DRAMAKILLER's blog: "EDUCATION ON DRUGS"

Oxycodone is an opioid analgesic medication synthesized from opium-derived thebaine. It was developed in 1916 in Germany, as one of several new semi-synthetic opioids with several benefits over the older traditional opiates and opioids; morphine, diacetylmorphine (heroin) and codeine. It was introduced to the pharmaceutical market as Eukodal or Eucodal and Dinarkon. Its chemical name is derived from codeine - the chemical structures are very similar, differing only in that the hydroxyl group of codeine has been oxidized to a carbonyl group (as in ketones), hence the "-one" suffix, the 7,8-dihydro-feature (codeine has a double-bond between those two carbons), and the hydroxyl group at carbon-14 (codeine has just a hydrogen in its place), hence oxycodone. Oxycodone was first synthesized in a German laboratory in 1916, a few years after the German pharmaceutical company Bayer had stopped the mass production of heroin due to addiction and abuse. It was hoped that a thebaine-derived drug would retain the analgesic effects of morphine and heroin with less addiction. To some extent this was achieved, as oxycodone does not have the same immediate effect as heroin or morphine nor does it last as long. It was first introduced to the US market in May 1939 and is the active ingredient in a number of pain medications commonly prescribed for the relief of moderate to severe pain, either with inert binders, e.g. (oxycodone, OxyContin) or supplemental analgesics such as paracetamol (acetaminophen), e.g. (Percocet, Endocet, Tylox, Roxicet) or aspirin (Percodan, Endodan, Roxiprin ). More recently, ibuprofen has been added to oxycodone under the name (Combunox). [edit]Clinical use In palliative care, oxycodone is viewed as a second line opioid to morphine, along with other second-line strong opioids such as hydromorphone and fentanyl.[1] There is no evidence that any opioids are superior to morphine in relieving the pain of cancer, and no controlled trials have shown oxycodone to be superior to morphine.[2] However, switching to an alternative opioid can be useful if adverse effects are troublesome, although the switch can be in either direction, i.e. some patients have fewer adverse effects on switching from morphine to oxycodone and vice versa. Oxycodone has the disadvantage of accumulating in patients with renal and hepatic impairment. In addition, and unlike morphine and hydromorphone, it is metabolized by the cytochrome P450 enzyme system in the liver, making it vulnerable to drug interactions.[3] It is metabolized to the very active opioid analgesic oxymorphone.[4] Some people are fast metabolizers resulting in reduced analgesic effect but increased adverse effects, while others are slow metabolisers resulting in increased toxicity without improved analgesia.[5][6] [edit]Manufacture and patents Formulations containing oxycodone and other analgesics. An extended-release formulation of oxycodone, OxyContin, was first introduced to the US market by Purdue in 1996. Purdue has multiple patents for OxyContin, but has been involved in a series of ongoing legal battles on the validity of these patents. On June 7, 2005, the United States Court of Appeals for the Federal Circuit, upheld a decision from the previous year that some of Purdue’s patents for OxyContin could not be enforced.[7] This decision allowed and led to the immediate announcement from Endo Pharmaceuticals that they would begin launching a generic version of all four strengths of OxyContin.[8] Purdue, however, had already made negotiations with another pharmaceutical company (IVAX Pharmaceuticals) to distribute their brand OxyContin in a generic form. This contract was severed, and currently Watson Pharmaceuticals is the exclusive U.S. distributor of Purdue-manufactured generic versions of OxyContin tablets in 10, 20, 30, 40, 60, and 80 milligram dosages in the United States.[9] On February 1, 2006, the Federal Circuit Court of Appeals issued a revised decision varied their prior decision.[10] The court concluded that the patents-in-suit are unenforceable, and the case is remanded for further proceedings. Purdue Pharma has since announced resolution of its infringement suits with Endo,[11] Teva,[12] IMPAX,[13] and Mallinckrodt.[14] Endo and Teva each agreed to cease selling generic forms of OxyContin, while IMPAX negotiated a temporary, and potentially renewable, license, and Mallinckrodt negotiated a temporary license ending in 2009. In 2001, OxyContin was the highest sold drug of its kind, and in 2000, over 6.5 million prescriptions were written.[15] [edit]OxyContin misbranding and fraud Critics have accused Purdue of putting profits ahead of public interest by understating or ignoring the addictive potential of the drug.[16][17][18] Purdue Pharma and its top executives pleaded guilty to felony charges that they misbranded and misled physicians and the public by claiming OxyContin was less likely to be abused, less addictive, and less likely to cause withdrawal symptoms than other opiate drugs.[19] The company also paid millions in fines relating to aggressive off-label marketing practices in several states.[20] [edit]Abuse Oxycodone is a drug subject to abuse.[21][22] The drug is included in the sections for the most strongly controlled substances that have a commonly accepted medical use, including the German Betäubungsmittelgesetz III (narcotics law), the Swiss law of the same title, UK Misuse of Drugs Act (Class A), Canadian Controlled Drugs and Substances Act (CDSA), Dutch Opium Law (List 1), Austrian Suchtmittelgesetz (Addictives Act), and others. It is also subject to international treaties controlling psychoactive drugs subject to abuse or dependence. The introduction of higher strength preparations in 1995 resulted in increasing patterns of abuse.[21] Unlike Percocet, whose potential for abuse is somewhat limited by the presence of paracetamol (acetaminophen), OxyContin and other extended release preparations contain mainly oxycodone. Abusers crush the tablets to defeat the time-release "micro-encapsulation" and then ingest the resulting powder orally, intra-nasally, rectally, or by injection. Research has shown that the brains of adolescent mice, which were exposed to OxyContin, can sustain lifelong and permanent changes in their reward system.[23][24] It is notable that the vast majority of OxyContin related deaths are attributed to ingesting substantial quantities of oxycodone in combination with another depressant of the central nervous system such as alcohol, barbiturates and related drugs.[25] Illegal distribution of OxyContin occurs through pharmacy diversion, physicians, doctor shopping, faked prescriptions, and robbery. In Australia during 1999 and 2000, more than 260,000 prescriptions for narcotics and codeine-based medications were written to almost 9,000 known abusers at a cost of more than AUD 750,000.[22] Oxycodone has been refered to as "hillbilly heroin" due to its recreational use in more rural parts of the U.S., especially Appalachia.[26] [edit]Regulation Regulation of oxycodone (and opioids in general) differs according to country, with different places focusing on different parts of the supply chain. [edit]Australia A General Practitioner can prescribe for short term treatment without consulting another practitioner or government body. Only twenty tablets are normally available per prescription on the Pharmaceutical Benefits Scheme, Australia's government-funded pharmaceutical insurance system, but with prior approval from Medicare Australia a patient can potentially get up to sixty tablets.[citation needed] Prescriptions for chronic pain or cancer patients require the prescriber to have referred the patient to another medical practitioner to confirm the need for ongoing treatment with narcotic analgesics. Pharmacists must record all incoming purchases of oxycodone products, and maintain a register of all prescription sales for inspection by their state Health Department on request. In addition, details of all Pharmaceutical Benefits Scheme prescriptions for oxycodone are sent to Medicare Australia. This data allows Medicare Australia to assist prescribers to identify doctor-shoppers via a telephone hotline. [edit]Canada Oxycodone is a controlled substance under Schedule I of the Controlled Drugs and Substances Act (CDSA). Every person who seeks or obtains the substance without disclosing authorization to obtain such substances 30 days prior to obtaining another prescription from a practitioner is guilty of an indictable offence and liable to imprisonment for a term not exceeding seven years. Possession for purpose of trafficking is guilty of an indictable offence and liable to imprisonment for life. [edit]Germany Only physicians (Ärzte) can prescribe oxycodone. Prescribing physicians need to have a special BtM number (controlled substance number). BtM prescriptions are handled very cautiously and the central Federal Opium Bureau (Bundesopiumstelle) records all traffic. [edit]Hong Kong Oxycodone is regulated under Schedule 1 of Hong Kong's Chapter 134 Dangerous Drugs Ordinance. It can only be used legally by health professionals and for university research purposes. The substance can be given by pharmacists under a prescription. Anyone who supplies the substance without a prescription can be fined $10,000 (HKD). The penalty for trafficking or manufacturing the substance is a $5,000,000 HKD fine and/or life imprisonment. Possession of the substance for consumption without license from the Department of Health is illegal with a $1,000,000 HKD fine and/or 7 years of jail time. [edit]United Kingdom Oxycodone is a Class A drug under the Misuse of Drugs Act. [27] It is available by prescription from a GP on the NHS for short-term severe pain and long-term for cancer patients. Possession without a prescription is punishable by up to seven years in prison, an unlimited fine, or both. Dealing of the drug illegally is punishable by up to life imprisonment, an unlimited fine, or both.[28] [edit]United States Oxycodone is a schedule II drug in the United States. Except when dispensed directly by a practitioner, other than a pharmacist, to an ultimate user, no controlled substance in schedule II, which is a prescription drug as determined under the Federal Food, Drug, and Cosmetic Act (21 U.S.C. 301 et seq.), may be dispensed without the written prescription of a practitioner, except that in emergency situations, such drug may be dispensed upon oral prescription (ie. telephone) in accordance with section 503(b) of that Act (21 U.S.C. 353(b). Prescriptions shall be retained in conformity with the requirements of section 827 of this title. No prescription for a controlled substance in schedule II may be refilled.[29] Some states may have more strict laws pertaining to the prescribing and dispensing of CII medications. [edit]Dosage and administration Oxycontin tablets of varying dosage Oxycodone can be administered orally, intranasally, via intravenous/intramuscular/subcutaneous injection or rectally. The bioavailability of oral administration averages 60–87%, with rectal administration yielding the same results. Oxycodone is approximately 1.5× - 2x as potent as morphine when administered orally.[30][31] However, 10-15mg of oxycodone produces an analgesic affect similar to 10mg of morphine when administered intramuscularly. Therefore, as a parenteral dose, morphine is approximately up to 50% more potent than oxycodone. [32] There are no comparative trials showing that oxycodone is more effective than any other opioid. In palliative care, morphine remains the gold standard,[2] however oxycodone can be useful as an alternative opioid if a patient has troublesome adverse effects with morphine. Percocet tablets [33](oxycodone with paracetamol/acetaminophen), are routinely prescribed for post-operative pain control. Tablets are available with 2.5, 5, 7.5, and 10 mg's of oxycodone and varying amounts of acetaminophen. Oxycodone is also used in treatment of moderate to severe chronic pain. OxyNorm is available in 5, 10, and 20 mg capsules and tablets, and also as a 1 mg/1 ml liquid in 250 ml bottles and as a 10 mg/1 ml concentrated liquid in 100 ml bottles. Available in Europe and other areas outside the United States, Proladone suppositories contain 15 mg of oxycodone pectinate and other suppository strengths under this and other trade names are less frequently encountered. Injectable oxycodone hydrochloride or tartrate is available in ampoules and multi-dose vials in many European countries and to a lesser extent various places in the Pacific Rim. For this purpose, the most common trade names are Eukodol and Eucodol. Roxicodone is a generically made oxycodone product designed to have an immediate release effect for rapid pain relief, and is available in 5 (white), 15 (green), and 30 (light blue) mg tablets. Generic versions of Roxicodone may differ in color from the brand name tablets. [edit]OxyContin Available in, 10 mg (white), 15 mg (grey), 20 mg (pink), 30 mg (brown), 40 mg (yellow), 60 mg (red), and 80 mg (green) in the U.S. and Canada; 160 mg (blue) in Canada only, and 5 mg (blue) in Europe. Because of its sustained-release mechanism, the medication is typically effective for eight to twelve hours.[3] The 160 mg tablets were removed from sale due to problems with overdose, but have been re-introduced for limited use under strict medical supervision. Generic OxyContin was introduced in 2005 (80 mg) and 2006 (10, 20, and 40 mg). However, because of numerous lawsuits noted above, generic manufacture ceased on December 31, 2007. Generic OxyContin has been reintroduced by Mallinckrodt Pharmacueticals in the strengths of 10mg, 20mg, 40mg and 80mg. This has been made possible by a royalties based contract with Purdue pharma.[1] [edit]Side effects The most commonly reported effects include constipation, fatigue, dizziness, nausea, lightheadedness, headache, dry mouth, anxiety, pruritus, euphoria, and diaphoresis.[34] It has also been claimed to cause dimness in vision due to miosis. Some patients have also experienced loss of appetite, nervousness, abdominal pain, diarrhea, dyspnea, and hiccups,[3] although these symptoms appear in less than 5% of patients taking oxycodone. Rarely, the drug can cause impotence, enlarged prostate gland, and decreased testosterone secretion.[35] In high doses, overdoses, or in patients not tolerant to opiates, oxycodone can cause shallow breathing, bradycardia, cold, clammy skin, apnea, hypotension, pupil constriction, circulatory collapse, respiratory arrest, and death.[3] [edit]Withdrawal related side effects There is a high risk of experiencing severe withdrawal symptoms if a patient discontinues oxycodone abruptly. Therefore therapy should be gradually discontinued rather than abruptly discontinued. Drug abusers are at even higher risk of severe withdrawal symptoms as they tend to use higher than prescribed doses. Withdrawal symptoms are also likely in newborns whose mothers have been taking oxycodone or other opiate based painkillers during their pregnancy. The symptoms of oxycodone withdrawal are the same as for other opiate based painkillers and may include the following symptoms.[36][37] Anxiety Nausea Insomnia Muscle pain Fevers Flu like symptoms

Under the Federal Controlled Substances Act of 1970, cannabis is classified as a schedule one substance. Schedule one substances are defined as currently having no accepted medical use in the USA and having a high potential for abuse. Cannabis is the name of the genus to which the plant belongs. Three species names for Cannabis are indica, sativa, and ruderlaris. The preparation made from the stems, buds, and leaves of Cannabis is known as marijuana. Cannabis' psychoactive effects are caused by potent psychotoxins, which are present throughout its various forms (i.e. marijuana). The most well known of these psychotoxins, which is also it's primary psychoactive component, is delta-9-tetrahydrocannibinol (THC). There are many forms of THC; at least eighty derivatives have been synthesized and studied pharmacologically. The effects of THC range from euphoria and relaxation to anxiousness. From the various studies that have been done on marijuana, there has emerged evidence for marijuana having positive medical effects on people. Throughout history, cannabis has been a plant that has been used for medicinal purposes all over the world. By classifying marijuana under schedule one, is the government failing to acknowledge the many therapeutic advantages of marijuana? This paper will discuss the historical and current uses of marijuana and come to a conclusion on whether or not the beneficial effects of marijuana are conclusive enough for it to be used medicinally. The chemistry behind THC remained a mystery until 1942, when H.J. Wollner and his co-workers first isolated and identified a natural tetrahydrocannabinol. In the mid to late 1940's, synthetic forms of THC began to appear under the trade names synhexyl, pyrahexyl, and parahexyl. THC is a highly lipid soluble molecule which is found throughout the male and female parts of the cannabis plant. The highest concentration of THC is present in the sticky resin that is produced by the flowering portion of the female plant. The THC content of marijuana varies depending on the section of the plant that is used. The presence of THC and THC metabolites remain in the body and can be detected in the urine for many days after use. In 1990, the serendipitous discovery of the cannabinoid receptor was revealed at the National Institute of Mental Health (NIMH). Today, although much progress has been made in molecular biology with regards to cannabinoids and cannabinoid receptors (CB1, CB2, CB1A), there is still much to be discovered. CB1 receptors are mainly found in specific areas of the brain, spinal cord, and peripheral nervous system. Within these areas, high density binding occurs in the cerebellum, basal ganglia, hippocampus and cerebral cortex, while low density binding occurs in the brainstem. CB2 receptors are found mainly in the immune system on the spleen, tonsils, B cells, minocytes, natural killer cells, T4 cells, and T8 cells. All cannabinoid receptors belong to the superfamily of G-protein coupled plasma membrane receptors. Currently, a number of carefully directed laboratory studies are under way to explore the mechanisms behind cannabinoids and its receptors to explore their roles in the positive and negative effects (short and long term) of using marijuana. In 1992, a paper in Science was published revealing the discovery of an endogenous ligand for the cannabinoid receptor. William Devane and Raphael Mechoulam of the Hebrew University discovered the endogenous ligand, which was later named anandamide. Long before any research was ever done on marijuana, people used it all over the world for a variety of reasons. The oldest record of medicinal use of marijuana comes from Chinese texts, around 5000 years ago. Its exact origins are still unknown but most experts hypothesize that it originated from somewhere in Central Asia, north of the Himalayan Mountains. The Latin term cannabis had a Greek origin (kannabis) whereas the English word hemp is derived from Middle English hempe and the earlier Old English form henep or haenep. The term marijuana may have arisen from the Portuguese marihuango or the Mexican-Spanish mariguana, both of which mean "intoxicant." Marijuana is a term that indicates a preparation made from the flowering or fruiting tops of the cannabis plant from which the resin has not been extracted. The use of the term cannabis is international, yet its products and the plant itself can be called many different names. The synonyms, excluding the street names, are almost legion and vary from country to country. For example, Central Africans refer to cannabis as mata, kwane, M bhanze, or dagga while Indians commonly refer to it as charas, bhang, ganja, or hashish. Central Asiatic nomads may have been the agents for cultural dispersion of the hemp plant throughout Asia. Warlike equestrian pastoralists inhabiting Scythia, a large ancient region in southeastern Europe and Asia used the hemp plant for textiles and intoxication. Herodotus, a famous Greek historian, stated that the "Scythian passion was inhaling the smoke of burning hemp plants." This was done by burning portions of the plant in metal censers beneath small tent structures that enclosed the vapors, which were then inhaled for ritualistic and euphoric purposes. Later it was discovered by Russian archaeologists that hemp fibers were used by the Scythians for certain types of clothing's. After 1700 B.C., nomads possessing use and knowledge of hemp migrated out of central Asia. Ancient Iranian literature implies that the hemp plant was used as an oil source. However, hemp's most significant use in southwest Asia, Egypt, the Mediterranean region, and Africa was for intoxicating purposes. The Assyrians in ancient Mesopotamia used hemp for fibers, incense, cultivation of sesame and flax for essential fats, and most notably, for drug sources. In the Mediterranean region, there is strong evidence that hemp intoxication was a popular social practice. In the first century of the Christian era, Dioscordes, a physician, wrote a book on medicinal herbs. He was unaware of the "dioecious nature of the hemp plant and therefore listed a separate species for both the female (Kannabis Emeros) and the male (Kannabis Agria)." He indicated that for females, cannabis could be used for strong rope, relieving earaches, and inducing menstrual flow. For the male, on the other hand, cannabis could be used for muscular ailments. Claudius Galen (130-193 A.D.), a renowned scholar and author, reported that hemp was a commonly consumed substance on the Italian Peninsula. It was noted that it caused dry mouth but if taken in excess, produced sluggishness (torpor). It was often customary to offer guests hemp seeds as a promoter of hilarity. Marijuana was used to some extent for ecstatic purposes and had limited drug use in the northerly regions of central and Western Europe. In the Chinese culture, one of the early medicinal uses of hemp was for "absent-mindedness." Shen Nung, the "father of husbandry," who probably lived some time between 3494 and 2657 B.C. experimented with cannabis for its drug potential. In his pharmacological book, he wrote that hemp should be prescribed for "female weakness, gout, rheumatism, malaria, beriberi, constipation, and absent-mindedness." In India, there is evidence of migrating tribes being the first to introduce hemp into the region. The earliest synonym for hemp in ancient India was bhanga. In old Indian folk songs, "ganga or bhanga was the invariable drink of heroes before performing great feats of heroism." The traditional hemp intoxication was a means of stimulating confidence, bravery, and success. In the XV Fargard of the Vendidad, a compilation of religious laws and myths, hemp is referred to as a substance that stimulates abortions. In the Din Yast, a devotional treatise dedicated to the goddess Kista, hemp is referred to as being used for inducing euphoric feelings and righteous actions. Despite of all the evidence supporting marijuana's historical use for medicinal purposes, there is still much to be learned about its risks and benefits. On March 17, 1999, the US Institute of Medicine (IOM) said that smoking marijuana has benefits for the terminally ill. They suggested that studies begin on producing inhalation devices to provide a safe alternative to the harmful effects of smoking. The study concluded that cannabinoids can be useful in treating pain, nausea and appetite loss caused by advanced cancer and AIDS. D-tetrahydrocannabinol (THC) also acts as a sedative and reduces anxiety, which in itself may have therapeutic effects. The results of the studies done by IOM also stated that there was no evidence for marijuana being a "gateway" to harder drugs, or that it is addictive. Recently it was discovered that THC mimics the lipid molecule anandamide, both of which bind to the same cannabinoid receptors, CB1 and CB2, in the body. Anandamide, an endogenous cannabimimetic eicosanoid, is a member of the a family of fatty acid ethanolamides. Danielle Piomelli (University of California at Irvine) and his colleagues have recently uncovered one of anandamide's endogenous roles. When the nerve terminal releases anandamide, it inhibits other nerve cells that trigger physical action. This inhibition occurs by blocking the action of the brain neurotransmitter dopamine. David W. Self, of the Yale University School of Medicine, says that "these findings promise to propel anandamide from candidate status to bona fide neurotransmitter and may also open the door to novel treatments for diseases that involve dysfunction of dopamine signaling." Studies done on the striatum region of the brain in mice showed that by blocking anandamide release and increasing dopamine release via stimulation make the mice more hyperactive than if anandamide had not been blocked at all. The striatum is densely seeded with both dopamine and anandamide receptors. From these studies, it can be concluded that anandamide acts as a dopamine "brake. There is some evidence that boosting anandamidelike activity by administering THC alleviates symptoms of Tourette's syndrome, although this research is still in its preliminary stages. The US National Institute of Health (NIH) and the British Medical Association released reports in 1997 on the potential therapeutic uses of cannabis and cannabinoids. Each one of the reports concluded that cannabinoids may be potentially useful as analgesics, antispasmodics, anti-emetics, appetite stimulants, and in treatment of epilepsy and glaucoma. Much of the evidence is from small controlled trials of oral dronabinol or nabilone. Although much evidence was gathered from these trials, doubt still lingers due to the difference between oral THC and smoked cannabis products. CB1 binding in the substantia gelatinosa could mediate analgesia while the high CB1 density in the basal ganglia could be the basis of antispasmodic effects of CB1 agonists. CB2 receptors so far are known to mainly appear on immune cells, especially on B cells. Activation of these receptors by cannabinoid agonists may cause the alleged immunosuppressant effect of cannabis. However, THC is unlikely to have a substantial effect at this receptor due to its low affinity for the CB2 receptor. More studies done with CB2 agonists and antagonists need to be done to help further see the effects of activating the CB2 receptor. In the case of Multiple Sclerosis (MS), marijuana seems to bring relief to sufferers like no other painkillers can. Multiple Sclerosis is a debilitating disease that causes damage to the brain and destruction of the protective fatty coating around nerve cells. Subsequently, sufferers of MS tend to experience burning sensations in the limbs, particularly at night. Conventional analgesics can do little to ease this pain. Sufferers say that smoking a joint before bedtime can be the difference between getting sleeping at night and staying awake due to the pain. Sufferers of MS also experience spasms as a result of nerve damage. Marijuana has shown to help control the incidence of spasms in MS sufferers, epilepsy sufferers, and those who have suffered spinal cord injuries. Although there have not been many studies done on this aspect of therapeutic marijuana, the studies that have been done so far suggest that the sufferers may be right. One of the first therapeutic uses of marijuana in the modern era has been its effects in suppressing nausea suffered by anti-cancer chemotherapy patients. The controversy in this case is whether or not marijuana needs to be smoked in order to achieve the full benefits. Unlike THC capsules or other legal nausea suppressors, smoking marijuana in the joint form allows the patients to have control over the dosage. This also allows patients to feel as though they have some sense of control over their bodies while suffering from cancer, a life-threatening illness that they have no control over. Another well-known effect of marijuana is its ability to increase appetite. This could be helpful for anyone who has a decreased appetite due to an illness, especially those with AIDS and cancer patients who are undergoing chemotherapy. Smoking marijuana seems to be a more effective method to increase appetite than ingesting the THC capsule due to the poor absorption of the capsule in the digestive tract. Cost of treatment plays a role in marijuana use because the alternative to smoking marijuana to increase appetite is taking human growth hormone (GH) supplements. Although GH supplements have another benefit in that they also increases lean mass muscle in emaciated AIDS patients, treatment with these supplements cost an average of $36,000 a year. On the other hand a one year's treatment with medicinal marijuana would cost the AIDS patient around $500. Another alternative that was approved by the FDA is the use of Marinol. Marinol is a drug that contains the active ingredient of marijuana, THC. The problem with Marinol is that it doesn't always work as well as smoking marijuana. It is difficult to take just the right dosage of Marinol. If too little is taken, the effects can not be felt but if too much is ingested, then Marinol acts as a sedative. More conclusive studies need to be conducted on the relationship between marijuana and appetite in order to weigh the risks and benefits. On a lighter note that relates to increased appetite is the recent discovery of chemicals found in chocolate that seem to target the same brain receptor system that is targeted by marijuana. One of the chemicals discovered has turned out to be anandamide. "Chocoholics" claim that not only is it the taste that makes them crave chocolate, it is the sensation of "feeling good' after eating chocolate that also plays a big part in the craving. Unlike THC, chocolate's chemicals turn on only a few circumscribed regions in the brain. A 130-pound person would have to eat about 25 pounds of chocolate to obtain a noticeable 'buzz.' Therefore, it is unlikely that one could eat so much chocolate as to experience a high. Yet, chocolate craving is a real physiological phenomena. The exact details of the mechanism by which this occurs is not yet understood. It is hypothesized that the chemicals in chocolate "intensify the sensory properties of chocolate." Or it could be that they elevate the mood directly. This could help explain why people tend to eat a vast amount of chocolate during physiological times of stress. In the long run, this discovery could lead to a new type of treatment for depression. A negative aspect of increased anandamide activity was recently shown by studies done by scientists at the University at Buffalo in New York. It has been known for thirty years that very heavy marijuana smoking has drastic effects on sperm production within the testis. The study showed that human sperm contains receptors for cannabinoids. For the first time, a study showed that cannabinoids can affect three key fertilization processes: 1) Prevention of sperm binding to the egg cover, or zona, 2) Regulation of very active sperm swimming patterns, called hyperactivation, and 3) Inhibition of the acrosomal reaction, the normal release of the sperm enzymes that enable sperm to penetrate the egg. These new findings suggest that the anandamides and THC in marijuana smoke may affect sperm functions required for fertilization in the female reproductive tract. In thirty trials done by Schuel, Burkman, and colleagues, results showed that after six hours, sperm exposed to THC or AM-356 (a synthetic equivalent of the natural anandamide) had a 67% reduction in premature acrosome reactions. Motility studies showed that higher levels of AM-356 inhibited hyperactive swimming while lower concentrations actually stimulated hyperactivation. These results suggest that fluctuations in anandamide concentration levels within the oviduct may regulate sperm swimming patterns and subsequently affect the timing of the sperm meeting the egg. Roger Pertwee, President of the International Cannabinoid Research Society, has conducted studies that have focused on CB1 activity and memory loss. Short-term memory loss has long since been a known effect of cannabis use. The effect of memory loss occurs at the hippocampus. The binding of THC to the CB1 receptors on the hippocampus fits with the ability of cannabis to affect short-term memory. In vitro work has shown that CB1 agonist can prevent long-term potentiation. In a study using a synthetic CB1 antagonist, SR141716A, improved memory in rats was observed. This finding raises the possibility that SR141716A could be used for improving memory in those aging and for those with cognitive disorders, supporting the theory that THC induces short-term memory loss. The use of medicinal marijuana for treatment of glaucoma has had mixed results. Although most patients will tell you that marijuana helps their glaucoma, studies have revealed conflicting conclusions. A study by Keith Green, of the Department of Ophthamology at the Medical College of Georgia, was conducted to see the clinical effects, including toxicological effects, of marijuana and it's many constituent components on the eye and the remainder of the body. The conclusions derived from this study yielded mixed results. In the case of glaucoma, it is widely accepted that the elevated intraocular pressure (IOP) that causes damage to the optic nerve is greatly reduced in 60 to 65 percent of users when marijuana is smoked. That is why until 1991, America's Food and Drug Administration (FDA) permitted ophthamologists to prescribe marijuana to patients for whom all other treatments had failed. However, more recent research shows that the continued use of marijuana at the high dose that is required to control glaucomatous pressure would lead to substantial systemic toxic effects (i.e. increased risk of lung cancer). Concurrently, new glaucoma drugs have been produced. These drugs act at different biological pathways to help reduce the IOP. Yet, no approved drug so far actually makes the eyes' drainage system more efficient than marijuana. In order to circumvent the systemic toxic effects, Keith Green says that "development of drugs based on the cannabinoid molecule or its agonists for use as topical or oral antiglaucoma medications seems to be worthy of further pursuit." A common theme that has been echoed in many of the studies or reviews of studies that have been done is that more research is needed in order for one to come to a clear conclusion about the therapeutic effects of marijuana. For groups who are interested in therapeutic uses, they advocate for proper trials of individual cannabinoids for specific disorders to be performed. Yet, regardless of whether all of the current research is conclusive or not, it has been noted throughout history that people feel relief and obtain pleasure from marijuana. One would find it difficult to discover another drug that has as many benefits as marijuana. In the past, records have shown that people smoked marijuana for its euphoric effects, painkilling quality, and for religious purposes. History has shown that the effects of marijuana can be beneficial. Yet, in the present day, due to advances in research and research techniques, skeptics are not so quick to call marijuana beneficial. The risks of abuse versus therapeutic benefits is the main issue behind the debate of legalizing marijuana. Results obtained from studies that deem marijuana as a "gateway drug," a drug that leads to the consumption of other illicit drugs, have so far proven inconclusive. Studies have shown that there are more benefits to smoking marijuana than there are risks. The results of these studies should be interpreted with caution because most of them produced mixed results. However, for those who use marijuana as a last resort to treat their pain, they should have the option of having access to it via legal channels. Whether physiological evidence supports use or not, those people who use marijuana to sooth illness obviously feel better by using it. If marijuana use is psychological, then so be it. The bottom line is that marijuana use for therapeutic purposes should feel effective to those who are using it. From the hundreds of studies done over the years, scientists and the general public have a general notion of what the short and long term effects are. If one is willing to take the risk and use marijuana to help them cope with their illness, then it is their choice to do so. There is an obvious necessity for more research to be done. Science is headed in the right direction by developing new drugs that mimic the effects of marijuana and by continuing its quest to learn more about it. Until drugs are developed that work as well as smoking marijuana, there should be no doubt that this wonder drug should be allowed for medicinal use. History has dictated that there definitely is a role for marijuana in society. Science has shown that there are more positives than negatives in smoking marijuana. Up to this point in time, all of the evidence presented so far has made it clear that when it comes to the issue of marijuana for therapeutic use, the benefits outweigh the risks.

They look so innocent---like Flintstone vitamins or sugar pills. Your five-year-old would pick them up and eat them, thinking them to be just candy. They come in all shapes and colors. MDMA (3, 4 methylenedioxymethamphetamine), also called Ecstasy, XTC, X, Versace, the hug drug, the love pill, and numerous other names reflecting the various imprints on the pills, is clearly out there in far greater volume than traditional law enforcement seizures have indicated. U.S. Customs had seized only 1,000 MDMA pills in 1995, then 400,000 in 1998 and this exploded into 9.3 million in 2000. Widespread use of this drug is of serious concern due to the risks of immediate and long-term issues from abusing MDMA—This despite the plethora of information on the net swearing that it’s totally safe and just to drink lots of water and stay cool, etc. Our concern is that young people know the truth about all drugs and at least have the opportunity not to fall victim to the drugs and the lies told about them being “safe.” MDMA is extremely popular with groups not so often encountered by law enforcement, especially narcotics officers. Thus, the problem has been growing rapidly during recent years, especially in the rave, techno music crowd, club scene, etc. Without a law enforcement presence on the scene party after party, many young people have lost the distinction between legal herbal ecstasy and illicit ecstasy, for example. Literally—“Everyone is doing it, and no one seems to care (parents or cops)”, they say. We need to care. MDMA was first synthesized in 1912, not as an appetite suppressant or an analog to anything, but as a precursor agent—an intermediate structural compound—possessing properties deemed to contain primary constituents for therapeutically active compounds (as per Cohen’s The Love Drug: Marching to the Beat of ECSTASY). MDMA (which is an analog of MDA; there are numerous related drugs, including MDMB, MDEA, etc.) is commonly, though incorrectly, referred to as a “mixture” of mescaline and amphetamine or commonly as hallucinogenic speed. It is a federal Schedule I drug because it has no approved medical use. It induces a five to seven hour euphoric effect (impairment may last 12 hours), characterized by increased activity, mood alteration and altered perception. MDMA is not a mixture of anything, but is a substance with its own chemical makeup. Though commonly called a “designer drug,” one created as a variation of an already existing and controlled drug to circumvent the controls, it wasn’t created in that fashion. As per Cohen, both MDA and MDMA were identified at about the same time; MDMA is a derivative of MDA and they are structurally similar. MDA wasn’t controlled until the early 70’s. MDMA was federally deemed a Schedule I substance in 1986. An element of the psychiatric world wanted to use it in their practice to open the minds of their patients, claiming that it reduced fear thresholds, opened the door to repressed memories and enable them to develop a bond with their doctors. In fact, in some cases it was given only to the patient; in other practices, the experience was “shared” by the doctor and patient. The product and the statistics The pills or capsules are expensive, commonly $15 to $25 a hit in many areas and $35 to $45 in some more remote areas. When the supply is low, suspects may mix meth with LSD or ketamine or the cough suppressant dextromethorphan (DXM) even GHB powder (anything that gives the hallucinogenic aspect) and represent it to be MDMA. Or, it may be mostly bunk (filler) or dangerous random chemicals or just caffeine and/or ephedrine mixtures (which would actually qualify as “herbal ecstasy” which is also sold at the raves as an extension of or addition to the MDMA). The average weight of an MDMA tablet is 300 milligrams but the actual content of MDMA ranges from 75 to 125 mg per tablet. There is no way to know the quantitative content of a particular pill from the little test kits being sold, leading to really dangerous jumps in dosage when pills come from different sources. In recent years, Israeli organized crime syndicates, some composed of Russian immigrants associated with Russian organized crime syndicates, have established relationships with the Western European traffickers and have gained control over a significant share of the European market. The Israeli syndicates are the primary sources to U.S. distribution groups. This is consistent with large seizures in Los Angeles, for example. This represents a “professionalization” of the MDMA market. Syndicates from other countries are moving into the field too. By the end of 2000, MDMA had made it clear that this is not “kiddy dope.” Bodies in trunks and drive-bys of MDMA dealers who went out on their own or cheated bosses sent a message; dope is dope and bad guys are bad guys. Meanwhile, the federal sentencing guidelines on MDMA were finally upgraded in early 2001. Now 800 pills can get you five years in federal prison (it took 11,000 before). Indicators of use and the paraphernalia Indicators of MDMA use or possession (and the pills themselves with their candy-like façade) appear totally innocent and are simply not recognized by police officers or parents in general. Common paraphernalia: --Tootsie roll pops (any lollipops on a stick) and baby pacifiers –because MDMA causes teeth grinding. The pacifiers are often one of the numerous beaded necklaces worn around their neck or arms. Now some are switching to “mouthguards” which are less noticeable (as cops are starting to zero in on the pacifier issue) and also because some are made to hold the tiny mouth glow sticks (that otherwise could be swallowed or bitten too easily). --Butterfly “wings” and emblems are the universal symbol of MDMA. Dealers often wear hats (which may have a hidden velcro pocket behind the emblem) or shirts with butterfly emblems or “E” or “X” displayed. --Vicks inhalants & Vicks w/face masks (or even cough drops)---fumes (from eucalyptus & menthol) are intensified by the high, resulting in a pleasurable sensation. Light shows and lights wands (hand held or mouth size) are common because visual images are also enhanced by MDMA. --Bags of small Tootsie Rolls. Dealers warm the Tootsie Rolls in hand, or in the microwave, or in the sun, unwrap them, push an MDMA pill into the roll and re-wrap it. This is to elude detection by police. Thus the phrase in reference to taking MDMA—“Doing rolls.” --Open bag of candy such as Skittles (MDMA pills floating loose, mixed with the candy). Again, to avoid detection. May be in a Pez container or mini-M&M canister. --Because of the muscle rigidity/spasms caused by using MDMA and because every touch and rub feels good while under the influence, users may carry Tiger Balm or other lotions for rubbing each other down. Rave parties typically have massage rooms and misting areas (to cool users off). --Be alert for other creative efforts, such as Tylenol capsules that have been emptied and refilled with MDMA powder. Tylenol (or other conventional capsules) in a plastic baggie or appearing damaged in any way would be an indicator. --Be aware of “candy flipping,” the simultaneous ingestion of MDMA and LSD. Other “flips” refer to polydrug use of MDMA and other drugs. Kitty flipping is MDMA and ketamine. Hippy flipping is MDMA and mushrooms, etc. Users start with just one pill, but may increase the number taken at one time due to its reduced impact per usage after the first few experiences. Some may build up tolerance to take as many as ten pills or more at one time with follow up doses during the night. Why MDMA is so popular today and its effects MDMA is not “the usual suspect.” It is a mind-expander, more than it is an “intoxicant.” Take a room full of total strangers, give each one an Ecstasy tablet and Voila!!! Each person now has 50 best friends. To parents (and many officers) the users may not appear “drunk” or drugged in the conventional way, and therefore it isn’t easy to notice. Or, perhaps more accurately, it is easy NOT to notice. As one user (Duke University Medical Center publication) put it, “You feel open, clear, loving. I can’t imagine being angry under its influence, or feeling selfish or mean or even defensive. You have a lot of insights into yourself, real insights, that stay with you after the experience is over. It doesn’t give you anything that isn’t already there. It is not a trip. You don’t lose touch with the world. You could pick up the phone, call your mother, and she’d never know.” As another one put it (on a 20/20 Show re raves), “I could give you (20/20 interviewer) one, and you’d like it. I could give one to the high school principal, and he’d like it. I don’t know anyone who wouldn’t like it.” But not everyone has such a wonderful experience on MDMA. Sadly these young people are often afraid to speak out and think there must be something “wrong” with them that they didn’t enjoy it or simply that they got a “bad drug.” Peer pressure is intense and peer pressure can be deadly. MDMA is not an extremely potent stimulant, though it gives energy and sustains the user through a long session of dancing and gyrating. And, true hallucinations, except with other drugs perhaps, are not characteristic of MDMA. In research, unknown drugs are given to an animal that is trained to recognize a certain class of drugs to see if the animal recognizes the drug being tested. This is a “drug discrimination test.” According to Duke University Medical Center, amphetamine-like drugs are almost never confused with hallucinogens. Confusion between classes doesn’t generally occur……except in the case of MDMA. Some of the animals trained to recognize amphetamines will also recognize MDMA, while some of the animals trained to recognize hallucinogens will recognize MDMA. The psychological effects of MDMA include: Entactogenesis (touching within)—Generalized feeling of peace and happiness and goodness. Common items or sensations may be abnormally beautiful or fascinating. Empathogenesis—a feeling of emotional closeness to other and to one’s self. There is a breakdown in communication barriers, enabling the user to open up to others. This quality gets today’s lonely kids past any potentially awkward of uncomfortable social situations. MDMA is a better socializer that getting drunk with alcohol. Sensory enhancement—Touch, vision, taste, smell, etc., are significantly enhanced or distorted. Textured objects or skin (their own or someone else’s) may be captivating. Tasting and smelling may be greatly enhanced. Calling MDMA the “Love Drug” is a bit of a misnomer as it tends to decrease sexual behavior in both human and animals; it results in “limp noodle syndrome” for men and may restrict orgasm in females as well. The “Hug Drug” is perhaps a better name. It’s more about that loving feeling than it is about sexual activity. Many in today’s scene “hang out” together rather than pair off as “dates.” But unplanned, undesired and unprotected casual sex can take place during recreational drug use and sexual predators may lurk around the rave and party venues looking for females out of control and easily victimized because of their use. And, Viagra is becoming more common in the scene. This is to counter the limp-noodle problem and because even some girls claim to be energized by taking Viagra. While users claim to find self esteem, acceptance of negative experiences, increased self-awareness, open-mindedness, immediate closeness in relationships, etc., the side effects include peripheral vasoconstrictions, tachycardia, pupil dilation, bruxism (teeth grinding), trismus (jaw muscle spasms), other muscle spasms, blurred vision, headaches, eyelid twitches, increase pulse and blood pressure, agitation, nystagmus, nausea, possible exhaustion, dehydration and death. Psychologically, it may cause anxiety, panic attacks, disorientation, depression, delusions, mood swings, lapses in memory and insomnia. Medically, it may cause acute renal (kidney) failure, liver damage, convulsions and seizures, coma, stroke, hyperthermia, cerebral edema, and incontinence. As for MDMA in therapeutic use: The claims are that it opens doors in the mind enabling people to release feelings and accept others and be more open, etc. The flip side of that (seldom discussed) is the possibility that it will open doors in the mind that shouldn’t be opened, at least not without proper counseling supervision. Given the vulnerable age of MDMA users, this could present a mental health danger in its own right. Proponents of MDMA don’t like to talk about the reports of confusion, anxiety, amnesia, panic attacks, depression, mania (excessive excitation), suicide, insomnia, nightmares, depersonalisation (the person feels that they are not real), derealisation (feeling that the surroundings are unreal), hallucinations, flashbacks, post-hallucinogen perceptual disorder, paranoia and other persistent false beliefs, other types of psychosis, automatic or repetitive behavior, dissociative disorders, irritability and aggression with mood swings, tolerance, dependence and increased risk of problems with other drugs (as discussed by Dr. Karl Jansen). Ecstasy could potentially upset the balance of the mind by releasing disturbing material from the unconscious. Psychodynamics maintains that anxiety provoking material “unacceptable” to the waking consciousness is repressed into the unconscious and that defenses are erected against this material. Some psychotherapies may involve bringing such material to the surface so that it can be “worked through” and discharged. ………It is also possible that some of the “liberated” material cannot be easily squashed back in. There may be little chance of ‘working through” the material. …………especially in the middle of an all-night dance fest or local fraternity party, etc. MDMA related deaths---Don’t hug this drug! Cohen’s book refers to numerous MDMA related deaths and notes that they may be the direct result of the effects of MDMA in and of itself, or resulting from the intoxicating effects of MDMA that lead to altered perception and judgment. They are commonly related to operation of a vehicle, or may involve sudden collapses, suicide or unusual activity such as climbing an electrical utility tower. He comments that the autopsies reveal striking changes to the liver, brain and heart. He cites several deaths from 1994 and 1995, including one of a young, first time user whose mother quotes him as saying he “hated drugs and called drug addicts and pushers the scum of the earth.” He cites a teenage waterskiing champion who died from the effects of MDMA. He includes the April 1995 death of a male sophomore at UC Santa Cruz who died from just two MDMA tablets (taken half an hour apart) at a San Francisco area rave. His family was horrified by numerous email messages circulating after his death, saying that it either wasn’t true or that his death was an aberration due to some carelessness on his own part. A 1999 newspaper article discussing how raves originated in England and then moved to the US, cites over 100 British deaths from MDMA. The following are representative of MDMA related deaths. An Asian female died, spring 1999, from MDMA ingestion in Santa Barbara. Alameda County has reported an MDMA related death this summer. Other deaths have occurred nationwide and are usually associated with “burning up” from the effects of MDMA. Users need to drink water continuously to stay hydrated. An 18-year-old Ojai female died on August 4, 1999, in Lake Nacimiento (San Luis Obispo County) while under the influence of a significant amount of MDMA and a small amount of alcohol. She was hanging on the back of the boat platform; she laid her head back and went underwater. She was found two days later; official cause of death was cardiac arrhythmia. An accident this spring involved four Asian female teens from the Walnut area of Los Angeles returning home from a rave. Two died and two were badly injured when the car suddenly just drove off the road. Survivors admitted using MDMA and the two dead females were positive for MDMA. The recent, highly publicized deaths of five teens returning from a rave in the mountains whose vehicle plunged off a 1,000-foot cliff “as though the road just continued” was indeed associated with drug use; all five came back positive for the related drug MDA and/or meth. June 1999, Old Orchard Beach, Maine, a 20-year-old female died after taking MDMA. It was about the third time she had tried the drug. Demetrius DuBose, former professional football player, had alcohol, cocaine and MDMA in his blood at the time he was shot and killed by San Diego police on July 24, 1999. Buffalo, New York, June 1999, two overdoses on MDMA left a 17-year-old female recovering and a 20-year-old female dead after taking it in a nightclub. Former Dallas Cowboys offensive tackle Mark Tuinei had reportedly been taking MDMA heavily during the weeks before his death, which was caused by either MDMA or heroin, according to the coroner. In early 2000 in Northern California, a young man ingested eight MDMA tablets at one time and became ill. He was taken out into the cold night air to cool down but died. Even after being on the cold sidewalk for a while and in the coroner’s refrigerator for several hours, his body temperature was still 106 degrees. In Boulder, Colorado, an MDMA pill given as a 16th birthday present resulted in death from hyponytremia (drinking too much water, trying to cool off from the drugs effects, and flooding life-sustaining sodium from the system). A 1998 Johns Hopkins University study found that MDMA causes permanent brain damage. MDMA causes lasting damage to the nerves that produce serotonin, an important chemical messenger in the human brain that is associated with mood and personality traits, according to the research. Some amount of the damage may regenerate within six or seven years, but the rest is permanent. While risk of death is real, the real threat may be potential damage to long-term mental health. One in ten could be affected. Dr. Michael Morgan, Sussex University, has been researching the serotonin levels in the brains of MDMA users. In an article by BBC reporter Julie Etchingham, Morgan stated, “In the early nineties, it was thought of as a soft drug, analogous to cannabis, but we now know that ecstasy is one of the worst drugs in terms of its long-term harm potential. It is more neurotoxic to the serotonin system than any other drug we know, and this kind of permanent brain damage is something you don’t see with other drugs. Ecstasy is one of the most pernicious and damaging drugs available—and at the same time the second most popular drug in use. It’s a major issue.” One female who had taken ecstasy nearly every weekend for six years, starting at age 13, told Etchingham that she started to suffer panic attacks and severe depression, becoming a basket case for her mother to care for, on and off anti-depressants, in and out of doctors offices. She developed agoraphobia and couldn’t do anything for over a year. Her serotonin levels were found to be two thirds below normal. Her doctors expect her to be on medication for the rest of her life. Another British study, by Drs. Stephany Biello and Richard Dafters, found that MDMA use can damage the users’ body clocks, giving them permanent jet lag. Their work suggests that MDMA disrupts the sensitive clock mechanism in the brain by damaging cells that contain serotonin. The say the research indicates that once a serotonin pathway is disrupted, it can never repair itself. The drug is linked to mood disorders, depression and sleep disruption and resulted in an inability to reset body clocks to certain stimuli. MDMA abuse very widespread MDMA is widely abused across the country, most commonly at rave parties, college campuses and in the club scene. The nicknames for it are as varied as the shapes, colors and imprints you may see. MDMA may come in powder form or in capsules, but most commonly it is in pressed pills. The imprints are generally cartoon characters, business logos, animals, initials, or shapes such as mushrooms or hearts. The pills may be any shape and any color. They are often small white round pills, but may be pink or orange or blue or green, etc. They may be of fine milled texture or may have a more coarse texture with multi-shaded color. The nicknames used generally describe the imprint or color and shape. Blue and white capsules may be called Smurfs, for example. Pills with the imprint of a crown are called Crowns or Royals. They are commonly hidden by mixing them with colorful candies. They are often “crotch packed” into clubs since most security guards are reluctant to do aggressive searches or carried in by females (often in their bras or panties) who are less likely to be searched. This isn’t a benign and safe drug

OXYCONTIN What does it look like? OxyContin is available in tablet form in 5 doses: 10, 20, 40, 80, and 160mg. (However, the manufacturer is no longer shipping 160mg). How is it used? As pain medication, OxyContin is taken every 12 hours because the tablets contain a controlled, time-release formulation of the medication. Most pain medications must be taken every three to six hours. Oxycontin abusers remove the sustained-release coating to get a rapid release of the medication, causing a rush of euphoria similar to heroin. What are its short-term effects? The most serious risk associated with opioids, including OxyContin, is respiratory depression. Common opioid side effects are constipation, nausea, sedation, dizziness, vomiting, headache, dry mouth, sweating, and weakness. Taking a large single dose of an opioid could cause severe respiratory depression that can lead to death. What are its long-term effects? Chronic use of opioids can result in tolerance for the drugs, which means that users must take higher doses to achieve the same initial effects. Long-term use also can lead to physical dependence and addiction -- the body adapts to the presence of the drug, and withdrawal symptoms occur if use is reduced or stopped.Properly managed medical use of pain relievers is safe and rarely causes clinical addiction, defined as compulsive, often uncontrollable use of drugs. Taken exactly as prescribed, opioids can be used to manage pain effectively.

What does it look like? A black or brown block of tar like substance. How is it used? Smoked. What are its short-term effects? Opium can cause euphoria, followed by a sense of well-being and a calm drowsiness or sedation. Breathing slows, potentially to the point of unconsciousness and death with large doses. Other effects can include nausea, confusion and constipation. Use of opium with other substances that depress the central nervous system, such as alcohol, antihistamines, barbiturates, benzodiazepines, or general anesthetics, increases the risk of life-threatening respiratory depression. What are its long-term effects? Long-term use can lead to drug tolerance, meaning the user needs more of the drug to get similar euphorix effects. Opium use can also lead to physical dependence and addiction. Withdrawal symptoms can occur if long term use is reduced or stopped.

What does it look like? White to dark brown powder or tar-like substance. How is it used? Heroin can be used in a variety of ways, depending on user preference and the purity of the drug. Heroin can be injected into a vein ("mainlining"), injected into a muscle, smoked in a water pipe or standard pipe, mixed in a marijuana joint or regular cigarette, inhaled as smoke through a straw, known as "chasing the dragon," snorted as powder via the nose. What are its short-term effects? The short-term effects of heroin abuse appear soon after a single dose and disappear in a few hours.After an injection of heroin, the user reports feeling a surge of euphoria ("rush") accompanied by a warm flushing of the skin, a dry mouth, and heavy extremities. Following this initial euphoria, the user goes "on the nod," an alternately wakeful and drowsy state. Mental functioning becomes clouded due to the depression of the central nervous system. Other effects included slowed and slurred speech, slow gait, constricted pupils, droopy eyelids, impaired night vision, vomiting, constipation. What are its long-term effects? Long-term effects of heroin appear after repeated use for some period of time.Chronic users may develop collapsed veins, infection of the heart lining and valves, abscesses, cellulites, and liver disease. Pulmonary complications, including various types of pneumonia, may result from the poor health condition of the abuser, as well as from heroin's depressing effects on respiration.In addition to the effects of the drug itself, street heroin may have additives that do not really dissolve and result in clogging the blood vessels that lead to the lungs, liver, kidneys, or brain. This can cause infection or even death of small patches of cells in vital organs. With regular heroin use, tolerance develops. This means the abuser must use more heroin to achieve the same intensity or effect. As higher doses are used over time, physical dependence and addiction develop. With physical dependence, the body has adapted to the presence of the drug and withdrawal symptoms may occur if use is reduced or stopped. Withdrawal, which in regular abusers may occur as early as a few hours after the last administration, produces drug craving, restlessness, muscle and bone pain, insomnia, diarrhea and vomiting, cold flashes with goose bumps ("cold turkey"), kicking movements ("kicking the habit"), and other symptoms. Major withdrawal symptoms peak between 48 and 72 hours after the last does and subside after about a week. Sudden withdrawal by heavily dependent users who are in poor health can be fatal.

What does it look like? Meth is a crystal-like powdered substance that sometimes comes in large rock-like chunks. When the powder flakes off the rock, the shards look like glass, which is another nickname for meth. Meth is usually white or slightly yellow, depending on the purity. How is it used? Methamphetamine can be taken orally, injected, snorted, or smoked. What are its short-term effects? Immediately after smoking or injection, the user experiences an intense sensation, called a "rush" or "flash," that lasts only a few minutes and is described as extremely pleasurable. Snorting or swallowing meth produces euphoria - a high, but not a rush. After the initial "rush," there is typically a state of high agitation that in some individuals can lead to violent behavior. Other possible immediate effects include increased wakefulness and insomnia, decreased appetite, irritability/aggression, anxiety, nervousness, convulsions and heart attack. What are its long-term effects? Meth is addictive, and users can develop a tolerance quickly, needing larger amounts to get high. In some cases, users forego food and sleep and take more meth every few hours for days, 'binging' until they run out of the drug or become too disorganized to continue. Chronic use can cause paranoia, hallucinations, repetitive behavior (such as compuslively cleaning, grooming or disasembling and assembling objects), and delusions of parasites or insects crawling under the skin. Users can obsessively scratch their skin to get rid of these imagined insects. Long-term use, high dosages, or both can bring on full-blown toxic psychosis (often exhibited as violent, aggressive behavior). This violent, aggressive behavior is usually coupled with extreme paranoia. Meth can also cause strokes and death.