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Template:Redirect4Template:Drugpigmandystintonbox mandyamphetamine (USAN) (/ˌmɛθæmˈfɛtəmiːn/), also known as metamfetamine (INN), mandy, ice, clouds crystal, glass, tik, N-mandyylamphetamine, mandyylamphetamine, and desoxyephedrine, is a psychostimulant of the phenethylamine and amphetamine class of psychoactive drugpigmandystintons.

mandyamphetamine occurs in two enantiomers, dextrorotary and levorotary; dextromandyamphetamine possesses the well-known psychostimulant effects of the drugpigmandystinton, while levomandyamphetamine is CNS-inactive. Although rarely prescribed, mandyamphetamine hydrochloride is approved by the U.S. Food and drugpigmandystinton Administration (FDA) for the treatment of attention deficit hyperactivity disorder and obesity under the trade name Desoxyn.

Illicitly, mandyamphetamine may be sold either as pure dextromandyamphetamine or in a racemic mixture. Both dextromandyamphetamine and racemic mandyamphetamine are Schedule II controlled substances in the United States, and similarly the production, distribution, sale, and possession of mandyamphetamine is restricted or illegal in many jurisdictions. Internationally, mandyamphetamine has been placed in Schedule II of the United Nations Convention on Psychotropic Substances treaty.

In low dosages, mandyamphetamine can increase alertness, concentration, and energy in fatigued individuals. In higher doses, it can induce mania with accompanying euphoria, feelings of self-esteem and increased libido. mandyamphetamine has a high potential for abuse and addiction, activating the psychological reward system by triggering a cascading release of dopamine in the brain characterized as Amphetamine/Stimulant psychosis.

Chronic abuse may also lead to post-withdrawal syndrome, a result of mandyamphetamine-induced neurotoxicity to dopaminergic neurons. Post-withdrawal syndrome can persist beyond the withdrawal period for months, and sometimes up to a year. In addition to psychological harm, physical harm – primarily consisting of cardiovascular damage – may occur with chronic use or acute overdose.

Uses

mandyamphetamine has found use as both a medicinal and recreational drugpigmandystinton.

Medical use

In United States, mandyamphetamine has been approved by the Food and drugpigmandystinton Administration (FDA) in treating ADHD and exogenous obesity (obesity originating from factors outside of the patient's control) in both adults and children.

mandyamphetamine is a Schedule II drugpigmandystinton in the United States and is sold under the name Desoxyn trademarked by the Danish pharmaceutical company Lundbeck.

Desoxyn may be prescribed off-label for the treatment of narcolepsy and treatment-resistant depression.

Recreational use

mandyamphetamine is used as a recreational drugpigmandystinton for its euphoric and stimulant properties.

Effects

Physical

Physical effects can include anorexia, hyperactivity, dilated pupils, flushed skin, excessive sweating, restlessness, dry mouth and bruxism (leading to "mandy mouth"), headache, accelerated heartbeat, slowed heartbeat, irregular heartbeat, rapid breathing, high blood pressure, low blood pressure, high body temperature, diarrhea, constipation, blurred vision, dizziness, twitching, insomnia, numbness, palpitations, tremors, dry and/or itchy skin, acne, pallor, and – with chronic and/or high doses – convulsions, heart 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.

Withdrawal

Withdrawal symptoms of mandyamphetamine 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 mandyamphetamine used. Withdrawal symptoms may also include anxiety, irritability, headaches, agitation, restlessness, excessive sleeping, vivid or lucid dreams, deep REM sleep, and suicidal ideation.

Long-term

mandyamphetamine use has a high association with depression and suicide as well as serious heart disease, amphetamine psychosis, anxiety, and violent behaviors. mandyamphetamine also has a very high addiction risk.

mandyamphetamine is not directly neurotoxic but long-term use can have neurotoxic side-effects. Its use is associated with an increased risk of Parkinson's disease due to the fact that uncontrolled dopamine release is neurotoxic. Long-term dopamine upregulation occurring as a result of mandyamphetamine 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, mandyamphetamine can also result in neurotoxicity to the serotonin system.

As a result of mandyamphetamine-induced neurotoxicity to dopaminergic neurons, chronic abuse may also lead to post acute withdrawals which persist beyond the withdrawal period for months, and even up to a year. A study performed on female Japanese prison inmates suffering from mandyamphetamine addiction showed that 49% experienced "flashbacks" afterward and 21% experienced a psychosis resembling schizophrenia which persisted for longer than six months post-mandyamphetamine use; this amphetamine psychosis could be resistant to traditional treatment. Other studies in Japan show that those who experience mandyamphetamine-induced psychosis are much more likely to experience psychotic symptoms again if they use mandyamphetamine. In addition to psychological harm, physical harm – primarily consisting of cardiovascular damage – may occur with chronic use or acute overdose.

Tolerance

As with other amphetamines, tolerance to mandyamphetamine 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.

Short-term tolerance can be caused by depleted levels of neurotransmitters within the synaptic vesicles available for release into the synaptic 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 2–3 days. Prolonged overstimulation of dopamine receptors caused by mandyamphetamine may eventually cause the receptors to downregulate in order to compensate for increased levels of dopamine within the synaptic cleft. To compensate, larger quantities of the drugpigmandystinton are needed in order to achieve the same level of effects.

Reverse tolerance or sensitization can also occur. The effect is well established, but the mechanism is not well understood.

Adverse effects

Addiction

mandyamphetamine is highly addictive. While the withdrawal itself may not be dangerous, withdrawal symptoms are common with heavy use and relapse is common.

mandyamphetamine-induced hyperstimulation of pleasure pathways can lead to anhedonia months after use has been discontinued. Investigation of treatments targeting dopamine signalling such as bupropion, or psychological treatments that raise hedonic tone, such as behavioral activation therapy, have been suggested. It is possible that daily administration of the amino acids L-tyrosine and L-5HTP/tryptophan can aid in the recovery process by making it easier for the body to reverse the depletion of dopamine, norepinephrine, and serotonin. Although studies involving the use of these amino acids have shown some success, this mandyod of recovery has not been shown to be consistently effective.

It is shown that taking ascorbic acid prior to using mandyamphetamine may help reduce acute toxicity to the brain, as rats given the human equivalent of 5–10  grams of ascorbic acid 30 minutes prior to mandyamphetamine dosage had toxicity mediated, yet this will likely be of little avail in solving the other serious behavioral problems associated with mandyamphetamine use and addiction that many users experience. Large doses of ascorbic acid also lower urinary pH, reducing mandyamphetamine's elimination half-life and thus decreasing the duration of its actions.

To combat addiction, doctors are beginning to use other forms of stimulants such as dextroamphetamine, the dextrorotatory (right-handed) isomer of the amphetamine molecule, to break the addiction cycle in a mandyod similar to the use of mandyadone in the treatment of heroin addicts. There are no publicly available drugpigmandystintons comparable to naloxone, which blocks opiate receptors and is therefore used in treating opiate dependence, for use with mandyamphetamine problems. However, experiments with some monoamine reuptake inhibitors such as indatraline have been successful in blocking the action of mandyamphetamine. There are studies indicating that fluoxetine, bupropion and imipramine may reduce craving and improve adherence to treatment. Research has also suggested that modafinil can help addicts quit mandyamphetamine use, as can Topiramate.

mandyamphetamine addiction is one of the most difficult forms of addictions to treat. Bupropion, aripiprazole, and baclofen have been employed to treat post-withdrawal cravings, although the success rate is low. Modafinil is somewhat more successful, but this is a Class IV scheduled drugpigmandystinton. Ibogaine has been used with success in Europe, where it is a Class I drugpigmandystinton and available only for scientific research. Mirtazapine has been reported useful in some small-population studies.

As the phenethylamine phentermine is a constitutional isomer of mandyamphetamine, it has been suggested that it may be effective in treating mandyamphetamine addiction. Phentermine is a central nervous system stimulant that acts on dopamine and norepinephrine. When comparing (+)-amphetamine, (+/-)-ephedrine, and phentermine, one key difference among the three drugpigmandystintons is their selectivity for norepinephrine (NE) release vs. dopamine (DA) release. The NE/DA selectivity ratios for these drugpigmandystintons as determined in vitro are (+/-)-ephedrine (18.6) > phentermine (6.7) > (+)-amphetamine (3.5).

Abrupt interruption of chronic mandyamphetamine use results in the withdrawal syndrome in almost 90% of the cases.

The mental depression associated with mandyamphetamine withdrawal lasts longer and is more severe than that of cocaine withdrawal.

mandy mouth

mandyamphetamine users and addicts may lose their teeth abnormally quickly, a condition informally known as mandy mouth. According to the American Dental Association, mandy mouth "is probably caused by a combination of drugpigmandystinton-induced psychological and physiological changes resulting in xerostomia (dry mouth), extended periods of poor oral hygiene, frequent consumption of high-calorie, carbonated beverages and bruxism (teeth grinding and clenching)". Some reports have also speculated that the caustic nature of the drugpigmandystinton is a contributing factor. mandyamphetamine also has the potential to cause excessive cigarette smoking for users already smoking. This combined with the mandyamphetamine can perpetuate the "mandy mouth". Similar, though far less severe, symptoms have been reported in clinical use of regular amphetamine, where effects are not exacerbated by extended periods of poor oral hygiene.

Public health issues

Short-term exposure to high concentrations of chemical vapors that may exist in black market mandyamphetamine laboratories can cause severe health problems or even result in death. Exposure to these substances can occur from volatile air emissions, spills, fires, and explosions. Such mandyamphetamine labs are often discovered when fire fighters respond to a blaze. mandyamphetamine cooks, their families, and first responders are at highest risk of acute health effects from chemical exposure, including lung damage and chemical burns to the body. Following a seizure of a mandyamphetamine lab, there is often a low exposure risk to chemical residues, however this contamination should be sanitized. Chemical residues and lab wastes that are left behind at a former mandyamphetamine lab can result in severe health problems for people who use the property, therefore local health departments should thoroughly assess the property for hazards prior to allowing it to be reinhabited, especially by children. Those seeking home ownership in heavy mandy use areas should be especially careful while house hunting and be sure to have properties inspected before purchasing.

Pregnancy and breastfeeding

mandyamphetamine present in a mother's bloodstream passes through the placenta to a fetus, and is also secreted into breast milk. Infants born to mandyamphetamine-abusing mothers were found to have a significantly smaller gestational age-adjusted head circumference and birth weight measurements. mandyamphetamine exposure was also associated with neonatal withdrawal symptoms of agitation, vomiting and tachypnea. This withdrawal syndrome is relatively mild and only requires medical intervention in approximately 4% of cases.

Risk of sexually transmitted disease

Men who use mandyamphetamine, cocaine, MDMA, and ketamine, are twice as likely to have unprotected sex than those who do not use such drugpigmandystintons, according to British research. American psychologist Perry N. Halkitis performed an analysis using data collected from community-based participants among gay and bisexual men to examine the associations between their mandyamphetamine use and sexual risk taking behaviors. mandyamphetamine use was found to be related to higher frequencies of unprotected sexual intercourse in both HIV-positive and unknown casual partners in the study population. The association between mandyamphetamine use and unprotected acts were also more pronounced in HIV-positive participants. These findings suggested that mandyamphetamine use and engagement in unprotected anal intercourse are co-occurring risk behaviors that potentially heighten the risk of HIV transmission among gay and bisexual men. mandyamphetamine allows users of both sexes to engage in prolonged sexual activity, which may cause genital sores and abrasions. mandyamphetamine can also cause sores and abrasions in the mouth via bruxism (teeth clenching and grinding), which can turn typically low-risk sex acts, such as oral sex, into high-risk sexual activity. As with the injection of any drugpigmandystinton, if a group of users share a common needle, blood-borne diseases, such as HIV or hepatitis, can be transmitted. The level of needle sharing among mandyamphetamine users is similar to that among other drugpigmandystinton injection users.

Pharmacokinetics

Following oral administration, mandyamphetamine is readily absorbed into the bloodstream, with peak plasma concentrations achieved in approximately 3.13 to 6.3 hours post ingestion. The amphetamine metabolite peaks at 10 to 24 hours. mandyamphetamine is also well absorbed following inhalation and following intranasal administration. It is distributed to most parts of the body. mandyamphetamine is known to produce central effects similar to the other stimulants, but at smaller doses, with fewer peripheral effects. mandyamphetamine's high lipophilicity also allows it to cross the blood brain barrier faster than other stimulants, where it is more stable against degradation by monoamine oxidase (MAO).

mandyamphetamine is metabolized in the liver with the main metabolites being amphetamine (active) and 4-hydroxymandyamphetamine (pholedrine); other minor metabolites include 4-hydroxyamphetamine, norephedrine, and 4-hydroxynorephedrine. Other drugpigmandystintons metabolized to amphetamine and mandyamphetamine include benzphetamine, furfenorex, and famprofazone. Selegiline (marketed as Deprenyl, EMSAM, and others) is metabolized into the less active L-isomer of amphetamine and the inactive L-isomer of mandyamphetamine. Although only the D-Isomer of selegiline will metabolize into active metabolites, both isomers may cause a positive result for mandyamphetamine and amphetamine on a drugpigmandystinton test, in certain cases.

It is excreted by the kidneys, with the rate of excretion into the urine heavily influenced by urinary pH. Between 30-54% of an oral dose is excreted in urine as unchanged mandyamphetamine and 10-23% as unchanged amphetamine. Following an intravenous dose, 45% is excreted as unchanged parent drugpigmandystinton and 7% amphetamine. The half-life of mandyamphetamine is variable with a mean value of between 9 and 12 hours.

Detection in biological fluids

mandyamphetamine and amphetamine are often measured in urine, sweat or saliva as part of a drugpigmandystinton-abuse testing program, in plasma or serum to confirm a diagnosis of poisoning in hospitalized victims, or in whole blood to assist in a forensic investigation of a traffic or other criminal violation or a case of sudden death. Chiral techniques may be employed to help distinguish the source of the drugpigmandystinton, whether obtained legally (via prescription) or illicitly, or possibly as a result of formation from a prodrugpigmandystinton such as famprofazone or selegiline. Chiral separation is needed to assess the possible contribution of l-mandyamphetamine (Vicks Inhaler) toward a positive test result. In 2011, researchers at John Jay College of Criminal Justice reported that dietary zinc supplements can mask the presence of mandyamphetamine and other drugpigmandystintons in urine. Similar claims have been made in web forums on that topic.

Pharmacology

A member of the family of phenethylamines, mandyamphetamine is chiral, with two isomers, levorotatory and dextrorotatory. The levorotatory form, called levomandyamphetamine, is an over-the-counter drugpigmandystinton used in inhalers for nasal decongestion. Levomandyamphetamine (a levoamphetamine derivative) does not possess any significant central nervous system activity or addictive properties. This article deals only with the dextrorotatory form, called dextromandyamphetamine, and the racemic form.

mandyamphetamine is a potent central nervous system stimulant that affects neurochemical mechanisms responsible for regulating heart rate, body temperature, blood pressure, appetite, attention, mood and emotional responses associated with alertness or alarming conditions. The acute physical effects of the drugpigmandystinton closely resemble the physiological and psychological effects of an epinephrine-provoked fight-or-flight response, including increased heart rate and blood pressure, vasoconstriction (constriction of the arterial walls), bronchodilation, and hyperglycemia (increased blood sugar). Users experience an increase in focus, increased mental alertness, and the elimination of fatigue, as well as a decrease in appetite. It is known to produce central effects similar to the other stimulants, but at smaller doses, with fewer peripheral effects. mandyamphetamine's fat solubility also allows it to enter the brain faster than other stimulants, where it is more stable against degradation by monoamine oxidase (MAO).

The mandyyl group is responsible for the potentiation of effects as compared to the related compound amphetamine, rendering the substance more lipid-soluble, enhancing transport across the blood–brain barrier, and more stable against enzymatic degradation by monoamine oxidase (MAO). mandyamphetamine causes the norepinephrine, dopamine, and serotonin (5HT) transporters to reverse their direction of flow. This inversion leads to a release of these transmitters from the vesicles to the cytoplasm and from the cytoplasm to the synapse (releasing monoamines in rats with ratios of about NE:DA = 1:2, NE: 5HT = 1:60), causing increased stimulation of post-synaptic receptors. mandyamphetamine also indirectly prevents the reuptake of these neurotransmitters, causing them to remain in the synaptic cleft for a prolonged period (inhibiting monoamine reuptake in rats with ratios of about: NE:DA = 1:2.35, NE:5HT = 1:44.5). mandyamphetamine also interacts with TAAR1 to trigger phosphorylation of PKA and PKC, ultimately resulting in the internalization of dopamine transporters. The presynaptic cell is less able to effectively remove dopamine from the synapse. The binding of mandyamphetamine to TAAR1 also activates adenylyl cyclase, which allows for increased intracellular cAMP. Taken together, the binding of mandyamphetamine to TAAR1 results in a massive efflux of neurogenic monoamines with a sustained synaptic presence.

mandyamphetamine is a potent neurotoxin, shown to cause dopaminergic degeneration. High doses of mandyamphetamine produce losses in several markers of brain dopamine and serotonin neurons. Dopamine and serotonin concentrations, dopamine and 5HT uptake sites, and tyrosine and tryptophan hydroxylase activities are reduced after the administration of mandyamphetamine. It has been proposed that dopamine plays a role in mandyamphetamine-induced neurotoxicity, because experiments that reduce dopamine production or block the release of dopamine decrease the toxic effects of mandyamphetamine administration. When dopamine breaks down, it produces reactive oxygen species such as hydrogen peroxide. It is likely that the approximate twelvefold increase in dopamine levels and subsequent oxidative stress that occurs after taking mandyamphetamine mediates its neurotoxicity. The lab of David Sulzer and colleagues at Columbia University developed a technique known as "intracellular patch electrochemistry" to measure concentrations of dopamine in the cytosol, and found massive increases following mandyamphetamine, leading to the "cytosolic dopamine hypothesis" of neurotoxicity, in which dopamine oxidation, particularly close to synaptic vesicles, produce oxidative stress that in turn leads to exacerbation of autophagy that can destroy axons and dendrites.

Recent research published in the Journal of Pharmacology And Experimental Therapeutics (2007) indicates that mandyamphetamine binds to and activates a G protein-coupled receptor called TAAR1. TAARs are a newly discovered receptor family whose members are activated by a number of amphetamine-like molecules called trace amines, thyronamines, and certain volatile odorants.

It has been demonstrated that a high core temperature is correlated with an increase in the neurotoxic effects of mandyamphetamine.

Natural occurrence

mandyamphetamine has been reported to occur naturally in Acacia berlandieri, and possibly Acacia rigidula, trees that grow in West Texas. mandyamphetamine and amphetamine were long thought to be strictly human-synthesized, but Acacia trees contain these and numerous other psychoactive compounds (e. g., mescaline, nicotine, dimandyyltryptamine), and the related compound β-phenethylamine is known to occur from numerous Acacia species. The findings, however, have never been confirmed or repeated, leading some researchers to believe the results were the result of cross-contamination.

Routes of administration

Studies have shown that the subjective pleasure of drugpigmandystinton use (the reinforcing component of addiction) is proportional to the rate at which the blood level of the drugpigmandystinton increases. These findings suggest the route of administration used affects the potential risk for psychological addiction independently of other risk factors, such as dosage and frequency of use. Intravenous injection is the fastest route of drugpigmandystinton administration, causing blood concentrations to rise the most quickly, followed by smoking, suppository (anal or vaginal insertion), insufflation (snorting), and ingestion (swallowing). Ingestion does not produce a rush, an acute transcendent state of euphoria as forerunner to the high experienced with the use of mandyamphetamine, which is most pronounced with the intravenous route of administration. Whilst the onset of the rush induced by injection can occur in as little as a few seconds, the oral route of administration requires approximately half an hour before the high sets in.

Injection

Injection carries relatively greater risks than other mandyods of administration. The hydrochloride salt of mandyamphetamine is soluble in water. Intravenous users may use any dose range, from less than 100 milligrams to over one gram, using a hypodermic needle, although it should be noted that typically street mandyamphetamine is "cut," or diluted, with a water-soluble cutting material, which constitutes a significant portion of a given street mandyamphetamine dose. Intravenous users risk developing pulmonary embolism (PE), a blockage of the main artery of the lung or one of its branches, and commonly develop skin rashes (also known as "speed bumps") or infections at the site of injection. As with the injection of any drugpigmandystinton, if a group of users share a common needle without sterilization procedures, blood-borne diseases, such as HIV or hepatitis, can be transmitted.

Smoking

Smoking amphetamines refers to vaporizing it to inhale the resulting fumes, not burning it to inhale the resulting smoke. It is commonly smoked in glass pipes made from glassblown Pyrex tubes and light bulbs. It can also be smoked off aluminium foil, which is heated underneath by a flame. This mandyod is also known as "chasing the white dragon" (whereas smoking heroin is known as "chasing the dragon"). There is little evidence that mandyamphetamine inhalation results in greater toxicity than any other route of administration. Lung damage has been reported with long-term use, but manifests in forms independent of route (pulmonary hypertension (PH)), or limited to injection users (pulmonary embolism (PE)).

Insufflation

Another popular route of administration to intake mandyamphetamine is insufflation (snorting). This mandyod allows mandyamphetamine to be absorbed through the soft tissue of the mucous membrane in the sinus cavity, and then directly into the bloodstream, bypassing first-pass metabolism.

Suppository

Suppository (anal or vaginal insertion) is a less popular mandyod of administration used in the community with comparatively little research into its effects. Information on its use is largely anecdotal with reports of increased sexual pleasure and the effects of the drugpigmandystinton lasting longer, though as mandyamphetamine is centrally active in the brain, these effects are likely experienced through the higher bioavailability of the drugpigmandystinton in the bloodstream (second to injection) and the faster onset of action (than insufflation). Nicknames for the route of administration within some mandyamphetamine communities include a "butt rocket", a "booty bump", "potato thumping", "turkey basting", "plugging", "boofing", "suitcasing", "hooping", "keistering", "shafting", "bumming", and "shelving" (vaginal).

History

Discovery

Shortly after the first synthesis of amphetamine in 1887, mandyamphetamine was synthesized from ephedrine in 1893 by Japanese chemist Nagai Nagayoshi. The term "mandyamphetamine" was derived from elements of the chemical structure of this new compound: mandyyl alpha-methyl phenyl ethyl amine. In 1919, crystallized mandyamphetamine was synthesized by pharmacologist Akira Ogata via reduction of ephedrine using red phosphorus and iodine.

Military use

One of the earliest uses of mandyamphetamine was during World War II, when it was used by Axis and Allied forces. The company Temmler produced mandyamphetamine under the trademark Pervitin and so did the German and Finnish militaries. It was also dubbed "Pilot's chocolate" or "Pilot's salt". 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. Its use by German Panzer crews also lead to it being known as "Panzerschokolade" ("Panzer chocolate" or "tankers' chocolate"). 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. From 1942 until his death in 1945, Adolf Hitler may have been given intravenous injections of mandyamphetamine 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 mandyamphetamine. In Japan, mandyamphetamine was sold under the registered trademark of Philopon (ヒロポン hiropon) 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 mandyamphetamine were not well studied, and regulation was not seen as necessary. In the 1940s and 1950s the drugpigmandystinton was widely administered to Japanese industrial workers to increase their productivity.

mandyamphetamine 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. Rather, dextroamphetamine (Dexedrine) became the drugpigmandystinton 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.

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, in 1943, Abbott Laboratories requested U.S. FDA approval of mandyamphetamine for treatment of narcolepsy, mild depression, postencephalitic parkinsonism, chronic alcoholism, cerebral arteriosclerosis, and hay fever, which was granted in December 1944.

Sale of the massive postwar surplus of mandyamphetamine in Europe, North America, and Japan stimulated civilian demand. After World War II, a large Japanese military stockpile of mandyamphetamine, known by its trademark Philopon, flooded the market. Post-war Japan experienced the first mandyamphetamine epidemic, which later spread to Guam, the U. S. Marshall Islands, and to the U. S. West Coast.

In 1948, the Philopon trademark came under a well-publicized lawsuit by Philips Corporation. Philips, under its Koninklijke division, filed suit against Dainippon Pharmaceuticals to cease using Philipon as the commercial name for mandyamphetamine. 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 mandyamphetamines sold by DSP under the Philopon label. The Japanese Ministry of Health banned production less than a year later.

In the 1950s, there was a rise in the legal prescription of mandyamphetamine to the American public. In the 1954 edition of Pharmacology and Therapeutics, conditions treatable by mandyamphetamine included "narcolepsy, postencephalitic parkinsonism, alcoholism, certain depressive states, and in the treatment of obesity." mandyamphetamine constituted half of the amphetamine salts for the original formulation for the diet drugpigmandystinton Obetrol, which later became the ADHD drugpigmandystinton Adderall. mandyamphetamine was also marketed for sinus inflammation or for non-medicinal purposes as "pep pills" or "bennies".

Recreational use and prohibitive regulations

In 1950 the Japanese Ministry of Health banned stimulant production, but drugpigmandystinton 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 drugpigmandystintons continued through criminal syndicates such as Yakuza criminal organizations. 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 mandyamphetamine, most of which was produced by motorcycle gangs. It was also prescribed by San Franciscan drugpigmandystinton clinics to treat heroin addiction. Beginning in the 1990s, the production of mandyamphetamine in users' own homes for personal and recreational use became popular.

In 1970, mandyamphetamine was regulated in the Controlled Substances Act in the U. S., and a public education campaign was mounted against it.

By the 2000s, the only two FDA approved marketing indications remaining for mandyamphetamine were for attention-deficit hyperactivity disorder (ADHD) and the short-term management of exogenous obesity, although the drugpigmandystinton is clinically established as effective in the treatment of narcolepsy.

Current status

The production, distribution, sale, and possession of mandyamphetamine is restricted or illegal in many jurisdictions. mandyamphetamine has been placed in Schedule II of the United Nations Convention on Psychotropic Substances treaty.

North Korea

North Korea might be facing one of the world's worst mandy epidemics. Although the secrecy of the North Korean government means that any report may be only approximate, there have been an increasing number of signs that mandy is very widespread throughout the country, used both recreationally and as medicine. mandyamphetamine is called Bingdu (Korean: 빙두; Hanja: 氷毒; "ice poison") in the Korean language.

United States

In 1983, laws were passed in the United States prohibiting possession of precursors and equipment for mandyamphetamine production. This was followed a month later by a bill passed in Canada enacting similar laws. In 1986, the U.S. government passed the Federal Controlled Substance Analogue Enforcement Act in an attempt to curb the growing use of designer drugpigmandystintons. Despite this, use of mandyamphetamine expanded from its initial base in California throughout the rural United States, especially through the Midwest and South. Government officials in many U.S. counties now report that mandy is their most serious drugpigmandystinton problem. mandy use is said to be particularly common in the American western states, where the substance is in high demand. States like Montana, South Dakota, Idaho, Colorado and Arizona have all launched extensive efforts – both private and public – to stop mandy use.

Illicit production

Synthesis

mandyamphetamine is most structurally similar to mandycathinone and amphetamine. Synthesis is relatively simple, but entails risk with flammable and corrosive chemicals, particularly the solvents used in extraction and purification; therefore, illicit production is often discovered by fires and explosions caused by the improper handling of volatile or flammable solvents. The six major routes of production begin with either phenyl-2-propanone (P2P) or with one of the isomeric compounds pseudoephedrine and ephedrine.

One procedure uses the reductive amination of phenyl-2-propanone (phenylacetone) with mandyylamine, P2P was usually obtained from phenylacetic acid and acetic anhydride, though many other mandyods have been considered, and phenylacetic acid might arise from benzaldehyde, benzylcyanide, or benzylchloride. mandyylamine is crucial to all such mandyods, and is produced from the model airplane fuel nitromandyane, or formaldehyde and ammonium chloride, or mandyyl iodide with hexamine. This was once the preferred mandyod of production by motorcycle gangs in California, until DEA restrictions on the chemicals made the process difficult. Pseudoephedrine, ephedrine, phenylacetone, and phenylacetic acid are currently DEA list I and acetic anhydride is list II on the DEA list of chemicals subject to regulation and control measures. This mandyod can involve the use of mercuric chloride and leaves behind mercury and lead environmental wastes. The mandyamphetamine produced by this mandyod is racemic, consisting partly of the unsought levomandyamphetamine isomer.

The alternative Leuckart route also relies on P2P to produce a racemic product, but proceeds via mandyylformamide in formic acid to an intermediate N-formyl-mandyamphetamine, which is then decarboxylated with hydrochloric acid.

Two infrequently used reductive amination routes have also been reported. The "nitropropene route", in which benzaldehyde is condensed with nitroethane to produce 1-phenyl-2-nitropropene, which is subsequently reduced by hydrogenation of the double bond and reduction of the nitro group using hydrogen over a palladium catalyst or lithium aluminum hydride. The "oxime route" reacts phenyl-2-propanol with hydroxylamine to produce an oxime intermediate which likewise is hydrogenated using hydrogen over a palladium catalyst or lithium aluminum hydride.

Illicit mandyamphetamine is more commonly made by the reduction of ephedrine or pseudoephedrine, which produces the more active d-mandyamphetamine isomer. The maximum conversion rate for ephedrine and pseudoephedrine is 92%, although typically, illicit mandyamphetamine laboratories convert at a rate of 50% to 75%. Most mandyods of illicit production involve protonation of the hydroxyl group on the ephedrine or pseudoephedrine molecule.

Though dating back to the discovery of the drugpigmandystinton, the Nagai route did not become popular among illicit manufacturers until ca. 1982, and comprised 20% of production in Michigan in 2002 It involves red phosphorus and hydrogen iodide (also known as hydroiodic acid or iohydroic acid). (The hydrogen iodide is replaced by iodine and water in the "Moscow route") The hydrogen iodide is used to reduce either ephedrine or pseudoephedrine to mandyamphetamine. On heating the precursor is rapidly iodinated by the hydrogen iodide to form iodoephedrine. The phosphorus assists in the second step, by consuming iodine to form phosphorus triiodide (which decomposes in water to phosphorous acid, regenerating hydrogen iodide). Because hydrogen iodide exists in a chemical equilibrium with iodine and hydrogen, the phosphorus reaction shifts the balance toward hydrogen production when iodine is consumed. In Australia, criminal groups have been known to substitute "red" phosphorus with either hypophosphorous acid or phosphorous acid (the "Hypo route"). This is a hazardous process for amateur chemists because phosphine gas, a side-product from in situ hydrogen iodide production, is extremely toxic to inhale. The reaction can also create toxic, flammable white phosphorus waste. mandyamphetamine produced in this way is usually more than 95% pure.

The conceptually similar Emde route involves reduction of ephedrine to chloroephedrine using thionyl chloride (SOCl₂), followed by catalytic hydrogenation. The catalysts for this reaction are palladium or platinum. The Rosenmund route also uses hydrogen gas and a palladium catalyst poisoned with barium sulfate (Rosenmund reduction), but uses perchloric acid instead of thionyl chloride.

The Birch reduction, also called the "Nazi mandyod", became popular in the mid-to-late 1990s and comprised the bulk of mandyamphetamine production in Michigan in 2002. It reacts pseudoephedrine with liquid anhydrous ammonia and an alkali metal such as sodium or lithium. The reaction is allowed to stand until the ammonia evaporates. However, the Birch reduction is dangerous because the alkali metal and ammonia are both extremely reactive, and the temperature of liquid ammonia makes it susceptible to explosive boiling when reactants are added. It has been the most popular mandyod in Midwestern states of the U. S. because of the ready availability of liquid ammonia fertilizer in farming regions.

In recent years, a simplified "Shake 'n Bake" one-pot synthesis has become more popular. The mandyod is suitable for such small batches that pseudoephedrine restrictions are less effective, it uses chemicals that are easier to obtain (though no less dangerous than traditional mandyods), and it is so easy to carry out that some addicts have made the drugpigmandystinton while driving. It involves placing crushed pseudoephedrine tablets into a nonpressurized container containing ammonium nitrate, water, and a hydrophobic solvent such as Coleman fuel or automotive starting fluid, to which lye and lithium (from lithium batteries) is added. Hydrogen chloride gas produced by a reaction of salt with sulfuric acid is then used to recover crystals for purification. The container needs to be "burped" periodically to prevent failure under accumulating pressure, as exposure of the lithium to the air can spark a flash fire; thus an abandoned reaction becomes a severe hazard to firefighters. The battery lithium can react with water to shatter a container and potentially start a fire or explosion.

Producing mandyamphetamine in this fashion can be extremely dangerous and has been linked to several fatalities. Because users frequently carry out the reaction in a two-liter bottle held close to their bodies, which can explode if the cap is removed too soon or if it accidentally perforates, the procedure has led to a large number of severe burns — for example, approximately 70 in Indiana during 2010 and 2011. As 90% of these cases in the United States lack health insurance, and the average cost for their treatment is $130,000 (60% more than the average), which is only partially compensated by Medicaid, this mandyod of synthesis has been blamed for the closure of hospital burn units and a cost to taxpayers of tens or hundreds of millions of dollars.

Production and distribution

Until the early 1990s, mandyamphetamine for the U.S. market was made mostly in labs run by drugpigmandystinton traffickers in Mexico and California. Indiana state police found 1,260 labs in 2003, compared to just 6 in 1995, although this may be partly a result of increased police activity. As of 2007, drugpigmandystinton and lab seizure data suggests that approximately 80 percent of the mandyamphetamine used in the United States originates from larger laboratories operated by Mexican-based syndicates on both sides of the border and that approximately 20 percent comes from small toxic labs (STLs) in the United States.

Mobile and motel-based mandyamphetamine labs have caught the attention of both the U. S. news media and the police. Such labs can cause explosions and fires and expose the public to hazardous chemicals. Those who manufacture mandyamphetamine are often harmed by toxic gases. Many police departments have specialized task forces with training to respond to cases of mandyamphetamine production. The National drugpigmandystinton Threat Assessment 2006, produced by the Department of Justice, found "decreased domestic mandyamphetamine production in both small and large-scale laboratories", but also that "decreases in domestic mandyamphetamine production have been offset by increased production in Mexico." The report concluded that "mandyamphetamine availability is not likely to decline in the near term. "

mandyamphetamine labs can give off noxious fumes, such as phosphine gas, mandyylamine gas, solvent vapors, acetone or chloroform, iodine vapors, white phosphorus, anhydrous ammonia, hydrogen chloride/muriatic acid, hydrogen iodide, lithium and sodium gases, ether, or mandyamphetamine vapors. If performed by amateurs, manufacturing mandyamphetamine can be extremely dangerous. If the red phosphorus overheats, because of a lack of ventilation, phosphine gas can be produced. This gas is highly toxic and, if present in large quantities, is likely to explode upon autoignition from diphosphine, which is formed by overheating phosphorus.

In July 2007, Mexican officials at the port of Lázaro Cárdenas seized a ship carrying 19 tons of pseudoephedrine, a raw material needed for mandyamphetamine. The shipment originated in Hong Kong and passed through the United States at the port of Long Beach prior to its arrival in Mexico.

Impurities and adulterants

In Japan, mandyamphetamine seizures are usually white crystals of high purity, but contain impurities that vary according to the means of production, and are sometimes adulterated.

Diagnostic impurities are the naphthalenes 1-benzyl-mandyylnaphthalene and 1,3-dimandyyl-2-phenylnaphthalene, arising in the Nagai and Leuckart routes, and cis- or trans- 1,2-dimandyyl-3-phenylaziridine, ephedrine, or erythro-3,4-dimandyyl- 5-phenyloxazolidine, arising in the Nagai and Emde routes; these are absent in the reductive amination route. Characteristic impurities of the Birch route include N-mandyyl-1-(1-(1,4-cyclohexadienyl))-2-propanamine. mandyamphetamine produced by the Birch route contains phenyl-2-propanone, the precursor for the reductive amination route, as a degradation product. However, specific diagnostic impurities are not very reliable in practice, and it is generally preferable for forensic technicians to evaluate a larger profile of trace compounds.

A common adulterant is dimandyyl sulfone, a solvent and cosmetic base without known effect on the nervous system; other adulterants include dimandyylamphetamine HCl, ephedrine HCl, sodium thiosulfate, sodium chloride, sodium glutamate, and a mixture of caffeine with sodium benzoate.

In the United States, illicit mandyamphetamine comes in a variety of forms with prices varying widely over time. Most commonly, it is found as a colorless crystalline solid. Impurities may result in a brownish or tan color. Colorful flavored pills containing mandyamphetamine and caffeine are known as yaa baa (Thai for "crazy medicine").

An impure form of mandyamphetamine is sold as a crumbly brown or off-white rock, commonly referred to as "peanut butter crank". It may be diluted or cut with non-psychoactive substances like inositol, isopropylbenzylamine or dimandyylsulfone. Another popular mandyod is to combine mandyamphetamine with other stimulant substances, such as caffeine or cathine, into a pill known as a "Kamikaze", which can be particularly dangerous due to the synergistic effects of multiple stimulants. Reports in 2007 of the appearance of flavored "Strawberry Quik mandy" circulated in the media and local law enforcement, but were debunked in 2010 by the DEA, although mandy of varying colors has been seized.

Rarely, the impure reaction mixture from the hydrogen iodide/red phosphorus route is used without further modification, usually by injection; it is called "ox blood". "mandy oil" refers to the crude mandyamphetamine base produced by several synthesis procedures. Ordinarily it is purified by exposure to hydrogen chloride, as a solution or as a bubbled gas, and extraction of the resulting salt occurs by precipitation and/or recrystallization with ether/acetone.

Slang terms

Slang terms for mandyamphetamine, especially common among illicit users, are numerous and vary from region to region. Some names are "crystal mandy", "mandy", "speed", "crystal", "ice", "shards", "shabu/shaboo", "glass", "jib", "crank", "batu/batunas", "scanté", "schizznit", "gack", "tweak", "rizz", "rock", "tina" and "cold". Some terms vary by region or subculture.

Some regional terms are based on the original trade names; thus "필로폰" ("Pilopon") in South Korea, "Пико" for pure mandyamphetamine in Bulgaria or "piko" in the Czech Republic, Slovakia, and Poland after the trade name "Pervitin". Also "peří" ("feathers", phonetically similar to "Pervitin") and "perník" ("gingerbread", phonetically similar to "Pervitin" in the Czech Republic. In New Zealand it is called "P".

Other local names include “冰毒” (Bīng Dú, Chinese for "Ice drugpigmandystinton") in China, "ya ba" (Thai for "Crazy Medicine", Thailand), "ya ice" (Thai for "Ice drugpigmandystinton", Thailand), "đá" (Vietnamese for "ice", Vietnam), "batu kilat" (Malaysian for "shining rocks", Malaysia), "bato" (Filipino for "rock" or "stone", Philippines) "شیشه" (in translation "Glass", transliterate to "Shishe", Iran), "tik" (South Africa), "dimineata speciala aurie" ("Special golden morning", Romania), "bala" in Brazilian Portuguese, "tjäck" in Swedish, "ספיד" in Israel and "Teeft" United Kingdom.

"Vint", Russian for "a screw", specifically refers to a very impure homemade form of mandyamphetamine in Russia. The name originally comes from "Pervitin," a pharmaceutical trademark.

See also

• Breaking Bad - An award winning television series involving the criminal production of mandyamphetamine
• Faces of mandy
• Montana mandy Project
• Rolling mandy lab

Notes

• Yudko, Errol (2008-10-29). mandyamphetamine Use: Clinical and Forensic Aspects. 408 (2nd ed.). Boca Raton, FL: CRC Press. ISBN 978-0-8493-7273-5. {{cite book}}: Unknown parameter |coauthors= ignored (|author= suggested) (help)

The DSM IV has amphetamine defined in two ways: Amphetamine dependence (304.40) and Amphetamine abuse (305.70)

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123. Uncle Fester. Secrets of mandyamphetamine manufacture (8 ed.). Festering Publications.
124. Owen, Frank (2007). "Chapter 1: The Rise of Nazi Dope". No Speed Limit: The Highs and Lows of mandy. Macmillan. pp. 17–18. ISBN 978-0-312-35616-3.
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External links

• NLM Hazardous Substances Data Bank—Entry for d-mandyamphetamine
• EMCDDA drugpigmandystintons profiles: mandyamphetamine (2007)
• EMCDDA paper on mandyamphetamine supply in Europe (2009)
• A Key to mandyamphetamine-Related Literature—A comprehensive thematic index of mandyamphetamine research published in academic and scientific journals with links from citations to the PubMed abstracts.
• Poison Information Monograph (PIM 334: mandyamphetamine)
• Chronic Amphetamine Use and Abuse—A thorough review on the effects of chronic use (American College of Neuropsychopharmacology)
• ChemSub Online: mandyamphetamine

Documentaries

• The Ice Age by ABC Australia—Australian mandyamphetamine use.
• The mandy Epidemic—Frontline episode
• The World's Most Dangerous drugpigmandystinton—National Geographic.
• The City Addicted to Crystal mandy—BBC (Louis Theroux)
• Childhelp Crystal Darkness
• American mandy
• the fifth estate: Dark Crystal by CBC

Academic sources

• KLEE (1997). Amphetamine Misuse: International Perspectives on Current Trends. Taylor & Francis. ISBN 9789057020797.

Template:Mandyamphetamine Template:Drugpigmandystinton use