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DRUGSThe Straight FactsDesignerDrugs

DRUGS The Straight FactsAlcoholAntidepressantsBody Enhancement ProductsCocaineDate Rape DrugsDesigner DrugsDiet PillsEcstasyHallucinogensHeroinInhalantsMarijuanaNicotinePrescription Pain RelieversRitalin and Other Methylphenidate-Containing DrugsSleep Aids

DRUGSThe Straight FactsDesignerDrugsM. Foster OliveConsulting EditorDavid J. TriggleUniversity ProfessorSchool of Pharmacy and Pharmaceutical SciencesState University of New York at Buffalo

CHELSEA HOUSE PUBLISHERSVP, NEW PRODUCT DEVELOPMENT Sally CheneyDIRECTOR OF PRODUCTION Kim ShinnersCREATIVE MANAGER Takeshi TakahashiMANUFACTURING MANAGER Diann GrasseStaff for DESIGNER DRUGSASSOCIATE EDITOR Beth RegerPRODUCTION EDITOR Megan EmeryASSISTANT PHOTO EDITOR Noelle NardoneSERIES & COVER DESIGNER Terry MallonLAYOUT 21st Century Publishing and Communications, Inc.©2004 by Chelsea House Publishers,a subsidiary of Haights Cross Communications.All rights reserved. Printed and bound in the United States of America.www.chelseahouse.com3 5 7 9 8 6 4 2Library of Congress Cataloging-in-Publication Data.Olive, M. Foster.Designer drugs / M. Foster Olive.p. cm. — (Drugs, the straight facts)Includes index.Summary: Explains what designer drugs are, their effects on the mind andbody, how they are made and distributed, and laws regarding these drugs.ISBN 0-7910-7638-51. Designer drugs—Juvenile literature. 2. Drug abuse—Juvenile literature.[1. Designer drugs. 2. Drug abuse.] I. Title. II. Series.RM316.O458 2003362.29'9—dc22 2003020140

Table of ContentsThe Use and Abuse of DrugsDavid J. Triggle, Ph.D. 61. Designer Drugs and the Brain 82. Methamphetamine 183. Ecstasy 304. GHB 425. Rohypnol 546. Ketamine 627. Painkiller Analogues 72Bibliography and Further Reading 83Websites 86Additional Resources 88Index 90

The Use and Abuse of DrugsThe issues associated with drug use and abuse in contemporarysociety are vexing subjects, fraught with political agendasand ideals that often obscure essential information that teensneed to know to have intelligent discussions about how tobest deal with the problems associated with drug use andabuse. Drugs: The Straight Facts aims to provide this essentialinformation through straightforward explanations of how anindividual drug or group of drugs works in both therapeuticand non-therapeutic conditions; with historical informationabout the use and abuse of specific drugs; with discussion ofdrug policies in the United States; and with an ample list offurther reading.From the start, the series uses the word “drug” to describepsychoactive substances that are used for medicinal or nonmedicinalpurposes. Included in this broad category aresubstances that are legal or illegal. It is worth noting thathumans have used many of these substances for hundreds, ifnot thousands of years. For example, traces of marijuana andcocaine have been found in Egyptian mummies; the use ofpeyote and Amanita fungi has long been a component ofreligious ceremonies worldwide; and alcohol production andconsumption have been an integral part of many humancultures’ social and religious ceremonies. One can speculateabout why early human societies chose to use such drugs.Perhaps, anything that could provide relief from the harshnessof life—anything that could make the poor conditions andfatigue associated with hard work easier to bear—was considereda welcome tonic. Life was likely to be, according to theseventeenth century English philosopher Thomas Hobbes,“poor, nasty, brutish and short.” One can also speculate aboutmodern human societies’ continued use and abuse of drugs.Whatever the reasons, the consequences of sustained drug useare not insignificant—addiction, overdose, incarceration, anddrug wars—and must be dealt with by an informed citizenry.The problem that faces our society today is how to break6

the connection between our demand for drugs and the willingnessof largely outside countries to supply this highlyprofitable trade. This is the same problem we have facedsince narcotics and cocaine were outlawed by the HarrisonNarcotic Act of 1914, and we have yet to defeat it despitecurrent expenditures of approximately $20 billion per year on“the war on drugs.” The first step in meeting any challengeis always an intelligent and informed citizenry. The purposeof this series is to educate our readers so that they canmake informed decisions about issues related to drugs anddrug abuse.SUGGESTED ADDITIONAL READINGDavid T. Courtwright, Forces of Habit. Drugs and the Making ofthe Modern World. Cambridge, Mass.: Harvard UniversityPress, 2001. David Courtwright is Professor of History atthe University of North Florida.Richard Davenport-Hines, The Pursuit of Oblivion. A GlobalHistory of Narcotics. New York: Norton, 2002. The authoris a professional historian and a member of the RoyalHistorical Society.Aldous Huxley, Brave New World. New York: Harper & Row,1932. Huxley’s book, written in 1932, paints a picture of acloned society devoted only to the pursuit of happiness.David J. Triggle, Ph.D.University ProfessorSchool of Pharmacy and Pharmaceutical SciencesState University of New York at Buffalo7

1Designer Drugsand the BrainDesigner drug (noun): “A synthetic version of a controlledsubstance (as heroin) that is produced with a slightly alteredmolecular structure to avoid having it classified as anillicit drug.”—Merriam-Webster’s DictionaryWHAT ARE DESIGNER DRUGS?The term designer drug was coined in the mid- to late 1980s whendoctors, scientists, and law enforcement agencies noted that, overthe past few decades, the number of people who were attemptingto illegally synthesize mind-altering drugs in underground “clandestine”laboratories was increasing dramatically. These “basementchemists” were taking the chemical structures of knownlegal drugs, such as the narcotic painkiller Demerol®, and alteringthem slightly (even by one or two atoms) to produce closelyrelated analogues (molecules with very similar chemical structures).The idea behind this illegal synthesis was to create a“designer drug” that was hundreds or thousands of times morepotent than the original legal drug. For a few hundred dollars inchemicals and lab supplies, drug makers and dealers could produceliterally millions of dollars’ worth of illegal drugs. Also, sincethe chemical structure of the drug had been altered slightly, it wasstill perfectly legal.8

The term designer drugs was originally used todescribe the illegal analogues of the popular painkillersmeperidine (Demerol) and fentanyl (Sublimaze®). However,in the 1980s, various analogues of the powerful stimulantamphetamine also started to emerge, most notably Ecstasyand methamphetamine. Since these drugs were largely usedby teenagers and young adults at dance clubs, parties, andall-night raves, the term designer drugs was often replaced bythe name “club drugs.” Today, the terms club drugs anddesigner drugs are often used interchangeably.The term designer drugs was a parody of the termdesigner jeans, according to J. Morgan and his colleagues intheir discussion about designer drugs in the book SubstanceAbuse—A Comprehensive Textbook. During the 1970s and1980s, Levi Strauss, Inc., was the leading manufacturer ofdenim blue jeans and was dominating the blue jean market.Hoping that consumers would pay little attention to thedifference, other clothing designers started to produce“designer jeans” that were cheaper imitations, or copycats, ofthe original Levi brand.Making designer drugs was legal for years, because atthe time, U.S. drug laws only prohibited synthesizing exactcopies of approved drugs, while altering the chemical structureslightly and producing a closely related analogue wasstill perfectly legal. Thus, a basement drug laboratorycould synthesize huge amounts of a designer drug withoutgetting into trouble with the law. The same was true afterthe U.S. government banned the sale of AK-47 assault rifles,leading gunmakers to manufacture copycats with slightmodifications so they were not technically AK-47s, but servedthe same purpose.In 1970, the U.S. government passed the ControlledSubstances Act, which classified all drugs into one of fivecategories, or “schedules.” In effect, this law classified drugs9

10DESIGNER DRUGSaccording to how medically useful, safe, and addictive theyare. The schedules are defined as follows:Schedule I—The drug or other substance has (1) ahigh potential for abuse, (2) no currently acceptedmedical use in treatment in the United States, and(3) a lack of accepted safety for use of the drug orother substance under medical supervision. Examples:Ecstasy, heroin, marijuana, and the hallucinogens peyote,mescaline, psilocybin, and LSD.Schedule II—The drug or other substance has (1) ahigh potential for abuse, (2) a currently accepted medicaluse in treatment in the United States or a currentlyaccepted medical use with severe restrictions, and(3) abuse of the drug or other substances may lead tosevere psychological or physical dependence. Examples:cocaine, PCP, morphine, fentanyl and meperidine,codeine, amphetamine and methamphetamine, Ritalin®.Schedule III—The drug or other substance has (1) apotential for abuse less than the drugs or other substancesin Schedules I and II, (2) a currently acceptedmedical use in treatment in the United States, and(3) abuse of the drug or other substance may lead tomoderate or low physical dependence or high psychologicaldependence. Examples: ketamine, anabolicsteroids, some barbiturates.Schedule IV—The drug or other substance has(1) a low potential for abuse relative to the drugs orother substances in Schedule III, (2) a currentlyaccepted medical use in treatment in the UnitedStates, and (3) abuse of the drug or other substance

Designer Drugs and the Brain11may lead to limited physical dependence or psychologicaldependence relative to the drugs or othersubstances in Schedule III. Examples: Valium®, Xanax®,some barbiturates.Schedule V—The drug or other substance has (1) a lowpotential for abuse relative to the drugs or other substancesin Schedule IV, (2) a currently accepted medicaluse in treatment in the United States, and (3) abuse ofthe drug or other substance may lead to limited physicaldependence or psychological dependence relative to thedrugs or other substances in Schedule IV. Example:codeine cough syrup.Schedule I drugs are the most highly restricted and tightlyregulated, whereas Schedule V drugs are the least restricted.Note that, in some circumstances, some drugs can be classifiedunder more than one schedule. For example, althoughmorphine is a Schedule II drug, it is considered Schedule IIIif it comes in a concentration of less than 2 milligrams permilliliter of water.During the 1980s, it became evident that some “designerdrugs” were more potent and dangerous than the originaldrugs they were designed to imitate, leading to many overdoses.Also, the drugs often contained impurities that madethem extremely toxic. Thus, in 1986, the United States governmentamended the Controlled Substances Act toinclude the Controlled Substances Analogues EnforcementAct. This law made it illegal to manufacture any drug thatwas “substantially similar” to the chemical structure of analready legal drug. Thus, simply replacing an atom or two inthe chemical structure of a narcotic painkiller was no longera legal way to create a drug that had similar effects to onesalready made by pharmaceutical companies.

12DESIGNER DRUGSOne thing is unique about designer/club drugs—theyare all purely synthetic and made by chemical reactions inlaboratories, often in garages or basements in residentialneighborhoods. By contrast, other well-known illegal drugscome from natural sources such as plants. For example,cocaine is made from the coca plant, heroin is made from theopium poppy, marijuana comes from the cannabis plant,nicotine comes from tobacco leaves, etc. Thus, unlike illegaldrugs that require significant interstate and internationaltrafficking of the plant products (for example, from SouthAmerica, Europe, or the Middle East) before it gets to theuser, the route from designer drug maker to designer druguser could be as short as a few city blocks.DRUGS AND THE BRAINDesigner drugs are mind-altering and can produce hallucinations.For these reasons, they are often called “psychoactive” or“psychedelic.” Designer drugs produce their effects by alteringthe way nerve cells (neurons) in the brain communicate witheach other (Figure 1.1).Under normal circumstances, neurons carry electricalsignals along wire-like nerve fibers called axons. At the endof each axon is a mushroom-shaped nerve ending calleda synaptic terminal. When the electrical signal from theaxon reaches the synaptic terminal, it causes chemicalmessengers (called neurotransmitters) to be released andsecreted onto nearby neurons. This junction between asynaptic terminal and a nearby neuron is called a synapse.There are literally trillions of synapses in the brain, andeach neuron can have as many as 100,000 different synapseson it. After neurotransmitters are released, they diffuseaway from the synaptic terminal into the synapse andencounter proteins (called receptors) on the nearby neuronsthat are designed to recognize specific neurotransmitters(Figure 1.2). These receptors can cause the nearby nerve cell

Designer Drugs and the Brain13Figure 1.1 Neurons (nerve cells) transmit informationthroughout the brain and the body. A typical neuron is shownhere. Electrical impulses are received by the dendrites andtransmitted to the next neuron via the axon. The myelin sheathinsulates the axon and increases the speed at which electricalimpulses can travel.to either become activated (passing along the electrical signal)or inhibited (not passing along the signal).Designer drugs, as well as other drugs like alcohol, cocaine,and heroin, produce their effects on the brain by altering the

14DESIGNER DRUGSFigure 1.2 Serotonin is one of the brain’s neurotransmitters. Thisimage depicts serotonin transmission between neurons and the drugEcstasy’s effects on that transmission. Serotonin is normally removedfrom the synapse shortly after being released. Ecstasy blocks thismechanism, increasing the amount of serotonin in the synapse. Thiscauses the postsynaptic neuron to be overstimulated by serotonin.Serotonin is one of many neurotransmitters that nerve cells can secrete.Other common neurotransmitters include dopamine, glutamate,gamma aminobutyric acid (GABA), noradrenaline, and endorphins.actions of neurotransmitters and consequently how neuronscommunicate with each other. However, different drugs canalter the actions of neurotransmitters in different ways. Somedrugs, like Ecstasy and methamphetamine, cause neurons torelease excess neurotransmitters like dopamine and serotonin.

Designer Drugs and the Brain15Other drugs, like GHB and Rohypnol®, can interact directlywith the neurotransmitter receptors to either enhance or blockthe effects of the brain’s own neurotransmitters. Still otherdrugs can alter the metabolic breakdown or clearance ofcertain neurotransmitters after they are released from thesynaptic terminal, thereby altering how long the neurotransmitteraffects the activity of other nearby neurons.The brain has numerous regions that are specialized for particularfunctions (see Table 1.1, Figure 1.3a, and Figure 1.3b). Theeffect a particular drug has on a person’s thinking or behaviormay depend on which region it is acting upon.Table 1.1 Brain Regions and FunctionsREGIONFrontal cortexMotor cortexSensory cortexVisual cortexCerebellumBrainstemHypothalamusLimbic system*FUNCTIONInvolved in planning, thinking, anddecision-makingControls movement of the face,arms, and legsInvolved in perception of touchProcesses sight and visionControls motor coordination, balanceControls basic bodily functions likechewing, swallowing, heart rate, andbreathingControls metabolism, sleep, eating,and drinkingControls emotions, memory, andmotivation*Note: The limbic system is made up of several brain structures,including the hippocampus, amygdala, and basal forebrain(Figure 1.3b).

16DESIGNER DRUGSFigure 1.3a This diagram illustrates a cross-section of the humanbrain, showing some of the major structures. The brainstem,which governs functions such as breathing, heart rate, chewing,and swallowing, is made up of structures including the pons,locus ceruleus, raphe nuclei, and midbrain reticular formation.

Designer Drugs and the Brain17Figure 1.3b This cross-section of the human brain showsadditional major structures. Note that the limbic system,which controls emotions, is made up of structures includingthe amygdala and hippocampus at the “core” of the brain.

2MethamphetamineCOMMON STREET NAMESMeth, Crystal Meth, Speed, Ice, Fire, Glass, L.A. Glass, Quartz,Crank, Chalk, Tweak, Tina, Jib, Yaba, Crazy Medicine, Poor Man’sCocaine, Hitler’s Drug, Devil’s Drug, Blue Mollies, Go-Fast, MexicanCrack, Shabu, Sketch, Stove Top, West Coast, Yellow Bam.HISTORY AND LEGAL STATUSMethamphetamine is a potent stimulant that was first synthesized bya Japanese scientist in the early 1900s as an analogue of amphetaminefor use as a nasal decongestant, antiasthma drug, and weightloss aid. However, it was not used commercially until the 1940swhen it was manufactured and marketed as “Methedrine” by thepharmaceutical company Burroughs Wellcome.During World War II, methamphetamine was given frequentlyto soldiers to help fight fatigue and hunger, and to increase physicalendurance. However, by the time the war ended, many soldierswere addicted to the drug and wanted to continue using it.Methamphetamine addiction became especially prevalent inJapan, where after the war Japanese soldiers were given access tomilitary supplies of the drug to feed the addiction they developedduring the war.In the 1950s, many college students, athletes, and long-haul truckdrivers started to use methamphetamine because of its ability to givethe user energy and keep the user awake for long periods of time.During the 1960s, recreational use of methamphetamine increaseddramatically when injectable forms became available that produced18

a much stronger “rush” than was previously obtainable. Addictionto methamphetamine continued to escalate.In 1970, the U.S. government passed the original ControlledSubstances Act, and under this law methamphetaminewas classified as a Schedule II drug in its injectable form and aSchedule III in its noninjectable (pill) form. However, a yearlater, both forms of methamphetamine were reclassified asSchedule II drugs. Today, it is still sold under the name Desoxyn®for a few medical uses, such as for the treatment of attention-deficit/hyperactivitydisorder (ADHD) and narcolepsy.Throughout the 1980s and 1990s, the supply of methamphetaminecontinued to increase to meet the demands of anever-growing population of meth addicts. Methamphetaminerelatedoverdoses and deaths also increased. To stem the risingtide of meth-related overdoses and deaths, Congress passedthe Comprehensive Methamphetamine Control Act in1996, which established more rigid controls of ingredients inmethamphetamine (such as pseudoephedrine—see discussionthat follows) and imposed stiffer penalties for the manufacture,distribution, and possession of the drug.WHAT METHAMPHETAMINELOOKS LIKE AND HOW IT IS TAKENMethamphetamine most often comes in the form of white orclear crystals, which give it its nickname “ice” or “glass.”Methamphetamine crystals can also be brown in color. Thesecrystals are most often smoked with a pipe or snorted (Figure 2.1)and can easily be dissolved in water and injected intravenously.Methamphetamine crystals are also taken rectally. Meth powderand crystals often contain contaminants and impurities(including lead) from the chemical synthesis process that areoften toxic. Approximately 50 milligrams (mg) of methamphetaminewill give the user a significant high, although theabsolute content of meth in a given batch of powder or crystalsvaries, making it difficult to know the precise amount of the19

20DESIGNER DRUGSFigure 2.1 Methamphetamine can come in a crystallized formand be snorted with a “pipe” (shown here). Methamphetamine inthis form is known as “ice” or “glass.” The drug is also found inpill or tablet form, but produces a less immediate high, becausethe drug does not directly enter the bloodstream when taken orally.drug that is being taken. Methamphetamine crystals cost anywherefrom $300 to $4,000 per ounce, depending on wherethey are being sold.Methamphetamine can also come in the form of coloredpills or tablets (Figure 2.2), which many users consider saferthan raw powder because they are less likely to be lacedwith contaminants. However, pill and tablet forms of methamphetamineoften do contain impurities. These forms oftenproduce less of a “rush” (the immediate pleasurable feelingproduced by a drug) compared to when the drug is injected orsmoked. This is because the pills must be absorbed through thegastrointestinal (GI) tract prior to entering the bloodstreamand subsequently the brain.Most methamphetamine in the United States comes from

Methamphetamine21Figure 2.2 Methamphetamine can be found in pill form,as shown here. Many users incorrectly believe that pills areless likely to be laced with other drugs or contaminants.underground “clandestine” laboratories in the western UnitedStates (primarily California) and Mexico. These labs are foundin apartments, hotel rooms, basements, garages, rented storagespaces, and even moving vans. Lab operators often make theirlabs “mobile” so they can easily be packed up and transported.Meth labs are also often “booby trapped” with explosives todestroy the evidence in case they are discovered, and meth laboperators often arm themselves with guns and other weapons todefend their prized source of income.

22DESIGNER DRUGSFigure 2.3 The chemical structures of the common coldand allergy medicines ephedrine and pseudoephedrine (illustratedhere) are very similar to, and can be used to synthesize,the illegal stimulants amphetamine and methamphetamine.Methamphetamine is much more potent than amphetamine.Methamphetamine is synthesized, or “cooked,” by a simplechemical reaction from its precursor pseudoephedrine (Figure2.3), a stimulant commonly found in over-the-counter allergyand cold medications (such as Sudafed®). Because methamphetamineis made relatively easily from pseudoephedrine,many pharmacies and drug stores now restrict the amount ofpseudoephedrine-containing medications that individual customerscan buy to avoid the possibility of “stockpiling” pseudoephedrinefor the purpose of making methamphetamine.Meth dealers and makers in the United States have also been

Methamphetamine23known to hijack shipments of pseudoephedrine-containingdrugs en route to pharmacies in other countries, divertingthem to the United States instead.PSYCHOLOGICAL AND PHYSICALEFFECTS OF METHAMPHETAMINEWhen methamphetamine is smoked or injected intravenously,it produces a rapid intense “rush,” “flash,” or euphoria (verypleasurable sensation) within 3–5 minutes of taking the drug.This rush only lasts a few minutes and is not usually experiencedafter snorting the drug or taking it orally in pill form.After the rush wears off (usually after a few more minutes), theuser becomes extremely alert, active, energetic, and restless,Yaba—MethamphetamineFrom the Far EastRecently there has been a large influx into the United Statesof newer methamphetamine tablets from countries in the FarEast, notably Thailand and Burma. These tablets are brightlycolored, often stamped with letters like “WY” and are calledby their Thai name “yaba.” While the presence of the tablet isso new that use patterns are not yet known, the tablets aremostly found in Asian communities in California. The tabletsare sent from traffickers in Southeast Asia to the United Statesby mail, overnight couriers, or on cargo ships. Because theycome in convenient pill forms, many users take the drugsat dance clubs and raves. The colored pills look very similarto Ecstasy tablets (see Chapter 3). In addition to containing25 – 30 milligrams of methamphetamine, yaba tablets alsocontain 45–65 milligrams of caffeine to give the user anextra energy boost. The pills may also be flavored to tastelike candy. Some users even dissolve yaba pills in alcoholicdrinks and coffee (so-called “bikers’ coffee”).

24DESIGNER DRUGSand experiences very pleasurable feelings. These effects maytake longer (15 –20 minutes) to achieve if the drug is snortedor taken orally. Regardless of how it is taken, the effects ofmethamphetamine last anywhere from 6–24 hours (muchlonger than the effects of cocaine, which last 30–60 minutes).When people start to use methamphetamine repeatedly,however, its psychological effects start to change. Repeated usecauses tolerance to the psychological and physical effects of thedrug—that is, the drug becomes less effective each time it istaken, causing the user to progressively need more and more of itto achieve the same desired high he or she has become accustomedto. However, some repeated users of methamphetaminemay become increasingly sensitive (or “sensitized”) to itseffects. Repeated methamphetamine use can lead to “psychosis”(a lost sense of reality accompanied by hallucinations, delusions,and paranoia). A common delusion experienced by meth users isthe belief that their skin is crawling with insects (“crank bugs”),so users may frequently pick at their skin, causing sores to form.Repeat users also commonly experience insomnia, mood swings,and personality disturbances, and because methamphetaminesuppresses appetite, significant weight loss. Meth users mayalso become violent and aggressive, or engage in odd repetitivebehaviors, such as being obsessed with dismantling andreassembling cars or other mechanical devices.In addition to its effects on the brain, methamphetaminecauses dramatic increases in heart rate and blood pressure. Thisis because methamphetamine causes increases in the secretionof dopamine, epinephrine, and norepinephrine in the heart andcirculatory system, raising the user’s heart rate to as much as200 beats per minute (normal heart rate is around 70 beats perminute). Irregular heartbeats (arrhythmias) are also common.In addition, methamphetamine causes blood vessels to constrict,resulting in higher blood pressure in many parts of the body,including the brain. This “cerebral hypertension” eventuallycauses damage to the vessels, greatly increasing the risk for stroke

Methamphetamine25or hemorrhage. Chronic methamphetamine use can also causean inflammation of the lining of the heart.Other effects caused by methamphetamine include headaches,decreased appetite, dry mouth, dilated pupils, trembling,chest pains, increased respiration and shortness of breath, hyperthermia(elevated body temperature), insomnia, and nausea andvomiting. In more severe cases (i.e., overdoses) it can produceseizures and convulsions, stroke, heart attacks, and death. Therisk of encountering these more serious side effects are greatlyincreased when methamphetamine is used in combination withother drugs like cocaine, marijuana, alcohol, and heroin.HOW METHAMPHETAMINEWORKS IN (AND DESTROYS) THE BRAINIn the brain, methamphetamine causes massive amountsof the neurotransmitters dopamine, norepinephrine, andserotonin to be released from neurons in the brain, particularlyin the limbic system and frontal cortex. Scientists believethe increased dopamine release in these brain regions isresponsible for methamphetamine’s ability to keep peopleawake, alert, energetic, active, and possibly addicted.Methamphetamine acts on a variety of brain regions to producea number of different effects (Table 2.1).Table 2.1 Methamphetamine’s Effects on the BrainEFFECTBRAIN REGION(S)Euphoria and pleasureDecreased appetite, hyperthermiaParanoia, hallucinationsIrritation, aggression, violenceIncreased respirationLimbic systemHypothalamusFrontal cortex,visual cortexFrontal cortexBrainstem

26DESIGNER DRUGSProlonged release of large amounts of dopamine in thebrain can be toxic to neurons, however, causing dopaminereleasingneurons to die. This damage may be permanent, asevidenced by brain scans on methamphetamine addicts thatshow that this damage is still present three years after ceasingto use the drug. Because dopamine-releasing neurons die offin regions of the limbic system, symptoms of impaired movementand muscle control can appear that are strikingly similarto Parkinson’s disease (see Chapter 7). The death ofdopamine neurons in the frontal cortex is believed to causethe paranoia and psychosis (hallucinations and delusions)seen in many chronic methamphetamine users.STATISTICS AND PATTERNS OFMETHAMPHETAMINE USE AND ABUSEIn the past, methamphetamine use and abuse in the UnitedStates was most prevalent in individuals who needed to remainawake and alert due to the nature of their occupations—long-haul truckers, for example—and in some “fringe”members of society. Today, however, it is predominantly usedby white males in their 20s and 30s and is becoming morepopular with teenagers at dance clubs and “raves.” For thesereasons, methamphetamine can be considered a “club drug.”Methamphetamine use is also increasing among homelesspeople, prostitutes, and runaway youths.Recent surveys indicate that as much as 4% of the U.S. population,including high school students, have tried methamphetamineat least once. Surveys of emergency room reportsindicate that over the past decade, upward of 3,000–4,000methamphetamine-related deaths have occurred. There has alsobeen a constant trend of more than 10,000 ER “mentions” ofmethamphetamine since 1994 (Figure 2.4). In addition, thousandsof meth labs have been raided and seized by law enforcementagencies in the United States in the past several years.Historically, most methamphetamine use was concentrated

Methamphetamine27Figure 2.4 Although methamphetamine use has decreased slightlysince 1994, the number of times methamphetamine is mentionedin emergency room patient reports in the United States is well intothe tens of thousands, as can be seen in this graph. Many of thesepatients die from complications resulting from methamphetamine use.in the western and southwestern United States. The drug isstill one of the most widely used illegal drugs in such citiesas San Francisco, Los Angeles, San Diego, and Honolulu.However, increased methamphetamine use is starting toappear in Midwest states like Iowa and Nebraska, and evenlarge cities on the East Coast such as New York City, indicatingthat its use is spreading across the entire country.METHAMPHETAMINE ADDICTIONMethamphetamine is highly addictive, and people havereported becoming addicted to the drug after only taking ita few times. While some meth addicts take the drug once or

28DESIGNER DRUGStwice a day, other addicts may go on meth “binges” or“runs,” taking the drug every 2–3 hours for several dayswithout sleep. Heavy methamphetamine users tend to havepoor hygiene and appear pale, and show a progressiveMETHAMPHETAMINEAND ADOLF HITLERMethamphetamine was widely used by soldiers in World War IIbecause its potent stimulant effects kept them awake and alertfor longer periods of time and increased their physical endurance.One infamous user of methamphetamine during wartime wasone of the most evil men of the twentieth century—Adolf Hitler.Hitler started receiving daily injections of methamphetaminefrom his personal physician Dr. T. Morrell in 1942, and it wasreported he could not function without his daily doses. Hitleralso took many other drugs (perhaps over two dozen), includingCola-Dalmann tablets that contained caffeine. Hitler alsodispensed methamphetamine to his troops so they couldfight for days on end without sleep or food and outlast theendurance of enemy troops.Hitler eventually developed hand tremors and problemscontrolling movement, which he would attempt to hide bycovering one hand with the other, or by placing his hands in hispockets. These symptoms strongly resembled Parkinson’sdisease (see Chapter 7), which many scientists speculate mayhave been caused by brain degeneration brought about byHitler’s methamphetamine use. Other historians, however,speculate that Hitler’s Parkinson’s disease may have beencaused by a virus or by the spirochete that causes syphilis.Hitler’s tremendous paranoia, lack of compassion andjudgment, and violent and aggressive tendencies are oftenattributed to his repeated use of methamphetamine. Thesepersonality changes may have ultimately helped change thecourse of World War II and history itself.

Methamphetamine29decline in their ability to function in social and job-relatedsituations. (This inability can persist for months or yearseven after stopping use.)One of the most devastating effects of methamphetamineaddiction can be seen in pregnant women who are addicted.Exposure of a fetus to methamphetamine has been shown tocause limb malformations, abnormal reflexes, and behavioralproblems in the newborn. Moreover, meth-addicted expectantmothers experience more premature deliveries and complicationsduring delivery than do non-using expectant mothers.Another consequence of methamphetamine addiction isincreased risk for HIV infection and AIDS, since many methusers inject the drug intravenously and share needles. In fact,illegal drug use is one of the fastest-growing ways HIV is spreadto other people.Once a methamphetamine addict stops taking the drug,the withdrawal symptoms can be very severe and includedepression and anxiety, increased appetite, fatigue, paranoia,irritability, aggressive behavior, and intense craving for thedrug. Some of these symptoms can be eased with sedativedrugs like Valium or antidepressants like Prozac®.Although there are currently no pharmacological treatmentsfor methamphetamine addiction, psychological treatmentssuch as psychotherapy, cognitive-behavioral therapy (whichinvolves changing one’s thought patterns, expectations, andbehavior), and improving coping skills can be mildly effectivein helping meth addicts stay clean.

3EcstasyCOMMON STREET NAMESX, XTC, E, Adam, Eve, Clarity,Stacy,Love drug,Lover’s Speed,HugDrug, Versace, Essence, Decadence, Dex, M&M, Roll, Bean,Bens, B-Bombs, Disco Biscuit, Go, Morning Shot, Scooby Snacks,Sweeties, Wheels.HISTORY AND LEGAL STATUSEcstasy, also known by its chemical name, 3,4-methylenedioxymethamphetamine(MDMA), was first synthesized in 1912 bychemists at the Merck pharmaceutical company in Germany, whowere searching for amphetamine analogues to use as new appetitesuppressants. These chemists also synthesized a similar drug called3,4-methylenedioxyamphetamine (MDA), which, as it turns out, isan active metabolite of MDMA. As MDMA and MDA are veryclosely related to amphetamine and methamphetamine (Figure 3.1),Ecstasy is considered one of the original “designer drugs.”Merck patented MDMA and MDA in 1914, but World Wars Iand II sidetracked any further research on the drugs. Interest in thetwo drugs was revived in the 1950s by the U.S. military, but neverwent further than the animal testing stage.Ecstasy remained largely unused as a recreational drugthrough the 1960s and early 1970s. However, in the late 1970s, abiochemist at the University of California at Berkeley namedAlexander Shuglin was approached by a student who claimed tohave used MDMA to fix a stuttering problem. Shuglin decidedto synthesize the drug and take it himself. He wrote a scientific30

Figure 3.1 The chemical structure of Ecstasy (MDMA) is verysimilar to those of its cousins, amphetamine and methamphetamine.The structure of Ecstasy is shown here, with the structure ofamphetamine enclosed in the box. Ecstasy contains an additionalcarbon ring and a methane (CH 3) group.article that described the extremely pleasurable and controllablestate of consciousness he obtained by taking thedrug, and the mild, pleasurable hallucinations thataccompanied these feelings. Based on his experience withthe drug, Shuglin suggested that MDMA should be usedby psychologists, psychiatrists, and counselors to helppatients “open up” and explore their own feelings. Asmall underground group of psychotherapists followedhis advice and used MDMA successfully in their practicesfor several years.But by the early 1980s, reports of Ecstasy’s psychedeliceffects leaked out to the public, and recreational Ecstasy useblossomed on college campuses in states such as California andTexas. This prompted the Drug Enforcement Administration31

32DESIGNER DRUGS(DEA) to begin investigating the use, abuse, and trafficking ofMDMA, which spawned media coverage and further publicawareness of the drug. In 1986, the DEA indicated its intent toclassify Ecstasy as a Schedule II controlled substance, citingthat it still had potential for medical use in psychiatry. However,the director of the DEA, concerned about the potential foraddiction to Ecstasy, deemed it necessary to classify it as aSchedule I controlled substance, the most restricted classificationa drug can receive.By the late 1980s, use of Ecstasy had spread across theUnited States and into England and the rest of Europe. Ironically,however, even though Ecstasy use likely originated in theUnited States, most (at least 80%) of the Ecstasy found in theUnited States is now produced in European countries like theNetherlands and Belgium. In 2001, U.S. Customs reported seizingmore than 7 million Ecstasy tablets that were illegallyshipped to the United States. Penalties for Ecstasy manufacturing,trafficking, and possession currently include many years inprison and hundreds of thousands of dollars in fines.WHAT ECSTASY LOOKS LIKE AND HOW IT IS TAKENEcstasy most commonly comes in the form of a small pill(Figure 3.2). These pills come in a large variety of shapes andcolors with various designs imprinted on them. A typicalEcstasy pill costs between $10 and $25 and contains 75–150milligrams of MDMA. Since these pills look so much likecandy, they are often concealed by mixing them into a bagof M&Ms® or Skittles®, or even placing the pills inside aPez® dispenser. The pills are usually chewed or taken with adrink. In rarer instances, the pills are crushed into a powderand snorted or injected intravenously, or the pills are insertedinto the rectum (“shafting”).Despite being in pill form, Ecstasy tablets often containimpurities that can be toxic and cause serious adverse reactions.Such impurities may include other amphetamine derivatives,

Ecstasy33Figure 3.2 Ecstasy tablets come in many colors, with hundreds ofdifferent designs imprinted on them. The designs range from sportsand car logos to catchy names, cartoon characters, and popularsymbols, making them all the more appealing to teenagers.ephedrine, and even heroin. Increasing reports of contaminatedbatches of Ecstasy pills has prompted the need for “drug testkits,” which test for such impurities, to be sold with the drug.Many rave parties now have booths set up where users can havetheir Ecstasy pills tested for contaminants.PSYCHOLOGICAL AND PHYSICAL EFFECTS OF ECSTASYEcstasy has both stimulant and hallucinogenic properties. Theeffects of the drug begin approximately 20–60 minutes aftertaking it and usually last for 3–4 hours, but sometimes longer.

34DESIGNER DRUGSThe most well-known effect of Ecstasy is its ability toproduce intense feelings of happiness, well-being, confidence,loss of inhibitions, and closeness to others. Ecstasy alsoproduces strong feelings of empathy (the ability to identifywith and share other people’s feelings) and often makes theusers feel like they “love and want to hug everyone” (henceits name, the “hug” or “love” drug). Ecstasy can also producea mild “rush” or euphoria, although not nearly as intense asHERBAL ECSTASY—NOT REALLY ECSTASYIn recent years, a new drug called “Herbal Ecstasy” has been promotedas a natural and safer alternative to Ecstasy that may helpwith weight loss. Herbal Ecstasy supplements are sold in healthfood and drug stores, and marketed mainly to teenagers andyoung adults as being able to produce euphoria, increased energy,and heightened sexual sensations. They are also marketed as anaid in combating asthma. Common names for Herbal Ecstasyinclude Cloud 9, Rave Energy, X, Herbal X, Ultimate X-phoria,and Herbal Bliss.Herbal Ecstasy is actually nothing more than a stimulantcontaining ephedrine and caffeine. The manufacturers claim theproduct is natural because the ephedrine it contains comes fromthe Chinese herb ephedra (also called “ma huang ”) or otherephedrine extracts, and the caffeine it contains comes from thekola nut. Herbal Ecstasy can also contain other herbs such asginseng, ginkgo biloba, green tea, and nutmeg. However, theFood and Drug Administration (FDA) has warned that HerbalEcstasy is just as dangerous as other synthetic ephedrine andcaffeine products and can potentially result in irregular heartbeat,heart attack, stroke, psychosis, and death. These dangers areincreased in patients with heart conditions, those who are takingantidepressants, or people who are overly sensitive to stimulants.

Ecstasy35that felt after taking cocaine or methamphetamine. Otherpsychological effects of Ecstasy include increased excitement,laughter, relaxation, and talkativeness, and decreased feelingsof anxiety, alienation, and aggression.Because Ecstasy can produce mild hallucinations, it isoften referred to as a psychedelic drug having effects similarto those of LSD. Unlike other psychedelic drugs, however,Ecstasy does not produce vivid perceptual and visual distortions,like walls and ceilings turning into liquid. Rather, theperception of colors, sound, music, and touch appears to beintensified by Ecstasy. In addition, the perception of time maybe slowed or otherwise altered.Despite the pleasurable effects Ecstasy produces in manyindividuals, some people report negative psychological effectswhile on the drug, including feelings of confusion, depression,anxiety, paranoia, and depersonalization. These problems canalso occur when the person “comes down” from the high andthe drug begins to wear off. Insomnia and irritability oftenoccur as well.In spite of the pleasurable effects that it brings about,Ecstasy is nevertheless a very dangerous drug. Ecstasy canproduce sharp increases in body temperature (called malignanthyperthermia), which can lead to excess sweating, dehydration,and heat exhaustion, especially when the drug is taken atdances and clubs where room temperatures are abnormallyhigh. Malignant hyperthermia is the most common cause ofdeath associated with Ecstasy use. Another common cause ofEcstasy-related death is hyponatremia. Hyponatremia occurswhen a person drinks too much fluid (in an attempt to avoiddehydration), which results in kidney failure, swelling ofthe brain, and coma. Ecstasy also increases heart rate andblood pressure, thereby increasing the risk of heart attack,stroke, or brain hemorrhage. Other common physical sideeffects of Ecstasy include dilated pupils, jaw clenching andgrinding of the teeth (which is why many users chew on

36DESIGNER DRUGSpacifiers), muscle tension, headaches, nausea and vomiting,tremors, anxiety, shortness of breath, faintness, chills, andblurred vision.HOW ECSTASY WORKS IN(AND DESTROYS) THE BRAINEcstasy produces its effects by causing massive amounts ofserotonin and dopamine to be released from neurons in thebrain. In addition, Ecstasy inhibits the ability of neuronsto reabsorb these neurotransmitters after they are secreted.This has the overall effect of dramatically increasing thestimulation of serotonin receptors on nearby neurons.Ecstasy affects numerous brain regions, as described inTable 3.1:Table 3.1 Ecstasy’s Effect on the BrainEFFECTEuphoria, pleasure, empathyHyperthermia, decreasedappetiteHallucinations, heightenedperceptionsJaw clenchingBRAIN REGION(S)Limbic system, frontalcortexHypothalamusFrontal cortex, visualcortex, sensory cortexBrainstemEcstasy also stimulates the sympathetic nervous system(nerves located outside the brain and spinal cord), causingincreases in heart rate and blood pressure.It is becoming increasingly evident that repeated use ofEcstasy actually damages the brain. Scientists believe thatEcstasy interferes with cellular and metabolic processes,

Ecstasy37specifically in serotonin-containing neurons, which eventuallywither and die with repeated Ecstasy use. This destruction ofserotonin neurons in brain regions such as the limbic systemand frontal cortex has been linked to depression, memoryloss, and decreased cognitive ability.ECSTASY AS A DATE RAPE DRUGEcstasy is not as commonly used as a date rape drug asGHB or Rohypnol, primarily because it does not incapacitatethe victim or make him or her unable to ward offsexual advances. In addition, Ecstasy is relatively insoluablein many liquids. Also, Ecstasy actually tends to makemale users impotent and unable to achieve an erection.This impotence is increasingly common in men whorepeatedly use Ecstasy. This has spurred the popularity of anew drug combination, Viagra® (a drug that helps men achieveerections) and Ecstasy, which male users take so they canremain sexually functional while high on Ecstasy. Thiscombination is quite risky, however, with numerous sideeffects such as heart problems, high blood pressure, andeven death, especially when taken with another drugcalled amyl nitrate (“poppers”).Nevertheless, there have been reports of Ecstasy powderbeing slipped into an unsuspecting person’s drink. In suchinstances, a person under the influence of Ecstasy mightexperience confusion and impaired judgment, and may engagein behaviors that he or she would not normally engage in.Thus, Ecstasy is often still considered a date rape drug.STATISTICS AND PATTERNSOF ECSTASY USE AND ABUSEAs mentioned earlier, Ecstasy was given to patients by somepsychotherapists in the 1980s to help them improve theircommunication skills and explore their own feelings. However,once the public became aware of Ecstasy’s powerful

38DESIGNER DRUGSpsychological effects, illegal use increased dramatically, especiallyamong high school and college students (Figure 3.3).In fact, recent polls and surveys indicate that between 7 and11% of high school students have tried Ecstasy at least once,and this number is even higher among college students andyoung adults. As with other designer and club drugs, themajority of users tend to be Caucasian, although the drug isgaining popularity in African Americans, Hispanics, and otherethnic groups. Ecstasy users often tend to be from middle- orupper-class families, and thus Ecstasy is often referred to as a“yuppie” drug. Ecstasy use is vastly popular at dance clubs,DRUGS AND ANIMAL RESEARCHResearch on animals has helped scientists to discover thetoxic effects of Ecstasy on the brain. As in humans, whenexperimental animals like monkeys and rats are repeatedlygiven Ecstasy, nerve fibers containing the neurotransmitterserotonin start to die. Normally, the cerebral cortex (whichincludes the frontal, sensory, motor, and visual cortices)contains thousands of serotonin-releasing nerve fibers, whichcontrol mood and thinking abilities. In one scientific study,monkeys were given two 5-milligram doses of Ecstasy a dayfor four days, in an attempt to mimic the kind of “Ecstasybinge” that human Ecstasy users often engage in. A separateset of “control” monkeys was given only saline. When thebrain tissue of the monkeys was examined two weeks aftergiving them Ecstasy, many of the serotonin nerve fibers(depicted as pink in the photograph on the facing page) inthe cerebral cortex had died or withered away. The scientistsalso examined the brains of a separate set of monkeys thathad received the same Ecstasy treatment seven years beforehandand found that many of the serotonin nerve fibers in thecerebral cortex were still missing, although some had grownback. Scientists have recently found that Ecstasy also

Ecstasy39parties, and raves, and its use is on the rise at such venues asschools and shopping malls.Ecstasy-related visits to hospital emergency rooms haveskyrocketed in recent years, with approximately 250 reportsof Ecstasy-related emergencies in 1994 to more than 4,500 in2000. The majority of the visits are Ecstasy-induced malignanthyperthermia, the risk of which is increased whenEcstasy is combined with other drugs such as LSD (“candyflipping”), psychedelic mushrooms (“hippie flipping”),methamphetamine (“up Ecstasy”), heroin (“down Ecstasy”),and cocaine, Rohypnol, cough syrup, and antidepressants.destroys nerve fibers in the brain that release dopamine, aneurotransmitter involved in motor control and motivation. Itis thought that the ability of Ecstasy to destroy nerve fibers inthe brain is linked to its ability to reduce memory capabilityand alter moods and motor function in human Ecstasy users.Please see Publisher’s note at the end of this chapter.

40DESIGNER DRUGSFigure 3.3 This graph shows the annual numbers of new users ofEcstasy, LSD, and PCP from 1965–2000. Starting in the 1990s,Ecstasy use increased in an extraordinary fashion and surpassed eventhe highest levels of LSD and PCP used. During this same timeframe,the use of other hallucinogens stayed approximately the same.ECSTASY ADDICTIONEcstasy is mostly used as a recreational drug and is considerednot as addictive as drugs like cocaine, methamphetamine, orheroin. However, there is growing evidence that Ecstasy canindeed become addictive if taken repeatedly. Repeat Ecstasyusers often report that they develop tolerance to its effects andrequire higher doses to achieve the same high as previouslyexperienced. In addition, some heavy Ecstasy users reportintense cravings for the drug when they have not taken it for afew days. However, since Ecstasy is a relatively new drug and isoften abused in combination with other drugs like heroin andalcohol, specific treatment programs for Ecstasy addiction arenot well established.

Ecstasy41RAVESEcstasy and other designer drugs are often taken at “raves,”which are all-night dance parties held in warehouses or otherlarge buildings. Raves feature loud dance music, lights, lasers,and other visual effects. Although they are often promoted asbeing alcohol and drug free, they are frequently a haven forillegal drug use. Raves came to the United States from GreatBritain in the late 1980s and have become extremely popularin major metropolitan areas in the United States. Often soldat raves are overpriced water bottles and sports drinks (tocombat the dehydration brought on by Ecstasy and otherstimulants), pacifiers (to prevent teeth clenching by Ecstasyusers), and glow sticks and menthol nasal sprays to enhancethe effects of Ecstasy.As mentioned earlier, Ecstasy can cause muscle stiffnessand rigidity, so raves often have massage rooms. Many ravesalso have misting rooms with fans, where rave-goers can cooloff from the hyperthermic effects of Ecstasy. Given that raveshave these special rooms designed for Ecstasy users, it is notsurprising that as many as 90% of all rave-goers have reportedtrying Ecstasy.Publisher’s Note:Recently, one of the central studies showing evidence that Ecstasycan damage brain cells was retracted because methamphetamine,not Ecstasy, was mistakenly used in the study’s trial experiments.Nevertheless, there is still significant evidence that shows theharmful effects of Ecstasy. These deleterious effects includedamage to serotonin neurons, problems forming new memories,depression, and heatstroke. More studies must be conducted toprovide irrefutable evidence about Ecstasy’s specific effects on thebrain, however.

4GHBCOMMON STREET NAMESG, Gamma-G, Georgia Home Boy, Grievous Bodily Harm, Salty Water,Scoop, Soap, Goop, Liquid X/Ecstasy (not to be confused with thereal Ecstasy—see Chapter 3).HISTORY AND LEGAL STATUSGHB, short for its chemical name gamma hydroxybutyrate, is apotent sedative and a depressant of the central nervous system. GHBwas first synthesized in the 1920s, although it was not specificallydesigned to mimic another existing drug. In the 1960s, GHB wasdeveloped for possible use as an anesthetic. However, the makers ofGHB later withdrew it from consideration for approval by the U.S.FDA because of severe side effects reported by patients.Despite these early warning signs of the potential dangers ofGHB, several nutritional supplement companies started promotingGHB in the 1980s as a way for bodybuilders to stimulate theproduction of growth hormones, enhance muscle mass, and reducebody fat. However, scientific studies have yet to prove that GHBcan indeed increase muscle mass or assist in weight loss. GHB couldeasily be found in bulk quantities in many health food stores duringthis time and was also promoted as a way to ease anxiety anddepression because of its potent sedative properties.However, many reports of severe side effects and overdosesbecame evident, and in 1990, the FDA declared GHB to be unsafe forover-the-counter use and restricted its use to physician-supervisedadministration. Because of the FDA ban on GHB, street chemists42

and underground laboratories began to synthesize GHBillegally to fill the continued demand for the drug. GHB useas an anesthetic still remains legal in many European countries,despite being banned in the United States.By the mid-to-late 1990s GHB had made its way into theclub, dance, and rave scene. Many adolescents found that GHBgave them a pleasurable “high” and enhanced sexual experiences.However, reports of GHB overdoses and use as a daterape drug, particularly when used in combination with alcohol,prompted the FDA in 1997 to reissue a warning againstGHB use. Recipes and kits for making the drug began to appearon the Internet around this time.In 2000, the FDA classified GHB as a Schedule I controlledsubstance. Punishment for possession, sale, or use of GHB becameas severe as for other Schedule I drugs, including up to 20 yearsin prison. However, GHB was also subclassified as a ScheduleIII controlled substance, allowing for its medical use inpatients with narcolepsy (see box on page 50).WHAT GHB LOOKS LIKE AND HOW IT IS TAKENRaw GHB comes in the form of a fine white or light sandy-coloredpowder. This powder is rarely pure GHB—often the drug powdercontains residues of the ingredients that are used to make it. Theseingredients (GBL and BD—see discussion on page 47) are alsocommonly found in engine degreasers and floor strippers, andingestion of these substances is extremely toxic to the human body.Thus, since the drug is made illegally in underground laboratories,there is no quality control, and any batch of GHB has the potentialto contain one or more of these extremely toxic chemicals.GHB powder easily dissolves in water or alcohol, and GHBis usually in this liquid form when it is distributed to the user.A standard “dose” of GHB costs anywhere from $5–$25.The liquid has a salty taste, much like baking soda, thus itsnickname “salty water.” The presence of chemicals otherthan GHB itself causes the taste to become very bitter and43

44DESIGNER DRUGSchemical-like. Some users tend to drink GHB by the capful,while others prefer to mix it into alcoholic beverages or otherdrinks to hide its salty taste. Since the liquid has no color orodor, it is easy to conceal in plastic water or sports drinkbottles, or even mouthwash bottles or eye droppers.PSYCHOLOGICAL AND PHYSICAL EFFECTS OF GHBThe effects of GHB usually start to take place 15–30 minutesfollowing ingestion and can last for 3–6 hours. A typical doseof GHB can range from 1–5 grams. However, since theconcentration of actual GHB in the mixture varies from batchto batch and vial to vial, it is extremely difficult for the userto know the precise dose he or she is taking. Thus, thedifference between getting high and ending up in a coma canbe only a few drops.GHB has effects on the brain that are very similar to thatof alcohol. In fact, many people take GHB to achieve its alcohollikeeffects with less risk of a hangover. A low dose of GHB(less than a gram) causes the user to feel very similar to having1–3 drinks—loss of inhibitions, feeling less anxious, andbecoming more energetic, sociable, and talkative. Users may alsoexperience mild muscle relaxation after a low dose of GHB.A more moderate dose of GHB (1–2 grams) causes overallfeelings of relaxation, well-being, and euphoria. Users alsoreport an increased appreciation for music or dancing, as wellas increased sexual drive and enhanced sexual experiences. Maleusers often report that GHB enhances their erectile capacity andintensifies orgasms. The user may also start to feel a slight lossof both balance and motor skills. Physiologically, this dose ofGHB slows the user’s heart rate and lowers his or her bloodpressure and respiration.Stronger doses of GHB (2 grams or more) start to producesigns of an overdose—such as slurred speech, severe motorimpairment, and an overwhelming urge to sleep. In fact, thesleepiness produced by GHB can be so strong that it produces

GHB45a coma-like state for which paramedics are needed to resuscitatethe victim. Other effects of high doses of GHB include visualhallucinations, delusions, out-of-body experiences, vertigo (dizziness),disorientation, depression, and amnesia. Respiration isseverely decreased at these higher doses, with reports of breathingrates as low as 6–10 breaths per minute. High doses of GHB canalso cause one to lose control of the bladder or bowels. Othereffects that are experienced at high doses include nausea andvomiting, seizures, respiratory arrest, coma, and even death, especiallywhen GHB is mixed with other drugs like methamphetamine.All of these effects can have a quick onset, and unlike drinkingalcoholic beverages, once the user starts to feel these effects, he orshe is unable to “slow down” to avoid any further complications.The effects of GHB are strongly enhanced, and muchmore dangerous, when it is used in combination with alcohol.Thus, the likelihood of the user experiencing one of GHB’smore severe effects (such as seizure, coma, or death) is greatlyincreased when it is combined with alcohol. In fact, morethan 80% of all GHB-related deaths involve the combineduse of GHB and alcohol. GHB overdoses can also result from“boosting” (taking another dose before the effects of the firstdose wear off). Since 1990, the Drug Enforcement Agencyhas documented more than 70 deaths that were related toGHB overdoses.As mentioned earlier, raw GHB powder is often mixed withother chemicals, including those found in engine degreasers andfloor strippers. With repeated GHB use, these chemicals canerode the lining of the user’s mouth and esophagus.HOW GHB WORKS IN THE BRAINSurprisingly, GHB is naturally present in most cells of thehuman body at very low concentrations. Although the functionof the body’s own GHB is not clear, scientists believe it maybe involved with cellular metabolism. GHB is also found in thebrain and is believed to act as a neurotransmitter. It is believed

46DESIGNER DRUGSthat taking GHB drastically increases the messages carriedby the brain’s own GHB. GHB may also interact with a wellknownchemical messenger in the brain called GABA (gammaamino butyric acid).Table 4.1 lists the brain regions where GHB is believed toproduce its effects.Table 4.1 GHB’s Effect on the BrainEFFECTDrowsiness and sleepEuphoria, positive feelings,reduced inhibitionsHallucinations, increasedsexual driveLoss of balance, motorimpairmentReduced respirationAmnesiaBRAIN REGION(S)Frontal cortex, brainstem,hypothalamusFrontal cortex, limbicsystemVisual cortex, limbicsystemCerebellumBrainstemHippocampus(limbic system)GHB may also act directly on muscles to produce relaxationand decreased heart rate.GHB AS A DATE RAPE DRUGAlthough the most well-known date rape drug is Rohypnol(see Chapter 5), the effects of GHB have also been exploitedand used to commit sexual assault. In fact, the number ofGHB-related sexual assaults in recent years has paralleled oreven surpassed those involving Rohypnol. The number ofGHB-related sexual assaults may be vastly underestimatedbecause GHB is metabolized rapidly by the body and is oftennot detectable in blood or urine when the victim reports the

GHB47assault to the police. In addition, the victim is often not evenaware that the drug was ingested.GHB, GBL, and BD (GHB analogues) are used as daterape drugs for the following reasons:• They are colorless and odorless in liquid, and can easilybe added to a person’s drink without his or her knowledge.Although the drugs have a slightly salty taste, onceblended with an alcoholic drink, the taste becomesextremely difficult to detect.• They have effects that are greatly enhanced when mixedwith alcohol, making the victim vulnerable to sexualassault even after one drink.• They increase sexual drive and reduce inhibitions.•They cause impaired judgment and decision-makingabout sexual activity.• They can cause the user to “pass out,” making him or herunable to consent to or ward off sexual advances.• They produce amnesia, so the victim may not even recallthat a sexual assault has taken place and may not immediatelygo to the police.GHB ANALOGUESAfter GHB was banned by the FDA in 1990 for over-thecounteruse, GHB chemists tried to circumvent the ban bydeveloping closely related chemicals called gamma butyrolactone(GBL) and 1,4-butanediol (BD). The chemical structures ofGHB, GBL, and BD are shown in Figure 4.1. When GBL or BDis ingested, it is rapidly converted by the body to form GHB,and the effects become identical to that of taking regular GHB.Due to the 1990 FDA ban, manufacturers of nutritionalsupplements previously selling GHB quickly reformulatedtheir product so it contained GBL and/or BD instead of the

48DESIGNER DRUGSFigure 4.1 This diagram shows the chemical structure of GHBand its analogues BD and GBL. Notice the strong similarity betweenGHB and BD. Once ingested, both BD and GBL are rapidly convertedto GHB by the body.now illegal GHB. Such products were given names likeLongevity, Renewtrient, Revitalize, and Blue Nitro. However,GBL and BD are no less dangerous than GHB itself. The FDAhas issued warnings against the potential health hazards ofand addiction to GBL and BD, and GBL is now considered aSchedule I controlled substance (BD is yet to be classified).GBL is an active ingredient in liquid paint strippers, polishes,and engine degreasers, while BD can also be found in variousplastics, including floor coverings.GHB OVERDOSES INSPIRE A FEDERAL LAWUp until 2000, most laws regarding GHB and its analogueswere primarily up to the legislature of each individual state. As

GHB49a consequence, enforcement of laws regarding GHB was difficult.However, on February 18, 2000, President Bill Clintonsigned a new federal bill into law regarding the use of GHB.The bill, HR 2130, was inspired by the lobbying effortsof the families of two teenagers, Hillory J. Farias andSamantha Reid, who both overdosed on GHB in the late1990s. The bill became known as the Hillory J. Fariasand Samantha Reid Date Rape Drug Prohibition Act of2000. The law made GHB and GBL Schedule I controlledsubstances, which are the most restricted controlled substancesunder DEA jurisdiction. This classification nowmakes it a crime to possess, manufacture, or sell GHB orits analogues, with up to 20 years in prison for violatingthe law. The bill also mandates nationwide educationalprograms for students, teachers, nurses, sexual assaultcounselors, and emergency room staff on the dangers ofdate rape drugs (including GHB), symptoms of overdose,and penalties for their use.Below are excerpts from Websites devoted to the memoryof Hillory J. Farias and Samantha Reid:Hillory J. Farias. 1978–1996. “Hillory J. Farias was17 years old when someone slipped the deadly drugGHB into her soda. Also Hillory never drank, neverparticipated in any drug use. She was very wellrespected by all of her classmates. She was going to bea senior in high school, she didn’t attend her prom,never had a date. Hillory was cheated from having ahappy and productive life. Hillory was the last personanyone would hurt. But it happened, and if it canhappen to her, it could happen to you. Girls are notthe only victims, men as well have been victimized,so please be careful. Remember a large percentageof victims know the person who drugged them.”(fariasfamily.homestead.com/Hillory.html)

50DESIGNER DRUGSSamantha Reid. 1984–1999. “Samantha left for themovies on Jan. 16, 1999, with two of her girlfriendsand two male friends from high school. GHB and/orGBL was slipped into her Mountain Dew soft drinkthat night. Samantha was taken to the hospital withno vital signs and died after 18 hours on life support.The boys from high school are now serving 5 1/2 to15 years in prison for the manslaughter death ofSamantha.” (www.ghbkills.com)ARE THERE MEDICAL USES FOR GHB?One of the ironic things about many abused drugs is that theyoften have a medicinal value and can actually be used to treatvarious diseases and disorders, given the proper medicalsupervision. However, the risks of abuse and overdose makethem poor treatment options.One peculiar effect of GHB is that it seems to reducethe symptoms of narcolepsy, a relatively rare sleep disorder.People with narcolepsy are excessively sleepy all the timeand often have a condition called cataplexy, in which theperson can suddenly and unexpectedly lose all muscletone and fall immediately into rapid eye movement (REM)sleep (the stage of sleep during which dreaming occurs).Thus, a person with narcolepsy can immediately go frombeing awake right into REM sleep. (Normally, it takes atleast 60 minutes to enter into REM after falling asleep.)These rapid transitions from waking to REM sleep canresult in frightening hallucinations. Interestingly, boutsof cataplexy are usually brought on by laughter or strongemotional experiences.In clinical studies, GHB has been shown to effectivelyreduce the symptoms of narcolepsy. These findings are quite

GHB51STATISTICS AND PATTERNS OF GHB USE AND ABUSEGHB is currently extremely popular in the dance club andrave scene. It is also popular among the gay community aswell as with exotic dancers and strippers. It is primarily used forits ability to produce euphoria, intoxication, and enhancedsexual feelings. Others use it as a sleep aid or to enhancebodybuilding. Still others use it intentionally as a daterape drug. Abusers of other drugs, such as cocaine ormethamphetamine, often take GHB to reduce the withdrawalironic and paradoxical, given that GHB itself can cause excessivesleepiness and loss of muscle tone similar to that observedin narcoleptic patients. Scientists speculate that the sleepinducingeffects of GHB may counteract the abnormal sleeptendency seen in narcolepsy that contributes to the disease.This is similar to the paradoxical way in which the stimulantRitalin is used to treat hyperactivity disorders in children.Scientists are currently investigating how the body’s own GHBsystems may contribute to the development of narcolepsy,and they are exploring possible GHB-like medications thatcan be used to treat the disorder without all the dangerousside effects. Because there are so few effective medicationsto treat narcolepsy, in July 2002, the FDA approved the useof GHB under the trade name Xyrem® for the treatment ofthe disease.GHB has also been reported to have other medical benefits,such as a sleep aid for people suffering from temporaryinsomnia and for treating alcohol withdrawal and alcoholism.However, the risks and dangers of taking GHB, especially incombination with alcohol, have prohibited the FDA fromapproving its use for conditions other than narcolepsy.

52DESIGNER DRUGSsymptoms that occur after the effects of these stimulantswear off.Regardless of the purpose, GHB is primarily taken byteenagers and young adults ages 18–25. A recent surveyfound that in 2001, approximately 1% of eighth grade studentshad tried GHB in the past year, whereas 1.6% of highschool seniors had tried the drug. On college campuses, theuse of GHB is even more prevalent, with as many as 20%of all college students having tried GHB or knowingsomeone who has.To determine the prevalence of GHB-related overdoses,the Drug Abuse Warning Network (DAWN) recently surveyedreports from emergency rooms across the United States formentions of GHB. As seen in Figure 4.2, the number of timesGHB has been mentioned in emergency room visit reports hasskyrocketed in the past decade, with around 55 in 1994 tomore than 4,000 in 2000. Of GHB-related emergencies, mostvictims appear to be middle-class, male Caucasians. Morethan 75% of all GHB-related emergency room visits have alsoinvolved the use of alcohol, showing how dangerous the combinationof the two drugs can be. GHB-related emergencyroom visits that involve the co-use of cocaine, Ecstasy, andmarijuana occur less frequently than with alcohol.GHB ADDICTIONAlthough GHB is primarily used for recreational purposes,cases of addiction to GHB have been reported. Some GHBusers go on binges during which they take GHB around theclock (every 2–4 hours) for a few days. As the user takesadditional doses, he or she develops tolerance to the effectsof the drug (GHB becomes less effective with subsequentdoses, so the user takes even more). Eventually, the bingeGHB user exhibits signs of withdrawal, such as anxiety,insomnia, delirium and hallucinations, muscle crampingand tremors, and tachycardia (abnormally fast heart rate).

GHB53Figure 4.2 The number of emergency room cases resulting fromGHB use has increased significantly since the early 1990s. Ascan be seen on this graph, the number of emergency room reportsmore than doubled in the course of two years (1998 and 2000).Although fewer cases were reported in 2001 than 2000, GHB useis still a problem.* The estimate for this year was significantly different (p

5RohypnolCOMMON STREET NAMESRoofies, Rophies, Ruffies, Roche, Roach, Rope, Ropies, Rib, Circles,Mexican Valium, R-2, Date Rape Pill, Forget-Me Pill.HISTORY AND LEGAL STATUSRohypnol is the trade name for flunitrazepam (pronounced “floonigh-trays-eh-pam”),a drug that belongs to a class of drugs calledbenzodiazepines (pronounced “ben-zoh-di-ayz-eh-peens”). Other wellknownbenzodiazepines include Valium and Xanax. Benzodiazepinesare primarily prescribed by doctors to treat anxiety, panic attacks,and insomnia.Rohypnol was first manufactured and patented by the pharmaceuticalcompany Hoffman-La Roche in 1963 as a way to treat insomniaand anxiety. Rohypnol was intended to be an analogue of Valiumand other benzodiazepine drugs. In 1984, Rohypnol becameclassified as a Schedule IV controlled substance by the DEA. However,due to increasing reports of Rohypnol abuse and misuse, it wasreclassified as a Schedule III drug in 1995, requiring morethorough record keeping by manufacturers, pharmacies, anddoctors. Further increases in illegal use of the drug in the UnitedStates during the late 1990s has prompted the DEA to considerclassifying it as a Schedule I controlled substance throughout theUnited States, although to date only several states have actuallydone so. Despite heavy restrictions on its use in the United States,Rohypnol is still sold legally by prescription for the treatment ofinsomnia and as a sedative prior to surgery in many Latin American54

and European countries. Rohypnol is difficult to synthesizeand is not made in underground “clandestine” laboratories.In the 1990s, Rohypnol became known as the “date rapedrug” because of its ability to physically and mentally incapacitatethe user, allowing sexual advances to proceed virtuallyunimpeded. Extensive use of Rohypnol in sexual assaultsand “date rapes” led Congress to pass the Drug-Induced RapePrevention and Punishment Act of 1996. This law increasedprison time for persons convicted of using Rohypnol (or othercontrolled substances) to commit a violent crime such asrape. Importation and distribution of one or more grams ofRohypnol became punishable by up to 20 years in prison,whereas possession of smaller amounts of the drug becamepunishable by up to 3 years in prison and a fine.WHAT ROHYPNOL LOOKS LIKEAND HOW IT IS TAKENRohypnol was originally manufactured in the form of a smallround white pill, each a little over a centimeter in diameter(see Figure 5.1), with the word Roche stamped on it. Each pillcontained 1–2 milligrams of the drug. On the street, thesepills cost anywhere from $2–$10 each. While many illicitusers of Rohypnol chose to take the pill orally, some groundthe pills into a fine white powder so it could be snorted ormixed into a drink.In response to the alarming increases in reported daterapes that used Rohypnol to incapacitate the victim, Rohypnolmanufacturer Hoffman-La Roche decided to change the shapeand color of the pill in the late 1990s. Rohypnol was changed toa green oval tablet with the number “542” stamped on it. However,the manufacturers also added something else—a dye.According to Hoffman-La Roche, if the newer Rohypnol pillswere crushed into a powder and slipped into someone’s drink,the dye would turn the drink blue or green, alerting the potentialvictim that his or her drink had been tampered with (unless, of55

56DESIGNER DRUGSFigure 5.1 Rohypnol tablets are very small (just over a centimeterin diameter) due to their strong potency. This photo is of the olderwhite Rohypnol tablets. Newer Rohypnol tablets are green andoval shaped.course, he or she is drinking a blue or green drink). Hoffman-LaRoche also reduced the dosage of Rohypnol from 1–2 milligramsdown to one milligram or less. However, many of the older whitepills are still available on the street.PSYCHOLOGICAL AND PHYSICALEFFECTS OF ROHYPNOLUnlike many other designer drugs, which users take for theirpleasurable and psychedelic effects, Rohypnol does not tend toproduce strong feelings of well-being, euphoria, or hallucinations.It does, however, produce an intoxicated feeling, andreduces anxiety and inhibitions, similar to the effects of Valium.The chemical structures of Rohypnol and Valium arevery similar (see Figure 5.2), although Rohypnol is 10 timesmore potent than Valium.

Rohypnol57Figure 5.2 The chemical structures of Rohypnol andValium are shown here. The chemical structure of Rohypnolis quite similar to that of Valium, but Rohypnol is 10 timesmore potent.The effects of Rohypnol are felt approximately 15–20 minutesafter taking the drug and can last up to eight hours. The userwill feel drowsy, dizzy, and confused, and may experienceextreme sleepiness. Many times the user will become physicallyand mentally incapacitated, unable to think or move. Despitethe strong depressant effects of Rohypnol, some users mayinitially feel agitated or aggressive. Users often experience“anterograde amnesia,” meaning that he or she will be unable

58DESIGNER DRUGSto remember many events that occurred while being under theinfluence of the drug. Some Rohypnol users take the drugbecause it lessens the “crash” or depression that follows thehigh of a stimulant like cocaine or amphetamine.Physical effects of Rohypnol include gastrointestinaldisturbances (an upset stomach), slurred speech, decreasedblood pressure, muscle relaxation, motor incoordination, andurinary retention (inability to urinate).All of the psychological and physical effects of Rohypnol aredramatically increased when the drug is taken in combinationwith alcohol. In some instances, the combination can be lethal.HOW ROHYPNOL WORKS IN THE BRAINRohypnol, like all benzodiazepines, produces its effect bydepressing the activity of nerve cells in the brain. It does so byinteracting with a protein called the GABA-A receptor. GABAis the main chemical messenger in the brain that causes nervecells to become less active. Rohypnol binds to the same proteinas GABA (the GABA-A receptor) and increases the ability ofGABA to reduce neuronal activity. Other drugs that also act onthe GABA-A receptor include alcohol and barbiturates.Rohypnol is believed to produce its effects by acting onnumerous brain regions, as described in Table 5.1.Table 5.1 Rohypnol’s Effect on the BrainEFFECTDrowsiness, confusion,dizziness, and sleepMotor impairmentSlurred speechAmnesiaBRAIN REGION(S)Frontal cortex, brainstem,hypothalamusCerebellumFrontal cortex, brainstemHippocampus(limbic system)

Rohypnol59Rohypnol can also act directly on other parts of the body(such as the stomach, intestines, bladder, arteries) to producegastrointestinal disturbances, reduced blood pressure, andurinary retention.ROHYPNOL—THE ORIGINAL DATE RAPE DRUGAlthough other club drugs (such as GHB and ketamine) canbe used to help commit sexual assault, Rohypnol is consideredthe original “date rape” drug because it was the first to be usedspecifically for that purpose. Sexual predators could easily slipthe older white tasteless Rohypnol powder into a victim’sdrink unnoticed, and in less than an hour, the victim wouldbecome virtually unconscious and mentally paralyzed so theattacker could commit rape without much resistance. Often,the rape victims cannot remember the incident because of theprofound amnesia caused by Rohypnol, especially when combinedwith alcohol. The extensive use of Rohypnol in sexualassaults and date rapes in the 1990s prompted Congress topass the Drug-Induced Rape Prevention and Punishment Actof 1996, which severely increased punishment for use ofRohypnol for the purposes of committing sexual assault. Thislaw also prompted Hoffman-La Roche to add a dye to the pill toallow it to be seen after being dissolved in a drink.STATISTICS AND PATTERNS OFROHYPNOL USE AND ABUSERohypnol is mainly used by teenagers and young adults atdance clubs, parties, and raves. A survey conducted in 2001showed that 1.1% of eighth graders had used Rohypnol at leastonce, while 1.7% of high school seniors had used the drug.But, unlike other designer drugs, the majority of users appearto be Hispanic as opposed to Caucasian. This is not surprising,given that Rohypnol is easily obtained from Mexico. SinceRohypnol can reduce the “crash” that follows the high of

60DESIGNER DRUGSdrugs like cocaine or heroin, it is also used by cocaine andheroin addicts.There are two common myths that are believed to increasethe usage of Rohypnol among young people: (1) it is a pharmaceuticalpill sold in sealed bubble packaging, so it is safe and freeof contaminants, and (2) it cannot be detected in urine samples.ILLEGAL SALE OF ROHYPNOLRohypnol is illegal in the United States. So, how does it get inthe country? The answer is smugglers. Since the pills are verysmall, Rohypnol tablets can easily be smuggled through the mail,in luggage, or on airplanes. Rohypnol is also easily availablefrom pharmacies in Mexico, and smugglers often hide the drug incars as they cross the border from Mexico to the United States.The year 1995 produced the largest number of Rohypnolseizures by the DEA thus far, with more than 160,000 illegalpills confiscated. In one instance, over 52,000 Rohypnol pills,concealed in plastic bags located inside a car door, wereseized by the Louisiana State Police. Also in 1995, the U.S.Border Patrol seized over 57,000 Rohypnol tablets (along with53 pounds of marijuana) en route from Mexico to Florida.Seizures of Rohypnol in the United States have declinedover subsequent years, with just under 5,000 pills beingseized by the DEA in 2000. In May 2000, DEA agents seizedapproximately 900 pills of Rohypnol that were hidden in acar crossing the border from Mexico into Texas. A few monthslater, a Tijuana, Mexico, pharmacy operator was arrested bythe DEA for illegally shipping Rohypnol pills from a Mexicanpharmacy to nearby San Ysidro—a town minutes north ofTijuana in southern California.In 2001–2002, however, business began to pick up again,and during this time the DEA seized several overnight deliverypackages originating from Colombia that contained up to11,000 Rohypnol pills each.

Rohypnol61Both of these are false—Rohypnol pills are often crushed bydealers into a powder, and this powder may contain many contaminantsincorporated by drug dealers. In addition, advancesin medical technology can now detect Rohypnol metabolites inbodily fluids for 2–3 days after taking the drug.Rohypnol is especially dangerous and potentially lethalwhen used in combination with other drugs such as alcohol. In1994, the number of emergency room reports that mentionedRohypnol was only 13, but this number grew to over 500 bythe late 1990s; many of these instances also involved the useof alcohol.Because Rohypnol is banned in the United States, thereis an emerging trend for young people to start abusing twoother Rohypnol-like drugs that are still legal in the UnitedStates: clonazepam (Klonopin®) and alprazolam (Xanax). BothKlonopin and Xanax are benzodiazepines that are used forthe treatment of anxiety and insomnia. Although they areless potent than Rohypnol, they can produce similar effectswhen mixed with alcohol and also have been reported toenhance the effects of heroin.ROHYPNOL ADDICTIONAlthough many benzodiazepine drugs such as Valium or Xanaxare successfully used for treating problems like anxiety andinsomnia, repeated use of these drugs can produce psychologicaland physical dependence. Rohypnol is no exception. Peoplewho take Rohypnol repeatedly can become addicted and mayexperience seizures, headaches, anxiety, irritability, delirium andhallucinations, and insomnia when they stop taking the drug.These symptoms may last up to one week after stopping chronicuse of Rohypnol. The most common treatment for Rohypnoladdiction is medically supervised “tapering off,” during whichtime the user continues to take the drug, but in decreasingdoses over a period of many weeks to reduce the severity ofwithdrawal symptoms.

6KetamineCOMMON STREET NAMESK, Special K, Vitamin K, Lady K, Super K, Kat, Kit Kat, Cat Valium,Bump, Jet, Ket, Ketalar, Ketaject, Psychedelic Heroin, Super acid,Super C, Green, Purple, Kelly’s Day, Honey Oil, Blind Squid.HISTORY AND LEGAL STATUSKetamine was first synthesized in the 1960s by the Parke-Davispharmaceutical company, where scientists were developinganalogues of phencyclidine (PCP) for use as general anesthetics forsurgery. Like PCP, ketamine proved to be a potent anesthetic, andParke-Davis patented it for use in both humans and animals in 1966.Around that same time it was first reported that ketamine had profoundpsychedelic effects and was named a “dissociative” anesthetic. By thelate 1960s, ketamine became available by prescription under thetrade name Ketalar®, and was also being used as a field anesthetic bythe United States during the Vietnam War. Ketamine’s anestheticproperties were also used widely in veterinary clinics, pediatric burncases, and for some dental surgery.Throughout the 1970s, 1980s, and 1990s the recreationaluse of ketamine became popular in many parts of the world,primarily because of its psychedelic effects. Some psychologistseven used ketamine as an aid in psychotherapy since itgave people “insightful thinking.” In the late 1990s, ketaminebecame popular with teenagers and young adults at “raves,”parties, and dance clubs.In 1995, the DEA added ketamine to its “emerging drugs”62

list, signifying that further restrictions on its use mightbe needed. Indeed, in 1999 ketamine was classified by theDEA and FDA as a Schedule III controlled substance,making it illegal to possess without a prescription orveterinary license.WHAT KETAMINE LOOKS LIKEAND HOW IT IS TAKENKetamine is most commonly sold to pharmacies and veterinaryclinics in a clear liquid form (Figure 6.1). Illegal users ofketamine inject the drug intravenously or intramuscularly,mix it into a drink, or dip tobacco or marijuana cigarettesinto the liquid prior to smoking them. Ketamine liquid iscolorless, odorless, and tasteless. This liquid can be easilyconverted to a white powder by allowing the liquid to evaporateand then collecting the powder residue. This powder canalso be mixed into drinks, snorted, or smoked. A typical doseof ketamine costs $20–$25 on the street.Ketamine dealers have been known to obtain the drugby breaking into veterinary clinics or pharmacies and stealingtheir supply of the drug. Dealers also get ketamine by divertingshipments of the drug from pharmacies and veterinary clinicsin Mexico.PSYCHOLOGICAL AND PHYSICALEFFECTS OF KETAMINEThe chemical structure of ketamine is similar to that of thepotent psychedelic PCP (Figure 6.2). Not surprisingly, ketamineproduces many psychedelic effects that are similar tothose produced by PCP. However, ketamine’s effects aremuch shorter in duration—a “trip” on ketamine may lastonly 30–60 minutes, whereas a trip on PCP may last severalhours. The onset of ketamine’s actions is quite rapid (i.e.,within minutes), especially if snorted or injected intravenously.63

64DESIGNER DRUGSFigure 6.1 Ketamine was originally used in both humans andanimals as an anesthetic during surgery. Vials containing theliquid form of ketamine, like the ones pictured here, are stillwidely used for veterinary purposes.Lower doses of ketamine (25 –100 milligrams) produce anexperience that many users call “K-Land,” which has beendescribed as a dreamy, relaxed state where the perceptionof colors and music is enhanced, and mild and pleasurablehallucinations are present. Hallucinations tend to be visualin nature, such as walls and carpets glowing different colors,ceilings turning to liquid, distorted body parts or shapes, andmany other illusions. Other hallucinations may include feelingsof floating or flying in space, being made out of rubber or wood,spinning and rotating rooms, melting into other people orthings, or insight into the meaning of life. Lower doses ofketamine also produce mild amnesia, symptoms of dizziness,and altered perception of sound, taste, and smell.

Ketamine65Figure 6.2 The chemical structure of ketamine (top) is relatedto the psychedelic PCP (bottom). Both chemicals produce stronghallucinations and psychedelic effects. However, while the effectsof ketamine may only last an hour, the effects of PCP can lastseveral hours after the drug is taken.Higher doses of ketamine (more than 100 milligrams)produce more profound psychological effects, sometimesknown as the “K-Hole.” Here, users often experience “outof-body”or “near-death” experiences, where they feel like

66DESIGNER DRUGSthey are floating high above and looking down on theirown body, or traveling through a dark tunnel toward abright light. They may also lose their sense of time—thepassage of time may appear to be slowed or even stopped. Itis for these reasons that ketamine is known as a “dissociative”drug—the user feels “disassociated” and detachedfrom his or her own body and consciousness. These dissociativeexperiences can also be quite frightening and resultin a “bad trip,” similar to that experienced by some LSDusers. Higher doses of ketamine can also produce profoundmemory loss, feelings of depression, confusion, delirium,and paranoia. Motor abilities may be severelyimpaired, and the user may feel as if he or she is unable tomove or talk. Occasionally, users of high doses of ketaminecan become violent when they feel an exaggerated senseof strength and invulnerability.Physical effects of high doses of ketamine includedecreased respiration and heart rate, increased blood pressure,and the possibility of vomiting and convulsions. These can leadto cardiac and respiratory arrest, coma, and death. The risk ofketamine overdose is much greater when it is mixed with otherdrugs such as alcohol, Ecstasy, caffeine, or cocaine. Overdosesof ketamine have been reported when people “boost” thedrug (take another dose before the first dose wears off) toprolong its psychedelic effects.Since ketamine is an anesthetic, most users report profoundfeelings of numbness. Ketamine users can easily burnthemselves on a stove or lamp while on the drug and not evenknow it.Ketamine is rapidly metabolized by the body, so the hallucinogeniceffects of ketamine wear off within an hour or soafter taking the drug. However, users say they often experiencerepeated “flashbacks,” or sudden memories of the visions or feelingsexperienced while on the drug. These flashbacks can persistfor days, weeks, months, or even a year after a particular trip.

Ketamine67HOW KETAMINE WORKS IN THE BRAINOne of the major neurotransmitters in the brain is an aminoacid called glutamate. When neurons secrete glutamate onto aneighboring nerve cell, that neighboring nerve cell becomesactivated and passes along the electrical signal to other regionsof the brain. Glutamate can activate several types of receptorson nerve cells, and one of the primary subtypes of glutamatereceptors is called the N-methyl-D-aspartate (NMDA) receptor.When NMDA receptors are inhibited or “blocked” by certaindrugs, nerve cells in the brain that use glutamate as a neurotransmittercannot communicate properly.Ketamine acts as a blocker (or “antagonist”) of the NMDAreceptor. PCP also acts as an antagonist of the NMDA receptor,as does alcohol, although much less potently. NMDA receptorsare present in numerous brain regions, and ketamine isthought to produce its effects by blocking NMDA receptors ina number of brain regions, as shown in Table 6.1.Table 6.1 Ketamine’s Effect on the BrainEFFECTDistorted thoughts, vision,and hearingDizzinessDifficulty moving, impairedcoordinationNumbnessAmnesiaAltered breathing,heart rateBRAIN REGION(S)Frontal cortex, visualcortexFrontal cortex, brainstemMotor cortex, basalganglia, cerebellumSpinal cord, sensorycortexHippocampus(limbic system)Brainstem

68DESIGNER DRUGSKETAMINE AS A DATE RAPE DRUGKetamine has a variety of properties and produces a numberof effects that make it an increasingly popular date rape drug.These properties and effects are as follows:• It is colorless, odorless, and tasteless, and can easily beslipped into someone’s drink without his or her noticing.• It often causes the user to feel as if he or she cannot move,making him or her unable to ward off unwanted sexualadvances.• It impairs the user’s senses and judgment for up to 24 hoursafter taking the drug, even though the initial trip wears offwithin an hour or so.• It produces amnesia, so the victim may not even recall thata sexual assault has taken place and may not immediatelygo to the police.STATISTICS AND PATTERNSOF KETAMINE USE AND ABUSEAs with other designer and club drugs, ketamine is primarilytaken by teenagers and young adults ages 18–25. A survey ofmiddle and high school students found that in 2001, approximately1.3% of eighth grade students had tried ketamine in thepast year, whereas 2.6% of high school seniors had tried the drug.Ketamine users tend to be predominantly male and Caucasian.Ketamine is often taken with other drugs, such as cocaine,marijuana, alcohol, and Ecstasy, which greatly increases the riskfor overdose. Ketamine tends to be taken by people with ahistory of experimenting with numerous other drugs. Ketamineis also occasionally taken by physicians and veterinarians, whohave easy access to the drug and want to experiment with itspsychedelic effects.

Ketamine69Figure 6.3 Although the number of emergency room mentions ofketamine use is not as high as the rates of methamphetamine andGHB use (see Figures 2.4 and 4.2), ketamine use has increasedsignificantly in the last ten years. The number of emergency roommentions of ketamine nearly doubled between 1999 and 2001.* The estimate for this year was significantly different (p

70DESIGNER DRUGSmost addictive substances, repeated use of ketamine canproduce tolerance, requiring the user to take more and more ofthe substance to achieve its desired effects. Also, chronic use ofketamine can lead to physical and/or psychological dependence,resulting in withdrawal symptoms once the user stops takingKETAMINE USE INTRANQUILIZER DARTSThe ability of ketamine to render the user unable to move orexperience pain has resulted in a very effective use for thedrug in animals—tranquilizer darts. Through a blowgun,rifle, or similar method, a dart or syringe loaded with a highdose of ketamine can be launched from a distance towarda large animal to incapacitate it for transport, research, orveterinary care. When the dart strikes the animal, it empties itscontent into the muscle (similar to an intramuscular injectionin humans), and within minutes the animal is knocked out.Ketamine darts have been used by zookeepers, wild animalresearchers, and veterinarians to tranquilize horses, bears,elephants, monkeys, tigers, lions, leopards, bobcats, mountainlions, large birds, poisonous snakes, and many other animals.Although ketamine causes the animal’s muscles to becomerigid, it retains its ability to breathe. Also, as in humans, thedrug is metabolized very rapidly, and the effects wear offwithin an hour.Obviously, we do not know what, if any, psychedelicexperiences an animal may have in response to a ketaminedart. (Perhaps they experience K-Land and K-Hole justlike humans.) Animals rarely become violent or agitatedafter being injected with ketamine, so it is unlikely toproduce the psychotic symptoms observed in somehuman users.

Ketamine71the drug. As with other designer and club drugs, specific treatmentprograms for ketamine addiction have not yet beendeveloped, although they might become needed if currenttrends of use and abuse continue.

7Painkiller AnaloguesWhile most people treat headaches and muscle aches by takingaspirin, Tylenol®, Motrin®, or other over-the-counter pain relievers,chronic and severe pain requires more potent painkillers. Some ofthe most potent pain relieving drugs that have been discoveredare “narcotic analgesics,” such as morphine, codeine, Vicodin®,OxyContin®, Demerol, Dilaudid®, and others. These drugs arewidely used for the treatment of severe pain and are also usedas anesthetics for surgical procedures and childbirth. As narcoticanalgesics were originally derived from the opium poppy(Figure 7.1), they are often referred to as “opiate” or “opioid”drugs. However, pharmaceutical companies can now synthesizenarcotic analgesics in chemical laboratories and are no longerdependent on using raw opium as the primary ingredient.Most, if not all, opiate drugs are highly addictive, and it isestimated that over 2 million Americans use prescription narcoticanalgesics for nonmedical (i.e., recreational) purposes. Thispercentage tends to be greater among women. The most commonaddictive opiate drug that is sold on the street is heroin, butpatients who use prescription narcotic analgesics for pain, aswell as the doctors who prescribe them, can also become addicted.In the late 1970s and early 1980s, two commonly prescribedopiate painkillers, fentanyl and meperidine, fell into the handsof underground drug chemists who tried to synthesize illegalanalogues. These fentanyl and meperidine analogues were amongthe first “designer drugs.”72

Figure 7.1 The opium poppy, shown here, is the source of suchdrugs as opium and heroin. Opium poppies are grown in variousregions of the world, including the Middle East, Southeast Asia,and Central and South America. To harvest the opium, growers“nick” the poppies with a knife and let the sappy, raw opium dripout. The opium is then scraped off the poppy and processed intoillegal opiate drugs like heroin.73

74DESIGNER DRUGSFENTANYL AND ITS ANALOGUESFentanyl was introduced to the United States in 1968 by theJanssen Pharmaceutical Company and marketed under thetrade name Sublimaze. Its primary purpose was for use as anintravenous anesthetic and analgesic. It is 100 times more potentthan morphine in reducing pain, and its duration of action is only30 minutes (compared to morphine, which lasts several hours).Over the years, fentanyl has proved to be an extremely usefuldrug, and to date, it is still widely used for surgeries, childbirth,pain associated with cancer and other diseases, and the treatmentof trauma-related injuries. Although fentanyl solutions are oftengiven intravenously, pill forms of the drug are also available.Due to the success of fentanyl, Janssen and other pharmaceuticalcompanies started to produce other legal fentanylanalogues with a wider range of potency and duration ofaction, including:• Alfentanil—also known as Alfenta®, it is very shortacting(5–15 minutes), 20–30 times more potent thanmorphine, and used for dental, diagnostic, and otherminor surgical procedures.• Sufentanil—also known as Sufenta®, it is extremelypotent (2,000–4,000 times more potent than morphine),and is used for heart surgery and childbirth.• Carfentanil—also known as Wildnil®, it is 10,000times more potent than morphine and is often usedby veterinarians and wild animal researchers toimmobilize large animals.• Lofentanil—another extremely potent fentanylderivative that is 6,000 times stronger than morphineand is very long-acting (i.e., hours), so it is used onlyfor prolonged surgical procedures and treatment ofmultiple trauma-related injuries.

Painkiller Analogues75In 1979–1980, some illegal fentanyl analogues appearedthat were being sold as substitutes for heroin on the street.Suddenly, a series of more than a dozen mysterious deathsoccurred in southern California. Upon autopsy, the victimsstrongly looked as if they had overdosed on heroin; however,no traces of heroin could be found in their bodies. Later,forensic chemists identified a fentanyl analogue (alphamethyl-fentanyl)that was present in all of the victims. As itturns out, alpha-methyl-fentanyl was being sold on thestreets under the name “China White” (Figure 7.2), becauseit resembled (and contained) pure synthetic heroin that wasproduced in Southeast Asia.Later in the 1980s, other fentanyl analogues started to befound in the tissues of heroin users and overdose victims. Onesuch analogue was 3-methyl-fentanyl (see Figure 7.3), which is6,000 times more potent than morphine. This drug was foundin the tissue of 16 overdose victims in Pennsylvania in 1988. Inall, more than 150 deaths have been attributed to overdoses ofillegal fentanyl analogues. It is likely that victims overdosebecause they think they are injecting heroin and are ignorantto the potency of the fentanyl analogues that they are actuallytaking. Alpha-methyl-fentanyl became classified as a ScheduleI controlled substance in 1982, and 3-methyl-fentanyl wassimilarly classified in 1985.Fentanyl analogues often come as a fine or coarse powderthat is either white or yellowish-white (when sold as “ChinaWhite”), tan (when sold as “Synthetic Heroin”), or light brown(when sold as “Mexican Brown”). Other names for fentanyl orits analogues include “Goodfella” and “Tango and Cash.” Drugdealers often cut (dilute) fentanyl analogues with largeamounts of powdered sugar so that the actual drug content isvery small (as low as 1%). When dealers “cook” the fentanylanalogues, the sugar content can become caramelized, giving ita brownish color. The drugs are mostly injected intravenouslybut can also be snorted or smoked.

76DESIGNER DRUGSFigure 7.2 China White powder, shown here, is a syntheticform of heroin that is very pure. China White that was taintedwith illegal fentanyl analogues, which are hundreds of timesmore potent than heroin, caused numerous overdoses in heroinaddicts in the late 1970s and early 1980s.Users of fentanyl analogues report that these drugs producea rapid “rush” or euphoria that is similar to that felt with heroin,followed by a sedated, dream-like state. As analgesics, they alsoproduce a profound loss of pain sensation and have commonunwanted side effects such as sleepiness and constipation.However, because they are so potent, fentanyl analogues can

Painkiller Analogues77Figure 7.3 The chemical structure of fentanyl and its illegalanalogues alpha-methyl-fentanyl and 3-methyl-fentanyl areshown here. Fentanyl was originally designed and marketedas an anesthetic, as it is 100 times stronger than morphine.It is still in use today as a pain reliever for certain surgeries,childbirth, and cancer.easily produce unexpected respiratory paralysis (stoppedbreathing) and subsequently death. Some law enforcementagents have reported that fentanyl analogue overdose victimsoften still have the needle in their arm when they are found,likely because the onset of death was so quick.Opiate painkillers act on a neurotransmitter receptor

78DESIGNER DRUGScalled the mu (like the Greek letter m, pronounced “mew”)opioid receptor. Mu opioid receptors are present on the surfaceof many neurons of the brain and spinal cord, and normallyserve as receptors for the body’s own painkillers such asendorphins. When a person takes fentanyl, meperidine,morphine, or other opiate drugs, the drug binds to the muopioid receptors, causing neurons in the spinal cord tobecome inactive. When pain signals from nerve endingsin the skin, muscle, or organs arrive at the spinal cord, thesesignals are not transmitted to the brain, and therefore pain isnot experienced. There are also high concentrations of muopioid receptors in regions of the brainstem that controlbreathing, so when a person takes an opiate drug, neuronsthat control breathing become less active and respiration isdecreased. Mu opioid receptors are also present in the frontalcortex and limbic system, where opiate drugs act to produceboth pleasurable and sedating effects. Finally, mu opioidreceptors are present in the intestines, where opiate drugs actto inhibit bowel movements and produce constipation.MEPERIDINE AND ITS ANALOGUESMeperidine (Figure 7.4) was introduced in the 1930s as analternative to morphine for relieving pain. Its advantage overmorphine was that its duration of action was shorter and it hadfewer unwanted side effects such as sedation and constipation.However, meperidine turned out to be less potent thanmorphine as a painkiller. This inspired underground chemists totry to synthesize more potent analogues of meperidine, with hopesthat increasing the potency might give heroin addicts another wayto get high. One such analogue was developed in 1977 by a collegestudent in Bethesda, Maryland, who also had a drug habit.(Ironically, he started making meperidine analogues with a homechemistry kit that his parents gave him.) The analogue he synthesizedwas 1-methyl-4-phenyl-propionoxypiperidine, or MPPPfor short. MPPP was sometimes referred to as New Heroin.

Painkiller Analogues79Figure 7.4 The chemical structure of meperidine, its analogueMPPP, and the closely related neurotoxin MPTP, are all shownhere. Meperidine, an anesthetic, was also used as an alternativeto morphine. It proved advantageous because it has a shorterlength of duration and fewer side effects than morphine.This college student was able to successfully make MPPPfrom meperidine for months for his own use. However, oneday while cooking up some MPPP, he was in a hurry andskipped a step or two in the synthesis process. Later, when hedecided to inject himself with this latest batch of MPPP, heimmediately knew something was wrong when his whole armbegan to burn. Within a few days, his arms and legs becamecompletely paralyzed, and he was unable to move or speak. His

80DESIGNER DRUGSparents took him to several psychiatrists and neurologists whoeventually diagnosed him with Parkinson’s disease, a diseasethat primarily occurs in people over 65 years old and is largelyincurable. The college student’s life was forever changed.Unaware of it at the time, the college student’s “sloppychemistry” had, in addition to synthesizing MPPP, inadvertentlycreated some additional by-products that were very toxic. Itturns out that one of the by-products, called 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP), is very toxic to neurons inPARKINSON’S DISEASE—NATURAL AND EXPERIMENTALParkinson’s disease is a devastating brain disorder that occursin approximately one out of every 100 people. The disease ismarked by extreme muscle stiffness, slowness or inability towalk, difficulty initiating movements of the arms and legs,and occasionally tremors. Although the disease usually strikeselderly people over the age of 65, it can also occur in youngerpeople. Notable celebrities that have this “early onset” formof Parkinson’s disease include boxer Muhammad Ali (who wasin his early 40s when diagnosed) and actor Michael J. Fox(who was actually 30 when he was originally diagnosed, butdid not go public about the disease for another seven years).The cause of Parkinson’s disease is still unknown. However,researchers have pinpointed the brain regions and neurotransmittersinvolved in the disease. For some reason, neuronscontaining the neurotransmitter dopamine that are locatedin a brain region called the substantia nigra (literally, “blacksubstance”) start to die in patients with Parkinson’s disease.These neurons send their dopamine-releasing axon fibers tothe striatum (also known as the caudate nucleus and putamen),a brain region involved in voluntary control of movements.When neurons in the substantia nigra die, a shortage ofdopamine in the striatum results, and the patient begins tolose control over muscle movements, walking, etc. Drugs that

Painkiller Analogues81the brain that use the neurotransmitter dopamine. Circuits inthe brain that use dopamine are primarily involved in thecontrol of motor skills such as movements of the arms, legs,and face. This MPTP-laced heroin explained why this youngman showed signs of Parkinson’s disease.In 1982, many more cases of drug addicts becoming“frozen” after injecting themselves with (what they thought tobe) heroin were reported by various emergency rooms inthe San Francisco Bay area. Neurologists, psychiatrists, andmimic the action of dopamine, or are converted to dopamineonce taken, such as L-dopa, are currently used to treatParkinson’s disease, but with limited success.When heroin laced with toxic MPTP enters the body, itis metabolized to form MPP+, which is very toxic to neuronscontaining dopamine, such as those in the substantia nigra. Inaddition, it is a relatively selective toxin, so it does not destroyneurons containing other types of neurotransmitters. Whenheroin addicts injected that bad batch of heroin containingthe meperidine analogue MPTP, it was converted to MPP+and destroyed many neurons in their substantia nigra, resultingin a dopamine shortage in their striatum and subsequentlycausing symptoms resembling Parkinson’s disease.Despite the misfortunes of these addicts, MPTP hasproved an invaluable tool for studying the biology of Parkinson’sdisease. When MPTP is injected into experimental rats,mice, or monkeys, neurons in the substantia nigra ofthese animals start to die, and the animals develop motorproblems that closely resemble the symptoms of Parkinson’sdisease. Researchers hope to use MPTP in animals tounravel the mystery of what causes Parkinson’s disease inhumans, in the hope that they can develop a cure for thisdevastating disease.

82DESIGNER DRUGSscientists were able to trace contaminants found in the victims’bodies to a bad batch of heroin that was being sold in the area.These unfortunate heroin addicts also developed a form ofParkinson’s disease.Statistics on the patterns of use of fentanyl and meperidineanalogues are relatively scarce. Although abuse of prescriptionpainkillers is on the rise, the use of fentanyl and meperidineanalogues is not. Law enforcement agencies believe theuse of painkiller analogues is not nearly as prevalent today as itwas in the 1970s and 1980s because of increased law enforcementefforts to shut down illegal underground laboratoriesand tighter restrictions and documentation of fentanyland meperidine prescriptions and shipments. In addition,heroin addicts tend to shy away from fentanyl andmeperidine analogues because of the frightening reportsthat they cause frequent overdoses and degeneration of neuronsin the brain.

Bibliography and Further ReadingChapter 1: Designer Drugs and the BrainBuchanan, J.F., and C.R. Brown. “‘Designer drugs.’ A problem in clinical toxicology.”Medical Toxicology and Adverse Drug Experience 3, 1988. 1–17.Henderson, G.L. “Designer Drugs: Past History and Future Prospects.”Journal of Forensic Science 33 (1988): 569–575.Morgan, J.P. “Designer Drugs.” In: Substance Abuse—A ComprehensiveTextbook (Lowinson JH, Ruiz P, Millman RB, Langrod JG, eds). 3 rd ed.Baltimore: Williams & Wilkins, 1997, 264–269.Ziporyn, T. “A growing industry and menace: makeshift laboratory’s designerdrugs.” Journal of the American Medical Association 256 (1986): 3061–3063.Chapter 2: MethamphetamineThe DAWN Report. Rockville, Md.: Drug Abuse Warning Network, Office ofApplied Studies, Substance Abuse and Mental Health ServicesAdministration (SAMHSA), December 2000.Emergency Department Trends from the Drug Abuse Warning Network: FinalEstimates 1994–2001, Rockville, Md.: Office of Applied Studies, SubstanceAbuse and Mental Health Services Administration (SAMHSA), August2002.Fact Sheet: Methamphetamine. Rockville, Md.: Office of National DrugControl Policy Information Clearinghouse, May 1999.Monitoring the Future 2002—Data from In-School Surveys on 8 th ,10 th and 12 thGrade Students, Rockville, Md.: National Institute on Drug Abuse and theUniversity of Michigan, December 2002.Research Report: Methamphetamine Abuse and Addiction, Bethesda, Md.:National Institute on Drug Abuse, NIH Publication 98-4210, April 1998.Chapter 3: EcstasyCole, J.C., and H.R. Sumnall. “Altered States: the Clinical Effects of Ecstasy.”Pharmacology and Therapeutics 98 (2003) 35–58.The DAWN Report. Rockville, Md.: Drug Abuse Warning Network, Office ofApplied Studies, Substance Abuse and Mental Health ServicesAdministration (SAMHSA), December 2000.Emergency Department Trends from the Drug Abuse Warning Network: FinalEstimates 1994–2001, Rockville, Md.: Office of Applied Studies, SubstanceAbuse and Mental Health Services Administration (SAMHSA), August2002.Fact Sheet: MDMA (Ecstasy). Rockville, Md.: Office of National Drug ControlPolicy Information Clearinghouse, May 1999.83

Bibliography and Further ReadingMonitoring the Future 2002—Data from In-School Surveys on 8 th ,10 th and 12 thGrade Students, Bethesda, Md.: National Institute on Drug Abuse and theUniversity of Michigan, December 2002.Chapter 4: GHBThe DAWN Report. Rockville, Md.: Drug Abuse Warning Network, Office ofApplied Studies, Substance Abuse and Mental Health ServicesAdministration (SAMHSA), December 2000.Emergency Department Trends from the Drug Abuse Warning Network: FinalEstimates 1994–2001, Rockville, Md.: Office of Applied Studies, SubstanceAbuse and Mental Health Services Administration (SAMHSA), August2002.Fact Sheet: Gamma Hydroxybutyrate. Rockville, Md.: Office of National DrugControl Policy Information Clearinghouse, November 2002.Monitoring the Future 2002—Data from In-School Surveys on 8 th ,10 th and 12 thGrade Students, Bethedsa, Md.: National Institute on Drug Abuse and theUniversity of Michigan, December 2002.Chapter 5: RohypnolThe DAWN Report. Rockville, Md.: Drug Abuse Warning Network, Office ofApplied Studies, Substance Abuse and Mental Health ServicesAdministration (SAMHSA), December 2000.Emergency Department Trends from the Drug Abuse Warning Network: FinalEstimates 1994–2001, Rockville, Md.: Office of Applied Studies, SubstanceAbuse and Mental Health Services Administration (SAMHSA), August2002.Fact Sheet: Rohypnol. Rockville, Md.: Office of National Drug Control PolicyInformation Clearinghouse, February 2003.Monitoring the Future 2001—Data from In-School Surveys on 8 th ,10 th and 12 thGrade Students, Bethesda, Md.: National Institute on Drug Abuse and theUniversity of Michigan, 2002.Chapter 6: KetamineCurran, H.V., and C. Morgan. “Cognitive, Dissociative and PsychotogenicEffects of Ketamine in Recreational Users on the Night of Drug Use and 3Days Later.” Addiction 95 (2000): 575–590.The DAWN Report. Rockville, Md.: Drug Abuse Warning Network, Officeof Applied Studies, Substance Abuse and Mental Health ServicesAdministration (SAMHSA), December 2000.84

Dillon, P. Copel, and J.K. Jansen. “Patterns of Use and Harms Associated withNon-Medical Ketamine Use.” Drug and Alcohol Dependence 69 (2003): 23–28.Emergency Department Trends from the Drug Abuse Warning Network: FinalEstimates 1994–2001, Rockville, Md.: Office of Applied Studies, SubstanceAbuse and Mental Health Services Administration (SAMHSA), August2002.Monitoring the Future 2002—Data from In-School Surveys on 8 th ,10 th and 12 thGrade Students, Bethesda, Md.: National Institute on Drug Abuse and theUniversity of Michigan, December 2002.Research Report: Hallucinogens and Dissociative Drugs, Bethesda, Md.:National Institute on Drug Abuse, NIH Publication No. 01-4209, March2001.Wenker, C.J. “Anesthesia Of Exotic Animals.” The Internet Journal ofAnesthesiology. Volume 2, Number 3, 1998.Chapter 7: Painkiller AnaloguesLangston, J.W., and J. Palfreman. The Case of the Frozen Addicts. New York:Pantheon Books, 1995.Morgan, J.P. “Designer Drugs.” Substance Abuse–A Comprehensive Textbook.3 rd ed., eds. J.H. Lowinson, P. Ruiz, R.B. Millman, and J.G. Langrod.Baltimore, Md.: Williams & Wilkins, 1997, 264–269.Research Report: Prescription Drugs: Abuse and Addiction, Bethesda, Md.:National Institute on Drug Abuse, NIH Publication No. 01-4881, July 2001.85

Websiteswww.health.orgU.S. Department of Health and Human Services and the Substance Abuseand Mental Health Services Administration (SAMHSA)’s NationalClearinghouse for Alcohol and Drug Information. Provides informationabout prevention, treatment, and recovery.www.whitehousedrugpolicy.govThe U.S. government’s Office of National Drug Control Policy. Legal issuesand fact sheets.www.drugabuse.govThe National Institute on Drug Abuse’s Website. An extensive Websitecontaining information for children and parents, teachers and students,and researchers and health professionals.www.dea.govWebsite of the U.S. Drug Enforcement Administration. Contains legalinformation about drug use and abuse.www.clubdrugs.orgA Website targeted toward teenagers, part of the National Instituteon Drug Abuse. Focuses on club drugs such as Ecstasy, GHB, Rohypnol,ketamine, methamphetamine, and LSD.www.streetdrugs.orgExtensive Website devoted to education about many drugs, current trends,and law enforcement policies.www.methamphetamineaddiction.comContains information about methamphetamine addiction, treatmentoptions, and personal stories of recovery. Sponsored by the NarcononArrowhead treatment program.www.ecstasyaddiction.comInformation about Ecstasy (MDMA) addiction, treatment options,and personal stories of recovery. Sponsored by the Narconon Arrowheadtreatment program.86

www.projectghb.orgInformation about GHB, the effects of the chemical, and date rape, as wellas personal accounts.www.designer-drugs.comPersonal Website of Donald A. Cooper, Drug Enforcement Administration,McLean, Virginia. Contains information about various synthetic, or“designer,” drugs.87

Additional ResourcesIf you would like more information about drug use and abuse, or to speakto someone confidentially, please call the following hotlines:American Council for Drug Education800-488-DRUG (800-488-3784)National Institute of Drug Abuse888-644-6432National Council on Alcoholism and DrugDependence, Inc.’s Hope Line800/NCA-CALLNational Treatment and Referral Hotline11-800-662-HELPOr visit the Substance Abuse and Mental Health ServicesAdministration (SAMHSA)’s treatment facility locator Website athttp://findtreatment.samhsa.gov/facilitylocatordoc.htmto find a treatment facility near you.For Parents and Teachers:If you would like information about how to talk to your children or studentsabout drugs and alcohol, or to learn more about drug abuse in teens, pleasevisit the following Websites:A Family Guide to Keeping Youth Mentally Healthy and Drug Free,provided by the Substance Abuse and Mental Health ServicesAdministration (SAMHSA)http://family.samhsa.gov/Partnership for a Drug Free Americawww.drugfreeamerica.orgParents. The Anti-Drugwww.theantidrug.comDrug Strategies: Treating TeensWeb companion to the Drug Studies publication:Treating Teens: A Guide to Adolescent Drug Programshttp://www.drugstrategies.org/teens/index.html88

Talk With Your KidsInformation on talking with your children about various tough issues,including drug abuse.http://www.talkingwithkids.org/Drugstory.org. Information about Drug Prevention and Treatment,sponsored by the Office of National Drug Control Policyhttp://www.drugstory.org/prevention_treatment/index.asp89

IndexADHD. See Attentiondeficit/hyperactivitydisorderAlcohol, 13, 41,43–45, 51–52,58–59, 61, 66,68–69Alfenta. See FentanylAlfentanil. SeeFentanylAli, Muhammad, 80Alpha-methylfentanyl.See FentanylAlprazolam. SeeXanaxAmphetamine, 10, 31,58analogues of, 9, 18,30, 32, see alsoindividual drugsuses of, 18Anabolic steroids, 10Analoguesillegal, 8–9production of, 8–9,12, 18, 47–48, 62,72–82Aspirin, 72Antidepressants, 40Attention-deficit/hyperactivitydisorder (ADHD)and desoxyn, 19Barbiturates, 10–11,58Basement chemists,21and the productionof analogues, 8,12Benzodiazepines, 54,58, 61Brain, 24axons of, 12–13and designer drugs,8–17Ecstasy effects on,36–38functions of, 15–17GHB’s effects on,44–46Ketamine’s effectson, 67methamphetamine’seffects on,24–26myelin sheath of, 13neurons of, 12–15,25–26, 36–37,58, 67, 78, 80–81neurotransmittersof, 12, 14–15, 25,36, 38–39, 45, 67,77, 80–81, seealso individualtypesRohypnol’s effectson, 58–59structures of,16–17, 38synaptic terminalof, 12, 14Brain regions, 80–81brainstem, 15–16,25, 36, 46, 58, 67cerebellum, 15–16,46, 58, 67frontal cortex, 15,25–26, 36–37,46, 58, 67hypothalamus, 15,25, 36, 46, 58limbic system, 15,17, 25–26,36–37, 46, 58, 67motor cortex, 15,67sensory cortex, 15,36, 67visual cortex, 15,25, 36, 46, 67Brave New World(Huxley), 7Burroughs Wellcome,18Carfentanil. SeeFentanylClinton, Bill, 49Clonazepam. SeeKlonopinClub drugs. SeeDesigner drugsCocaine, 10, 13, 40,51–52, 58, 60, 66,68source of, 12Codeine, 10, 72Codeine cough syrup,11, 40ComprehensiveMethamphetamineControl Act, 19Controlled SubstanceAct (1970), 19drug classificationsin, 9–12Controlled SubstancesAnalogues EnforcementAct, 11Courtright, David T.Forces of Habit.Drugs and themaking of themodern world, 7Dance clubs. SeeRaves90

Date rape drugsEcstasy, 37GHB, 43, 46–47,51, 59Ketamine, 59, 68Rohypnol, 46, 55, 59Davenport-Hines,RichardThe Pursuit of Oblivion.A global historyof narcotics, 7Demerol(Meperdine), 8–10,72action of, 78analogues of, 78–82overdose of, 82patterns of use andabuse, 82side effects of, 78statistics of, 82structure of, 79Designer drugs (clubdrugs), 26, 30, 56,68, 71–72and the brain, 8–17dangers of, 11, 59defined, 8–12psychedelic effectsof, 12, 55psychoactive effectsof, 12, 55Desoxynand attentiondeficit/hyperactivitydisorder, 19and narcolepsy, 19Dilaudid, 72Dopamine, 80–81action of, 14and Ecstasy, 36, 39and methamphetamine,24, 26Drug-Induced RapePrevention andPunishment Act of1996, 55, 59Drugsabuse of, 6–7and animalresearch, 38history of, 6–7use of, 6–7Ecstasy (3, 4-methylenedioxymethamphetamine,MDMA)(3, 4-methylenedioxyamphetamine,MDA), 9–10, 23,30–41, 52, 66, 68action of, 14, 36–39addiction to, 32,40–41common streetnames of, 30costs of, 32dangers of, 35, 37,39, 41as date rape drug,37forms of, 32–33history of, 30–32legal status of,30–32looks of, 32–33patterns of use andabuse of, 32,37–40physical effects of,31, 33–37, 39,41psychedelic effectsof, 31, 35psychologicaleffects of,33–36–38and serotonin, 14statistics of, 37–40structure of, 31uses of, 30–31, 37,40Endorphins, 14, 78Ephedrine, 32, 34and methamphetamine,22Epinephrineand methamphetamine,24Farias, Hillory J.and GHB overdose,49Fentanyl (Sublimaze),9–10, 72analogues of, 74–78,82common streetnames for, 75forms of, 74–76medical uses of, 74,77overdoses of, 75, 77,82patterns of use andabuse, 82physical effects of,76psychologicaleffects of, 76, 78side effects of, 76, 78statistics of, 82structures of, 77Flunitrazepam. SeeRohypnolForces of Habit. Drugsand the making ofthe modern world(Courtright), 791

IndexFox, Michael J., 80GABA. See Gammaaminobutyric acidGamma aminobutyricacid (GABA), 14and GHB, 46Gamma hydroxybutyrate.See GHBGHB (gammahydroxybutyrate),42–53, 69action of, 15, 42,44–46addiction to, 48,52–53analogues of, 47–48common streetnames, 42dangers of, 42, 52–53as date rape drug,43, 46–47, 49, 51,59and federal law,48–50forms of, 43–44history of, 42–43legal status of,42–43looks of, 43–44medical uses of,42–43, 47–48,50–51overdose of, 42–45,48–50, 52–53patterns of use andabuse of, 50–52physical effects of,42, 44–45, 47, 50psychologicaleffects of, 44–45,47, 51statistics of, 51–52structure of, 48withdrawal symptomsof, 52–53Glutamate, 14Harrison Narcotic Actof 1914, 7Herbal Ecstasy, 34Heroin, 10, 13, 32,40–41, 60–61, 72,75–76, 78, 81–82source of, 12, 73Hitler, Adolfand methamphetamines,28Hoffman-La Roche,54–56, 59Huxley, AldousBrave New World, 7Janssen PharmaceuticalCompany, 74Ketamine, 10, 62–71action of, 67addiction to, 69–71common streetnames, 62costs of, 63dangers of, 69as date rape drug,59, 68forms of, 63–64history of, 62–63legal status of,62–63looks of, 63medical uses of, 62,64, 66, 70overdose of, 66, 68patterns of use andabuse of, 68–69physical effects of,63–66, 68psychedelic effectsof, 62–66psychologicaleffects of, 63–66,68, 70statistics of, 68–69structure of, 63, 65uses of, 62Klonopin(Clonazepam), 61Lofentanyl. See FentanylLSD, 10, 35, 39–40,66Malignant hyperthermiaand Ecstasy, 35,39–41Marijuana, 10, 52, 68source of, 12MDA. See EcstasyMDMA. See EcstasyMeperdine. SeeDemerolMerck, 30Mescaline, 10Methamphetamine,9–10, 18–29, 31,40, 45, 51, 69action of, 14, 24–26addiction to,18–19, 27–29common streetnames, 18costs of, 20dealers of, 22forms of, 19–23history of, 18–19and Adolf Hitler,2892

legal status of,18–19looks of, 19–23overdose of, 19,26–27patterns of use andabuse of, 26–27physical effects of,23–26, 28–29psychologicaleffects of, 23–26,29statistics of, 26–27uses of, 18withdrawal symptomsof, 29Methedrine, 18Morgan, J.Substance Abuse—A ComprehensiveTextbook,9Morphine, 10–11, 72,74, 77–78Morrell, T., 28Motrin, 72MPPP. See DemerolMPTP. See DemerolNarcolepsyand desoxyn, 19and GHB, 50–51Narcotics, 8, 11, 72New Heroin. SeeDemerolNicotinesource of, 12Noradrenaline, 14and methamphetamine,24Opium, 72–73,77–78Oxycontin, 72Painkiller analogues,8–9, 72–82Parke-Davis, 62Parkinson’s disease,26, 80–82PCP, 10, 40, 63, 65analogs of, 62Peyote, 10Prozac, 29Pseudoephedrine(Sudafed)and methamphetamine,19, 22–23Psilocybin, 10Psychedelic mushrooms,39Pursuit of Oblivion.A global history ofnarcotics, The(Davenport-Hines),7Raves (dance clubs),23, 39–40, 51, 59,62, 69Reid, Samanthaand GHB overdose,49–50Ritalin, 10, 51Rohypnol (flunitrazepam),40, 54–61action of, 15, 58–59addiction to, 61common streetnames of, 54costs of, 55dangers of, 61as date rape drug,46, 55, 59forms of, 55–56,59, 61history of, 54–55illegal sale of, 60legal status of,54–55looks of, 55–56myths of, 60–61patterns of use andabuse of, 59–61physical effects of,56–58psychologicaleffects of, 56–58statistics of, 59–61structures of,56–57withdrawal symptomsof, 61Schedule V drugsdefined, 11examples of, 11Schedule IV drugsdefined, 10–11examples of, 10–11,54Schedule I drugsdefined, 10–11examples of, 10, 31,43, 48–49, 75Schedule III drugsdefined, 10examples of, 10, 19,43, 54, 63Schedule II drugsdefined, 10examples of, 10, 19,32Serotoninaction of, 14and Ecstasy, 14,36–38Shuglin, Alexanderand MDMA, 30–31Sublimaze. SeeFentanyl93

Substance Abuse—AComprehensive Textbook(Morgan), 9Sudafed. See PseudoephedrineSufenta. See FentanylSufentanil. See FentanylTriggle, David J.,on the use and abuseof drugs, 7Tylenol, 72Valium, 11, 29, 54,56–57, 61Viagra, 37Vicodin, 72Vietnam Warand the use of ketamine,62Wildnil. See FentanylWorld War Iand the use of MDMAand MDA, 30World War IIand the use of MDMAand MDA, 30and the use ofmethamphetamine,18Xanax (alprazolam), 11,54, 61Yaba methamphetamine,2394

Picture Creditspage:13: Lambda Science Artwork14: Lambda Science Artwork16: Lambda Science Artwork17: Lambda Science Artwork20: Courtesy of the Drug EnforcementAdministration21: Courtesy of the Drug EnforcementAdministration22: ©Noelle Nardone27: Office of Applied Studies, SAMHSA, DrugAbuse Warning Network, 200131: ©Noelle Nardone33: Courtesy of the Drug EnforcementAdministration/Design NN39: Courtesy of the National Institute onDrug Abuse40: Office of Applied Studies, SAMHSA48: ©Noelle Nardone53: Office of Applied Studies, SAMHSA, DrugAbuse Warning Network, 200156: Courtesy of the Drug EnforcementAdministration57: ©Noelle Nardone64: Courtesy of the Drug EnforcementAdministration65: ©Noelle Nardone69: Office of Applied Studies, SAMHSA, DrugAbuse Warning Network, 200173: ©Associated Press, AP76: Courtesy of the Drug EnforcementAdministration77: ©Noelle Nardone79: ©Noelle NardoneCover: Courtesy of the Drug Enforcement AdministrationAlfenta is a registered trademark of Johnson & Johnson; Demerol is a registered trademark ofSanofi-Synthelabo Inc.; Desoxyn is a registered trademark of Abbott Laboratories; Dilaudid isa registered trademark of Knoll Pharmaceutical; Ketalar is a registered trademark of WarnerLambert Company; Klonopin is a registered trademark of Hoffman-La Roche Inc.; M&M is aregistered trademark of Mars Inc.; Motrin is a registered trademark of Johnson & Johnson;OxyContin is a registered trademark of Purdue Pharma Inc.; Pez is a registered trademarkof Pez Candy Inc.; Prozac is a registered trademark of Eli Lilly and Company; Ritalin is aregistered trademark of Novartis; Rohypnol is a registered trademark of Hoffman-La Roche Inc.;Skittles is a registered trademark of Mars Inc.; Sublimaze is a registered trademark ofJohnson & Johnson; Sudafed is a registered trademark of Warner Lambert Company; Sufentais a registered trademark of Johnson & Johnson; Tylenol is a registered trademark of McNeilConsumer Brands; Valium is a registered trademark of Hoffman-La Roche Inc.; Viagra is aregistered trademark of Pfizer Inc.; Vicodin is a registered trademark of Knoll PharmaceuticalsCompany; Wildnil is a registered trademark of Johnson & Johnson; Xanax is a registeredtrademark of Pharmacia & Upjohn Company; Xyrem is a registered trademark of OrphanMedical Inc.95

About the AuthorM. Foster Olive received his Bachelor’s in Psychology from the University ofCalifornia at San Diego, and went on to receive his Ph.D. in neurosciencefrom UCLA. He is currently an associate investigator at the Ernest GalloClinic & Research Center, a non-profit research institute affiliated with theDepartment of Neurology at the University of California at San Francisco.His research focuses on the neurobiology of stress and addiction, and ispublished in numerous academic journals including Pharmacology,Biochemistry and Behavior, Psychopharmacology, and the Journal ofNeuroscience. Foster and his family live in the San Francisco Bay Area innorthern California.About the EditorDavid J. Triggle is a University Professor and a Distinguished Professor inthe School of Pharmacy and Pharmaceutical Sciences at the State Universityof New York at Buffalo. He studied in the United Kingdom and earned hisB.Sc. degree in chemistry from the University of Southampton and a Ph.D.degree in chemistry at the University of Hull. Following post-doctoral workat the University of Ottawa in Canada and the University of London in theUnited Kingdom, he assumed a position at the School of Pharmacy at Buffalo.He served as Chairman of the Department of Biochemical Pharmacologyfrom 1971 to 1985 and as Dean of the School of Pharmacy from 1985 to 1995.From 1995 to 2001 he served as the Dean of the Graduate School and asthe University Provost from 2000 to 2001. He is the author of several booksdealing with the chemical pharmacology of the autonomic nervous systemand drug-receptor interactions, some 400 scientific publications, and hasdelivered over 1,000 lectures worldwide on his research.96