped packet of heroin are pulled out. They mixed the heroin in a plastic cup with boiled water and a powdered antihistamine that enhances the effect, and drew it equally into three syringes. Aleksandr's 14-year-old daughter lingered in the hallway, ignoring the all-too-common scene. The two bottles into which Sveta deposits the used needles and syringes sat beside a bag filled with 30 or more new replacements. Back at the clinic, Dr. Batma said exchanging needles is not enough. Heroin cannot be overcome without an extensive rehabilitation program. But there are none in Kyrgyzstan, where half the population lives below the poverty line and the national annual budget is only $300 million. Heroin and Needles: A Post-Soviet Ray of Hope By DOUGLAS FRANTZ \5 Heroin process Heroin's long journey to America's streets begins with the planting of the seed of an opium poppy. The flower's botanical name is papaver somniferum. The Sumerians called it Hul Gil, the 'flower of joy.' The flower is grown mainly by impoverished farmers on small plots in remote regions of the world. It flourishes in dry, warm climates and the vast majority of opium poppies are grown in a narrow, 4,500-mile stretch of mountains extending across southern Asia from Turkey through Pakistan and Laos. Heroin is also increasingly becoming an export from Latin America, notably Colombia. About three months after the poppy seeds are planted, brightly-colored flowers bloom at the tips of greenish, tubular stems. As the petals fall away, they expose an egg-shaped seed pod. Inside the pod is an opaque, milky sap. This is opium in its crudest form. The sap is extracted by slitting the pod vertically in parallel strokes with a special curved knife. As the sap oozes out, it turns darker and thicker, forming a brownish-black gum. A farmer collects the gum with a scraping knife, bundles it into bricks, cakes or balls and wraps them in a simple material such as plastic or leaves. Then the opium enters the black market. A merchant or broker buys the packages for transport to a morphine refinery. "Most traffickers do their morphine refining close to the poppy fields, since compact morphine bricks are much easier to smuggle than bundles of pungent, jelly-like opium," writes Alfred W. McCoy in The Politics of Heroin. At the refinery, which may be little more than a rickety laboratory equipped with oil drums and shrouded in a jungle thicket, the opium is mixed with lime in boiling water. A precipitate of organic waste sinks to the bottom. On the surface a white band of morphine forms. This is drawn off, reheated with ammonia, filtered and boiled again until it is reduced to a brown paste. Poured into molds and dried in the sun, it is now morphine base, which has the consistency of dense modeling clay. Morphine base is smokable in a pipe - a practice introduced by the Dutch in the 17th century - or ready for further processing into heroin. The first to process heroin was C.R. Wright, an English researcher who unwittingly synthesized heroin (diacetylmorphine) in 1874 when he boiled morphine and a common chemical, acetic anhydride, over a stove for several hours. The modern technique entails a complicated series of steps in a good laboratory. In his book, Opium A History, Martin Booth describes the process: "First, equal quantities of morphine and acetic anhydride are heated in a glass or enamel-lined container for six hours at 85ÉC. The morphine and the acid combine to form impure diacetylmorphine. Second, water and chloroform are added to the solution to precipitate impurities. The solution is drained and sodium carbonate added to make the heroin solidify and sink. Third, the heroin is filtered out of the sodium carbonate solution with activated charcoal and purified with alcohol. [Fourth,] this solution is gently heated to evaporate the alcohol and leave heroin, which may be purified further ..." Purification in the fourth stage, involving ether and hydrochloric acid, is notoriously risky. "In the hands of a careless chemist the volatile ether gas may ignite and produce a violent explosion that can level a clandestine laboratory," writes McCoy. The final product is a fluffy, white powder known in the trade as number four heroin. When the heroin emerges from laboratories in places such as Bangkok or Hong Kong, it enters a multi-layered chain of distribution. Top brokers usually deal in bulk shipments of 20 to 100 kilos. A broker in New York might divide a bulk shipment into wholesale lots of 1 to 10 kilos for sale to underlings. A kilo of Southeast Asian heroin in 1997 costs $100,000 to $120,000, according to the Drug Enforcement Administration. Oddly, for a shadowy commerce, the one-kilo bricks are brightly packaged and imprinted with brands worthy of Madison Avenue. Heroin originating in Burma's Shan State, for example, sports a red-lettered logo, "Double UO Globe Brand", framed by a pair of lions. By the time heroin is peddled on city streets in small "bags" at $5 to $100, its value has ballooned more than ten- fold since its arrival in the United States. Not many years ago virtually all the heroin sold on America's streets was so heavily diluted that it was rarely more than 10 percent pure. Purity has risen sharply in the mid-'90's - routinely hitting 50 to 60 percent - as dealers have tried to expand their market beyond those addicts who inject heroin into their veins with hypodermic needles. Higher purity means "you can inhale it, you can smoke it, you can get high without the threat of AIDS or those nasty intravenous needles." says DEA administrator Thomas Constantine, in a recent Washington Post story. Greater purity also reflects a relatively high level of worldwide production. Last year the illicit output of raw opium amounted to a record 4,300 tons, an increase of almost 1000 tons since 1992, according to U.S. estimates. Burma's 1996 share of more than 2500 tons made it, far and away, the world leader. By an age-old rule of thumb, every 10 tons of raw opium reduces to one ton of heroin. In other words, the worldwide opium output in 1996 translates into 430 tons of heroin. About half of that is destined for the United States. home | interviews | how can we crack down? | maps & charts | transforming poppies to heroin | heroin in the brain | opium throughout history | viewer reactions | press | tapes & transcripts | explore FRONTLINE | pbs online | wgbh New Content Copyright © 1998 PBS and WGBH/Frontline \6 Heroin - Chasing the dragon Origins and history by Strang J, Griffiths P, Gossop M National Addiction Centre ABSTRACT: The history of heroin smoking and the subsequent development and spread of 'chasing the dragon' are examined. The first heroin smoking originated in Shanghai in the 1920s and involved use of porcelain bowls and bamboo tubes, thereafter spreading across much of Eastern Asia and to the United States over the next decade. 'Chasing the dragon' was a later refinement of this form of heroin smoking, originating in or near Hong Kong in the 1950s, and refers to the ingestion of heroin by inhaling the vapours which result when the drug is heated-typically on tin-foil above a flame. Subsequent spread of 'chasing the dragon' included spread to other parts of South East Asia during the 1960s and 1970s, to some parts of Europe during the late 1970s and early 1980s, and to much of the Indian sub-continent during the 1980s. At the time of writing, 'chasing the dragon' has now been reliably reported from many parts of the world but not from others with an established heroin problem-such as the United States and Australia. The significance of this new form of heroin use is examined, including consideration of the role of the different effect with this new form of use, the different types of heroin, and changing public attitudes to injecting. Opioids \7 Ibogaine A Brief History Ibogaine, Psychotherapy, and the Treat- ment of Substance-Related Disorders. Ibogaine is not a substitute for narcotics or stimulants, is not addicting and is given in a single admin modality (SAM). It is a chemical dependence interrupter. Retreatment may occasi- onally be needed until the person being treated with Ibogaine is able to extinguish certain conditioned respo- nses related to drugs they abuse. Early data suggests that a period of approximately two years of intermittent treatments may be required to attain the goal of long- term abstinence from narcotics and stimulants for many patients. The majority of patients treated with Ibogaine remain free from chemical dependence for a period of three to six months after a single dose. Approximately ten percent of patients treated with Ibogaine remain free of chemical dependence for two or more years from a single treatment and an equal percentage return to drug use within two weeks after treatment. Multiple admins of Ibogaine over a period of time are generally more effective in extending periods of abstinence. A BRIEF HISTORY. Ibogaine, a naturally occurring alkaloid found in Tabernanthe iboga and other plant species of Central West Africa, was first reported to be effective in interrupting opiate narcotic dependence disorders in U.S. patent 4,499,096 (Lotsof, 1985); cocaine dependence disorders in U.S. patent 4.587,243 (Lotsof, 1986) and poly-drug dependence disorders in U.S. patent 5,152,994 (Lotsof, 1992). The initial studies demo Ibogaine's effects on cocaine and heroin dependence were accom- plished in a series of focus group experiments by H. S. Lotsof in 1962 and 1963. Additional data on the clinical aspects of Ibogaine in the treatment of chemical dependence were reported by Kaplan (1993), Sisko (1993), Sanchez-Ramos & Mash (1994), and Sheppard (1994). Prior to Ibogaine's evaluation for the interruption of various chemical dependencies, the use of Ibogaine was reported in psychotherapy by Naranjo (1969, 1973) and at the First International Ibogaine Conference held in Paris (Zeff, 1987). The use of Ibogaine-containing plants has been reported for centuries in West Africa in both religious practice and in traditional med (Fernandez, 1982; Gollnhofer & Sillans 1983, 1985) An overview of the history of Ibogaine research and use was published by Goutarel et al. (1993). Claims of efficacy in treating dependencies to opiates, cocaine, and alcohol in human subjects were supported in preclinical studies by researchers in the US, the Netherlands and Canada. Dzoljic et al. (1988) were the first researchers to publish Ibogaine's ability to attenuate narcotic withdrawal. Stanley D. Glick et al. (1992) at Albany Medical College published original research and a review of the field concerning the attenuation of narcotic withdrawal. Maisonneuve et al. (1991) determined the pharmacological interactions between Ibogaine and morphine, and Glick et al. (1992) reported Ibogaine's ability to reduce or interrupt morphine self-administration in the rat. Woods et al. (1990) found that Ibogaine did not act as an opiate, and Aceto et al. (1991) established that Ibogaine did not precipitate withdrawal signs or cause dependence. Cappendijk and Dzoljic (1993) published Ibogaine's effect in reducing cocaine self-administration in the rat. Broderick et al. (1992) first published Ibogaine's ability to reverse cocaine-induced dopamine increases and later, on Ibogaine's reduction of cocaine-induced motor activity and other effects (1994). Broderick et al.'s research supported the findings of Sershen et al. (1992), that Ibogaine reduced cocaine-induced motor stimulation in the mouse. Sershen (1993) also demonstrated that Ibogaine reduced the consumption of cocaine in mice. Glick (1992) and Cappendijk (1993) discovered in the animal model that multiple administrations of Ibogaine over time were more effective than a single dose in interrupting or attenuating the self-administration of morphine and cocaine, supporting Lotsof's findings in human subjects (1985). Popik et al. (1994) determined Ibogaine to be a competitive inhibitor of MK-801 binding to the NMDA receptor complex. MK-801 has been shown to attenuate tolerance to opiates (Trujillo & Akil 1991) and alcohol (Khanna et al. 1993). MK-801 has also shown a blockade of "reverse tolerance" of stimulants (Karler et al. 1989). Ibogaine's effects on dopamine, a substance hypothesized to be responsible for reinforcing pleasurable effects of drugs of abuse, and the dopamine system were found by Maisonneuve et al. (1991), Broderick et al. (1992) and Sershen et al. (1992). Ibogaine binding to the kappa opiate receptor was reported by Deecher et al. (1992). Thus we begin to see a broad spectrum of mechanisms by which Ibogaine may moderate use of substances so diverse as opiate narcotics, stimulants and alcohol. Ibogaine is currently under review by the National Institute on Drug Abuse. On March 8, 1995 an Ibogaine Review meeting was held to determine if the Medications Development Division of NIDA would proceed to multi-site clinical studies. That decision is now being awaited. The FDA has already approved one human Ibogaine research project and is considering changes that may allow the research to move more quickly. Additionally the National Inst on Drug Abuse may proceed to multi-site human studies to determine if Ibogaine is effective in treating cocaine dependency. The ministry of Health in the Rep of Panama has approved experimental Ibogaine treatments at therapeuic doses which puts it about two years head of the US. Researchers in Israel and Turkey are also considering human trials for opiates and alcoholism. Ibogaine is not an LSD-like drug and appears according to early reports to be effective in the treatment of various forms of chemical dependence including opiates, stimul- ants, alcohol, nicotine or combinations of the above. The real surprise seemed to come when prelimiary treatment of methadone dependent persons also appeared to be effective in the same 2-4 day Lotsof procedure for the treatment of addiction. The substance has a psycho pharmacological effects including both Freudian and Jungian perceptions plus its ability to diminish narcotic withdrawal. Ibogaine's actions breaks down into three component parts. The first is a four to six hour period emulating dreaming in which either visual presentations or thoughts dealing with past events are experienced. The second is a cognitive or intellectual period in which those experi- ences are evaluated and the third is a period of residual stimulation eventually resulting in sleep. It is after the patient wakes when the effects are noticed in a lack of a desire in the majority of patients to seek or use the drugs they were abusing. However, it should be noted that the responses to the drug are very individual just as the patient has individual characteristics. --------------------------------------------------------- IBOGAINE, PSYCHOTHERAPY, AND THE TREATMENT OF SUBSTANCE- RELATED DISORDERS. Barbara E. Judd, CSW. Presented at The Eighth Intl Conf on Drug Related Harm Wash, DC 11/94 Introduction. I have been working with chemically dependent patients, some having dual diagooses, for twelve years in outpatient settings. My observations have been that the earliest phase of recovery, the first ninety days, is the most difficult for the therapist and the patient. I would like to compare and contrast certain issues seen as obstacles by patients, some of whom were treated with the Lotsof method and some treated in traditional outpatient settings. My observations are based on a small sample of patients seen in the U.S. and overseas. These observations are inconclusive and my work is ongoing. My involvement with Ibogaine began in June 1993, when I was approached by the International Coalition for Addict Self-Help (ICASH) and requested to provide aftercare for five patients who were treated with Ibogaine and were eager to share their experience and struggles. Four of the group were white males ranging in age from early thirties to mid forties. One was a female in her thirties. Their dependencies were to heroin, Methadone and/or cocaine. Additional substance use included marijuana, alcohol and psychedelics. This group met once a week for the duration of one year. Concurrent treatment was provided to one member of this grp on an individual basis. This patient, refered to as "M" is still presently under my care. "M" is 33 yrs old and formally heroin/methadone/cocaine dependent. He has been using drugs since the age of fourteen. My most recent involvement with Ibogaine has been with NDA International, Inc. when I participated in the treatment of three patients using the Lotsof method in Panama. All three patients were white males in the 30-40 age range. Two of the patient'. major drugoof choice was cocaine which was taken, orally, nasally or by IV injec- tion by one patient; the other by oral or nasal admin only. The third patient was heroin/cocaine dependent and occasionally used methadone in attempts to curb his habit. All patients had used drugs from 6-16 years. One of the most difficult aspects of treatment is getting the patient to enter treatment. The three major obstacles are the fear of detoxification, lack of insight, and the inability of patients to control their urges to use drugs. These are the areas where I have observed the benefits of Ibogaine treatment versus traditional methods Fear of Detoxification Across the board, addicts who enter outpatient treatment programs report that their fear of detoxing from drugs has prevented them from attending treatment. Although withdrawal from cocaine is not as severe or obvious as that from opiate narcotics, there is a fear of the psychological pain of never being able to use again. There is also a dread that once drug free, feelings that have been blocked by self-medicating will surface and be too overwhelming for the patient to handle. Most heroin addicts are petrified of withdrawal symptoms and are afraid of hospital detoxification. Outpatient clients have stated to me that they have delayed treatment to avoid this anticipated discomfort. My observations with Ibogaine treated patients have been that patients are eager to be treated when they know that Ibogaine promises to eliminate painful withdrawal, takes one administration with up to seventy-two hours of supervised care, and promises to interrupt their urges to use drugs. Three patients: Panama Patient "1" had used approximately $100 each per day of heroin and cocaine by IV admin for twenty of the thirty days prior to Ibogaine treatment. Patient "2", prior to treatment was using $80 per day of cocaine and alcohol. Patient "3" was using $50 of cocaine on a daily basis via IV injection and smoking. He had previously been heroin dependent. I observed during treatment with the Lotsof method, all of the three patients treated appeared calm and comfortable and exhibited no signs of withdrawal. This is significant considering the extent of the level of their drug use prior to treatment with Ibogaine. For these patients to have had little discomfort during withdrawal, speaks to the importance of the use of Ibogaine in the beginning of the recovery process. As patient "M" had stated, "Ibogaine is a much more humane and dignified approach to detox". Obstacles Within Traditional Treatment Returning to the obstacles of treatment, the second being the patients' lack of insight. Insight is necessary for patients to be able to focus and develop goals while in recovery. Patients in traditional outpatient groups who have less than ninety days clean, spend more time struggling with their urges to use and dealing with their defenses, specifically denial. They do develop insight into their problems, however, it takes at least one year of group treatment meetings one or two times a week on a regular basis. In contrast, my involvement with providing aftercare for the Ibogaine treated group showed these patients as having tremendous insight into their own issues, their feelings, and what might have caused them to use in the first place. After their Ibogaine treatment, patients began to see their drug use as destructive. This realization, coupled with psychotherapy, has allowed these patients to work on how to stay clean and to focus on what they must do to maintain a less destructive lifestyle. The reason for this insight developed by these patients appears to be the release of repressed material during the visualization stage of Ibogaine treatment. This material includes both images and racing thoughts, which somehow get processed to allow patients to have a better understanding of their emotional histories. The urge to use drugs again, is the highest cause for people to drop out of traditional treatment. Relapse, I think, is clearly inherent in the definition of substance-related disorders. In working with people treated with or without Ibogaine, my observations have been that relapse at some point is certain. However, according to members in the Ibogaine group, Ibogaine had reduced their urges to use, anywhere from two months to more than one year. This advantage allowed these patients to get a head start in their recovery, whereas clients in traditional outpatient treatment have a great deal of confusion around how to control their urges. Consequently, those patients have to learn very basic and concrete ways to stay clean as taught by self-help meetings, and emphasized in psychotherapy. The Ibogaine aftercare group did not appear to need self-help type assistance to reduce their urges, but seemed to benefit well from psychotherapy. Conclusion In conclusion, there is difficulty treating the drug addicted patient, particularly in the early stages of recovery, because of their fear of detox, their lack of insight, and their urges to relapse. Thus far, there is no opportunity for Ibogaine treatment within the United States. It is my recommendation that there be future research done with Ibogaine, so that some of the above mentioned observations are supported by more conclusive data. The prospects for a painless withdrawal method makes Ibogaine an attractive alternative to traditional treatment methods. Because Ibogaine interrupts substance related disorders, it gives patients a head start in their recovery. It also increases the patients' receptiveness to psychotherapy, which is a necessary component to the recovery process. \8 Ketamine (special K) Causes hallucinations and mood changes. Behavioral effects of ketamine, an NMDA glutamatergic antagonist, in non-human primates by Shiigi Y, Casey DE Mental Illness Research, Education and Clinical Center (MIRECC) VISN 20 and Mental Health Division, VA Medical Center, Portland, Oregon, USA ABSTRACT: Rationale: The dopamine hypothesis is the most widely investigated theory underlying schizophrenia and the mechanisms of action for antipsychotic drugs. However, recent studies call into question this proposal. Thus, the focus has turned towards other mechanisms, one of which has been glutamatergic systems. Phencyclidine (PCP), a potent NMDA receptor antagonist, causes a schizophrenic-like psychosis in normal volunteers and exacerbates psychotic symptoms in patients with schizophrenia. Ketamine, like PCP, is a non-competitive NMDA receptor antagonist, which is short acting and has been used as a dissociative anesthetic as well as a research tool in psychosis. Objective: To clarify the role of NMDA antagonists further and to develop an animal model of these actions, ketamine was studied across a range of behaviors in Cebus monkeys. Methods: Thirty-two (six male, 26 female) Cebus monkeys, which were previously sensitized to neuroleptics, were tested with a wide range of doses of ketamine that spanned the clinical effect range from threshold effects to full anesthesia. Behaviors scored included sedation/arousal, locomotor activity, extrapyramidal symptoms of parkinsonism and dystonia, as well as reactivity. Results: Ketamine produced dose-related increases in parkinsonian bradykinesia and dystonia as well as salivation. There were dose-related decreases in locomotor activity and reactivity to environmental stimuli. These effects had short time courses and steep dose-response curves. Conclusions: These results suggest that ketamine-induced behavioral effects in non-human primates offer a model for studying a glutamatergic role in motor and mental function such as attention or perception. --------------------------------------------------------- Ketamine FAQ December 1994, v1.0 KETAMINE HYDROCHLORIDE FAQ PAGE The following is an early draft of a FAQ concerning recreational use of Ketamine Hydrochloride. The authors of this FAQ in no way condone or suggest the use of Ketamine in anyway contrary to its intended use nor do they condone any illegal behaviors. The following was compiled from reference information and the anecdotes of those who have used Ketamine and is neither considered to be without flaw nor is it intended to be a guide to use, and the authors are not responsible in anyway for misinterpretations or misuse of Ketamine as a result of reading this material. This information may be shared as an educational document provided this disclaimer is included and the contents of the FAQ are delivered intact. *****WARNING: In the rave and club scene these days, especially in Europe, a substance is often sold under the names of Special K or Ketamine. This substance more often than not is Ketamine mixed with several other drugs, among which may be heroin, coke, or ecstasy. Any combination of drugs with ketamine is extremely dangerous and has minimum psychedelic value. The following FAQ is concerned only with use of pure Ketamine Hydrochloride and any major deviations in experience contrary to this listing often involve use of mixed substances. It is strongly encouraged that Ketamine or Special K not be obtained, and especially not used in club settings. ***** DRUG : Ketamine Hydrochloride STREET NAMES : K, Ket, Ketamine, Special K, Vitamin K BRIEF : Ketamine is an anaesthetic used primarily for veterinary purposes. Ketamine blocks nerve paths without depressing respiratory and circulatory functions, and therefore acts as a safe and reliable anaesthetic. It is commonly injected intramuscularly, but can also be taken orally and nasal pharyngealically. Ketamine is only available to physicians, and is not commonly sold as an illicit drug, and is scheduled in several states. The most common trade name for Ketamine are Ketaset and Ketalar, which are intramuscular veterinary Ketamine HCls. PSYCHEDELIC INDICATIONS : Ketamine does not treat music so well. Expect a narrowing of your auditory bandwidth. Music will sound neat but not correct and not transcending. You will selectively lose frequencies. Use mellow music with a psychedelic flavor, and keep the volume less than loud because your perception of overall volume will increase. Visual hallucinations are most notable in low light. Touch is exceptional. Smells and tastes will be nulled. Do not expect to talk, although you may. Expect general reflection but not exceptional emotionality. DOSAGE : Due to its anaesthetic nature, K can produce wide ranging effects from different amounts. There seems to be a crucial line where the patient will lose grasp of his/her primary senses, and this will be termed a Line Dose. A further line exists where the patient will lose complete consciousness. In general, boosting is not adequate and it does not seem worthwhile to boost the original dose more than ten minutes after initial dose. General tolerance is appreciable and several weeks between uses are required to return to original tolerance. For most types, effects are linear with dose, and good experience can be had at low dosages. ORAL DOSE : A Line Dose is about 1.0 mg/lb. body mass. Anaesthetic doses are above 4.0 mg/lb. A maximum oral dose of 3 mg/lb. should be set for adequate recovery. Above line dose, increasing doses yield little psychedelic advantage except for greater temporary memory loss. A good first dose is 300-350 mg for average weight woman, and 350-375 mg for average weight men. A minimum dose of 150-175 mg will give a good psychedelic experience. IM DOSE : Intramuscular doses begin at perhaps .4 mg/lb. for a Line Dose. Anaesthetic doses to IM are about 1 mg/lb. Two injections should be made instead of one. Sterility of the bottle and needle are imperative. 100 mg seems to be a good IM dose for everyone. Expect soreness in the injection region for several days or weeks. IV DOSE : I do not recommend IV doses but have read reports of successful IV dosing. In the IV case you will probably lose motor control before you finish injecting so beware. NASAL DOSE : Nasal doses are highly unlinear next to oral and IM doses. The effects are quite different as well at low doses. At Line Doses, oral consumption is probably a better bet than nasal doses. A Line Dose nasally would again be about 1.0 mg/lb. A minimum dose nasally would be about .25 mg/lb, but will be short and much different from a comparable oral dose. 75-100 mg would be a good starter for most weights. Ketamine is relatively comfortable in the nasal region. PREP : IV and IM require fully sterile Ket bottle and needle. Powder for nasal use can be gotten from gentle boiling off of solution. To prepare an oral dose from a powder, place powder in a cup and pour about 1 cm of hot water (tap should be ok) in it and stir to solution. Fill remainder of cup with an acid such as orange juice. SETTING : As with all anaesthetics, Ketamine will make the patient nauseaous to varying degrees, directly related to dosage. Therefore, the patient should find him/herself in a place where he/she can stay for several hours, with most ammenities close at hand (any movement will compound nauseau). A non-Ketting person is a great help, and will be fun to talk to, and convenient for changing music, etc. Darkness will eliminate some very strange visual experiences. Music is very powerful. Warmth can also be important, as although your respiratory system will not be depressed, you may become cold from inactivity. A blanket is a good idea. Dope should be handy for nauseau, and a bucket should be available as a precaution. Vomitting should be rare, but in the case, it is not a good idea to have to travel to the bathroom. You should try to make sure that your co-trippers start when you do, as it is a rapid starting drug. Nasal doses can usually accomodate real scenes, i.e. clubs or company, but expect things to be very strange. TIMING : Taken intramuscularly, Ketamine will bring you up quickly in less than two minutes. Orally, with a medium-full stomach, expect 15-20 minutes, and as little as five minutes on an empty stomach. Nasal doses allow 5-10 minutes. The acceleration is great but not alarming. Expect to be semi-unconscious on a Line-Dose for about an hour intramuscualrly, and slightly longer when taken orally. You will come down quickly as well past the first line, and will begin to assimilate senses over about an half-hour. When taken orally, a soft trip will linger for approximately 2-3 hours after that and can be lots of fun. You will feel light, lanky, and queasy for several hours, and may be somewhat light-headed, though not incapacable the following day. Nitrous has had success in bringing Ketamine down quickly, despite its anaesthetic nature. THE TRIP : Before reaching the first line, fragmentation will occur- the world will begin to spin, but it won't be dizzying. Music will become fragmented. Chaos will ensue. At some point, you will find yourself complete removed from your surroundings and your body. Descriptions of the post-line experience vary substantially, but most include talk of alternate planes of existence, oneness, past and future revelations, and strange fabrics of all sorts. It will be very difficult to communicate at this point, and you probably will not be able to see or hear others in the room. Some revelations will be extremely heavy and some scary, but that fear does not seem to come back with you and is therefore difficult to describe as scary. You will probably find yourself coming back across the line again visibly, attempting to put an object in focus or define it. It is at this point that you will likely want to get in touch with your co-trippers. This is the "Wow" period. It is very important here that you do not try to move for awhile. The trip will continue mildly for an hour or so after this, with more conventional focuses. PRECAUTIONS : An overdose of Ketamine will knock you out as if in an operating room. This would prove to be a waste of a tripping experience, and will probably make you ill to your stomach. The danger dosage is much higher however, at 10 mg/lb. Interactively, Ketamine should not be used with respiratory depressants, primarily alcohol, barbituates, and Valium. Ketamine has been used with no ill interactive effects with dope, acid, nitrous, dextromethorphan, and MDMA, although no combinations are recommended and are highly unnecessary given the totality of ketamine. It does not have a build-on effect with halucinagins and will generally overpower other drugs. Nitrous in the up and down periods can be effective. Unpracticed trippers may be overpowered by the awesome revelations of Ketamine and may be somewhat overwhelmed, although in general fear seems to be unable to compound here (such as in an LSD trip or with other drug paranoias) and will probably be only episodic. Food should not be consumed within an hour and one-half before the trip, and should be avoided for longer periods of time if possible. A peculiar sort of loneliness can occur over the line, so it is a good idea to stay in close quarters with people you are close with, and best to have a sober monitor or experienced Ketter at hand. TRIPS BY DOSE : Doses that do not push one over the consciousness line can be very fun if you get close. In general, a 150 mg minimum would be required to realize an effect. Under that amount, you will only feel a very operable up and down over about an half-hour that will give you no insight into Ketamine. At higher doses, the up will last longer, but in less than linear fashion. In general it seems that oral doses last longer. Trips over 450 mg. can be severe on the stomach and have rapidly diminishing returns over lower doses, and are therefore not recommended, although 450 mg. itself is a very sound and powerful trip. REPORTS : A number of sources claim Vitamin K to be a boring drug. Some complain that it removes you so completely from your body that it is difficult to even work with. Others have found Vit K to be very potent and shapable, an experience that can be tailormade by dosage and setting. There is little question that there is no comparable experience on any other drugs. Most agree that it has a good to very good recovery with little negative effect on the following day and mild hangover. Setting is agreed to be crucial. Most agree that Ketamin not be used by inexperienced trippers unless they want a complete out-of-body experience that is sure to change their life. \9 Kung-Sa Born on 17 Feb 34 in Hpa-perng village, Lashio. Orphaned at five, he was taken in, cared for and tutored by his grandfa ther. He was captured by the Burmese in early 1969. He was once married to a Thai, Khe Yoon. He surren- dered the opium drug trade in early 96 and adopted the Burmese name of Htet Aung for business purposes in 11/96. Khun Sa now sick (3/2000) is expected to return home to his favourite house being prepared Subin Khuenkaew and Cheewin Sattha. Next month Kung-sa is expected to return to his former stronghold in Homong, opposite Mae Hong Son, to live out the rest of his days. Following months of speculation about his return, sources among border security authorities and the former drug warlord's followers, said a house in Homong, known to be one of his favourites, is being cleaned and renovated in anticipation of his return in early Apr 2000. A family member said Khun Sa, is paralysed on the right side and can hardly speak. "He wishes to spend his final days in Homong. This is the place where he lived his most successful years," the relative said. Homong is 40km inside eastern Shan State, Burma. Opposite Muang district, the area was once an advanced settlement along the Thai-Burmese border, with a hosp, telephones, a hotel and even a karaoke bar. Before his capitulation to the Burmese military junta in early 1996, Khun Sa built a stupa 3km south of Homong and had told close aides it was to be his final resting place. Homong has been under the control of Burmese soldiers since early 1996. A source at the Office of Narcotics Control Board said he was aware of the rumours but could not confirm them. He said that it would be difficult for Khun Sa to regain his status as a drug warlord with the United Wa State Army now firmly in control of the drugs trade in the Golden Triangle. The charismatic Khun Sa, half-Chinese half-Shan, once controlled most of the opium and heroin trade in the drug-producing area where the borders of Burma, Laos and Thailand meet. Early this month, the HKG South China Morning Post quoted an unidentified source as saying the State Peace and Development Council, the ruling junta in Rangoon, had given permission for his return to Homong. ----------------------------------------------- Khun Sa (aka. The Prince of Death or Mr. K), wanted by the US govt for heroin trafficking, was the world's largest single supplier of heroin until he "surrendered" to SLORC in Jan 1996. The U.S. govt credits Khun Sa with providing a full two-thirds of the world's heroin supply when he was in business. Rather than rotting and languishing in some Third-World piss-stained jail cell, "Mr. K," as he's referred to by his close associates, instead lives opulently with the generals in Yangon. He has a number of hotel interests and runs the capital's bus system. It's golf twice a week with the generals and a military escort when he leaves home. His choice of rest doesn't need to be marred by how busy they might be. Soldiers simply clear the place out. Mr. K and his 10 aides--who followed him from his Ho Mong hdqrs can then dine in peace before taking Khun's four cars back to the compound for some afternoon pitch-and-putt in the back yard. Then, after a little nap, it's time to get that annoying diabetes checked out by his very own live-in Taiwanese doctor. Nonetheless, his best buddies say that Mr. K is both bored and stressed by Yangon and yearns for the mountains of Shan State and his former glory as a ruthless drug warlord. Not that he's left them entirely; his Khun Sa gang runs a network of methamphetamine factories where his poppies used to grow. Much of the dope ends up in Thai high schools and the glove boxes of long-dist truckers. Myanmar - The Khun Sa Gang (formerly the Shan United Army, or Mong Tai) The Mong Tai army was the private play-toy of ruthless drug-lord-turned-hotel-mogul Chang Chi Fu, also known by the thespian title Khun Sa (the Prince of Death; see below). It broke up into factions in June 1995, charging their leader with spending too much time tinkering with his dope business and not enough fighting for freedom. (Khun Sa theatrically claimed the defections occurred because he is half Chinese.) And govt troops seized the drug warlord's mountain stronghold at Ho Mong in January 1996. The cagey guerrilla commander cut a deal with SLORC in which he turned over his territory and what was left of his army to the govt in exchange for amnesty. Problem is, it seems he didn't tell his guerrillas. One Mong Tai army officer who made it into Thailand shortly before SLORC took the base said, "We were told our commanders were negotiating with SLORC for a cease-fire--but it turned out they were allowing the Burmese troops to take over our bases." Oh, well. Khun Sa has maintained all along that he was never an opium trader but a freedom fighter, and that he taxed drug runners moving through his territory to help fund the Shan liberation cause. An unknown number of the former soldiers remain loyal to Khun Sa and have been tasked with building and operating at least a dozen methamphetamine factories in the jungle along Myanmar's borders with Thailand and Laos. Khun Sa's Boy Soldiers. Theres hundreds of kids with guns whacking SLORC troops and rival drug armies, most of them between 10-14 years old. With the drug warlord's army now defunct, at least 500 of the kids don't have a home. SLORC's policy? They've asked that local families adopt the kids as farm laborers. Most won't take the kids in. Who knows, they may become the next rage in the States, like pet rocks and Vietnamese pygmy pigs. Want to adopt one of Khun Sa's boy guerrillas? Check with the Myanmar emb in BKK or Wash, DC. (see adrs and phone nbrs on foll page). A partial listing of Myanmar's insurgent groups, illegal political parties and rebels. All Burma Students Democratic Front (ABSDF) Burmese Communist Party (BCP) Chin National Front (CNF) Democratic Alliance of Burma (DAB) Karenni Liberation Army (KLA) Karenni Peoples United Liberation Front (KPULF) Kayah New Land Revolution Council (KNLRC) Kuomintang (KMT) Ma Ha Faction of the Wa Army Mon Liberation Front (MLF) National Democratic Front (NDF) National Coalition Govt of the Union of Burma (NCGUB) Pa-O Shan State Independence Party (PSSIP) Palaung State Liberation Organization (PSLO) Tai National Army (TNA) Shan United Revolutionary Army (SURA) Shan United Army (SUA) United Pa-O Organization (UPO) \10 Laws In NYS: Possessio,n is a misdemenor with a max sentence of a yr in pprison. Dealing is a felony as when you hand someone a controlled substance regardless if any value is exchanged, carries a penalty of 1-3 yr for a 1st offense and a 4 1/2 to 9 yr for others. --------------------------------------------------------- From the late 1800's through the 20th cen, drugs have degraded our way of life. Drug laws have failed to correct the trends The first laws controlling drug use were passed in the last quarter of the 19th century. 1868 Pharmacy Act of 1868 required registration of those dispensing drugs. 1875-90 Western States prohibit opium dens. 1906 Pure Food and Drug Act prohibited adulteration and mislabeling; lead to decline of patent medicines 1909 Opium Exclusion Act 1909 Shanghai Opium Convention 1911 International Conference on Opium 1913 International Opium Convention ratified by U.S. Senate. 1914 Harrison Narcotics Act taxed and regulated distribution and sale of narcotics 1919 Supreme Court sustained the Harrison Act in U.S. v. Doremus. 1920 Volsted Act, National alcohol prohibition. Narcotics Drugs Import and Export Act 1922 Federal Narcotic Control Board established. 1929 Porter Narcotic Farm Act established two narcotics hospitals for addicts in Federal prisons in response to addicts crowding. 1930 Federal Bureau of Narcotics created in the Treasury Department under a Comissioner of Narcotics, an enforcement structure that remained in place for 35 years. 1932 Uniform State Narcotics Act endorsed by Federal Bureau of Narcotics as an alternative to Federal laws; by 1937 every State prohibits marijuana use. 1935/1936 First Federal hospitals/prisons open in Lexington and Fort Worth under the Porter Act. 1937 Marijuana Tax Act 1942 Opium Poppy Control Act 1951 Boggs Act imposed harsher penalties 1956 Narcotics Control Act (Boggs-Daniels) increased penalties, defined sole role of Federal Government to be suppression of illegal drug traffic. 1962 White House Conference on Narcotics and Drug Abuse and President's Advisory Comission on Narcotics and Drug Abuse (The Prettyman Commission) recommended dismantling FBN with new focus on treatment and preventing the diversion of dangerous drugs from legal channels 1963 Community Mental Health Centers Act provided first Federal assistance to local treatment of addiction under rubric of mental illness. Pharmacy Act of 1868 1875-90 Western States Prohibits Opium Dens Pure Drug and Food Act Opium Exclusion Act Shanghai Opium Convention International Conference on Opium Ratification of Opium Convention Harrison Narcotics Act U.S. vs Doremus Volsted Act Narcotics Drugs Import and Export Act Federal Narcotics Control Board Porter Narcotic Farm Act Federal Bureau of Narcotics Created Uniform State Narcotics Act First Federal Hospitals/Prisons Open Marijuana Act Opium Poppy Control Act Boggs Act Narcotics Control Act White House Conference on Narcotics and Drug Abuse Community Mental Health Centers Act \11 Methcathinone Methcathinone is a dangerous addictive drug that is cheap and easy to manufacture. The drug is made from a mixture of battery acid, Drano, and over-the-counter asthma medication and can be manufactured in home kitchens. Methcathinone is a white or off-white crystalline powder. What are the street names/slang terms for it? Cat, Goob, Jeff, Speed, Bathtub speed, Mulka, Gagers, gaggers, The C, Wild cat Wonder star, Cadillac express, Ephedrone The most common means of taking methcathinone is snorting. Other routes of admin inc taking it orally mixed in a liquid such as coffee or soft drinks, intravenous injection, and smoking it either in a crack pipe or added to tobacco or marijuana cigarettes. Methcathinone is often used in binges lasting from two to six days, during which methcathinone is used repeatedly. What are its short-term effects? Short-term effects of methcathinone include: stimulation of heart rate and respiration; feeling of euphoria; loss of appetite; increased alertness, dilated pupils, and temperature may be slightly elevated. Acute intoxication at higher doses may also result in insomnia, tremors and muscle twitching, fever, headaches, convulsions, irregular heart rate and respirations, anxiety, restlessness, paranoia, and hallucinations and delusions. What are its long-term effects? While research on the long-term effects of methcathinone use is just beginning in the United States, anecdotal reports from users in treatment in this country, and from published research in Russia, paint a similar picture. Chronic use of methcathinone produces a range of problems typical of addiction to powerful stimulant drugs including paranoia and delusions, hallucinations, including a sensation of bugs crawling under the skin, anxiety followed by depression, tremors and convulsions, anorexia, malnutrition, and weight loss, sweating, dehydration, and electrolyte imbalance, stomach pains and nausea, nose bleeding and eventual destruction of nasal tissues and erosion of the nasal septum, elevated blood pressure and heart rate body aches. In addition, following a binge, users report a "crash" that often includes severe psychological depression, and suicide ideation. In extreme cases, deaths have been reported, and are related to heart failure, lethal overdoses, drug-related violence, and manufacturing accidents. What is its federal classification? Methcathinone was classified as a schedule I controlled substance under the Federal Controlled Substances Act on May 1, 1992, under the emergency scheduling procedure. The classification was made permanent effective October 15, 1993. Source: Indiana Prevention Resource Center ------------------------ What is it: The designer drug 'methcathinone HCl' is also known as Cat, Jeff, Mulka or Ephedrone. It is a schedule-1 stimulant, making it flat-out illegal like Heroin or LSD (Methamphetamine, on the other hand, is LEGAL with a valid triplicate prescription.) Chemically, Methcathinone is 2-(methylamino) propio- phenone. The name Methcathinone is derived from the name of the drug cathinone, obviously, which in turn is derived from "cathine", an alternate name for norpseude- phedrine, an isomer of phenpropanolamine. The name "Ephe- drone" is obviously derived from the fact that "Ephed- rone" is the ketone of the alcohol that is Ephedrine. Theory: The KMnO4 Synthesis: Theory and Background This synthesis uses KMnO4, a damn strong oxidizer that under most conditions might not be the ideal reactant for this synthesis, but when treated with some degree of respect, will work extremely well. This synthesis relies on two principles understandable by anyone who's had chemistry at the college level.. or any experience with chemicals at all. Even baking a cake. There's two other synthesises making their way about the net, that I am aware of. The first uses the less potent CHROMATES [which are more toxic] at room temperature, and the second uses KMnO4 with a variety of other weird things and conditions - albeit at room temperature. Seeking to avoid the chromates while also avoiding using a lot of more advanced technique and equipment, leaves only one option. Slowing KMnO4 down to a reasonable rate. 1. The reaction in the FAQ is dilluted considerably... 2. The reaction in the FAQ is done way colder than any other cat synth. Presto, the two key elements to changing the rate of a reaction. The end result is quite pleasing and economical, and the reaction is about as fast as the chromate recipe. Other than that, the only commentary on the recipe is that its a standard alcohol to ketone oxidization proceedure for the most part. Yield, when measured is likely to vary according due to a few things: 1. The efficiency of the pseudephedrine extraction employed. 2. Temp of the reaction - higher temps are far more apt to yield side product [deamination?] which will be lost. 3. Care taken during solvent "wash" of final product. 4. Realize that KCl is a very likely to be present in the final product. and adjust estimated yield from weight accordingly. Prep: The objective of this proc is to produce methcathi- none in a reletively pure form. This was done as evid- enced by a residue/burn test, and quite a few testimon- ials from users. A secondary objective was to not require complicated lab proceedures - avoiding even an acid-base extraction and to stray away from toxic byproducts. Upon completion, your methcathinone should be "pure" with a small potassium supplement... The methcathinone produced by this proc is no doubt not as pure as that which may be produced using a typical acid-base solvent extraction, but certainly rivals it nicely. And the conditions reqd for this method are far less demanding, as none of the toxic chromates are used. NEEDED FOR PREPARATION: Collander w/reletively small holes Shaved Ice Pseudephedrine tablets, 100 of 30mg each. Potassium Permaganate crystals, of reasonably pure origin [no lead, other toxic metals allowed.] Purified water [TAP WATER WILL *NOT* FUNCTION ADEQUATELY IN MOST CASES] Refridgerator chilled to just over 0c. Turkey Baster or other method of measuring water in mililiter quantities. An area heated or chilled to "room temp" (ROUGHLY 25c or 75f) Isopropanol for quenching KMnO4. Ethanol optional for speeding drying process. Acetone for the washing of crystals. ------------------ Most kitchens do NOT come equipped with a scale capable of measuring individual grams, let alone miligrams. And in many states, possession of such a finely tuned instrument, while not a crime, certainly is admissable as one of many items of evidence to be used in a criminal investigation. Definitly something to be avoided. Keep all the ingredients and all the labware in its "everday- use" place, and there's no evidence to support the existance of a cat lab. And no need to manufacture the stuff in the high desert regions either, since weird scents are for the most part avoided. CLEANING THE PSEUDEPHEDRINE TABLETS: [kudo's to POPeye for his doc "Getting the Red out"] 100 of the 30mg generic pseudephedrine tablets were placed into a collander containing about the same "volume" of crushed ice. They were swirled around in this collander over a sink (with running water to wash the color down the drain) until all the ice had melted and washed thru. The tablets were then rinsed once with distilled water, and removed to a glass jar for extracting. * NOTE: The running water kept the drain clean, but wasn't ever in contact * with the tablets themselves. This confused a number of people. Obviously, * its not necessary for this... just convienent I guess. * Do not wash the tablets UNDER WATER with crushed ice. Rather, place * them in the colander with crushed ice, thats it, and stir them around,.. * The very cold ice does a minimum of disolving WHILE its abrasion removes the coloring. MEASURING OUT & PREPARING THE KMnO4 FOR REACTION: KMnO4 is saturated at 25c in water - 100ml of solution holds 7.43g This time I will be using just under 3g of pseud- ephedrine (if extract was perfect would be exactly 3g pseudephedrine). Keep in mind that when preparing the saturated solution you need room temperature and time - you need to let the crystals settle!!! Excess (undis- olved) KMnO4 will stay "swirled in" the solution. Let it settle for a while at room temp, _then_ measure the 15mL or so... Failure to do this will result in a failed synthesis. If you are too impatient to do this, then you should purchase a miligram-quantity scale. In acid conditions, 1 mole of KMnO4 will oxidize 5 hydrogens. In basic conditions, 1 mole of KMnO4 will oxidize 3 hydrogens. We won't be specifically using either, because KMnO4 also works nicely under neutral conditions. It can be reasonably anticipated that the Pseudephedrine HCl will posess somewhat of an acidic character, so we will 'assume' acidic conditions, which also will allow us to avoid using TOO MUCH KMnO4... small amounts of pseud- ephedrine will go unnoticed in the final product, but gooey messes will not, for obvious reasons. The Pseudephedrine/KMnO4 ratio should be 2.5Mole to 1Mole, according to previous calcs. 3g pseudephedrine is 18.15mMole, therefore 7.26mMole of KMnO4, or 1.148g will be needed for the reaction. This means that 15.45mL of concentrated solution at room temp will be needed. Obvi- ously us kitchen chemists can't be that precise, so aim a little high, as previous margins were set about 10% low... use AT LEAST 15.45mL prepared at AT LEAST 25c. This 15.5 or so mL of solution is then diluted with 250mL H2O, and is started chilling in a refridgerator, with just over 0c the goal. EXTRACTING AND PREPARING THE PSEUDEPHEDRINE HCl FOR REACTION: Place the just washed and probably slightly red pseudephedrine tablets in a jar, and pour 150mL of water over them. Now heat this in a microwave at low power until it gets "hot" but not boiling. Stir the crap until the tablets fall all to pieces, then let the powdery FILLER material settle, leaving pseudephedrine in solution all by its lonesome, or at least mostly by its lonesome. Slowly pour this THRU coffee filter into another jar. When this is done, scrape/shake/get any powder caught in the filler and stick it in the FIRST jar, the one that might have some sludge at the bottom still. Now add another 150mL of water, heat until "hot", stir, then let settle. Pour this thru the coffee filter. Get the powder stuck in the filter (again) back with the sludge and add still another 150mL and heat until "hot". This time pour thru the filter, and your done. It is worth noting that the filler material clogs the filters and will dramatically increase time for filteration to take place, like from 30 seconds to 30 minutes. The enlightened will at once realize that the easiest way to avoid this is to decant the top layer thru the filter first, waiting until necessary to dump the sludge onto the filter. Place the pseudephedrine solution in the fridge to chill, next to the KMnO4 solution. Label the jar so that in the event you are raided during the proc more evidence will exist to prosecute you. * It should be noted at this point that much feedback has been recieved * from "failed" synthesis caused entirely by not letting the mixture chill * long enough. If your impatient, place it in the freezer until ice begins * to form then allow it to warm just enough to melt before mixing * remember, the ___ONLY___ reason this works at all is because the dilution * and temperature are such that the permaganate oxidizes the alcohol to a * ketone and then GETS USED UP before it can do anything else. * NOW THE FUN BEGINS (THE REACTION): And for the next few hours, nothing happens. This is a good time to stop for lunch. After a few hours, the two cold solutions are mixed together, stirred, and replaced in the fridge overnight (8-12 hours). In the morning, instead of a PURPLE color in the jar, there is a mostly clear layer, and a brownish gunk on the bottom, which agitates easily. Because its safer to err on the side of caution, 100mL of 70% isopropyl alcohol is added and stirred. If a purple color remains, odds are that an EXCESS of KMnO4 was used and the synthesis will fail, or that not enough time was allowed for the reaction to take place. Do not allow more than 12 hours in any case, instead give the KMnO4 something else to chew on [the isopropyl alcohol]. This is the sole reason for the addition of isopropanol. Ethanol or methanol were not used because they tend to oxidize further to substances not so easily seperated from the product. Acetone from the isopropanol will evaporate easily. Let the mixture sit for roughtly 2 hours on a shelf, and at the end of this period it should be around room temp. Time to room temp will vary with dimensions and thickness of the container, of course. This mixture is filtered thru two coffee filters stacked on top of each other with the intention of catching all the little maganeese particles that have precipitated. In an ideal world, you can do this on the first try and get a perfectly clear liquid on the bottom. In a less than ideal world, it was necessary to again RECOOL SLIGHTLY the filtered mix, and filter this thru another pair of coffee filters. My hunch is that the slight cooling in the fridge, and/or the extra time allowed the rest of the maganeese to 'clump' together into pieces too big to escape unfiltered. * many have found two, three, or even four refiltrations to be necessary * apparently the choice in coffee filter places a dramatic role. The truly * patient chemist could use a PAPER filter, provided it is free of anything * that would end up in the mixture [coloring, etc] This final solution was found to be basic with a pool test kit, no suprise if you figure that the HCl part of the Pfed was used up in the oxidation as 'acid'. Results will vary on the final pH. If its already acidic, you dont need to add any more acid (heheh). Most have found a pool test kit woefully inadequate, and have suggested using pH paper. I almost wonder if the amateur pH meter made from boiling red cabbages wouldnt be better, as it is also wider range. See below. MAKING GLITTERING WHITE CRYSTALS: If not yet, during this part of the proceedure you will definitly smell the meth- cathinone. It has a stronger odor than methamphetamine, BUT the odor of methcathinone is pleasant, even to those who have not experienced the drug (some people LEARN to like certain smells, but cat just smells plain good.) * The smell has been most closely likened to pistacio ice cream, of all things. Will ceases never wonder... Considering the fact that there's either isopropanol or acetone in the above mixture, its probably not a wise idea to just load your rig straight from it and shoot. And considering you might want to give some of your creation away, it'd sure be nice to have a transportable form. * NOTE: A *very small* amount of conc. HCl is required. Add it one drop at a time with stiring. Now to make sure the stuff is indeed the HCl form... Add HCl with stiring to adjust the pH to slightly acidic, i.e. just under 7 (like 5 - 6.5). This will ensure that Methcathinone HCl is produced, and not the freebase, which can decompose easily. While the original FAQ suggesting using a pool test kit to measure the change in pH across a very narrow range, many people haven't got this to work, and instead a less sensitive agent [pH paper?] is reccomended. Perhaps even the classic "red cabbage" pH tester will work... see any kids chemistry book for more details on this plant-based pH test... In any case, if its concentrated HCl, add it ONE DROP AT A TIME with stiring and checking of the pH. If you add too much HCl, the crystals wont seem to dry out properly. Fear not, place them in a freezer or some such, then take them out let them thaw & dry more, they will eventually freeze *after* the excess HCl moves into the atmosphere. Pour the stuff into a glass (PYREX!) brownie dish. Place on a stove and heat gently from below _while_ blowing lightly with a hair dryer (avoid splashing - it wastes drugs and leaves residue.) Eventually there will start to be a really really thick gooey mess. Adding methanol or ethanol to this thins it while speeding the drying process - a definite plus. In my case, ethanol was used, although methanol may be preferable. Doing this is probably a must to dry the crystals at a reasonable temperature in a reasonable amount of time, unless you happen to have a vaccuum pump lying around.... *** While it would seem that adding liquid would increase drying time, this is not the case because the alcohol helps remove water from the crystals - almost dry crystals can be heated very hot and still not dry. For best results do not add the extra alcohol until the drying stuff is kinda thick, or the first crystals have started to form. Be careful not to overheat the crystals. If they MELT, you've almost definitly screwed up.... :) Washing the crystals with acetone _is_ a possibility but can dramatically reduce yields, as Methcathinone HCl is apparently pretty soluable in the stuff. Just save the acetone and let it dry all alone, somewhere, for a product that is smokable but too oily to chop & sniff... Methcathinone is easily recovered from an 'acetone-wash' by slow evaporation, and such recovered globs, hunks, crystals, slime, ooze, whatever you get should be saved and washed again, to recover any lost crystals. Strangely, certain solvents will affect the potency of the end product. Disolution of the base in methanol will result in racemization! If you are especially (dis/) pleased with the results of a particular batch and can't figure out why, think back to what solvents were used in drying and/or washing. ************************TESTING************************** BURN: A burn-test of acetone-washed methcathinone left almost NO residue. The methcathinone HCl was heated over methane flame in a spoon. It first melted, then began boiling, and finally literally BURST INTO FLAMES and was gone except for a spot where the spoon was possibly corroded. A burn-test of the oily methcathinone from the acetone wash which evaporated (and would have been lost had I not kept the byproduct of the acetone wash) performed the same way! Its oily nature prevented clean chopping, but upon washing with ethyl-ether good product was formed from this oily cat. A burn-test of ether cleaned acetone-wash extract left nothing behind but a slight discoloring of the shiny part of the spoon, probably due again to reaction with the HCl or reaction with air catalysed by the salt nature of the crystals (?) TASTE: Bitter. No evidence of numbing of the tounge or sinuses was evidenced. Snorting the product produced intense burning feelings in the nostrils, stronger than saline solution or (laughably, I did this once to prove a point) sugar (which doesnt feel at all!), about as much sting as with methamphetamine, and no where near as much sting as was once obtained from snorting diphenhydramine concentrated from benedryl (a very stupid experiment in nasal congestion...) SMELL: Typical of a ketone - sweet. Once report says it smells like "pistaccio ice cream" when wet. The dry crystals dont smell all that much, but it doesnt take a genius to realize that once they get dogs trained for this stuff detection will be simple. melting point of the HCl form is 182-184c according to listing below. **********************COMMENTARY************************* Methcathinone was used as an antidepressant in the former soviet union. This almost makes good sense, as even in abuse doses the 'hangover' is nowhere near as severe as with the amphetamines. Indeed, bupropion, a close chem relative, is used as an antidepressant in todays US. Methcathinone was considered by one company for marketing in the US as an antidepressant in the 1950's, but was shelved due to "severe side effects". If you've ever taken Imipramine or another TCA, or know of the pharma- cology of the MAOI antidepressants, you really wonder about the truth of this statement. The "severe side effect" that shelved the project was no doubt addiction and abuse, not an actual physiological side effect... If I had to characterize the drug, I would say it induces mania more so than methamphetamine, but psychosis much less. The initial dose produced some paranoia, but subsequent doses did not make this worse (?) and in fact seemed to lessen it. This is definitly a drug for goofing off, unlike methamphetamine which makes one 'serious'. Methamphetamine may dramatically help certain peoples academic and or business careers, but it doesnt appear likely that methcathinone would do this, as it increases distractability rather than decreases it. "The drug didn't catch on in Ann Arbor. 'it would be hard to go to classes on cat,' Boyer theorized" -L.A. Times article on methcathinone abuse crackdowns ****************ANECDOTAL REPORTS OF USE***************** No dilation of the pupils was noticed at any level (?!?), however both pulse rate and blood pressure were up quite a bit. Upon sniffing, mouth instantly "watered", and thru the experience my mouth did not become dry. So +/-choli- nergic side effects appear absent, unlike either amphetamines or cocaine. When the drug wears off, sleep is much easier to obtain. The first night after a day of CATting I slept very well, but after the next day of the same I awakened after only 2 hours of sleep and had to take diphenhydramine to return to sleep. Withdrawl is characterized by sadness and feelings of despair, along with a lack of energy. Others have reported a physical withdrawl, but these reports come from the highDose michaganCatNut crowd. Alternately felt hopeless or giddy and almost euphoric. Caffeine appears to dramatically alleviate the depression. "I hadn't known I was hooked. I felt like I had a temperature of 1 million degrees. I could hardly breathe. My whole body ached" -Grimes on his experience in a detox tank in the Marquette county jail. ************************SOURCES************************** Pseudephedrine - From the tablets, silly. HCl - Any hardware store, as "muratic acid". KMnO4 - searsWater Softener Section, to regenerate iron filters water softener section of Home Depot ($6/lb?). - found it at a farm supply store. About $3.00 per llb. - Used to stain bacteria/biologicals for slides [if going this route, dont buy a kilogram obviously] Acetone - Hardware stores (used as paint thinner, to clean grease of off things, etc) **********************EXTENSIONS************************* Equimolar amounts of phenpropanolamine, norephedrine or norpseudephedrine may be easily substituted to produce CATHINONE instead of methcathinone. Data indicates this is a less potent drug, but this is easily remedied by taking more (obviously) and diff people may or may not prefer a slightly diff side effect profile, etc etc etc. > I notice all the generic phenpropanolamine I've come across contains vitamin c. Would it be necessary to extract that first to make cathinone? Yes, you must remove the vitamin C. There is little doubt in my mind that such a compound could make a simple oxidation into a gooey hell. Antoxidant that it is, Vitamin C may be in there to keep the stuff from oxidizing on the shelves... some catHeads have noticed that ground sudafed from Burroughs Wellcome has a very mild methcathinone smell to it.... weird, no? > What other Aminoketones are popular / widely used, and can I make them myself? Diethylpropion - Tenuate, a C-4 (USA) diet pill If you can produce diethylphenpropanolamine, you can use it in the above reaction to produce Diethylpropion, although the time involved makes it doubtful that you'd want to - this drug is not all that potent or interesting. DEPPA could probably be produced in decent yields via a controlled temperature reaction with base, PPA and chloroethane, although I have no idea what conditions would be ideal. Expected sideproducts would be unchanged PPA, EtPPA, and (Et3)PPA+ ions... Bupropion - Wellbutrin, an unscheduled (USA) antidep- ressant Nope. meta-Chloro,N-tert-butyl-Cathinone, or bupropion, would no doubt be problematic due to the meta-chloro grouping - difficult to produce in a home environment, if not damn near impossible, and probably a point of side reactions if the ephedrine of the compound were to be oxidized. Additionally, abuse potential for Bupropion is probably lower than that of even caffeine. Caged rhesus monkeys will slam it, but think about the condition of their life: In such a miserable state anything must be a relief. **********************OTHER DATA************************* Zingel, K.Y., Dovensky, W., Crossman, A. and Allen, A., "Ephedrone: 2-Methylamino-1-Phenylpropane-1-One (Jeff)," Journal of Forensic Sciences, v. 36, No.3, May 1991, pp.915-920 Synthesis & Info from above article follows: [I really *do not* like this synthesis] A 2000-mL Erlenmeyer flask, equipped with a magnetic stirring bar, was charged with methylene chloride (200 mL), acetic acid (10 mL) water (100 mL), potassium permanganate (2g) and ephedrine hydrochloride (2g). The solution was stirred at room temperature for 30 min. This was followed by the addition of sufficient sodium hydrogen sulfite to reduce the precipitated manganese dioxide. The aqueous phase was made basic with 5N sodium hydroxide (NaOH) and the methylene chloride was separated. The organic layer was extracted with 0.5N sulfuric acid (H2SO4). Isolation of the acid layer followed by basifi- cation with sodium bicarbonate and extraction with methylene chloride (50 mL, three times), removed the product into the organic phase. The solvent was concentrated by rotary evaporation, followed by column chromatography through neutral alumina with methylene chloride. Solvent removal through rotary evaporation produced a colorless liquid which was disolved in hexane. Gaseous hydrochloric acid was bubbled into the hexane to precipitate the amine hydrochloride to produce a 1-g (50%) yield of 2-methylamino-1-phenyl- propan-1-one hydrochloride. Ephedrone, like methamphetamine, processes one asymmetric center. Depending upon the synthetic precursor, l-ephedrine (1R,2S) or d-pseudoephedrine (1S,2R), the product expected would be d-ephedrone (2S) or l-ephedrone (2R), respectively. However, depending on the heat of the reaction or harsh extraction conditions the enolizable ketone will result in a racemic d,l-ephedrone. * Young, R. and R.A. Glennon. "Cocaine-Stimulus General- ization to Two New Designer Drugs: Methcathinone and 4-Methylaminorex" Pharmacol. Biochem. Behav. 45(1) 229-231, 1993 * Glennon, R.A., Yousif, M., Kalix, P. "Methcathinone: A new and potent amphetamine-like agent." Pharmacol. Biochem. Behav. 26:547-5451, 1987. * British Patent, 768,772 (1954). [This is the "classic" recipe using the chromates as oxidizers] A solution composed of 0.99g of sodium dichromate and 133g of concentrated sulfuric acid dissolved in 4.46 cc of water is added slowly with stirring to 1.65g of l-ephedrine dissolved in 4.7 cc of water and 0.55 cc of concentrated sulfuric acid at room temperature. The mixture is stirred at room temperature for an additional 4 to 6 hours and then made alkaline with sodium hydroxide soloution. the aqueous mixture is extracted with two volumes of chloroform and then with two volumes of ether. The organic extracts containing the free base of 1-a-methylaminoprophenone are combined, treated with an excess of dry hydrogen chloride and the solvents evaporated. The residual 1-a-methylaminopropiophenone hydrochloride is stirred with petroleum ether, collected and purified by dissolving in ethanol and reprecipitating with ether. m.p. 182-184 o C. * Goldstone, M.S., "Cat - Methcathinone - A New Drug of Abuse" Journal of the American Medical Association v269 no 19 p2508 (letter) 1993 This article basically warns of methcathinone appearing on the streets. Notable claims are that the typical dosage is .5 to 1 gram a day (!!!) and that addicts describe long-lasting intoxicating effects of up to 6 days (I would assume this is repeated administration...). The article also states that "cat" costs US$100 per gram (!whatever!), and goes on to reccomend benzodiazepines for addicts (yay!) but antipsychotics for those who have overdone it and schiz'd out (boo!). The article also indicates that tolerance develops and disapates rapidly, something that happens with just about any stimulant, even caffeine... [abstract follows immidiatly below, copied indirectly from MEDLINE] TI - Methcathinone: a new & potent amphetamine-like agt. AB - The purpose of the present investigation was to examine the effect of N-monomethylation of phenylisopropylamine derivatives on amphetamine- like activity. In tests of stimulus generalization using rats trained to discriminate 1.0 mg/kg of (+)-amphetamine from saline, the N- monomethyl derivatives of 1-(X-phenyl)-2-aminopropane, where X = 2,4- dimethoxy (2,4-DMA), 3,4-dimethoxy (3,4-DMA), 2,4,5-trimethoxy (2,4,5,-TMA), and 2-methoxy-4,5-methylenedioxy (MMDA-2), did not produce amphetamine-appropriate responding at the doses evaluated. However, the N-monomethyl derivative of cathinone (i.e., methcathinone), like cathinone, resulted in stimulus generalization. Further studies with this agent revealed that (a) in the amphetamine- trained animals, methcathinone (ED50 = 0.37 mg/kg) is more potent than racemic cathinone or racemic amphetamine (ED50 = 0.71 mg/kg in both cases), (b) methcathinone is capable of inducing release of radioactivity from [3H]dopamine-prelabeled tissue of rat caudate nucleus in a manner similar to that observed with cathinone, amphetamine, and methamphetamine, and (c) methcathinone is more potent than cathinone as a locomotor stimulant in mice as determined by their effect on spontaneous activity. The results of the present study provide evidence for a structural analogy between the prototypic psychostimulants amphetamine/methamphetamine and cathinone/methcathinone, and lend further support to the concept that amphetamine and cathinone correspond in their pharmacological effects. Regarding CATHINONE and the Khat Plant: Teri Randall "Khat Abuse Fuels Somali Conflict, Drains Economy" JAMA Jan 6, 1993 Vol 269, No. 1, p. 12 & 15 This article contains a number of political interpretations, but also states: "Its users report euphoria and increased alertness, although their concentration and judgement are objectively impaired" [This fits nicely with my observation that Methcathinone is not useful as a drug for treating ADHD - amphetamine will improve ability to concentrate] \12 Methcathinone questions The following have been paraphrased for brevity. > What brand of pseudephedrine is best??? HINT: The smaller the pill, the less filler material it has. Your safest bet on this one is to find out for yourself. Compared to just about anything else in this world, pseudephedrine is cheap. Purchase and find out. > Is there any faster or less labor-intensive method of drying a batch? An informed netter replies: You are absolutely right. I "understand" that placing the "stuff" into a glass casserole dish, then immersing in a double boiler setup does the job much nicer, while still being well within the means of the average kitchen. The main things to keep in mind are the addition of ethanol to thin the stuff while drying, and the use of a large surface area, to promote moving solvent into the air, both water and ethanol. > What of I.V. usage of the drug produced from this method? I wouldn't reccomend it as this method avoids an acid-base extraction. While certainly less toxic than the chromates, injection of "other" material ought to be avoided. > This is the same method of making cat that you wrote up some time ago, but you said that it (the synthesis you typed up) was crap. Is this synthesis the same as the one you were using? (I never read yours) Not the same by any stretch of the imagination. All the difference in the world results from using exact amounts of KMnO4, highly diluted, and in an extremely chilled condition. > The FAQ said 70% isopropanol, can this % be varied? Yes, that is just fine [esp. since its being added to a water-containing solution anyways :) The purpose is to provide "something else" [another alcohol] to be oxidized so that the Methcathinone won't get chewed up if any oxidizer remains... Do not substitue another alcohol for this *unless* it is a "secondary" alcohol. Primary alcohols like ethanol and methanol can oxidize further to substances that will not evaporate from the mixture as easily. The isopropanol will oxidize to acetone, which evaporates easily. > What drug-salts of methcathinone are there? The HCl form is the easiest and probably safest sniffable form. Its also pretty resistant to decomposition [esp. compared to freebase form]. Obviously other forms could be easily made, but why bother? > Will "Hardware store HCl" work? Yes, in fact any aqeuous solution of HCl alone will work. Concentration doesn't even really matter provided that pH is monitored - add the amount needed to achieve the desired pH change. > When your putting the jars in the fridge do you also put the lid on them or does it even matter? Unless the reagents are attacked by dripping WeenieDogs it shouldn't matter all that much. Best to place it safe and use lids anyways. > What is "filler material"? The other crap in any medicine tablet / pill / capsule that holds it together. Were your antibiotics to come without 'filler material', they would also arrive in a little plastic baggie just like the illegal drugs. > If you want to make life easier for kitchen chemists, a "tablespoon" is about 15mL Oh. Cool. Thanks. Nevertheless, a tablespoon is usually metalic, and therefor probably not to cool to use with permaganate solution :) CONCLUSION The original author of this synthesis does not have an internet address. She has given me permission to "maintain" this file, by adding Q&A, tips, comentary, etc at my discression to it. If you have a comment, question, or tip, simply post it in alt.drugs.chemistry so that the world will benefit. From klday@unity.ncsu.edu Jan 98. Methcathinone HCl FAQ v2.2 \13 Mushroom toxins Mushroom toxins 1. Name of Toxin(s):Amanitin, Gyromitrin, Orellanine, Muscarine, Ibotenic Acid, Muscimol, Psilocybin, Coprine 2. Name of Acute Disease: Mushroom Poisoning, Toadstool Poisoning Mushroom poisoning is caused by the consumption of raw or cooked fruiting bodies (mushrooms, toadstools) of a number of species of higher fungi. The term toadstool (from the German Todesstuhl, death's stool) is commonly given to poisonous mushrooms, but for individuals who are not experts in mushroom identification there are generally no easily recognizable differences between poisonous and nonpoisonous species. Old wives' tales notwithstanding, there is no general rule of thumb for distinguishing edible mushrooms and poisonous toadstools. The toxins involved in mushroom poisoning are produced naturally by the fungi themselves, and each individual specimen of a toxic species should be considered equally poisonous. Most mushrooms that cause human poisoning cannot be made nontoxic by cooking, canning, freezing, or any other means of processing. Thus, the only way to avoid poisoning is to avoid consumption of the toxic species. Poisonings in the United States occur most commonly when hunters of wild mushrooms (especially novices) misidentify and consume a toxic species, when recent immigrants collect and consume a poisonous American species that closely resembles an edible wild mushroom from their native land, or when mushrooms that contain psychoactive compounds are intentionally consumed by persons who desire these effects. 3. Nature of Disease(s):Mushroom poisonings are generally acute and are manifested by a variety of symptoms and prognoses, depending on the amount and species consumed. Because the chemistry of many of the mushroom toxins (especially the less deadly ones) is still unknown and positive identification of the mushrooms is often difficult or impossible, mushroom poisonings are generally categorized by their physiological effects. There are four categories of mushroom toxins: protoplasmic poisons (poisons that result in generalized destruction of cells, followed by organ failure); neurotoxins (compounds that cause neurological symptoms such as profuse sweating, coma, convulsions, hallucinations, excitement, depression, spastic colon); gastrointestinal irritants (compounds that produce rapid, transient nausea, vomiting, abdominal cramping, and diarrhea); and disulfiram-like toxins. Mushrooms in this last category are generally nontoxic and produce no symptoms unless alcohol is consumed within 72 hours after eating them, in which case a short-lived acute toxic syndrome is produced. 4. Normal Course of Disease(s):The normal course of the disease varies with the dose and the mushroom species eaten. Each poisonous species contains one or more toxic compounds which are unique to few other species. Therefore, cases of mushroom poisonings generally do not resembles each other unless they are caused by the same or very closely related mushroom species. Almost all mushroom poisonings may be grouped in one of the categories outlined above. PROTOPLASMIC POISONS Amatoxins: Several mushroom species, including the Death Cap or Destroying Angel (Amanita phalloides, A. virosa), the Fool's Mushroom (A. verna) and several of their relatives, along with the Autumn Skullcap (Galerina autumnalis) and some of its relatives, produce a family of cyclic octapeptides called amanitins. Poisoning by the amanitins is characterized by a long latent period (range 6-48 hours, average 6-15 hours) during which the patient shows no symptoms. Symptoms appear at the end of the latent period in the form of sudden, severe seizures of abdominal pain, persistent vomiting and watery diarrhea, extreme thirst, and lack of urine production. If this early phase is survived, the patient may appear to recover for a short time, but this period will generally be followed by a rapid and severe loss of strength, prostration, and pain-caused restlessness. Death in 50-90% of the cases from progressive and irreversible liver, kidney, cardiac, and skeletal muscle damage may follow within 48 hours (large dose), but the disease more typically lasts 6 to 8 days in adults and 4 to 6 days in children. Two or three days after the onset of the later phase, jaundice, cyanosis, and coldness of the skin occur. Death usually follows a period of coma and occasionally convulsions. If recovery occurs, it generally requires at least a month and is accompanied by enlargement of the liver. Autopsy will usually reveal fatty degeneration and necrosis of the liver and kidney. Hydrazines: Certain species of False Morel (Gyromitra esculenta and G. gigas) contain the protoplasmic poison gyromitrin, a volatile hydrazine derivative. Poisoning by this toxin superficially resembles Amanita poisoning but is less severe. There is generally a latent period of 6 - 10 hours after ingestion during which no symptoms are evident, followed by sudden onset of abdominal discomfort (a feeling of fullness), severe headache, vomiting, and sometimes diarrhea. The toxin affects primarily the liver, but there are additional disturbances to blood cells and the central nervous system. The mortality rate is relatively low (2-4%). Poisonings with symptoms almost identical to those produced by Gyromitra have also been reported after ingestion of the Early False Morel (Verpa bohemica). The toxin is presumed to be related to gyromitrin but has not yet been identified. Orellanine: The final type of protoplasmic poisoning is caused by the Sorrel Webcap mushroom (Cortinarius orellanus) and some of its relatives. This mushroom produces orellanine, which causes a type of poisoning characterized by an extremely long asymptomatic latent period of 3 to 14 days. An intense, burning thirst (polydipsia) and excessive urination (polyuria) are the first symptoms. This may be followed by nausea, headache, muscular pains, chills, spasms, and loss of consciousness. In severe cases, severe renal tubular necrosis and kidney failure may result in death (15%) several weeks after the poisoning. Fatty degeneration of the liver and severe inflammatory changes in the intestine accompany the renal damage, and recovery in less severe cases may require several months. NEUROTOXINS Poisonings by mushrooms that cause neurological problems may be divided into three groups, based on the type of symptoms produced, and named for the substances responsible for these symptoms. Muscarine Poisoning: Ingestion of any number of Inocybe or Clitocybe species (e.g., Inocybe geophylla, Clitocybe dealbata) results in an illness characterized primarily by profuse sweating. This effect is caused by the presence in these mushrooms of high levels (3- 4%) of muscarine. Muscarine poisoning is characterized by increased salivation, perspiration, and lacrimation within 15 to 30 minutes after ingestion of the mushroom. With large doses, these symptoms may be followed by abdominal pain, severe nausea, diarrhea, blurred vision, and labored breathing. Intoxication generally subsides within 2 hours. Deaths are rare, but may result from cardiac or respiratory failure in severe cases. Ibotenic acid/Muscimol Poisoning: The Fly Agaric (Amanita muscaria) and Panthercap (Amanita pantherina) mushrooms both produce ibotenic acid and muscimol. Both substances produce the same effects, but muscimol is approximately 5 times more potent than ibotenic acid. Symptoms of poisoning generally occur within 1 - 2 hours after ingestion of the mushrooms. An initial abdominal discomfort may be present or absent, but the chief symptoms are drowsiness and dizziness (sometimes accompanied by sleep), followed by a period of hyperactivity, excitability, illusions, and delirium. Periods of drowsiness may alternate with periods of excitement, but symptoms generally fade within a few hours. Fatalities rarely occur in adults, but in children, accidental consumption of large quantities of these mushrooms may cause convulsions, coma, and other neurologic problems for up to 12 hours. Psilocybin Poisoning: A number of mushrooms belonging to the genera Psilocybe, Panaeolus, Copelandia, Gymnopilus, Conocybe, and Pluteus, when ingested, produce a syndrome similar to alcohol intoxication (sometimes accompanied by hallucinations). Several of these mushrooms (e.g., Psilocybe cubensis, P. mexicana, Conocybe cyanopus) are eaten for their psychotropic effects in religious ceremonies of certain native American tribes, a practice which dates to the pre- Columbian era. The toxic effects are caused by psilocin and psilocybin. Onset of symptoms is usually rapid and the effects generally subside within 2 hours. Poisonings by these mushrooms are rarely fatal in adults and may be distinguished from ibotenic acid poisoning by the absence of drowsiness or coma. The most severe cases of psilocybin poisoning occur in small children, where large doses may cause the hallucinations accompanied by fever, convulsions, coma, and death. These mushrooms are generally small, brown, nondescript, and not particularly fleshy; they are seldom mistaken for food fungi by innocent hunters of wild mushrooms. Poisonings caused by intentional ingestion of these mushrooms by people with no legitimate religious justification must be handled with care, since the only cases likely to be seen by the physician are overdoses or intoxications caused by a combination of the mushroom and some added psychotropic substance (such as PCP). GASTROINTESTINAL IRRITANTS Numerous mushrooms, including the Green Gill (Chlorophyllum molybdites), Gray Pinkgill (Entoloma lividum), Tigertop (Tricholoma pardinum), Jack O'Lantern (Omphalotus illudens), Naked Brimcap (Paxillus involutus), Sickener (Russula emetica), Early False Morel (Verpa bohemica), Horse mushroom (Agaricus arvensis) and Pepper bolete (Boletus piperatus), contain toxins that can cause gastrointestinal distress, including but not limited to nausea, vomiting, diarrhea, and abdominal cramps. In many ways these symptoms are similar to those caused by the deadly protoplasmic poisons. The chief and diagnostic difference is that poisonings caused by these mushrooms have a rapid onset, rather than the delayed onset seen in protoplasmic poisonings. Some mushrooms (including the first five species mentioned above) may cause vomiting and/or diarrhea which lasts for several days. Fatalities caused by these mushrooms are relatively rare and are associated with dehydration and electrolyte imbalances caused by diarrhea and vomiting, especially in debilitated, very young, or very old patients. Replacement of fluids and other appropriate supportive therapy will prevent death in these cases. The chemistry of the toxins responsible for this type of poisoning is virtually unknown, but may be related to the presence in some mushrooms of unusual sugars, amino acids, peptides, resins, and other compounds. DISULFIRAM-LIKE POISONING The Inky Cap Mushroom (Coprinus atramentarius) is most commonly responsible for this poisoning, although a few other species have also been implicated. A complicating factor in this type of intoxication is that this species is generally considered edible (i.e., no illness results when eaten in the absence of alcoholic beverages). The mushroom produces an unusual amino acid, coprine, which is converted to cyclopropanone hydrate in the human body. This compound interferes with the breakdown of alcohol, and consumption of alcoholic beverages within 72 hours after eating it will cause headache, nausea and vomiting, flushing, and cardiovascular disturbances that last for 2 - 3 hours. MISCELLANEOUS POISONINGS Young fruiting bodies of the sulfur shelf fungus Laetiporus sulphureus are considered edible. However, ingestion of this shelf fungus has caused digestive upset and other symptoms in adults and visual hallucinations and ataxia in a child. 5. Diagnosis of Human Illness:A clinical testing procedure is currently available only for the most serious types of mushroom toxins, the amanitins. The commercially available method uses a 3H-radioimmunoassay (RIA) test kit and can detect sub-nanogram levels of toxin in urine and plasma. Unfortunately, it requires a 2-hour incubation period, and this is an excruciating delay in a type of poisoning which the clinician generally does not see until a day or two has passed. A 125I-based kit which overcomes this problem has recently been reported, but has not yet reached the clinic. A sensitive and rapid HPLC technique has been reported in the literature even more recently, but it has not yet seen clinical application. Since most clinical laboratories in this country do not use even the older RIA technique, diagnosis is based entirely on symptomology and recent dietary history. Despite the fact that cases of mushroom poisoning may be broken down into a relatively small number of categories based on symptomatology, positive botanical identification of the mushroom species consumed remains the only means of unequivocally determining the particular type of intoxication involved, and it is still vitally important to obtain such accurate identification as quickly as possible. Cases involving ingestion of more than one toxic species in which one set of symptoms masks or mimics another set are among many reasons for needing this information. Unfortunately, a number of factors (not discussed here) often make identification of the causative mushroom impossible. In such cases, diagnosis must be based on symptoms alone. In order to rule out other types of food poisoning and to conclude that the mushrooms eaten were the cause of the poisoning, it must be established that everyone who ate the suspect mushrooms became ill and that no one who did not eat the mushrooms became ill. Wild mushrooms eaten raw, cooked, or processed should always be regarded as prime suspects. After ruling out other sources of food poisoning and positively implicating mushrooms as the cause of the illness, diagnosis may proceed in two steps. The first step, outlined in Table 1, provides an early indication of the seriousness of the disease and its prognosis. As described above, the protoplasmic poisons are the most likely to be fatal or to cause irreversible organ damage. In the case of poisoning by the deadly Amanitas, important laboratory indicators of liver (elevated LDH, SGOT, and bilirubin levels) and kidney (elevated uric acid, creatinine, and BUN levels) damage will be present. Unfortunately, in the absence of dietary history, these signs could be mistaken for symptoms of liver or kidney impairment as the result of other causes (e.g., viral hepatitis). It is important that this distinction be made as quickly as possible, because the delayed onset of symptoms will generally mean that the organ has already been damaged. The importance of rapid diagnosis is obvious: victims who are hospitalized and given aggressive support therapy almost immediately after ingestion have a mortality rate of only 10%, whereas those admitted 60 or more hours after ingestion have a 50-90% mortality rate. Table 2 provides more accurate diagnoses and appropriate therapeutic measures. A recent report indicates that amanitins are observable in urine well before the onset of any symptoms, but that laboratory tests for liver dysfunction do not appear until well after the organ has been damaged. 6. Associated Foods:Mushroom poisonings are almost always caused by ingestion of wild mushrooms that have been collected by nonspecialists (although specialists have also been poisoned). Most cases occur when toxic species are confused with edible species, and a useful question to ask of the victims or their mushroom-picking benefactors is the identity of the mushroom they thought they were picking. In the absence of a well- preserved specimen, the answer to this question could narrow the possible suspects considerably. Intoxication has also occurred when reliance was placed on some folk method of distinguishing poisonous and safe species. Outbreaks have occurred after ingestion of fresh, raw mushrooms, stir-fried mushrooms, home-canned mushrooms, mushrooms cooked in tomato sauce (which rendered the sauce itself toxic, even when no mushrooms were consumed), and mushrooms that were blanched and frozen at home. Cases of poisoning by home-canned and frozen mushrooms are especially insidious because a single outbreak may easily become a multiple outbreak when the preserved toadstools are carried to another location and consumed at another time. Specific cases of mistaken mushroom identity appears frequently. The Early False Morel Gyromitra esculenta is easily confused with the true Morel Morchella esculenta, and poisonings have occurred after consumption of fresh or cooked Gyromitra. Gyromitra poisonings have also occurred after ingestion of commercially available "morels" contaminated with G. esculenta. The commercial sources for these fungi (which have not yet been successfully cultivated on a large scale) are field collection of wild morels by semiprofessionals. Cultivated commercial mushrooms of whatever species are almost never implicated in poisoning outbreaks unless there are associated problems such as improper canning (which lead to bacterial food poisoning). A short list of the mushrooms responsible for serious poisonings and the edible mushrooms with which they are confused is presented in Table 3. Producers of mild gastroenteritis are too numerous to list here, but include members of many of the most abundant genera, including Agaricus, Boletus, Lactarius, Russula, Tricholoma, Coprinus, Pluteus, and others. The Inky Cap Mushroom (Coprinus atrimentarius) is considered both edible and delicious, and only the unwary who consume alcohol after eating this mushroom need be concerned. Some other members of the genus Coprinus (Shaggy Mane, C. comatus; Glistening Inky Cap, C. micaceus, and others) and some of the larger members of the Lepiota family such as the Parasol Mushroom (Leucocoprinus procera) do not contain coprine and do not cause this effect. The potentially deadly Sorrel Webcap Mushroom (Cortinarius orellanus) is not easily distinguished from nonpoisonous webcaps belonging to the same distinctive genus, and all should be avoided. Most of the psychotropic mushrooms (Inocybe spp., Conocybe spp., Paneolus spp., Pluteus spp.) are in general appearance small, brown, and leathery (the so-called "Little Brown Mushrooms" or LBMs) and relatively unattractive from a culinary standpoint. The Sweat Mushroom (Clitocybe dealbata) and the Smoothcap Mushroom (Psilocybe cubensis) are small, white, and leathery. These small, unattractive mushrooms are distinctive, fairly unappetizing, and not easily confused with the fleshier fungi normally considered edible. Intoxications associated with them are less likely to be accidental, although both C. dealbata and Paneolus foenisicii have been found growing in the same fairy ring area as the edible (and choice) Fairy Ring Mushroom (Marasmius oreades) and the Honey Mushroom (Armillariella mellea), and have been consumed when the picker has not carefully examined every mushroom picked from the ring. Psychotropic mushrooms, which are larger and therefore more easily confused with edible mushrooms, include the Showy Flamecap or Big Laughing Mushroom (Gymnopilus spectabilis), which has been mistaken for Chanterelles (Cantharellus spp.) and for Gymnopilus ventricosus found growing on wood of conifers in western North America. The Fly Agaric (Amanita muscaria) and Panthercap (Amanita pantherina) mushrooms are large, fleshy, and colorful. Yellowish cap colors on some varieties of the Fly Agaric and the Panthercap are similar to the edible Caesar's Mushroom (Amanita caesarea), which is considered a delicacy in Italy. Another edible yellow capped mushroom occasionally confused with yellow A. muscaria and A. pantherina varieties are the Yellow Blusher (Amanita flavorubens). Orange to yellow-orange A. muscaria and A. pantherina may also be confused with the Blusher (Amanita rubescens) and the Honey Mushroom (Armillariella mellea). White to pale forms of A. muscaria may be confused with edible field mushrooms (Agaricus spp.). Young (button stage) specimens of A. muscaria have also been confused with puffballs. 7. Relative Frequency of Disease:Accurate figures on the relative frequency of mushroom poisonings are difficult to obtain. For the 5-year period between 1976 and 1981, 16 outbreaks involving 44 cases were reported to the Centers for Disease Control in Atlanta (Rattanvilay et al. MMWR 31(21): 287-288, 1982). The number of unreported cases is, of course, unknown. Cases are sporadic and large outbreaks are rare. Poisonings tend to be grouped in the spring and fall when most mushroom species are at the height of their fruiting stage. While the actual incidence appears to be very low, the potential exists for grave problems. Poisonous mushrooms are not limited in distribution as are other poisonous organisms (such as dinoflagellates). Intoxications may occur at any time and place, with dangerous species occurring in habitats ranging from urban lawns to deep woods. As Americans become more adventurous in their mushroom collection and consumption, poisonings are likely to increase. 8. Target Population:All humans are susceptible to mushroom toxins. The poisonous species are ubiquitous, and geographical restrictions on types of poisoning that may occur in one location do not exist (except for some of the hallucinogenic LBMs, which occur primarily in the American SW and SE). Individual specimens of poisonous mushrooms are also characterized by individual variations in toxin content based on genetics, geographic location, and growing conditions. Intoxications may thus be more or less serious, depending not on the number of mushrooms consumed, but on the dose of toxin delivered. In addition, although most cases of poisoning by higher plants occur in children, toxic mushrooms are consumed most often by adults. Occasional accidental mushroom poisonings of children and pets have been reported, but adults are more likely to actively search for and consume wild mushrooms for culinary purposes. Children are more seriously affected by the normally nonlethal toxins than are adults and are more likely to suffer very serious consequences from ingestion of relatively smaller doses. Adults who consume mushrooms are also more likely to recall what was eaten and when, and are able to describe their symptoms more accurately than are children. Very old, very young, and debilitated persons of both sexes are more likely to become seriously ill from all types of mushroom poisoning, even those types which are generally considered to be mild. Many idiosyncratic adverse reactions to mushrooms have been reported. Some mushrooms cause certain people to become violently ill, while not affecting others who consumed part of the same mushroom cap. Factors such as age, sex, and general health of the consumer do not seem to be reliable predictors of these reactions, and they have been attributed to allergic or hypersensitivity reactions and to inherited inability of the unfortunate victim to metabolize certain unusual fungal constituents (such as the uncommon sugar, trehalose). These reactions are probably not true poisonings as the general population does not seem to be affected. 9. Analysis of Foods for Toxins:The mushroom toxins can with difficulty be recovered from poisonous fungi, cooking water, stomach contents, serum, and urine. Procedures for extraction and quantitation are generally elaborate and time-consuming, and the patient will in most cases have recovered by the time an analysis is made on the basis of toxin chemistry. The exact chemical natures of most of the toxins that produce milder symptoms are unknown. Chromatographic techniques (TLC, GLC, HPLC) exist for the amanitins, orellanine, muscimol/ibotenic acid, psilocybin, muscarine, and the gyromitrins. The amanitins may also be determined by commercially available 3H-RIA kits. The most reliable means of diagnosing a mushroom poisoning remains botanical identification of the fungus that was eaten. An accurate pre-ingestion determination of species will also prevent accidental poisoning in 100% of cases. Accurate post-ingestion analyses for specific toxins when no botanical identification is possible may be essential only in cases of suspected poisoning by the deadly Amanitas, since prompt and aggressive therapy (including lavage, activated charcoal, and plasmapheresis) can greatly reduce the mortality rate. 10. Selected Outbreaks:Isolated cases of mushroom poisoning have occurred throughout the continental United States. The occurred in Oregon in October,1988, and involved the intoxication of five people who consumed stir-fried Amanita phalloides. The poisonings were severe, and at this writing three of the five people had undergone liver transplants for treatment of amanitin-induced liver failure. Other recent cases have included the July, 1986, poisoning of a family in Philadelphia, by Chlorophyllum molybdites; the September, 1987, intoxication of seven men in Bucks County, PA, by spaghetti sauce which contained Jack O'Lantern mushroom (Omphalotus illudens); and of 14 teenage campers in Maryland by the same species (July, 1987). A report of a North Carolina outbreak of poisoning by False Morel (Gyromitra spp.) appeared in 1986. A 1985 report details a case of Chlorophyllum molybdites which occurred in Arkansas; a fatal poisoning case caused by an amanitin containing Lepiota was described in 1986. In 1981, two Berks County, PA, people were poisoned (one fatally) after ingesting Amanita phalloides, while in the same year, seven Laotian refugees living in California were poisoned by Russula spp. In separate 1981 incidents, several people from New York State were poisoned by Omphalotus illudens, Amanita muscaria, Entoloma lividum, and Amanita virosa. An outbreak of gastroenterititis during a banquet for 482 people in Vancouver, British Columbia, was reported by the Vancouver Health Department in June, 1991. Seventy-seven of the guests reported symptoms consisting of early onset nausea (15-30 min), diarrhea (20 min-13 h), vomiting (20-60 min), cramps and bloated feeling. Other symptoms included feeling warm, clamminess, numbness of the tongue and extreme thirst along with two cases of hive-like rash with onset of 3-7 days. Bacteriological tests were negative. This intoxication merits special attention because it involved consumption of species normally considered not only edible but choice. The fungi involved were the morels Morchella esculenta and M. elata (M. angusticeps), which were prepared in a marinade and consumed raw. The symptoms were severe but not life threatening. Scattered reports of intoxications by these species and M. conica have appeared in anecodotal reports for many years. Numerous other cases exist; however, the cases that appear in the literature tend to be the serious poisonings such as those causing more severe gastrointestinal symptoms, psychotropic reactions, and severe organ damage (deadly Amanita). Mild intoxications are probably grossly underreported, because of the lack of severity of symptoms and the unlikeliness of a hospital admission. mow@cfsan.fda.gov Jan 1992 with periodic updates Peyote cactus - A spineless cactus with hallucinogenic properties used in native american rituals. by Leo Mercado of The Peyote Foundation has a long history of use as a medicinal and sacramental herb. Prehistoric trade in and knowledge of the sacred cactus was apparently well established prior to the European conquest of Mexico. At that time, Spanish Inquisitors declared its use to be a punishable crime against God. Ironically, native peyotists, relying on the humble cactus for divine guidance and inspiration, became targets of oftentimes ruthless evangelism. As in the case of Teonanacatl, the sacred mushrooms of MesoAmerica, the fact that the peyote religion continues to exist despite centuries of persecution is a testament to its importance in the spiritual lives of many. Sacred Cactus Peyote (Lophophora williamsii) is a small (less than 12 cm in diameter), round cactus with fuzzy tufts instead of spines. It rarely rises more than an inch or so above the soil surface. The largest part of the cactus is actually underground in the long, carrot-like root. The above ground portion is the "button" which is cut and consumed either fresh or dried. Usually, anywhere from four, to a dozen buttons, are eaten or made into tea. Myths concerning the presence of strychnine in the flesh or fuzz of are often circulated in the common lore, but this substance is completely absent from peyote. Peyote is a native of the Chihuahan Desert, specifically, portions of the Rio Grande Valley in Southern Texas, and south as far as the state of San Luis Potosi in Mexico. Peyote has been an item of commerce for a very long time. Most recently (just over 100 years) it has been commercially harvested in the state of Texas, though its sale is now restricted by law to members of the Native American Church (NAC). (It is estimated that the NAC has at least 250,000 members.) The annual harvest of individual plants, or buttons, is in the millions. When properly harvested, several new heads tend to form from the old root, thereby generating new plants for the future. Unfortunately, plants are often cut deeply, leaving little or no root remaining in the ground. In addition to commercial harvesting, large sections of the "peyote gardens" of Texas are uprooted for new grazing land with much of the small, slow growing cacti such as peyote, being destroyed as a result. Consequently, the regions where peyote may be found have greatly diminished. Areas where peyote once flourished in commercially harvestable quantities are now very often lacking this cactus entirely. Peyote is something of an alkaloid factory, producing upwards of 50 chemically related compounds. The effects experienced after consuming this unique medicine range from a feeling of physical energy and well being when taken in small amounts (though this is often preceded by a brief period of lethargy), to actual visionary experience when larger quantities are consumed. Often, individuals may experience stomach discomfort or nausea during the first few hours though this is not always the case. Noticeable psychic effects usually last 10 hours or so after they begin. Experienced peyotists recognize and welcome the feeling of the medicine working with them as a spiritual and physical blessing. The positive, life enhancing benefits of the peyote medicine are probably as diverse as the many people who have found it to play an extremely important role in their lives. The Peyote Religion The religious use peyote is very ancient. One cache of dried peyote found in a Texas cave, has been dated at approximately 7000 years old. The use of peyote in ceremonies among Mexican tribes was a well established tradition by the time of the European entrance into the continent. This pre-historical religious us e eventually diffused into the North American regions. Along with this evangelistic migration came changes in the basic ceremonies associated with peyote. Mexican peyotism is perhaps best typified by the traditional practices of the Huichol tribe of the Sierra Occidental, along the pacific coast of Mexico. Annual pilgrimages to ritually hunt the sacred cactus are still a central part of tribal myth and ceremony. A group leader, or Mara-a- 'kame leads the humble seekers in their mythical quest "...to find our life.", as it has been said. Only peyote gathered in this ceremonial way is suitable for the spiritual requirements of the tribe. The Cora and Tarahumara are related groups of people who use peyote in religious ceremony. Cora people are known to trade for, or purchase peyote from their Huichol neighbors, as their own traditions do not require the desert pilgrimage to collect the sacrament. In the mid 1800's, simultaneous with native genocide, the peyote religion spread north, arriving at a time when indigenous people were badly in need of spiritual uplifting and cultural strength. In the last 100 years, the spread of peyotism has been prolific. The peyote ceremony which was introduced to the American Plains Indians is a formalized, all-night prayer meeting, usually held in a teepee, hogan, or peyote house especially set aside for that purpose. Christian elements are often significantly present, depending on the particular tribe or group leader. Most of North American peyotism can be properly identified with the Native American Church (NAC), a large, oftentimes un- associated group of mostly native believers. There are numerous divisions of the NAC (NAC of North America, NAC of Navajoland, NAC of S. Arizona, etc.), with each division being composed of several local chapters, or moons. Each chapter normally has officers who are trained in distinct clerical functions of the church. The leader of a peyote meeting is known as the Road Chief, or Road Man. This is the person who is charged with the responsibility of overseeing the main elements of the meeting and leading others on the Peyote Road, the way of learning to live life well. Other offices include Cedar Chief, Fire Chief, Drum Chief, and often, Earth Mother or Morning Water Woman. Though ceremonies among different chapters tend to vary slightly, many common elements are present in most NAC ceremonies. An eagle bone whistle, various feather fans, water drum, and prayer staff, are a few of the ceremonial items necessary to conduct the prayer meeting. Central tenets of the NAC usually involve avoidance of alcohol, devotion to family, and right living in general. Probably the most simple, and possibly historically primitive, form of peyotism is the vision quest, alone in nature. Usually this involves fasting, solitude, and quiet but steady contemplation. Peyote is eaten or consumed as a tea and a vigil is kept until such time as the communicant comes to a sense of physical and spiritual completion. This way of experiencing the personal qualities of the experience sounds very much like traditional stories of the first person who was given peyote by Creator Spirit. Several tribes relate the story of a man or woman lost in the desert. Their wandering leaves them exhausted, starving, and dehydrated. Just at the point of giving up all hope of life comes a voice which instructs them to reach out and take hold of the soft and cool plant which grows just within reach of their outstretched hands. They are then told to eat it to quench their thirst for water, food, and guidance back to their home. Native/Non-Native Use The Native American Church (NAC) and its various sub-groups, has become the most well known form of the peyote religion. Prior to the 1900's, the ceremonial use of peyote was more strictly limited to the areas of its natural growth, i.e. the Chihuahuan Desert. The Tarahumara and Huichol peoples are well known for their traditional use of peyote, as they live near or travel to areas where it grows abundantly. The evangelistic spread of what is commonly called Peyotism is well documented in works by Omer Stewart and others. (See "Peyote Religion: A History", by Omer C. Stewart, 1987, University of Oklahoma Press.) The old peyote complex of Mexico spread north by peyote evangelists from the growing regions influencing the botanical medicine kit of their northern brethren. Soon thereafter, individuals such as Quanah Parker, (son of captured homesteader Cynthia Ann Parker and a Comanche chief), and John Wilson, a Caddo medicine man, became peyote missionaries to North American tribes and cultures. Aside from North American peyotism being an inter-tribal affair, as documented by Stewart, there have at times been mixed or all-race NAC groups, anglo-american and afro-american groups or members. Most NAC chapters allow membership by sincere individuals of various genetic or cultural makeup. Some of the most influential leaders or supporters of NAC peyotism have been people of mixed or European descent. ( J. Wilson, Q. Parker, O.C. Stewart, J.S. Slotkin and others.) In order to clarify the issue of multi-ethnic religious use of peyote I offer the following excerpt from Stewart's "Peyote Religion: A History": "An unusual case of harassment under the Drug Control Act took place in Grand Forks, North Dakota, in October, 1984, when a white couple, Mr. and Mrs. John D. Warner, were arrested by the FBI for possessing peyote, a controlled drug. The two were members of the NAC of Tokio, North Dakota, and had been for a number of years, and Mrs. Warner was custodian of the supply of peyote for the Tokio congregation. The FBI had learned of the possession of peyote by the Warners from the president of the NAC of NA (North America) Emerson Jackson (Navajo), so it was he who brought them to trial. Jackson said that they were not bona fide members of the NAC because they were not Indians. He maintained that in 1982 a motion had been passed by the NAC of NA to the effect that membership in that organization be limited to persons with one-quarter Indian blood, thereby excluding this white couple. A jury in Grand Forks Federal Court found the defendants innocent of breaking the law, since they were able to prove that although they were not Indians, nevertheless they were members in good standing of the local congregation of peyotists. The charges were dismissed. This case not only illustrates harassment under the Drug Control Act, but it also brings up the legality of non-Indians as bona fide members of the NAC. From the beginning, attendance of non-Indians to peyote meetings has been a somewhat personal or tribal matter. For instance, very early in Oklahoma some Caddo refused to allow non-Indians to attend any of their meetings. But others, such as the Kiowa and Comanche, welcomed non-Indians, black or white, as long as they were seriously interested. With the formation of the NAC, the same attitude has generally prevailed, and the presence of non-Indians has been no problem. It was in the sixties when the hippie generation became interested in peyote and became a nuisance in the peyote gardens of Texas, bringing about the Texas law which forbids possession of peyote by persons not having one-quarter Indian blood and proof of membership in the NAC, that race became an issue in membership. Since then, if non- Indians wish to be allowed to possess peyote, they must show that their involvement in the peyote religion is genuine -that is that it is not just a recreational, frivolous, or passing interest but a real commitment. Then, as the case against the Warners shows, race is not an issue. Still, it is especially important for non-Indians to carry identification of membership in the NAC if they have occasion to carry peyote, and even so, non-Indians possessing peyote violate Texas law. The ruling of the NAC of NA that only Indians should be enrolled in the Native American Church is new and is not shared by most peyotists. The NAC of NA does not speak for all peyotists, as much as it would like to do so. All peyotists consider themselves members of the Native American Church, but most are not affiliated with the NAC of NA. Each congregation makes its own rules, just as each meeting is conducted by its own roadman. The internal strife within the NAC from 1956 to 1972 which swirled around Frank Takes Gun did not end with his eclipse. Divisiveness has become as much a characteristic of the peyote religion as it is of other religions. Today there are many peyote churches which have little to do with the NAC of NA. Some are large with wide jurisdiction; others are a single congregation." The reason I have taken the space to allow Stewart's elucidation is to point out the occasional difficulties in the sharing and practices of the peyote religion. Acceptance of the NAC by the surrounding culture, legislature, and even tribal America, has been a gradual and complex process. Unfortunately, misinformation has often been used in a purposefully demeaning way in order to argue against the practice and practitioners of the peyote way, Indian or non-Indian. The NAC was instituted by the courageous and purposeful work of individuals experienced in the Creator's Grace bestowed by peyote. Despite this, individual and often unaffiliated, legitimate peyotists often face potential or active discriminatory prejudice by virtue of their beliefs. Recently, more concern has properly been directed toward conserving the plant that is the essential Sacrament of peyotists. (see " The Peyote Gardens of Southern Texas: A Conservation Crisis?, "Cactus and Succulent Journal, Vol. 67/1995, by Dr. Edward F. Anderson) Again I quote Dr. Stewart; "The main problem today facing the Native American Church in whatever manner of organization is the present reduction in the supply of peyote. The original peyote gardens which furnished such a plentiful and inexpensive supply to the Indians of Oklahoma in the last century are becoming depleted "Another way to increase the supply of peyote would be to cultivate it. This would be expensive, necessitating greenhouses if it were not cultivated in the area of natural growth. Again, this would necessitate changes in the law, for at present it is unlawful to cultivate it, even in a greenhouse. As for the area of natural growth in Texas, all of the land is privately owned. Generally it is used for ranching, but there is still some oil activity. Recently viticulture has been attempted in the area with some success. And so the future of the little cactus, the essential ingredient of peyotism, its sacrament, is still in doubt." Actually several states do not prohibit the cultivation of peyote specifically (though federal law might apply), rather, most prohibit its possession outside of a religious context. Natural Populations of Peyote in Decline Peyote is a native of the Chihuahan Desert, specifically, portions of the Rio Grande Valley in Southern Texas, and south as far as the state of San Luis Potosi in Mexico. Peyote has been an item of commerce for a very long time. Most recently (just over 100 years) it has been commercially harvested in the state of Texas, though its sale is now restricted by law to members of the Native American Church (NAC). (It is estimated that the NAC has at least 250,000 members.) The estimated annual harvest of individual plants, or buttons, is in the millions. When properly harvested, several new heads tend to form from the old root, thereby generating new plants for the future. Unfortunately, plants are often cut deeply, leaving little or no root remaining in the ground. In addition to commercial harvesting, large sections of the "peyote gardens" of Texas are uprooted for new grazing land with much of the small, slow growing cacti such as peyote, being destroyed as a result. Consequently, the regions where peyote may be found have greatly diminished. Areas where peyote once flourished in commercially harvestable quantities are now very often lacking this cactus entirely. While there is a need for preservation efforts in its native habitat, is the responsibility of those people who honor the divine cactus to cultivate it. This is a tangible way of establishing a close relationship with the plant while helping to preserve the genetic diversity and well-being of the species. Cultivation Private collections of the living peyote cactus, (Lophophora williamsii), are usually kept as a labor of love or even in the form of an altar or earth shrine. The Huichol people of Mexico often maintain live peyote, captured in the "hunt" of their ancestral pilgrimage. Several Texas peyoteros, (licensed peyote dealers), keep a peyote garden for veneration by those who arrive in person to purchase their sacrament. It is also not uncommon for members of the various Native American Church chapters to keep peyote growing in or around their homes. A suprising number of unassociated individuals cultivate peyote. One of the leading academic publications for cacti and succulent enthusiasts inserts occassional reminders that peyote is technically illegal in private and institutional collections. In the United States this would appear to be so, except in the case of a bona fide religious context such as the practitioner who keeps a home garden or altar. In the Southwestern U.S., private collections are not as rare as one might think. Also, many international collections exist, many of which are commercially tended for their value to cacti and seed buyers. Now, however, this usually slow growing and ethno/spiritually important plant, finds itself in a tenuous situation throughout the areas of Southern Texas where it was once plentiful. The importance of what are usually private, if not secretive collections of peyote, is only now becoming clear. (See "The Peyote Gardens' of Southern Texas: A Conservation Crisis?," by Dr. Edward F. Anderson, Cactus and Succulent Journal Vol. 67, 1995) Peyote grows from either seed or clonal offshoots, often called pups, which often re-grow from the roots of harvested plants. Older, uncut specimens also produce pups from their base. Seed grown peyote is a precious and small crop for the first several years. In natural conditions, plants may take 4 or more years to reach dime-size. Under optimal conditions however, growth is considerably faster. The earliest one may expect harvestable-size plants (3 inches or so in diameter) from seed is about five years, much like the length of time involved in planting and eating fruit. Peyote seeds should be gently and evenly tamped into a fine, washed sand and soil combination, preferably with a slightly alkaline ph. (7.5 to 8, add lime if needed.) A small board works well for pressing seeds into soil so that the tops are even with soil surface. Keep moist and in indirect natural light.(or under grow lights) At 80 deg F., seeds should sprout well within two weeks. An excellent sprouting chamber can be made using a small, plastic tofu-type container. Place soil mix inside and after planting and misting cover with a ziploc veggie bag. These are fairly new items which have micro-pores for breathability. Your seedlings will thrive from the combination of high humidity and air exchange with this simple setup. Seedlings should be allowed to nearly dry out before being gently sprayed with more water. A few weeks after sprouting, consider giving them a feeding. My preferred ferilizer for peyote seedlings is a regular spraying of dilute (50% of recommended strength) liquid seaweed, available from a number of sources. If using another type, try to keep the nitrogen (N) level low and the phosphorous (P) level high. A 5-10-5 type formula is a good example. Remember to dilute the solutuion considerably (25% of normal strength) as these little guys don't need a whole lot of anything but time. Too much sunlight, fertilizer, water, or cold are the main things to avoid in your seedling project, aside from impatience of course. By the end of the first year, seedlings should be large enough to transfer individually to a more permanent location. This can be in seperate containers or in a nicely spaced, group garden. Plants with already established taproots can produce several new usable buttons within a year or two. Thus each established plant becomes a source of more offshoots. Buttons must be sliced at ground level, or above, in order for offshoots to be produced. Sliced tops may be left to callous for a week or two, then re-rooted by laying in a porous soil or vermiculite/perlite mix. Water regularly, but allow to dry out between soakings. New roots will form from the cut base until after a year or so. A large taproot forms, making it hard to tell that it was ever cut. Grafting For Growth Small offshoots or seedlings may be grafted onto faster growing cactus rootstock. This increases growth rates by several times. Single column, healthy specimens of Trichocereous pachanoi or Myrtillo geometrizans are favored as graft stock because of their finger-friendly, small or virtually non-existant spines. Slice about 1 inch below the growing tip. Next, bevel down surrounding ribs at an angle. You end up wit a pencil shape w/flat top. This prevents areoles from pruducing new shoots too near the new graft. Next, with finger on top holding, make another thin slice, an eigth of an inch or so, under the first cut. Your finger holds the sliver on after the knife has passed through. This prevents the soon-to-be grafting tip from being exposed to air too soon. Now slice a small peyote, preferably a small offshoot. Make sure and make all you cuts straight. (A sharp knife helps.) Quickly lift the sliced top from your rootstock and with the other hand place the freshly sliced peyote firmly on the center of the exposed stock tissue. You get points here for quick, smooth movements, as the less time the cuts are exposed the better. Gently secure the new peyote top to the stock using rubber bands or a firm, but not too heavy weight. Be careful to not move the new graft as you do this. In three days remove the bands or weight and your new graft should remain, now bonded to its host's vascular tissue. Using this method growth can be enhanced by a factor of 5 to 10 times, small buttons growing to mature size in one year. Large grafts can be sliced above the graft/stock joint in order to re-root on their own. Providing sufficient peyote base is left on the top of the host cactus, new offshoots will quickly appear from the now topless peyote, providing many new grafting candidates. Suggested Reading: "Peyote and Other Entheogenic Cacti", Gottlieb, A., Ronin Publishing, 1997 "The Peyote Book: A Study of Native Medicine", Mount, G.(Ed.), Sweetlight books, 1993 "Straight With the Medicine", d'Azevedo, W., Heyday Books, 1978 "Peyote Hunt: The Sacred Journey of the Huichol Indians", Myerhoff, B., Cornell Univ. Press, 1974 "People of the Peyote" Schaefer, S. and Furst, P., (Ed.), The Univ. of New Mexico Press, 1996 "Peyote Religion: A History", Stewart, O.C., Univ. of Oklahoma Press, 1987 "Peyote the Divine Cactus", Anderson, E.F., Univ. of Arizona Press, 1996 "The Peyote Cult", La Barre, W., Yale Univ. Publications in Anthropology, 1989 "Peyote, The Medicine Journal", newsletter of The Peyote Foundation, PO Box 778, Kearny, AZ 85237, USA "The Sacred Record", The Peyote Way Church of God, newsletter of the Church, Box 7x, Rt 1, Willcox, Az. 85643 USA "Flowers of Wiricuta: A Gringo's Journey to Shamanic Power", Pinkson, T.S., Wakan Press, 1995 "Psychedelics Encyclopedia", Stafford, P., Ronin Publishing, 1992 \14 HISTORY Hallucinogenic mushrooms have been part of human culture as far back as the earliest recorded history. Ancient paintings of mushroom-ed humanoids have been found in caves in the Saharan desert. Central and Southern America cultures built temples to mushroom gods and carved "mushroom stones". These stone carvings in the shape of mushrooms, or in which figures are depicted under the cap of a mushroom, have been dated to as early as 1000-500 B.C. The purpose of the sculptures is not certain, but these stones may have been religious objects. The Mixtec culture of central Mexico worshipped many gods, one known as Piltzintecuhtli, or 7 Flower (his name presented in the pictoral language as seven circles and a flower) who was the god for hallucinatory plants, especially the divine mushroom. The Vienna Codex (or Codex Vindobonensis) (ca 13th-15th century) depicts the ritual use of mushrooms by the Mixtec gods, showing Piltzintecuhtli and 7 other gods holding mushrooms in their hands.1 The Aztec people had a closely related god of the entheogens. Xochipilli, Prince of Flowers, was the divine patron of "the flowery dream" as the Aztecs called the ritual hallucinatory trance. The Aztecs used a number of plant hallucinogens including psilocybian mushrooms (teonanácatl), morning glory seeds, Salvia divinorum, Datura (tlapatl or toloache) , Peyote (peyotl), and mixitl grain. Psilocybian mushrooms were used in ritual and ceremony, served with honey or chocolate at some of their holiest events.2 With Cortez's defeat of the Aztecs in 1521, the Europeans began to forbid the use of non-alcohol intoxicants, including sacred mushrooms, and the use of teonanácatl ('wondrous mushroom', or 'flesh of the gods'3) was driven underground. In the mid 16th century, Spanish priest Bernardino de Sahagún wrote of the use of hallucinogenic mushrooms by the Aztecs in his Florentine Codex : "The first thing to be eaten at the feast were small black mushrooms that they called nanacatl and bring on drunkenness, hallucinations and even lechery; they ate these before the dawn...with honey; and when they began to feel the effects, they began to dance, some sang and others wept... When the drunkenness of the mushrooms had passed, they spoke with one another of the visions they had seen." According to Sahagún, the psychoactive mushrooms which were ingested by the Aztec priests and their followers were always referred to as teonanácatl though the term does not appear to be used by modern indians or shamans in mesoamerica. 4 The varieties most likely to have been used by the Aztecs are Psilocybe caerulescens and Psilocybe mexicana. Psilocybe cubensis, which is currently quite popular as it is easy to locate and cultivate, was not introduced to America until the arrival of the Europeans and their cattle. During the early 20th century there was dispute amongst western academics as to whether psychoactive mushrooms existed. Though Sahagun had mentioned teonanácatl in his diaries, an American botanist William Safford argued he had mistaken dried peyote buttons for mushrooms. This theory was strongly disputed by Austrian amateur botanist Dr. Blas Pablo Reko, who had lived in Mexico. Reko was convinced that not only did teonanacatl refer to psychoactive mushrooms as Sahagun had written, but that people were still using these mushrooms in Mexico. In the early 30's, Robert Weitlaner, an Australian amateur anthropologist witnessed a Mazatec mushroom ceremony (velada) just northeast of Oaxaca, Mexico. After hearing about the dispute between Safford and Reko, he contacted Reko, told him that the Otomi Indians of Puebla used mushrooms as inebriants, and sent him samples of the mushrooms. Reko forwarded the samples to Stockholm for chemical analysis, and to Harvard for botanical examination, but by the time the samples arrived they were too decayed to be properly identified. The samples had been received at Harvard by ethnobotanist Richard Evans Schultes. Schultes quickly became a supporter of the idea that Teonanácatl did indeed refer to mushrooms and in the Harvard Botanical Museum Leaflets of April and November 1937 he argued against Safford's conclusions and urged that further work be done to identify the mushrooms. In 1938, Schultes and Reko went to Mexico and after hearing reports of Mazatec veladas near Huautla de Jimenéz northeast Oaxaca and collected specimens of Panaeolus sphinctrinus, which was reported to be the primary psychoactive mushroom used by the Mazatecs. They also collected Psilocybe cubensis, Psilocybe caerulescens, and possibly a few specimens of Psilocybe mexicana,5 all of which were deposited in the Harvard herbarium. While P. sphincrinus was identified as psychoactive, only two analysis have since detected indole alkaloids in the species, while hundreds of other analyses have not detected any activity whatsoever. The mushrooms which were examined were probably a mixed collection labeled as one species. 6 The investigations of Schultes and Reko came to an end during World War II, and little more was learned until the early 1950's when amateur mycologist R. Gordon Wasson, and his wife Valentina Povlovna, became interested in the traditional use of mushrooms in Mexico. In 1953 Wasson and a small group travelled to Huautla de Jimenéz where they observed an all night ceremony under the guidance of a shaman named Don Aurelio. Two subsequent trips to Mexico led to meeting the Mazatec curandera Maria Sabina who on June 29th 1955 provided Wasson and his companion photographer Allan Richardson with Psilocybe caerulescens during a Velada. In 1956, Heim requested help from Sandoz in extracting the active ingredients of the mushrooms. Albert Hofmann, a research chemist at Sandoz, soon isolated psilocybin and psilocin and developed a synthesis technique. Wasson continued to travel to Oaxaca over the next few years, and with Roger Heim published a description of the Mazatec velada and seven varieties of psilocybian mushrooms in the May 13, 1957 issue of Life magazine. Popular information about the mushrooms soon spread. Experimentation with the mushrooms and the synthesized substances began and "magic mushrooms"7 were soon part of the 60's 'psychedelic' movement. ETYMOLOGY 1. the origin and history of words The name of the genus "Psilocybe" comes from the Greek words "psilos" (bare) and "kube" (head), warped into New Latin to form "psilocybe". Literally translated, this means "bare head", most likely referring to their appearance. The most psychoactive compounds found in Psilocybe mushrooms are psilocybin and psilocin, which are discussed at length in the next part. The original Greek spellings for these are "psilocybin" and "psilocin" while the Latin spellings are "psilocybine" and "psilocine". Both sets of spellings are used. The Latin spellings are predominant in Europe, while most scholars in the field prefer the Greek spellings. CHEMISTRY The primary active ingredients of Psilocybe mushrooms are psilocybin and psilocin, and to a lesser extent baeocystin and norbaeocystin. The ratio of psilocybin to psilocin varies from species to species. The primary difference between the two compounds is that psilocin is unstable and breaks down when the mushroom is dried, while psilocybin lasts much longer (a 115-year old mushroom sample was found to contain some). The two are equally psychoactive, since one molecule of psilocybin breaks down into one molecule of psilocin. Once ingested, the phosphorus part is chopped off ("dephosphorylated") by the enzyme alkaline phosphatase, turning it into our other friend: Psilocybin and psilocin are part of the tryptamine family (indole C8H7N & ethylamine side chain). Psilocybin is soluable in 20 parts water, while psilocin is only slightly soluable in water.8 They bear close resemblance to the neurotransmitter serotonin. How these substances work is still quite obscure. Primary effect seems to be the inhibition of neurotransmitter serotonin (5-hydroxytryptamine aka 5-HT), i.e. a 5-HT2A post-synaptic agonist that mimics the effects to 5-HT to put it in jargon. This is the working hypothesis for LSD-25 at the moment and it's probably true for psilocybin as well. These substances also present some cross-tolerance. Psilocybin, psilocin and psilocybian mushrooms have very low toxicity - in tests with mice, doses up to 200 mg of pure psilocybin/kg of body weight have been injected intravenously without lethal effects (that would be 13 grams of pure psilocybin per average human (65 kg / 140 lbs). The ED50:LD50 ratio is 641 according to the NIOSH Registry of Toxic Effects; compare this with 9637 for vitamin A, 4816 for LSD, 199 for aspirin and 21 for nicotine. According to Leo Hollister, Jonathon Ott, and John Allen, one would have to consume their body weight in fresh mushrooms or eat approximately 19 grams of the pure chemical substance to bring on death. As long as Psilocybin mushrooms are properly identified, poisoning is not a problem. Unlike psilocybin, baeocystin is somewhat unstable, and decays noticeably with age. And then we have baeocystin's close chemical cousin: The demethyl analogue of psilocybin In other words, baeocystin and norbaeocystin are just psilocybin with one methyl and two methyls respectively lopped off. When baeocystin and norbaeocystin are dephosphorylated, they turn into 4-hydroxy-N-methyltryptamine and 4-hydroxytryptamine respectively. All 4 substances are presumed hallucinogenic though some suspect they are less psychoactive than psilocin or psilocybin. And unfortunately for all you synthesis experts, while baeocystin and norbaeocystin do not have DEA control numbers they do both fall under the Controlled Substance Analogue Act. Baeocystin and norbaeocystin are generally present in smaller quantities than psilocyin and psilocybin, if they are present at all. Very little work seems to have been done with either substance (Chemical Abstracts averages a cite a year, with most being of the variety "baeocystin found in Psilocybe totallyobscuralis"). There has been speculation about a possible correlation between baeocystin content and nausea, but at least one bioassay suggests the effects are quite similar to those of psilocybin and psilocyin.9 These are just the four "biggies". A whole truckload of other indoles are known to exist in Psilocybe mushrooms. Here's a sample of what was found in a batch of Psilocybe baeocystis, excluding the ones mentioned above: Indole derivativeAmount (ug)5-Benzyloxy-3-indole acetic acid2N,N-Dimethyltryptamine hydrogen-oxalate [aka DMT]4Gramine403-Hydroxyethyl indole25-Hydroxy-3-indole acetic acid25-Hydroxyindole43-Hydroxymethylindole25- Hydroxytryptamine creatine sulfate [aka Serotonin]45-Hydroxytryptophane2Indole43- Indoleacetamide23-Indole acetic acid23-Indoleacetic acid ethyl ester23-Indoleacetonitrile23-Indolealdehyde403- Indoleacetaldehyde23-Indolecarboxylic acid43-Indolelactic acid2gamma-(Indole)-N-butyric acid4beta-Indole-3-acrylic acid2beta-(Indole-3)-propionic acid4Indoxylacetate2Indoxylbutyrate2Isatin25-Methoxy-2- carboxyindole25-Methoxydimethyltryptamine monooxalate [aka Bufotenine]45-Methoxyindole42-Methylindole23- Methylindole45-Methylindole45-Methyltryptophane2N- Methyltryptophane2Tryptamine hydrochloride4L-Tryptophane0.8From: A.Y. Leung, A.H. Smith & A.G. Paul, "Production of Psilocybin in Psilocybe baeocystis Saprophytic Culture" J Pharm Sci 54: 1576 (1965) There continue to be rumors that some psilocybian mushrooms contain small quantities of DMT, yet no chemical analysis that we know of has shown the presence of DMT. If it is to be found, it's in microscopic quantities, and as DMT is not orally active without an MAOI (monoamine oxidase inhibitor)...it is quite unlikely to have any noticeable effect. The effects of psilocybin can be potentiated (made stronger) by taking them with an MAOI such as harmine or harmaline which are found in the plant Peganum harmala (Syrian Rue). This combination roughly doubles the potency of mushrooms, according to most reports. Be extremely careful when combining MAOIs and tryptamines; when using non-reversible MAOIs or large quantities of reversible MAOIs, there are number of substances you must avoid to prevent a serious hypertensive crisis. See Foods to Avoid When Using MAO-Inhibitors, as well as Drugs to Avoid when using MAOIs. Long-term health effects are also unknown. If you wish to know more, consult the Tryptamine FAQ. PSYCHOLOGY "Nature's Perfect Entheogen" Psilocybin is juuust fine. I've tried several psychoactive drugs, including hash, LSD-25 and psilocybin. Hash usually doesn't do much - sends me into a half sleep with silly thoughts and spacey soundscape added to music... LSD doesn't do it to me either. It's probably OK if you are after low dose recreation - partying and such... High doses - too blunt, like a mental power tool. It cracks up open your head; Starring You and Your Brain for 12 hours. Every perception magnified thousandfold - it's.. it's a bit too intense. INTENSE! is the keyword. It doesn't accept any apologies or mistakes.. too harsh. I often felt like I had been immersed in some chemical, into a substance so pure and efficient it has no place in nature. Too pure. 12 hours of LSD-25 acid-bath makes you really tired... physically and mentally. But psilocybin, mm-mm, it's juuuuust fiiiine. Voyage to the spiritworld... visions and travels, awesome mental hallucinations. It's a direct ISDN-link to the mother earth, forgiving, gentle substance. You hear the chanting of the planet and the spirit of the mushroom. It's a product of the nature, untied to the actions of men and women roaming this planet. Your body disconnected from the circuit, you may often forget it exists. Six hours - not too short, not too long. Perfect. It should be noted that like all 'major' hallucinogens, psilocybin can precipitate psychotic episodes and uncover or aggravate previous mental illness. If you're stressed out or depressed, don't take mushrooms; if you have schizophrenia or something, DO NOT take mushrooms. ACID IS NOT FOR EVERY BRAIN .... ONLY THE HEALTHY, HAPPY, WHOLESOME, HANDSOME, HOPEFUL, HUMOROUS, HIGH-VELOCITY SHOULD SEEK THESE EXPERIENCES. THIS ELITISM IS TOTALLY SELF-DETERMINED. UNLESS YOU ARE SELF-CONFIDENT, SELF-DIRECTED, SELF-SELECTED, PLEASE ABSTAIN. -- Timothy Leary, Ph.D. I think this applies to mushrooms as well. Mushrooms and acid will open your doors of perception, and once open you can never truly close them again. They are more than a purely recreational drug. *) The famed "Fly Agaric" red toadstool with white warts. Amanita species cause 95% of all deaths from mushroom poisoning. The ones above are (reasonably) safe. The danger lies in incorrect identification. Death by Amanita poisoning is reportedly an excruciating way to die, since they destroy liver tissue and the body's own wastes then kill you. Worse yet, noticeable negative effects do not begin until 3 days after ingestion, and by then it's too late. (Note - Silymarin found in Milk Thistle seeds is one of the only substances known to protect against a majority of the liver damage caused by poisonous Amanita species, but it needs to be taken immediately after ingestion, long before any negative effects are noticed.) I would seriously recommend against toying with these; most reports say they're not even fun. If you insist, consult other sources for more information. \15 Opium Preface: Man started taking drugs from nature as; flowers leaves, roots, etc. to relive pain or heal the body. In his experimentation he found that taking certain botan- icals resulted in intoxication or euphoria and liked the feeling as a means to assuage his problem, misery, or condition, and he has continued ever since. As civiliza- tion progressed, man created and diversified his artifacts improving upon nature including his chemicals. As an aside, I find it ironic that the white man is trying desperately and expensively to rid himself of scag and coke, but it was he who brought it to the people and he who perpetuates it. It just got out of control. That's not the only thing I see he's fucked up in my lifetime. Notes for Update, See DRUG ABUSE PREVENTION LIBRARY. 94 annual report. About 70% of heroin seized in the U.S. comes from the Golden Triangle. Cost $10 in NY. 50% pure in 90, 92 90% pure, now its 94% pure at the same price. As of 10/94 Stephen Roye became the 60th American (31 women) to be arrested in Thailand for drug smuggling. More Americans are in Thai jails than any other country. In 1970 HK had an estimated 100,000 addicts out of a population of 4 million making it the highest percentage of drug users in the world. Opiates: NARCOTIC and opiates refers to opium and its derivatives: heroin, codeine, and morphine. Opium is a narcotic that acts on the central nervous system (CNS) but unlike other depressants as barbiturates and alcohol it produces euphoria in an individual and renders him insensitive to pain. NARCOTIC from the Greek indicating stupor. Opioids are synthetic substances with characteristics similar to opiates. Opium for abuse is produced when air dries the milky exudate of the incised unripe seedpod of the opium poppy (Papaver somniferum). The resulting brownish gum is then shaped into various shapes which eventually harden and is the source for many natural and semisynthetic narcotics. Three of the extracted alkaloids; codeine, papaverine, and morphine is used in the clinical relief of pain. Poppy straw concentrate is the alkaloid derived from the mature dried opium poppy. It is one of five categories of illicit drugs, a narcotic in the category of depress- ants (sedatives). A chemical substances that effects a physical and mild mental change in an individual. The chemical substance (alkaloid) in opium which causes euphoria is morphine and from that comes heroin, and methadone. Morphine was first extracted in 1803 and because it was found to be more effective drug, led to the decline of opium. Only morphine and codeine are still in clinical use. Uses and Effects: The opium alkaloids and their semisyn- thetic derivatives including heroin act on the CNS producing analgesia, change in mood and drowsiness. The effects of a person in pain are usually pleasant but nausea and vomiting sometimes occur. In usual doses the analgesic effects are achieved w/o loss of consciousness. Other effects as coughing is suppressed, the electric activity pattern of the brain resembles that of sleep, the pupils constrict, the secretory activity and motility of the GI tract are dimin ished, and hiliary and pancreatic secretions are reduced. The use of morphine as an antidiarrheal preceded its use as an analgesic by hundreds of years. Prepared in a tincture it remains the most effective constipation agent available. Naturally occurring opiates called endophins (as well as the real thing and cocaine) occupy the receptor sites so that they can't receive the neural transmitters's message of pain. Twenty minutes of aerobic exercise is enough to stimulate the body to produce more endophins, the body's natural painkillers. Pain require full attention and distraction will relieve pain. This phenomena is call LATERAL DISTRACTION. Applying ice to a bruise helps retard the swelling and send cold messages to the brain reducing the pain signals. Common Opiate Analgesics: Morphine's major effects are on the CNS and the bowels. As an analge sia morphine has three characteristics: it raises the threshold for pain perception, reduces anxiety and stress, and induces sleep. It is the standard which the analgesic effect of other drugs are measured. Other synthetic narcotic compounds are fentanyl (Sublimaze), butorpha nol (Standol), and nalbuphine (Nubain). All are administered by injection used primarily in surgery as anaesthesia. Daily use of opiates can result in dependency in three weeks or less. Opium and Effects: The opium alkaloids and their semisynthetic derivatives including heroin act on the CNS producing analgesia, change in mood and drowsiness. The effects of a person in pain are usually pleasant but nausea and vomiting sometimes occur. In usual doses the analgesic effects are achieved w/o loss of consciousness. Other effects as coughing is suppressed, the electric activity pattern of the brain resembles that of sleep, the pupils constrict, the secretory activity and motility of the GI tract are dimin ished, and hiliary and pancreatic secretions are reduced. The use of morphine as an antidiarrheal preceded its use as an analgesic by hundreds of years. Prepared in a tincture it remains the most effective constipation agent available. The Flower and Poppy: When the colorful poppy flower matures, the petals fall off and the pod swells. The mature seed pod of an opium poppy oozes white opiate sap after its scored with a multi-bladed knife. Later the sap will be scraped off after a few hours in the air when it coagulates into a brown colored raw opium. In the rugged mountains of the Golden Triangle of the 1990's, various tribes still harvest opium clandestinely as a cash crop or for local use. In some countries as Thailand, it is legal to do so only in remote areas where it is difficult to market alternative crops. Tribes that are still active in opium cultivation and harvesting are: Mae, VN plans to spend 4.5 million U.S. dollars to suppress heroine production in 94/95. Currently there is no law to control heroin but expects action by 96. It has about 170,000 addicts in 94. Opium is obtained from the unripe seedpods of the opium poppy (Papaver somniferum), a plant of the family Papaveraceae. (See poppy.) Opium is obtained by slightly incising the seed capsules of the poppy after the plant's flower petals have fallen. The slit seedpods exude a milky latex that coagulates and changes colour, turning into a gumlike brown mass upon exposure to air. This raw opium may be ground into a powder, sold as lumps, cakes, or bricks, or treated further to obtain such derivatives as morphine, codeine, and heroin. Opium and the drugs obtained from it are called opiates. The pharmacologically active principles of opium reside in its alkaloids, the most important of which, morphine, constitutes about 10 percent by weight of raw opium. Other active alkaloids such as papaverine and codeine are present in smaller proportions. Opium alkaloids are of two types, depending on chemical structure and action. Morphine, codeine, and thebaine, which represent one type, act upon the central nervous system and are analgesic, narcotic, and potentially addicting compounds. Papaverine, noscapine (formerly called narcotine), and most of the other opium alkaloids act only to relax involuntary (smooth) muscles. Opiates exert their main effects on the brain and spinal cord. Their principal action is to relieve or suppress pain. The drugs also alleviate anxiety; induce relaxation, drowsiness, and sedation; and may impart a state of euphoria or other enhanced mood. Opiates also have important physiological effects; they slow respiration and heartbeat, suppress the cough reflex, and relax the smooth muscles of the gastrointestinal tract. Opiates are addictive drugs--i.e., they produce a physical dependence (and withdrawal symptoms) that can only be assuaged by continued use of the drug. With chronic use, however, the body develops a tolerance to opiates, so that progressively larger doses are needed to achieve the same effect. The higher opiates--heroin and morphine--are more addictive than opium or codeine. Opiates are classified as narcotics because they relieve pain, induce stupor and sleep, and produce addiction. The habitual use of opium produces physical and mental deterioration and shortens life. An acute overdose of opium causes respiratory depression which can be fatal. Opium was for many centuries the principal painkiller known to medicine and was used in various forms and under various names. Laudanum, for example, was an alcoholic tincture (dilute solution) of opium that was used in European medical practice as an analgesic and sedative. Physicians relied on paregoric, a camphorated solution of opium, to treat diarrhea by relaxing the gastrointestinal tract. The narcotic effects of opium are mainly attributable to morphine, which was first isolated about 1804. In 1898 it was discovered that treating morphine with acetic anhydride yields heroin, which is four to eight times as potent as morphine in both its pain-killing properties and its addictive potential. The other alkaloids naturally present in opium are much weaker; codeine, for example, is only one-sixth as potent as morphine and is used mainly for cough relief. Since the late 1930s, various synthetic drugs have been developed that possess the analgesic properties of morphine and heroin. These drugs, which include meperidine (Demerol), methadone, levorphonal, and many others, are known as synthetic opioids. They have largely replaced morphine and heroin in the treatment of severe pain. Opiates achieve their effect on the brain because their structure closely resembles that of certain molecules called endorphins, which are naturally produced in the body. Endorphins suppress pain and enhance mood by occupying certain receptor sites on specific neurons (nerve cells) that are involved in the transmission of nervous impulses. Opiate alkaloids are able to occupy the same receptor sites, thereby mimicking the effects of endorphins in suppressing the transmission of pain impulses within the nervous system. The opium poppy was native to what is now Turkey. Ancient Assyrian herb lists and medical texts refer to both the opium poppy plant and opium, and in the 1st century AD, the Greek physician Dioscorides described opium in his treatise De Materia Medica, which was the leading Western text on pharmacology for centuries. The growth of poppies for their opium content spread slowly eastward from Mesopotamia and Greece. Apparently opium was unknown in either India or China in ancient times, and knowledge of the opium poppy first reached China about the 7th century AD. At first, opium was taken in the form of pills or was added to beverages. The oral intake of raw opium as a medicine does not appear to have produced widespread addictions in ancient Asian societies. Opium smoking began only after the early Europeans in North America discovered the Indian practice of smoking tobacco in pipes. Some smokers began to mix opium with tobacco in their pipes, and smoking gradually became the preferred method of taking opium. Opium smoking was introduced into China from Java in the 17th century and spread rapidly. The Chinese authorities reacted by prohibiting the sale of opium, but these edicts were largely ignored. During the 18th century European traders found in China an expanding and profitable market for the drug, and the opium trade enabled them to acquire Chinese goods such as silk and tea without having to spend precious gold and silver. Opium addiction became widespread in China, and the Chinese government's attempts to prohibit the import of opium from British-ruled India brought it into direct conflict with the British government. As a result of their defeat in the Opium Wars, the Chinese were compelled to legalize the importation of opium in 1858. Opium addiction remained a problem in Chinese society until the Communists came to power in 1949 and eradicated the practice. In the West, opium came into wide use as a painkiller in the 18th century, and opium, laudanum, and paregoric were active ingredients in many patent medicines. These drugs were freely available without legal or medical restrictions, but the many cases of addiction they caused did not arouse undue social concern. Morphine was first isolated from opium about 1804, and the hypodermic syringe was invented at mid-century. Their use in combination on hundreds of thousands of sick or wounded American soldiers in the Civil War produced unprecedented numbers of addicts. Heroin, which was first synthesized in 1898, proved even more addictive than morphine, and by the early decades of the 20th century the legal use of opiates of any kind had been curtailed. The traffic in such drugs then went underground, leading to a vast illicit trade in heroin by the late 20th century. In the meantime, the smoking of opium had greatly declined in the 20th century, partly because opium had been supplanted by more potent derivatives, and partly because of determined legal efforts in China and other developing nations to eradicate it. Though opium smoking has declined, opium remains the starting product for heroin, which has millions of addicts worldwide. The cultivation of opium, which was formerly centred in India, Turkey, and China and was sometimes carried on legally, shifted to other countries and became wholly illicit in the second half of the 20th century. By the century's end, the nations of Myanmar (Burma), Afghanistan, Laos, Iran, and Pakistan had become the leading producers and exporters of opium. \16 FAQ Natural (known as opiates): Morphine Codeine Semi-Synthetic (known as opioids): Heroin Hydrocodone (Hycodan) Hydromorphone (Dilaudid) Meperidine (Demerol) Oxycodone (Percodan) Synthetic (also known as opioids): Fentanyl (Sublimaze) Methadone (Dolophine) Propoxyphene (Darvon) Pentazocine (Talwin) Opioid Addiction and Withdrawal The FAQ will use morphine as the standard opioid and base all other opioids in relation to it. (like class inheritance in C++). glossary: opiate - narcotic analgesic derived from a natural source(opium poppy) opioid - narcotic analgesic that is either semi or fully synthetic - also refers to entire family of both opiates and opioids IM - intramuscular injection SC - subcutaneous injection Morphine Synopsis: Morphine is naturally occurring substance in the opium poppy, Papaver somniferum. It is a potent narcotic analgesic, and its primary clinical use is in the management of moderately severe and severe pain. After heroin, morphine has the greatest dependence liability of the narcotic analgesics in common use. Morphine is administered by several routes (injected, smoked, sniffed, or swallowed); but when injected particularly intravenously, morphine can produce intense euphoria and a general state of well-being and relaxation. Regular use can result in the rapid development of tolerance to these effects. Profound physical and psychological dependence can also rapidly develop, and withdrawal sickness upon abrupt cessation of heroin use; many of the symptoms resemble those produced by a case of moderately severe flu. Morphine is infrequently encountered in the North American street drug culture. However, mainly because of its availability in hospitals, there have been several documented cases of morphine dependence among health professionals. Drug Source Morphine is isolated from crude opium, which is a resinous prep of the opium poppy, Papaver somniferum. Trade Name Roxinal, MS Contin, Morphine Sulfate Street Names "M", morph, Miss Emma Drug Combinations Use of morphine plus cocaine, as well as of morphine plus methamphetamine, has been reported. However, such combinations are not frequently encountered. Medical Usessymptomatic relief of moderately severe to severe pain;relief of certain types of difficult or labored breathing;suppression of severe cough (rarely);suppression of severe diarrhea (e.g., that produced by cholera). Physical Appearance Morphine is legally available only in the form of its water-soluble salts. Most common are morphine sulfate and morphine hydrochloride. Both are fine white crystalline powders, bitter to the taste. Both are soluble in water and slightly soluble in alcohol. Dosage ~~~~~~ Medical For moderate to severe pain the optimal intramuscular dosage is considered to be 10 mg per 70 kg body weight every four hours. The typical dose range is from 5 to 20 mg every four hours, depending on the severity of the pain. The oral dose range is between 8 and 20 mg; but with oral administration morphine has substantially less analgesic potency (approximately one-tenth of the effect produced by subcutaneous injection) because it is rapidly destroyed as it passes through the liver immediately after absorption. The intravenous route is employed primarily for severe post-operative pain or in an emergency; in this case the dose range is between 4 and 10 mg, and the analgesic effect ensues almost immediately. Nonmedical Irregular or intermittent users (who are not substituting the drug for another narcotic analgesic) may start and continue to use doses within the therapeutic range (e.i., up to 20 mg). However, regular users who employ morphine for its subjectively pleasurable effects frequently increase the dose as tolerance develops. To take several hundred milligrams per day is common, and there are reliable reports of up to four or five grams (4000 - 5000 mg) per day. Routes Of Administration Morphine may be taken orally in tablet form, and can also injected subcutaneously, intramuscularly, or intravenously; the last is the route preferred by those who are dependent on morphine. Short Term Use ~~~~~~~~~~~~~~ Low Doses (single doses of 5 - 10 mg administered by S.C or IM injection in non-tolerant users) CNS, behavioral, subjective: suppression the sensation of and emotional response to pain; euphoria; drowsiness, lethargy, relaxation; difficulty in concentrating; decreased physical activity in some users and increased physical activity in others; mild anxiety or fear; pupillary constriction, blurred vision, impaired night vision, suppression of cough reflex. Respiratory: slightly reduced respiratory rate. Gastrointestinal: nausea and vomiting; constipation; loss of appetite; decreased gastric motility. Other: slight drop in body temperature; sweating; reduced libido; prickly or tingling sensation on the skin (particularly after intravenous injection). Duration 4 - 5 hours Dependency Potential high, continued use results in both psychological and physical dependencyCodeine Drug Source Codeine is found in opium in concentrations between %0.1 and %2. Because of the small concentration found in nature, most codeine found in medical products is synthesized from morphine via the methylation of the hydroxyl group found on the second non-aromatic ring. Trade Name There are no commercial name for products containing only codeine in US. Found under common name of codeine. Canada does have a codeine only syrup available under Paveral. Mainly found in combination products. Street Name T-three's (Tylenol #3 w/ codeine), schoolboy, cough syrup Medical Usesrelief of mild to moderate painrelief of non-productive coughrelief of diarrhea Drug Combinations Sold under many name brand products, the most popular being the Tylenol with Codeine series, the number on the tablet corresponds to the amount of codeine and caffeine found in the each tablet. Tylenol #1 w/ codeine - 8 mg codeine, 15 mg caffeine Tylenol #2 w/ codeine - 15 mg codeine, 15 mg caffeine Tylenol #3 w/ codeine - 30 mg codeine, 30 mg caffeine Tylenol #4 w/ codeine - 60 mg codeine, no caffeine note: all tablets contain same amount of acetaminophen (300 mg) Fiorinal (aspirin, caffeine, barbital, codeine) Many other brand name product combinations. Physical Appearance Tylenol w/ codeine series are imprinted with number on one side and other side is Tylenol label(McNeil). Controlled Substance Status As a single product codeine is a schedule II controlled substance in the US. When combined with other non-controlled substance, and depending on amount per dose unit, codeine combined products range from schedule III to V. Canada has OTC codeine products available if product has no more than 8 mg of codeine per unit dose. Some US areas may have codeine preps available OTC, but usually require release form. As an interesting fact, a travelers handbook noted that Greece has banned codeine in that country (no idea on what it's status is now) so be careful when traveling there. Dosage ~~~~~~ Medical Pain relief : 30mg - 220mg oral or equivalent dose SC or IM Diarrhea relief : 10mg - 20mg orally Cough suppressant : 5mg - 15mg orally Nonmedical Doses can range from 30mg up to 400mg. LD50 for codeine is 800mg in a average nontolerant person. At doses of > 250mg adverse effects tend to arise, including intense itching, flushed skin, dizziness, sedation, nausea and vomiting Routes Of Administration Usually taken orally but can be injected IM or SC. The IV route is not recommended as reactions such as facial swelling, pulmonary edema and convulsions can occur. Short Term Use ~~~~~~~~~~~~~~ CNS, Behavioral, Subjective: Effects begin at 30mg and tend to mimic those of morphine, except sedation and euphoria are less intense. Respiratory: same as morphine but less intense. Gastrointestinal: same as morphine but nausea and vomiting are less common and constipation less severe. Other: alleocodone is a schedule II drug, and when combined with other non-controlled drugs, is found from schedule III-IV. Dosage ~~~~~~ Medical as a cough suppressant 5mg - 10mg for pain relief 10mg - 30mg Nonmedical doses are similar to those for pain relief Routes Of Administration Usually taken orally but can be inject via three routes. Unknown if hydrocodone can be sniffed or smoked. Sniffing is likely possible. Short Term Use ~~~~~~~~~~~~~~ CNS, Behavioral, Subjective: Has similar effects as morphine but less sedation and euphoria Respiratory: Less depression than morphine. Gastrointestinal: Less likely to cause nausea and vomiting than morphine. Other: Hydrocodone is a weaker opioid than morphine but still a effective opioid with similar potency to oxycodone. Duration 3 - 4 hours Dependency Potential moderately low, much less potential than morphineHydromorphone Drug Source Synthetically produced from morphine. Trade Name Dilaudid Street Name Dillies Medical Usesrelief of moderate to severe painrelief of severe cough Drug Combinations most commonly used as a single product Physical Appearance usually bought as tablets, or injectable solution Controlled Substance Status Hydromorphone, like most single product opioids, is a schedule II opioid. Dosage ~~~~~~ Medical for pain relief 1mg - 2mg Nonmedical same as pain relief doses Routes Of Administration Can be administered orally, by three routes of injection, and by sniffing. Unknown if smoking is an effective route. Short Term Use ~~~~~~~~~~~~~~ CNS, Behavioral, Subjective: Hydrocodone has effects similar to morphine, except euphoria is similar to codeine, nausea and vomiting is quite rare, and sedation is practically non-existent Respiratory: Hydrocodone depresses respiration minimally. Gastrointestinal: Hydromorphone effects GI tract very little. Other: Although hydromorphone's euphoria pales with other opioids it's abuse potential comes from the fact the rush experienced from IV use is very similar to heroin's. Hydromorphone is one of the most used opioids in the relief of pain for the terminally ill. The reasons being it's minimal side effects, and high potency. Duration 3 - 4 hours Dependency Potential moderately highMeperidine Drug Source Meperidine is completely synthetic and can be produced with dichlorodiethyl methylamine and benzyl cyanide. Trade Name Demerol Street Name Demmies Medical Usesoriginally found to be useful for muscle spasms but the discovery of it's analgesic properties has resulted in it's almost exclusive use for relief of moderate to severe pain Drug Combinations usually found as a single product, with few combination products. Is found in combination with acetaminophen in Demerol APAP Physical Appearance Demerol tablets are small white tablets with the name Winthrop on one side Controlled Substance Status Schedule II substance in US Dosage ~~~~~~ Medical pain relief is achieved with approx. 50mg - 150mg injected or 200mg - 300mg oral Nonmedical doses similar to those used in medical settings are used in recreational use. Routes Of Administration orally, three injection routes, and sniffing are possible, unknown if smoking is possible Short Term Use ~~~~~~~~~~~~~~ CNS, Behavioral, Subjective: same as morphine but less sedation, less intense euphoria Respiratory: respiratory depression tends to be less common and less intense than morphine Gastrointestinal: nausea and vomiting are reportedly common with oral use, but less when administered via injection Duration 3 - 4 hours Dependency Potential reported to be less than or equal to that of morphineOxycodone Drug Source synthesized from codeine Trade Name only found as a compound product combined with aspirin or acetaminophen. Available in Canada as a single product in the form of a suppository Street Name Percs Medical Usesrelief of moderate to severe pain Drug Combinations Percodan is aspirin and oxycodone Percocet is acetaminophen and oxycodone Physical Appearance Percodan tablets are color coded according to quantity of oxycodone in each tablet, the pink have ~2.5mg and the orange and green having twice as much Controlled Substance Status Schedule II in US Dosage Medical 10 - 20mg oral for pain relief 5 - 15mg injection Nonmedical Doses similar to those used in a medical setting are used Routes Of Administration Can be administered orally, three injection routes, sniffed and possibly smoked. Short Term Use CNS, Behavioral, Subjective: Same as morphine but milder. Respiratory: Less respiratory depression than morphine Gastrointestinal: Less constipating than morphine Duration 3 - 4 hours Dependency Potential ModerateFentanyl Drug Source Synthetically produced Trade Name Sublimaze Street Name China white Medical Uses Mainly relief of moderate to severe pain and as a surgical anesthetic Drug Combinations none Physical Appearance Found as a injectable solution, and a transdermal patch Controlled Substance Status Schedule II in US Dosage Medical 50ug - 200ug Nonmedical same range as medical use Routes Of Administration can be administered via three injection routes, sniffed and smoked Short Term Use CNS, Behavioral, Subjective: euphoria is less than morphine Respiratory: same as morphine but has potential to cause respiratory muscles to go into spasm and result in respiratory arrest Gastrointestinal: less constipating that morphine Duration 1 - 2 hours Dependency Potential moderately highMethadone Drug Source synthetically produced Trade Name Dolophine Street Name Dollies Medical Uses occasionally used for pain relief, but main use is in opioid withdrawal treatment as a substitute drug Drug Combinations none Physical Appearance found as a fruity solution for oral use, in wafers, and tablets also found as a injectable solution Controlled Substance Status Schedule II in US Dosage Medical 3 - 5mg provides same pain relief as 10mg morphine Nonmedical rarely used non-medically, but doses used are approx. same as medical doses Routes Of Administration can be injected via three routes, taken orally, unknown if methadone can be smoked, can be sniffed Short Term Use CNS, Behavioral, Subjective: Oral use provides little euphoria and tends to block opioid receptors in brain, so commonly used as a maintenance drug during rehab. Respiratory: Produces little depression in contrast to morphine Gastrointestinal: produces constipation of less intensity than morphine Other: Developed by Nazi Germany during WWII as Germany was unable to acquire adequate supplies of morphine. Duration first dose last approx. 8 hours and subsequent doses last 18 - 24 hours. Dependency Potential oral use provides little euphoria so little abuse potential in that form. When injected, methadone give very similar effects to morphine so has similar addiction potential.Propoxyphene Drug Source Synthetically produced with similar structure to that of methadone Trade Name Darvon, Darvon N Street Name none Medical Uses for relief of mild pain Drug Combinations Darvon compound is aspirin and propoxyphene Physical Appearance Darvon N as pink oval pills Controlled Substance Status Schedule III in US Dosage ~~~~~~ Medical range from 50mg - 150mg of hydrochloride Nonmedical similar to medical dose ranges. Routes Of Administration can be taken orally, three possible injection routes, no info on possible intranasal or smoked administration Short Term Use CNS, Behavioral, Subjective: oral use provides very little euphoria, mild sedation; at larger doses sedation becomes quite prominent and symptoms such as staggering and slurred speech become apparent. Respiratory: little respiratory depression in medical dose range Gastrointestinal: little effect on GI tract Other: IV use is reported to give rush similar to heroin; poor analgesic with standard dose providing less pain relief than standard aspirin dose Duration 3 - 4 hours Dependency Potential lowPentazocine Drug Source synthetically produced Trade Name Talwin Street Name yellow footballs Medical Uses for relief of moderate to moderately severe pain Drug Combinations Talwin NX - pentazocine and nalaxone (opioid antagonist) Physical Appearance usually found in orange-yellow tablets Controlled Substance Status Schedule III Dosage ~~~~~~ Medical 50mg - 100mg for pain relief Nonmedical similar to medical dosage Routes Of Administration can be taken orally, three injection routes, and sniffedpossibly smoked Short Term Use CNS, Behavioral, Subjective: poor opioid, very little euphoria, mainly just sedates and clouds mind, little recreational use Respiratory: less depression than morphine Gastrointestinal: very little constipation or nausea, vomiting occurs Other: as a opioid agonist/antagonist has potential to cause psychotic effects such as hallucinations, severe confusion Duration 3 - 4 hours Dependency Potential moderate potential, similar to hydrocodoneOpioid Dependence And Withdrawal Opioids have specific withdrawal and dependence characteristics common to all opioids, varying according to the specific drug. All opioids cause both physical and psychological dependence with prolonged use. Depending on the opioid in question withdrawal can become evident after continued use in as little time as 2 weeks or as long as 2 months. Withdrawal is commonly overstated by media and tends to be similar to bad case of flu. This is due to the fact that most opioid users don't tend to be able to acquire enough drug to result in severe withdrawal. It must be noted that physical symptoms may be similar to flu, psychological symptoms can be quite painful. Depression, mood swings, hypersensitivity to pain are some common symptoms. Opioid withdrawal DOES NOT endanger life as does alcohol and other depressant withdrawal.If anyone has any info that they would like to share with me and possibly have included in this FAQ, please send all mail to my mailbox at mdh@debug.cuc.ab.ca