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NARCOTICS

A narcotic is a natural or synthetic drug related to morphine, according to "Core Concepts in Pharmacology" by Norman Holland and Michael Adams. Narcotics are sometimes prescribed by physicians for pain, although the term narcotic is also loosely used to describe illegal substances. The U.S. Drug Enforcement Agency (DEA) divides narcotics into scheduled categories (I through IV) based on the potential for abuse and medical uses.

History
The term "narcotic" is believed to have been coined by the Greek physician Galen to refer to agents that numb or deaden, causing loss of feeling or paralysis. It is based on the Greek word (narcosis), the term used by Hippocrates for the process of numbing or the numbed state. Galen listed mandrake root, altercus (eclata),[15][not in citation given] seeds, and poppy juice (opium) as the chief examples.[16][17] It originally referred to any substance that relieved pain, dulled the senses, or induced sleep.[18] Now, the term is used in a number of ways. Some people define narcotics as substances that bind at opioid receptors (cellular membrane proteins activated by substances like heroin or morphine) while others refer to any illicit substance as a narcotic. From a legal perspective, narcotic refers to opium, opium derivatives, and their semisynthetic substitutes.[19] Though in U.S. law, due to its numbing properties, cocaine is also considered a narcotic. Sense of "any illegal drug" first recorded 1926, Amer.Eng. The adj. is first attested c.1600.[20]

List of Illegal Drugs:


Ecstasy: Also referred to as
MDMA, Ecstasy is a partial derivative of amphetamine and possesses effects similar to other drugs within the classification. Users of Ecstasy will feel a heightened sense of euphoria and an increased feeling of emotion, as well as sensitivity.

After-effects
Effects reported by some users once the acute effects of MDMA have worn off include: Psychological

Anxiety and paranoia Depression[25][26][27][28] Irritability[26] Fatigue[27][28] Impaired attention, focus, and concentration, as well as drive and motivation (due to depleted serotonin levels)[25] Residual feelings of empathy, emotional sensitivity, and a sense of closeness to others (afterglow) Physiological Dizziness, lightheadedness, or vertigo[28] Loss of appetite[25] Gastrointestinal disturbances, such as diarrhea or constipation Insomnia[25] Aches and pains, usually from excessive physical activity (e.g., dancing)[25][27] Exhaustion[26][28] Jaw soreness, from bruxism[28][29][30] A slang term given to the depressive period following MDMA consumption is Tuesday Blues (or "Suicide Tuesday"), referring to the low mood that can be experienced midweek by depleted serotonin levels following MDMA use on the previous Friday or Saturday when raves or dance concerts were frequently scheduled. Some users report that consuming 5-HTP, LTryptophan and vitamins the day after use can reduce the depressive effect by replenishing serotonin levels (magnesium supplements are also used prior to or during use, in an attempt to prevent jaw/muscle clenching).[31] Chronic use Some studies indicate that repeated recreational users of MDMA have increased rates of depression and anxiety, even after quitting the drug.[48][49] A meta-analytic review of the published literature on memory show that ecstasy users may suffer short-term and long-term verbal memory impairmentwith 7080% of ecstasy users displaying impaired memory[citation needed] . Moreover, this research shows the amount of doses consumed does not significantly predict memory performance.[50] Other meta analyses have reported possibility of impairment of executive functioning.[51] Despite these findings many factors including total lifetime MDMA consumption, the duration of abstinence between uses, dosage, the environment of use, polydrug use/abuse, quality of mental health, various lifestyle choices, and predispositions to develop clinical depression and other disorders have made the results of many studies difficult to verify. A study that attempted to eliminate these confounding factors was published in February 2011 by Addiction, and found few differences in the cognitive functioning of MDMAusing ravers versus non-MDMA-using ravers, "In a study designed to minimize limitations found in many prior investigations, we failed to demonstrate marked residual cognitive effects in ecstasy users. This finding contrasts with many previous findings-including our own-and emphasizes the need for continued caution in interpreting field studies of cognitive function in illicit ecstasy users."[52] MDMA use has been occasionally associated [53] [54] with liver damage, excessive wear of teeth, and (very rarely) hallucinogen persisting [55] perception disorder.

Cocaine:

When in powder form, cocaine

is snorted or ingested by the user. Cocaine is a stimulant that leaves the user feeling more alert, talkative, strong and confident. Cocaine is extremely addictive and is a popular street drug. In a crystallized form, Cocaine is referred to as Crack; when solidified, the Cocaine is smoked by the user. Highs from crack are typically very short and powerful in nature. Crack cocaine is cheaper than the powderized form and highly addictive.

Discovery
For over a thousand years South American indigenous peoples have chewed the leaves ofErythroxylon coca, a plant that contains vital nutrients as well as numerous alkaloids, including cocaine. The coca leaf was, and still is, chewed almost universally by someindigenous communities. The remains of coca leaves have been found with ancient Peruvian mummies, and pottery from the time period depicts humans with bulged cheeks, indicating the presence of something on which they are chewing.[76] There is also evidence that these cultures used a mixture of coca leaves and saliva as an anesthetic for the performance oftrepanation.[77] When the Spanish arrived in South America, most at first ignored aboriginal claims that the leaf gave them strength and energy, and declared the practice of chewing it the work of theDevil.[citation needed] But after discovering that these claims were true, they legalized and taxed the leaf, taking 10% off the value of each crop.[78] In 1569, Nicols Monardes described the practice of the natives of chewing a mixture of tobacco and coca leaves to induce "great contentment": When they wished to make themselves drunk and out of judgment they chewed a mixture of tobacco and coca leaves which make them go as they were out of their wittes. [79] In 1609, Padre Blas Valera wrote: Coca protects the body from many ailments, and our doctors use it in powdered form to reduce the swelling of wounds, to strengthen broken bones, to expel cold from the body or prevent it from entering, and to cure rotten wounds or sores that are full of maggots. And if it does so much for outward ailments, will not its singular virtue have even greater effect in the entrails of those who eat it?[citation needed] Isolation and naming Although the stimulant and hunger-suppressant properties of coca had been known for many centuries, the isolation of the cocainealkaloid was not achieved until 1855. Various European scientists had attempted to isolate cocaine, but none had been successful for two reasons: the

knowledge of chemistry required was insufficient at the time.[citation needed] Additionally contemporary conditions of sea-shipping from South America could degrade the cocaine in the plant samples available to Europeans.[citation needed] The cocaine alkaloid was first isolated by the German chemist Friedrich Gaedcke in 1855. Gaedcke named the alkaloid "erythroxyline", and published a description in the journal Archiv

der Pharmazie.[80]

In 1856, Friedrich Whler asked Dr. Carl Scherzer, a scientist aboard the Novara (an Austrian frigate sent by Emperor Franz Joseph to circle the globe), to bring him a large amount of coca leaves from South America. In 1859, the ship finished its travels and Whler received a trunk full of coca. Whler passed on the leaves to Albert Niemann, a Ph.D. student at the University of Gttingen in Germany, who then developed an improved purification process.[81] Niemann described every step he took to isolate cocaine in his dissertation titled ber eine neue organische Base in den Cocablttern(On a New Organic Base in the Coca Leaves), which was published in 1860it earned him his Ph.D. and is now in the British Library. He wrote of the alkaloid's "colourless transparent prisms" and said that, "Its solutions have an alkaline reaction, a bitter taste, promote the flow of saliva and leave a peculiar numbness, followed by a sense of cold when applied to the tongue." Niemann named the alkaloid "cocaine" from "coca" (from Quechua "cuca") + suffix "ine".[81][82] Because of its use as a local anesthetic, a suffix "caine" was later extracted and used to form names of synthetic local anesthetics. The first synthesis and elucidation of the structure of the cocaine molecule was by Richard Willsttter in 1898.[28] The synthesis started from tropinone, a related natural product and took five steps.

Hallucinogens:

Also referred to

as psychedelic drugs, hallucinogens create a range of perceptual distortion and various psychological symptoms. When a user is under the influence of these drugs, mushrooms, LSD or peyote for example, the individual will observe vibrant colors, transforming shapes and enhanced visions. The term hallucinogen is a misnomer because these drugs do not cause hallucinations at typical doses. Hallucinations, strictly speaking, are perceptions that have no basis in reality, but that appear entirely realistic. A typical "hallucination" induced by a psychedelic drug is more accurately described as a modification of regular perception, and the subject is usually quite aware of the illusory and personal nature of

their perceptions. Deliriants, such as diphenhydramine and atropine, may cause hallucinations in the proper sense. Psychedelics, dissociatives, and deliriants have a long history of use within medicinal and religious traditions around the world. They are used in shamanic forms of ritual healing and divination, in initiation rites, and in the religious rituals of syncretistic movements such asUnio do Vegetal, Santo Daime, and the Native American Church. When used in religious practice, psychedelic drugs, as well as other substances like tobacco, are referred to as entheogens. Also, in some states and on some reservations, certain drugs like peyote are classified as part of a recognized religious ceremony, and if used in said ceremonies, are considered legal. In Canada, mescaline is listed as prohibited under schedule III of the Controlled Drugs and Substances Acts, but peyote is specifically exempt and legally available in Canada. Starting in the mid-20th century, psychedelic drugs have been the object of extensive attention in the Western world. They have been and are being explored as potential therapeutic agents in treating depression, posttraumatic stress disorder,obsessive compulsive disorder, alcoholism, opiate addiction, cluster headaches, and other ailments. Early military research focused on their use as incapacitating agents. Intelligence agencies tested these drugs in the hope that they would provide an effective means ofinterrogation, with little success. Yet the most popular, and at the same time most stigmatized, use of psychedelics in Western culture has been associated with the search for direct religious experience, enhanced creativity, personal development, and "mind expansion". The use of psychedelic drugs was a major element of the 1960s counterculture, where it became associated with various social movements and a general atmosphere of rebellion and strife between generations. Despite prohibition, the recreational, spiritual, and medical use of psychedelics continues today. Organizations, such as MAPS and theHeffter Research Institute, have arisen to foster research into their safety and efficacy, while advocacy groups such as the Center for Cognitive Liberty and Ethics push for their legalization. In addition to this activity by proponents, hallucinogens are also widely used in basic science research to understand the mind and brain. However, ever since hallucinogenic experimentation was discontinued in the late 1960s, research into the therapeutic applications of such drugs have been almost nonexistent, that is until this last decade where research has finally been allowed to resume. In some cases, this includes research in humans, like that conducted by Roland Griffithsand colleagues.

Amphetamines:

Amphetamines

and methamphetamines are stimulants commonly abused by young people at parties or raves. These types of illegal drugs enhance the users energy levels, allowing the individual to stay up all night. Aside from recreational use, these forms of stimulants can be used to medicate

individuals stricken with attention-deficit disorder. Side effects Side effects may consist of severe weight loss, also dependence may develop during use of this drug. Smoking this specific drug may induce a higher threat of dependence for first time users. Amphetamine can also raise the heart rate to dangerous levels. History Amphetamine was first synthesized in 1887 by the Romanian chemist Lazr Edeleanu in Berlin, Germany.[53] He named the compound phenylisopropylamine. It was one of a series of compounds related to the plant derivative ephedrine, which had been isolated from the plant Ma-Huang (Ephedra) that same year by Nagayoshi Nagai.[54] No pharmacological use was found for amphetamine until 1927, when pioneer psychopharmacologist Gordon Alles resynthesized and tested it on himself, in search of an artificial replacement for ephedrine. From 1933 or 1934 Smith, Kline and French began selling the volatile base form of the drug as an inhaler under the trade name Benzedrine, useful as a decongestant but readily usable for other purposes.[55] One of the first attempts at using amphetamine as a scientific study was done by M. H. Nathanson, a Los Angeles physician, in 1935. He studied the subjective effects of amphetamine in 55 hospital workers who were each given 20 mg of Benzedrine. The two most commonly reported drug effects were "a sense of well being and a feeling of exhilaration" and "lessened fatigue in reaction to work".[56] During World War II amphetamine was extensively used to combat fatigue and increase alertness in soldiers. After decades of reported abuse, the FDA banned Benzedrine inhalers, and limited amphetamine to prescription use in 1965, but non-medical use remained common. Amphetamine became a schedule II drug in the USA under the Controlled Substances Act in 1971. The related compound methamphetamine, in its crystallized form, was first synthesized from ephedrine in Japan in 1920 by chemistAkira Ogata, via reduction of ephedrine using red phosphorus and iodine. The pharmaceutical Pervitin was a tablet of 3 mgmethamphetamine that was available in Germany from 1938 and widely used in the Wehrmacht, but by mid-1941 it became a controlled substance, despite this new classification, methamphetamine and the cocaine-derivative referred to as "Codename D-IX" were distributed by military doctors across both the Western and Eastern theatres of war. During the course of the war over 200 millionPervitin pills were prescribed to Wehrmacht combatants.[57][58] In 1997 and 1998,[59][60] researchers at Texas A&M University claimed to have found amphetamine and methamphetamine in the foliage of two Acacia species native to Texas, A. berlandieri and A. rigidula. Previously, both of these compounds had been thought to be human inventions. These findings have never been duplicated, and the analyses are believed by many biochemists to be the result of experimental error, and as such the validity of the report has come into question. Alexander Shulgin, one of the most experienced biochemical investigators and the discoverer of many new psychotropic substances, has tried to contact the Texas A&M researchers and verify their findings. The authors of the paper have not responded; natural amphetamine remains an unconfirmed discovery

Rohypnol:

This type of illegal drug

is a tranquilizer similar to Valium or painkillers but approximately 10 times more potent. This classification of drugs is extremely addictive; Rohypnol is commonly abused either for its intoxicating, sedative or numbing characteristics. Interactions The use of flunitrazepam in combination with alcohol synergizes the adverse effects, and can lead to toxicity and death. Flunitrazepam is metabolized almost completely by cytochrome P450-3A4. Atorvastatin administration along with flunitrazepam results in a reduced elimination rate of this molecule. Grapefruit juice reduces intestinal 3A4 and results in less metabolism and higher plasma concentrations of flunitrazepam, which could result in overdose. Overdose Flunitrazepam is a drug that is frequently involved in drug intoxication, including overdose.[14][15] Overdose of flunitrazepam may result in excessive sedation, impairment of balance and speech. This may progress in severe overdoses to respiratory depression or coma and possibly death. The risk of overdose is increased if flunitrazepam is taken in combination with CNS depressants such as alcohol andopiates. Flunitrazepam overdose responds to the benzodiazepine receptor antagonist flumazenil, which thus can be used as a treatment. Presence in bodily fluids Flunitrazepam can be measured in blood or plasma to confirm a diagnosis of poisoning in hospitalized patients, provide evidence in an impaired driving arrest, or assist in a medicolegal death investigation. Blood or plasma flunitrazepam concentrations are usually in a range of 5-20 g/L in persons receiving the drug therapeutically as a nighttime hypnotic, 10-50 g/L in those arrested for impaired driving and 100-1000 g/L in victims of acute fatal overdosage. Urine is often the preferred specimen for routine drug abuse monitoring purposes. The presence of 7aminoflunitrazepam, a pharmacologically-active metabolite and in vitro degradation product, is useful for confirmation of flunitrazepam ingestion. In postmortem specimens, the parent drug may have been entirely degraded over time to 7-aminoflunitrazepam.[16][17][18]

Recreational use

A 1989 journal on Clinical Pharmacology reports that benzodiazepines, including flunitrazepam, accounted for the largest volume of forged drug prescriptions in Sweden, a total of 52% of drug forgeries being for benzodiazepines, suggesting that benzodiazepines was a major

prescription drug class of abuse. Nitrazepam and flunitrazepam accounted for the vast majority of forged prescriptions.[19] Flunitrazepam and other sedative hypnotic drugs are detected frequently in cases of people suspected of driving under the influence of drugs. Other benzodiazepines (anxiolytic orhypnotic) and zolpidem and zopiclone (as well as similar hypnotic and anxiolytic drugs from the nonbenzodiazepine families cyclopyrrolones, imidazopyridines, andpyrazolopyrimidines) are also found in high numbers of suspected drugged drivers. Many drivers have blood levels far exceeding the therapeutic dose range suggesting a high degree of abuse potential for benzodiazepines and similar drugs.[ Suicide In studies in Sweden, flunitrazepam was the second-most-common drug used in suicides, being found in about 16% of cases. In a retrospective Swedish study of 1587 deaths, in 159 cases benzodiazepines were found. In suicides when benzodiazepines were implicated, the benzodiazepines flunitrazepam and nitrazepam were occurring in significantly higher concentrations, compared to natural deaths. In four of the 159 cases, where benzodiazepines were found, benzodiazepines alone were the only cause of death. It was concluded that flunitrazepam and nitrazepam might be more the assailant, or the events surrounding the assault. It is difficult to estimate just how many flunitrazepam-facilitated rapes have occurred. Very often, biological samples are taken from the victim at a time when the effects of the drug have already passed and only residual amounts remain in the body fluids. These residual amounts are difficult, and sometimes impossible, to detect using standard screening assays used in most countries. If flunitrazepam exposure is to be detected at all, urine samples need to be collected within 72 hours and subjected to sensitive analytical tests. The problem is compounded by the onset of amnesia after ingestion of the drug, which causes the victim to be uncertain about the facts surrounding the rape. This uncertainty may lead to critical delays or even reluctance to report the rape and provide appropriate biological samples for testing. If a person suspects that he or she is the victim of a flunitrazepam-facilitated rape, he or she should get laboratory testing for flunitrazepam as soon as possible. In recent news, it has been discovered that scientists can now detect flunitrazepam and related compounds in urine at least up to 5 days after administration of a single dose of Rohypnol and up to a month in hair. An inability to remember events, including sexual encounters, is not conclusive evidence of having consumed a drugged drink: Psychotropic CNS depressant drugs such as alcohol can cause blackouts, sleepiness, and a reduction in inhibitions. Only a timely screening for flunitrazepam can demonstrate its use. It has been shown that alcohol alone is the psychotropic substance used in the vast majority of cases of drug-facilitated date-rape. A recent study conducted by doctors in the UK found that none of the subjects reporting spiked drinks had any traces of flunitrazepam or other medications popularly believed to be associated with drug-assisted rape, such as GHB. However, flunitrazepam was prohibited for prescription under the NHS in 1992 (The National Health Service (General Medical Services). Rohypnol (1 mg) is available under private prescription. The study results, however, suggest that binge drinking is more commonly a factor in drug-assisted rapes than pharmaceutical drugs.

Drug-facilitated robbery In the United Kingdom, the use of flunitrazepam and other "date rape" drugs have been connected to stealing from sedated victims. One expert quoted in a British newspaper estimated that up to 2,000 individuals are robbed each year after being spiked with powerful sedatives,[26] making drug-assisted robbery a more commonly reported problem than drugassisted rape. In a notable flunitrazepam-related case, Selina Hakki was convicted in December 2004 and sentenced to five years in prison for using flunitrazepam to drug wealthy men and rob them of their clothes and accessories in the UK.[27] Flunitrazepam is also known to induce anterograde amnesia making police interrogations more difficult.[28][29][30] Adverse effects of flunitrazepam include dependence, both physical and psychological; reduced sleep quality resulting in somnolence; and overdose, resulting in excessive sedation, impairment of balance and speech, respiratory depression or coma, and possibly death. Because of the latter, flunitrazepam is commonly used in suicide. When used in pregnancy, it might cause hypotonia. toxic than other benzodiazepines. Drug-facilitated sexual assault

Main article: Drug facilitated sexual assault

Flunitrazepam is known to induce anterograde amnesia in sufficient doses; individuals are unable to remember certain events that they experienced while under the influence of the drug. This effect is particularly dangerous when flunitrazepam is used to aid in the commission of sexual assault; victims may be unable to clearly recall the assault, the assailant, or the events surrounding the assault. It is difficult to estimate just how many flunitrazepam-facilitated rapes have occurred. Very often, biological samples are taken from the victim at a time when the effects of the drug have already passed and only residual amounts remain in the body fluids. These residual amounts are difficult, and sometimes impossible, to detect using standard screening assays used in most countries. If flunitrazepam exposure is to be detected at all, urine samples need to be collected within 72 hours and subjected to sensitive analytical tests. The problem is compounded by the onset of amnesia after ingestion of the drug, which causes the victim to be uncertain about the facts surrounding the rape. This uncertainty may lead to critical delays or even reluctance to report the rape and provide appropriate biological samples for testing. If a person suspects that he or she is the victim of a flunitrazepam-facilitated rape, he or she should get laboratory testing for flunitrazepam as soon as possible. In recent news, it has been discovered that scientists can now detect flunitrazepam and related compounds in urine at least up to 5 days after administration of a single dose of Rohypnol and up to a month in hair. An inability to remember events, including sexual encounters, is not conclusive evidence of having consumed a drugged drink: Psychotropic CNS depressant drugs such as alcohol can cause blackouts, sleepiness, and a reduction in inhibitions. Only a timely screening for flunitrazepam can demonstrate its use. It has been shown that alcohol alone is the psychotropic substance used in the vast majority of cases of drug-facilitated date-rape. A recent study conducted by doctors in the UK found that none of the subjects reporting spiked drinks had any traces of flunitrazepam or other medications popularly believed to be associated with drug-assisted rape,

such as GHB. However, flunitrazepam was prohibited for prescription under the NHS in 1992 (The National Health Service (General Medical Services). Rohypnol (1 mg) is available under private prescription. The study results, however, suggest that binge drinking is more commonly a factor in drug-assisted rapes than pharmaceutical drugs. Drug-facilitated robbery In the United Kingdom, the use of flunitrazepam and other "date rape" drugs have been connected to stealing from sedated victims. One expert quoted in a British newspaper estimated that up to 2,000 individuals are robbed each year after being spiked with powerful sedatives,[26] making drug-assisted robbery a more commonly reported problem than drugassisted rape. In a notable flunitrazepam-related case, Selina Hakki was convicted in December 2004 and sentenced to five years in prison for using flunitrazepam to drug wealthy men and rob them of their clothes and accessories in the UK.[27] Flunitrazepam is also known to induce anterograde amnesia making police interrogations more difficult.[28][29][30]

Adverse effects

Adverse effects of flunitrazepam include dependence, both physical and psychological; reduced sleep quality resulting in somnolence; and overdose, resulting in excessive sedation, impairment of balance and speech, respiratory depression or coma, and possibly death. Because of the latter, flunitrazepam is commonly used in suicide. When used in pregnancy, it might cause hypotonia.

Other effects
After discontinuation of flunitrazepam, a rebound effect may occur about 4 days after stopping flunitrazepam.[35] (See benzodiazepine withdrawal syndrome) Flunitrazepam impairs cognitive functions. This may appear as lack of concentration, confusion and anterograde amnesia. It can be described as a hangover-like effect, with impairment of mental arithmetic abilities. Impaired psychomotor functions is another adverse effect, affecting reaction time and driving skill. This may also be expressed as impaired coordination, impaired balance and dizziness. Other adverse effects include: Slurred speech Gastrointestinal disturbances, lasting 12 or more hours/Vomiting Respiratory depression in higher doses Special precautions Benzodiazepines require special precaution if used in the elderly, during pregnancy, in children, in alcohol- or drug-dependent individuals, and in individuals with comorbid psychiatric disorders.[36] Impairment of driving skills with a resultant increased risk of road traffic accidents is probably the most important adverse effect. This side-effect is not unique to flunitrazepam but also occurs with otherhypnotic drugs. Flunitrazepam seems to have a particularly high risk of road traffic accidents compared to other hypnotic drugs. Extreme caution should be exercised by drivers after taking flunitrazepam.

Flunitrazepam, similar to other benzodiazepines and nonbenzodiazepine hypnotic drugs, causes impairments in body balance and standing steadiness in individuals waking up at night or the next morning. Falls and hip fractures are frequently reported. The combination with alcohol increases these impairments. Partial, but incomplete tolerance develops to these impairments.

Cannabis (/knbs/; Cn-na-bis)

a genus of flowering plants that three putative varieties, Cannabis [1] sativa, Cannabis indica,[1] and Cannabis ruderalis. These three taxaare indigenous to Central Asia, [2] and South Asia. Cannabis has long been used for fibre (hemp), for seed and seed oils, for medicinal purposes, and as a recreational drug. Industrialhemp products are made from Cannabis plants selected to produce an abundance of fiber. To satisfy the UN Narcotics Convention, some Cannabis strains have been bred to produce minimal levels of THC, the principal psychoactive constituent responsible for the "high" associated with marijuana. Marijuana consists of the dried flowers of Cannabis plants selectively bred to produce high levels of THC and other psychoactive cannabinoids. Various extracts including hashish and hash oil are also produced from the plant. Popular usage The scientific debate regarding taxonomy has had little effect on the terminology in widespread use among cultivators and users of drug-type Cannabis. Cannabis aficionados recognize three distinct types based on such factors as morphology, native range, aroma, and subjective psychoactive characteristics. Sativa is the most widespread variety, which is usually tall, laxly branched, and found in warm lowland regions. Indica designates shorter, bushier plants adapted to cooler climates and highland environments. Ruderalis is the informal name for the short plants that grow wild in Europe and central Asia. Breeders, seed companies, and cultivators of drug type Cannabis often describe the ancestry or gross phenotypic characteristics ofcultivars by categorizing them as "pure indica," "mostly indica," "indica/sativa," "mostly sativa", or "pure sativa." One of the most popular and potent sativas in Africa is Malawi Gold, locally known as chamba. It is internationally known for its potency and its flavor.

is includes

Opium (poppy

tears, lachryma papaveris) is

the dried latex obtained from the opium poppy (Papaver somniferum). Opium contains approximately 12% morphine, analkaloid, which is frequently processed chemically to produce heroin for the illegal drug trade. The latex also includes codeine and non-narcotic alkaloids such aspapaverine, thebaine and noscapine. The traditional method of obtaining the latex is to scratch ("score") the immature seed pods (fruits) by hand; the latex leaks out and dries to a sticky yellowish residue that is later scraped off. The modern method is to harvest and process mature plants by machine. "Meconium" historically referred to related, weaker preparations made from other parts of the poppy or different species of poppies.[1] The production of opium itself has not changed since ancient times. Through selective breeding of the Papaver somniferum plant, the content of the phenanthrenealkaloids morphine, codeine, and to a lesser extent thebaine, has been greatly increased. In modern times, much of the thebaine, which often serves as the raw material for the synthesis for hydrocodone, hydromorphone, and other semi-syntheticopiates, originates from extracting Papaver orientale or Papaver bracteatum. Opium for illegal use is often converted into heroin, which is less bulky, making it easier to smuggle, and which multiplies its potency to approximately twice that of morphine. Heroin can be taken by intravenous injection, intranasally, or smoked (vaporized) and inhaled.

History
Cultivation of opium poppies for food, anaesthesia, and ritual purposes dates back to at least theNeolithic Age (new stone age). The Sumerian, Assyrian, Egyptian, Indian, Minoan, Greek, Roman,Persian and Arab Empires all made widespread use of opium, which was the most potent form of pain relief then available, allowing ancient surgeons to perform prolonged surgical procedures. Opium is mentioned in the most important medical texts of the ancient world, including the Ebers Papyrus and the writings of Dioscorides, Galen, and Avicenna. Widespread medical use of unprocessed opium continued through the American Civil War before giving way to morphine and its successors, which could be injected at a precisely controlled dosage. In China, recreational use of this drug began in the 15th century, but was limited by its rarity and expense. Opium trade became more regular by the 17th century, when it was mixed with tobacco for smoking, and addiction was first recognized.[citation needed] Opium prohibition in China began in 1729, yet was followed by nearly two centuries of increasing opium use. China had a positive balance sheet in trading with the British, which led to a decrease of the British silver

stocks. Therefore, the British tried to encourage Chinese opium use to enhance their balance, and they delivered it from Indian provinces under British control. In India, its cultivation, as well as the manufacture and traffic to China, were subject to the East India Company, as a strict monopoly of the British government.[2] For supervising and managing the business, there was an extensive and complicated system of government agencies. A massive confiscation of opium by the Chinese emperor, who tried to stop the opium deliveries, led to two Opium Wars in 1839 and 1858, in which Britain suppressed China and traded opium all over the country. After 1860, opium use continued to increase with widespread domestic production in China, until more than 25% of the male population were regular consumers by 1905. Recreational or addictive opium use in other nations remained rare into the late 19th century, recorded by an ambivalent literature that sometimes praised the drug. Global regulation of opium began with the stigmatization of Chinese immigrants and opium dens in San Francisco, California, leading rapidly from town ordinances in the 1870s to the formation of the International Opium Commission in 1909. During this period, the portrayal of opium in literature became squalid and violent, British opium trade was largely supplanted by domestic Chinese production, purified morphine and heroin became widely available for injection, and patent medicines containing opiates reached a peak of popularity. Opium was prohibited in many countries during the early 20th century, leading to the modern pattern of opium production as a precursor for illegal recreational drugs or tightly regulated legal prescription drugs. Illicit opium production, now dominated byAfghanistan, was decimated in 2000, when production was banned by the Taliban, but has increased steadily since the fall of the Taliban in 2001 and over the course of the war in Afghanistan.[3][4] Worldwide production in 2006 was 6610 metric tons[5]nearly one-fifth the level of production in 1906.

Methamphetamine (USAN)
(pron.: /mmftmin/), also known [2] [3] as metamfetamine(INN), meth, ice, cryst al,[4] glass,[4] tik,[5] Nmethylamphetamine,methylamphetamine, and desoxyephedrine, is a psychostimulant of thephenethylamine and amphetamine class of psychoactive drugs. Methamphetamine occurs in two enantiomers, dextrorotary and levorotary ; dextromethamphetamine possesses the wellknown psychostimulant effects of the drug, while levomethamphetamine is CNS-inactive. Although rarely prescribed,[6]dextromethamphetamine is approved by the U.S. Food and Drug Administration (FDA) for the treatment of ADHD and obesity under the trade name Desoxyn, while levomethamphetamine is a non-prescription over-the-counter nasal decongestant.

Illicitly, methamphetamine may be sold either as pure dextromethamphetamine or in aracemic mixture. Both dextromethamphetamine and racemic methamphetamine areSchedule II controlled substances in the United States, and similarly the production, distribution, sale, and possession of methamphetamine is restricted or illegal in manyjurisdictions. Internationally, methamphetamine has been placed in Schedule II of theUnited Nations Convention on Psychotropic Substances treaty.[7] In low dosages, methamphetamine can increase alertness, concentration, and energy in fatigued individuals. In higher doses, it can induce mania with accompanying euphoria, feelings of selfesteem and increased libido.[8][9] Methamphetamine has a high potential forabuse and addiction, activating the psychological reward system by triggering a cascading release of dopamine in the brain characterized by Amphetamine /Stimulant psychosis. Chronic abuse may also lead to post-withdrawal syndrome, a result of methamphetamineinduced neurotoxicity to dopaminergic neurons. Post-withdrawal syndrome can persist beyond the withdrawal period for months, and sometimes up to a year.[10] In addition to psychological harm, physical harm primarily consisting of cardiovascular damage may occur with chronic use or acute overdose.[11]

Uses Methamphetamine has found use as both a medicinal and recreational drug. Effects

Physical Physical effects can include anorexia, hyperactivity, dilated pupils, flushed skin, excessive sweating, restlessness, dry mouth andbruxism (leading to "meth [15] mouth"), headache, accelerated heartbeat, slowed heartbeat, irregular heartbeat, rapid breathing, highblood pressure, low blood pressure, high body temperature, diarrhea, constipation, blurred vision, dizziness, twitching, insomnia,numbness, palpitations, tremors, dry and/or itchy [16] skin, acne, pallor, and with chronic and/or high doses convulsions, heart [17] [18] [18][19][20][21][22][23] attack, stroke, and death. Psychological Psychological effects can include euphoria, anxiety, increased libido, alertness, concentration, increased energy, increased self-esteem, self-confidence, sociability, irritability, aggressiveness, psychosomatic disorders, psychomotor agitation,dermatillomania(compulsive skin picking), hair pulling, delusions of grandiosity, hallucinations, excessive feelings of power and invincibility, repetitive and obsessive behaviors, paranoia, and with chronic use and/or high doses amphetamine psychosis.[18][24] Withdrawal Withdrawal symptoms of methamphetamine primarily consist of fatigue, depression, and increased appetite. Symptoms may last for days with occasional use and weeks or months with chronic use, with severity dependent on the length of time and the amount of methamphetamine used. Withdrawal symptoms may also include anxiety, irritability, headaches, agitation, restlessness, excessive sleeping, vivid or lucid dreams, deep REM sleep, and suicidal ideation.[25]

Long-term Methamphetamine use has a high association with depression and suicide as well as serious heart disease, amphetamine psychosis,anxiety, and violent behaviors. Methamphetamine also has a very high addiction risk.[11] Methamphetamine is not directly neurotoxic but long-term use can have neurotoxic sideeffects. Its use is associated with an increased risk of Parkinson's disease due to the fact that uncontrolled dopamine release is neurotoxic.[10][26] Long-term dopamine upregulation occurring as a result of Methamphetamine abuse can cause neurotoxicity, which is believed to be responsible for causing persisting cognitive deficits, such as memory loss, impaired attention, and decreased executive function. Similar to the neurotoxic effects on the dopamine system, methamphetamine can also result in neurotoxicity to the serotonin system.[27] In a study of incarcerated Japanese women who experienced methamphetamine-induced psychosis, 49% experienced "flashbacks" afterward and 21% remained in their psychotic state for more than six months. Other studies in Japan show that those who experience methamphetamine-induced psychosis are much more likely to experience psychotic symptoms again if they use methamphetamine.[28] Tolerance As with other amphetamines, tolerance to methamphetamine is not completely understood but is known to be sufficiently complex that it cannot be explained by any single mechanism. The extent of tolerance and the rate at which it develops vary widely between individuals, and even within one person. It is highly dependent on dosage, duration of use, and frequency of administration. Tolerance to the awakening effect of amphetamines does not readily develop, making them suitable for the treatment of narcolepsy.[29] Short-term tolerance can be caused by depleted levels of neurotransmitters within the synaptic vesicles available for release into thesynaptic cleft following subsequent reuse (tachyphylaxis). Short-term tolerance typically lasts until neurotransmitter levels are fully replenished; because of the toxic effects on dopaminergic neurons, this can be greater than 23 days. Prolonged overstimulation ofdopamine receptors caused by methamphetamine may eventually cause the receptors to downregulate in order to compensate for increased levels of dopamine within the synaptic cleft.[30] To compensate, larger quantities of the drug are needed in order to achieve the same level of effects. Reverse tolerance or sensitization can also occur.[29] The effect is well established, but the mechanism is not well understood.

History
Crystal methamphetamine was firstsynthesized in 1919 by Akira Ogata Discovery Shortly after the first synthesis of amphetamine in 1887,[97] methamphetamine was synthesized from ephedrine 1893 by Japanese chemist Nagai Nagayoshi.[98] The term "methamphetamine" was derived from elements of the chemical structure of this new compound: methyl alpha-methyl phenyl ethyl amine. In 1919, crystallized methamphetamine was

synthesized by pharmacologist Akira Ogata via reduction of ephedrine using [97] red phosphorus and iodine. Military use One of the earliest uses of methamphetamine was during World War II, when it was used by Axis and Allied forces.[99] The company Temmler produced methamphetamine under the trademark Pervitin and so did the German and Finnish militaries. It was also dubbed "Pilot's chocolate" or "Pilot's salt".[100] It was widely distributed across rank and division, from elite forces to tank crews and aircraft personnel, with many millions of tablets being distributed throughout the war.[101] Its use by German Panzer crews also lead to it being known as "Panzerschokolade" ("Panzer chocolate" or "tankers' chocolate").[102][103] More than 35 million three-milligram doses of Pervitin and the closely related Isophan were manufactured for the German army and air force between April and July 1940.[104] From 1942 until his death in 1945, Adolf Hitler may have been given intravenous injections of methamphetamine by his personal physician Theodor Morell. It is possible that it was used to treat Hitler's speculated Parkinson's disease, or that his Parkinson-like symptoms that developed from 1940 onwards resulted from using methamphetamine.[105] In Japan, methamphetamine was sold under the registered trademark of Philopon ([106] hiropon[107]) by Dainippon Pharmaceuticals (present-day Dainippon Sumitomo Pharma) for civilian and military use. As with the rest of the world at the time, the side effects of methamphetamine were not well studied, and regulation was not seen as necessary. In the 1940s and 1950s the drug was widely administered to Japanese industrial workers to increase their productivity.[108] Methamphetamine and amphetamine were given to Allied bomber pilots during World War II to sustain them by fighting off fatigue and enhancing focus during long flights. The experiment failed because soldiers became agitated, could not channel their aggression and showed impaired judgment.[97] Rather, dextroamphetamine (Dexedrine) became the drug of choice for American bomber pilots, being used on a voluntary basis by roughly half of the U.S. Air Force pilots during the Persian Gulf War, a practice which came under some media scrutiny in 2003 after a mistaken attack on Canadian troops.[109] Medical and legal over-the-counter sales Following the use of amphetamine (such as Benzedrine, introduced 1932) in the 1930s for asthma, narcolepsy, and symptoms of the common cold, [97] in 1943, Abbott Laboratories requested U.S. FDA approval of methamphetamine for treatment of narcolepsy, milddepression, postencephalitic parkinsonism, chronic alcoholism, cerebral arteriosclerosis, and hay fever, which was granted in December 1944.[citation needed] Sale of the massive postwar surplus of methamphetamine in Europe, North America, and Japan stimulated civilian demand.[100] After World War II, a large Japanese military stockpile of methamphetamine, known by its trademark Philopon, flooded the market.[110] Post-war Japan experienced the first methamphetamine epidemic, which later spread to Guam, the U. S. Marshall Islands, and to the U. S. West Coast.[97] In 1948, the Philopon trademark came under a well-publicized lawsuit [110] by Philips Corporation. Philips, under its Koninklijke division, filed suit against Dainippon Pharmaceuticals to cease using Philipon as the commercial name for methamphetamine. Philips claimed the exclusive right to use the trademark as a portmanteau of Philips and Nippon, the

Japanese name of the country. DSP's attorneys challenged Philips' standing to sue as a foreign (Dutch) corporation. The matter was ultimately settled out of court in 1952, with Dainippon Pharmaceuticals agreeing to pay Philips a 5% royalty on worldwide sales of methamphetamines sold by DSP under the Philopon label. The Japanese Ministry of Health banned production less than a year later.[111] In the 1950s, there was a rise in the legal prescription of methamphetamine to the American public. In the 1954 edition of Pharmacology and Therapeutics, indications for methamphetamine included "narcolepsy, postencephalitic parkinsonism, alcoholism, certain depressive states, and in the treatment of obesity."[112] Methamphetamine constituted half of the amphetamine salts for the original formulation for the diet drug Obetrol, which later became the ADHD drug Adderall. Methamphetamine was also marketed for sinus inflammation or for non-medicinal purposes as "pep pills" or "bennies".[97] Recreational use and prohibitive regulations In 1950 the Japanese Ministry of Health banned stimulant production, but drug companies continued to produce stimulants and they wound up on the black market. From 1951 to 1954 a series of acts were passed by the Japanese government to try to stop production and sale of stimulants; however, the production and sale of stimulant drugs continued through criminal syndicates such as Yakuzacriminal organizations.[111] On the streets, it is also known as S, Shabu, and Speed, in addition to its old trademarked name. The 1960s saw the start of significant use of clandestinely manufactured methamphetamine, most of which was produced bymotorcycle gangs. It was also prescribed by San Franciscan drug clinics to treat heroin addiction.[97] Beginning in the 1990s, the production of methamphetamine in users' own homes for personal and recreational use became popular. In 1970, methamphetamine was regulated in the Controlled Substances Act in the U. S., and a public education campaign was mounted against it.[97] By the 2000s, the only two FDA approved marketing indications remaining for methamphetamine were for attention-deficit hyperactivity disorder (ADHD) and the short-term management of exogenous obesity, although the drug is clinically established as effective in the treatment of narcolepsy.[14]

Crack

cocaine is

the freebase form

of cocaine that can be smoked. It may also be termedrock, work,[1] hard, iron, cavvy, base, or just crack; it is said to be the most addictive form of cocaine,[2] although this has been contested. Crack rocks offer a short but intensehigh to smokers.[3][4] Crack appeared primarily in impoverished inner-city neighborhoods inNew York, Los Angeles, and Miami in late 1984 and 1985. Psychological effects

Crack cocaine is a substance that affects the brain chemistry of the user: causing euphoria,[7] supreme confidence,[8] loss of appetite,[7] insomnia,[7] alertness,[7] increased energy,[7] a craving for more cocaine,[8] and potential paranoia (ending after use).[7][9] Its initial effect is to release a large amount of dopamine,[3] a brain chemical inducing feelings of euphoria[citation needed]. The high usually lasts from 510 minutes,[3][7] after which time dopamine levels in the brain plummet, leaving the user feeling depressed and low.[3]When cocaine is dissolved and injected, the absorption into the bloodstream is at least as rapid as the absorption of the drug which occurs when crack cocaine is smoked, [7] and similar euphoria may be experienced. A typical response among users is to have another hit of the drug; however, the levels of dopamine in the brain take a long time to replenish themselves, and each hit taken in rapid succession leads to progressively less intense highs.[3] However, a person might binge for 3 or more days without sleep, while partying with hits from the pipe.[9] Use of cocaine in a binge, during which the drug is taken repeatedly and at increasingly high doses, leads to a state of increasing irritability, restlessness, and paranoia. [7] This may result in a full-blown paranoid psychosis, in which the individual loses touch with reality and experiences auditory hallucinations.[7] Stimulant drug abuse (particularly amphetamine and cocaine) can lead to delusional parasitosis (aka Ekbom's Syndrome: a mistaken belief they are infested with parasites). [10] For example, excessive cocaine use can lead to formication, nicknamed "cocaine bugs" or "coke bugs," where the affected people believe they have, or feel, parasites crawling under their skin.[10] (Similar delusions may also be associated with high fever or in connection with alcohol withdrawal, sometimes accompanied by visual hallucinations of insects.)[10] People experiencing these hallucinations might scratch themselves to the extent of serious skin damage and bleeding, especially when they are delirious.[9][10] Physiological effects The short-term physiological effects of cocaine include[7] constricted blood vessels, dilated pupils, and increased temperature, heart rate, and blood pressure. Large amounts (several hundred milligrams or more) intensify the user's high, but may also lead to bizarre, erratic, and violent behavior.[7] Large amounts can induce tremors,vertigo, muscle twitches, paranoia, or, with repeated doses, a toxic reaction closely resembling amphetamine poisoning.[7] Some users of cocaine report feelings of restlessness, irritability, and anxiety. In rare instances, sudden death can occur on the first use of cocaine or unexpectedly thereafter.[7] Cocaine-related deaths are often a result of cardiac arrest or seizures followed by respiratory arrest. An appreciable tolerance to cocaines high may develop, with many addicts reporting that they seek but fail to achieve as much pleasure as they did from their first experience. [7] Some users will frequently increase their doses to intensify and prolong the euphoric effects. While tolerance to the high can occur, users might also become more sensitive (drug sensitization) to cocaine's local anesthetic (pain killing) and convulsant (seizure inducing) effects, without increasing the dose taken; this increased sensitivity may explain some deaths occurring after apparent low doses of cocaine.[7] Addiction

Main article: Substance dependence

Crack cocaine is popularly thought to be the most addictive form of cocaine. [2] However, this claim has been contested: Morgan and Zimmer wrote that available data indicated that "...smoking cocaine by itself does not increase markedly the likelihood of dependence.... The claim that cocaine is much more addictive when smoked must be reexamined."[11] They argued that cocaine users who are already prone to abuse are most likely to "move toward a more efficient mode of ingestion" (that is, smoking). The intense desire to recapture the initial high is what is so addictive for many users. [3] On the other hand, Reinarman et al. wrote that the nature of crack addiction depends on the social context in which it is used and the psychological characteristics of users, pointing out that many heavy crack users can go for days or weeks without using the drugs. [12]

Psilocybin mushrooms are fungi that


contain psychoactive indole alkaloids. There are multiple colloquial terms for psilocybin mushrooms, the most common being shrooms andmagic mushrooms.[1] Biological genera containin g psilocybin mushrooms includeAgrocybe, Conocybe, Copelandia, Galerina, Gerronema, Gymnopilus, Hyphol oma, Inocybe,Mycena, Panaeolus, Pluteus, and Psilocybe. There are approximately 190 species of psilocybin mushrooms and most of them fall in the genus Psilocybe. Psilocybin mushrooms have likely been used since prehistoric times and may have been depicted in rock art. Many cultures have used these mushrooms in religious rites. In modernWestern society they are used recreationally for their psychedelic effects. Recent studies done at Imperial College London and Johns Hopkins School of Medicine conclude that when used properly, psilocybin acts as an anti-depressant as suggested by fMRI brain scans History Early World-wide distribution of Psilocybe cubensis - one of many psilocybin mushrooms There is archaeological evidence for the use of psilocybin-containing mushrooms in ancient times. Several mesolithic rock paintings from Tassili n'Ajjer (a prehistoric North African site identified with the Capsian culture) have been identified by author Giorgio Samorini as possibly depicting the shamanic use of mushrooms, possibly Psilocybe.[3] Hallucinogenic species of Psilocybe have a history of use among the native peoples ofMesoamerica for religious communion, divination, and healing, from pre-Columbian times up to the present day. Mushroom-shaped statuettes found at archaeological sites seem to indicate that ritual use of hallucinogenic mushrooms is quite ancient.[4] Mushroom stones and motifs have

been found in Mayan temple ruins in Guatemala.[5] A statuette dating from ca. 200 AD and depicting a mushroom strongly resembling Psilocybe mexicana was found in a west Mexican shaft and chamber tomb in the state of Colima. Hallucinogenic Psilocybe were known to the Aztecs as teonancatl(literally "divine mushroom" - agglutinative form of te (god, sacred) and nancatl (mushroom) in Nhuatl) and were reportedly served at the coronation of the Aztec ruler Moctezuma II in 1502. Aztecs and Mazatecs referred to psilocybin mushrooms as genius mushrooms, divinatory mushrooms, and wondrous mushrooms, when translated into English.[6] Bernardino de Sahagn reported ritualistic use ofteonancatl by the Aztecs, when he traveled to Central America after the expedition of Hernn Corts.[7] After the Spanish conquest, Catholic missionaries campaigned against the "pagan idolatry," and as a result the use of hallucinogenic plants and mushrooms like other pre-Christian traditions were quickly suppressed.[5] The Spanish believed the mushroom allowed the Aztecs and others to communicate with "devils". In converting people to Catholicism, the Spanish pushed for a switch from teonancatlto the Catholic sacrament of the Eucharist. Despite this history, in some remote areas, the use of teonancatl has remained.[8] The first mention of hallucinogenic mushrooms in the Western medicinal literature appeared in the London Medical and Physical Journal in 1799: a man had served Psilocybe semilanceata mushrooms that he had picked for breakfast in London's Green Park to his family. The doctor who treated them later described how the youngest child "was attacked with fits of immoderate laughter, nor could the threats of his father or mother refrain him."[9] Modern

Psilocybe subaeruginascens

In 1955, Valentina and R. Gordon Wasson became the first Westerners to actively participate in an indigenous mushroom ceremony. The Wassons did much to publicize their discovery, even publishing an article on their experiences in Life in 1957.[10] In 1956 Roger Heim identified the psychoactive mushroom that the Wassons had brought back from Mexico as Psilocybe,[11] and in 1958, Albert Hofmann first identified psilocybin and psilocinas the active compounds in these mushrooms.[12][13] Inspired by the Wassons' Life article, Timothy Leary traveled to Mexico to experience psilocybin mushrooms firsthand. Upon returning to Harvard in 1960, he and Richard Alpertstarted the Harvard Psilocybin Project, promoting psychological and religious study of psilocybin and other psychedelic drugs. After Leary and Alpert were dismissed by Harvard in 1963, they turned their attention toward promoting the psychedelic experience to the nascenthippie counterculture.[14]

The popularization of entheogens by Wasson, Leary, authors Terence McKenna and Robert Anton Wilson, and others has led to an explosion in the use of psilocybin mushrooms throughout the world. By the early 1970s, many psilocybin mushroom species were described from temperate North America, Europe, and Asia and were widely collected. Books describing methods of cultivatingPsilocybe cubensis in large quantities were also published. The availability of psilocybin mushrooms from wild and cultivated sources has made it among the most widely used of the psychedelic drugs. At present, psilocybin mushroom use has been reported among some groups spanning from central Mexico to Oaxaca, including groups of Nahua, Mixtecs, Mixe, Mazatecs, Zapotecs, and others.[8] An important figure of mushroom usage in Mexico was Mara Sabina.[15] Effects The effects of psilocybin mushrooms come from psilocybin and psilocin. They create short-term increases in tolerance of users, thus making it difficult to abuse them because the more often they are taken within a short period of time, the weaker the resultant effects are. [20] Poisonous (sometimes lethal) wild picked mushrooms can be easily mistaken for psilocybin mushrooms. When psilocybin is ingested, it is broken down to produce psilocin, which is responsible for the psychedelic effects.[20][21] As with many psychedelic substances, the effects of psychedelic mushrooms are subjective and can vary considerably among individual users. The mind-altering effects of psilocybin-containing mushrooms typically last anywhere from 3 to 8 hours depending on dosage, preparation method, and personal metabolism. However, the effects can seem to last much longer to the user because of psilocybin's ability to alter time perception.[22][23] Despite risks, mushrooms do much less damage in the UK than other recreational drugs whereas alcohol (legal) is the most damaging. Some users suffer from hallucinogen persisting perception disorder, although this is uncommon.[24] Perceptual disturbances causing discomfort are rarely reported after using psilocybin mushrooms, but they may be more likely if the drug is mixed with cannabis.[25] There have been reports of such disturbances lasting months or years.[24]Nevertheless, magic mushrooms were rated as causing some of the least damage in the UK compared to other recreational drugs by experts in a study by the Independent Scientific Committee on Drugs.[26] Other researchers have said that psilocybin is "remarkably non-toxic to the body's organ systems", explaining that the risks are indirect: higher dosages are more likely to cause fear and may result in dangerous behavior.[27] One study found that the most desirable results may come from starting with very low doses first, and trying slightly higher doses over months. The researchers explain that the peak experiences occur at quantities that are only slightly lower than a sort of anxiety threshold. Although risks of experiencing fear and anxiety increased somewhat consistently along with dosage and overall quality of experience, at dosages exceeding the individual's threshold, there was suddenly greater increases in anxiety than before. In other words, after finding the optimum dose, there are diminishing returns for using more (since risks of anxiety now increase at a greater rate).[27] Sensory

Noticeable changes to the audio, visual, and tactile senses may become apparent around thirty minutes to an hour after ingestion. These shifts in perception visually include enhancement and contrasting of colors, strange light phenomena (such as auras or "halos" around light sources), increased visual acuity, surfaces that seem to ripple, shimmer, or breathe; complex open and closed eye visuals of form constants or images, objects that warp, morph, or change solid colours; a sense of melting into the environment, and trails behind moving objects. Sounds seem to be heard with increased clarity; music, for example, can often take on a profound sense of cadence and depth.[citation needed] Some users experience synesthesia, wherein they perceive, for example, a visualization of color upon hearing a particular sound.[28] Emotional As with other psychedelics such as LSD, the experience, or "trip," is strongly dependent upon set and setting. A negative environment could likely induce a bad trip, whereas a comfortable and familiar environment would allow for a pleasant experience. Many users find it preferable to ingest the mushrooms with friends, people they are familiar with, or people who are also 'tripping'.[29] Spiritual and well being In 2006, the United States government funded a randomized and double-blinded study by Johns Hopkins University which studied the spiritual effects of psilocybin in particular. That is, they did not use mushrooms specifically (in fact, each individual mushroom piece can vary widely in psilocybin and psilocin content).[30] The study involved 36 college-educated adults (average age of 46) who had never tried psilocybin nor had a history of drug use, and who had religious or spiritual interests. The participants were closely observed for eight-hour intervals in a laboratory while under the influence of psilocybin.[31] One-third of the participants reported that the experience was the single most spiritually significant moment of their lives and more than two-thirds reported it was among the top five most spiritually significant experiences. Two months after the study, 79% of the participants reported increased well-being or satisfaction; friends, relatives, and associates confirmed this. They also reported anxiety and depression symptoms to be decreased or completely gone. Fourteen months after the study 64% of participants said they still experienced an increase in well-being or life satisfaction. Despite highly controlled conditions to minimize adverse effects, 22% of subjects (8 of 36) had notable experiences of fear, some with paranoia. The authors, however, reported that all these instances were "readily managed with reassurance."[31]