Methamphetamine (contracted from N -methylamphetamine ) is a potent central nervous system (CNS) stimulant primarily used as a medicine recreational and more rare as second-line treatment for hyperactivity deficit attention and obesity. Methamphetamine was discovered in 1893 and exists as two enantiomers: levo-methamphetamine and dextro-methamphetamine. Methamphetamine correctly refers to certain chemicals, racemic free bases, which are the same mixture of levomethamphetamine and dextromethamphetamine in their pure amine form. It is rarely prescribed for concerns involving human neurotoxicity and potential for recreational use as an aphrodisiac and euphoria, among other concerns, as well as the availability of safer replacement drugs with comparable efficacy of treatment. Dextromethamphetamine is a much stronger CNS stimulant than levomethamphetamine.
Both methamphetamine and dextromethamphetamine are illegally traded and sold because of their potential for recreation. The highest prevalence of illegal methamphetamine use occurs in parts of Asia, Oceania, and in the United States, where racemic methamphetamine, levomethamphetamine, and dextromethamphetamine are classified as controlled substance II. Levomethamphetamine is available as an over-the-counter (OTC) drug for use as an inhalation nasal decongestant in the United States. Internationally, the production, distribution, sale and ownership of methamphetamine is restricted or prohibited in many countries, because of its placement in Schedule II of the United Nations Convention on the Agreement of Psychotropic Substances. While dextromethamphetamine is a more potent drug, racemic methamphetamine is sometimes produced illegally due to the ease of relative synthesis and the limited chemical precursors.
In low doses, methamphetamine can improve mood, increase alertness, concentration and energy in tired individuals, reduce appetite, and increase weight loss. At higher doses, it can induce psychosis, skeletal muscle damage, convulsions and bleeding in the brain. The use of chronic high doses can trigger unexpected and rapid mood swings, stimulatory psychosis (eg, paranoia, hallucinations, delirium, and delusions) and violent behavior. Recreational, methamphetamine's ability to increase energy has been reported to improve mood and increase sexual desire in such a way that users can engage in continuous sexual activity for several days. Methamphetamine is known to have high addictive responsibilities (ie, most likely long-term use or high doses will lead to the use of compulsive drugs) and high dependency responsibilities (ie most likely withdrawal symptoms will occur when the use of methamphetamine stops). Excessive use of methamphetamine can cause post-acute-withdrawal syndrome, which can persist for months after a typical withdrawal period. Unlike amphetamines, methamphetamine is neurotoxic in dopaminergic neurons of the midbrain of humans. It has also been shown to damage serotonin neurons in CNS. This damage includes adverse changes in the structure and function of the brain, such as the reduction of gray matter volume in some brain regions and adverse changes in markers of metabolic integrity.
Methamphetamine is included in the substituted phenethylamine class and substituted substituted chemical substitution. It is related to other dimethylphenethylamines as position isomers of this compound, which share the general chemical formula: C 10 H 15 N 1 .
Video Methamphetamine
Usage
Medical
In the United States, dextromethamphetamine hydrochloride, under the trade name
Because methamphetamine is associated with a high potential for abuse, it is regulated under the Controlled Substance Act and is listed under Schedule II in the United States. Methamphetamine hydrochloride distributed in the United States is required to include a box warning regarding the potential for recreational abuse and addiction liability.
Recreation
Methamphetamine is often used recreatively because of its effect as a powerful euphoriant and stimulant as well as aphrodisiac quality.
According to the National Geographic TV documentary on methamphetamine, all subcultures known as parties and games are based on sexual activity and the use of methamphetamine. Participants in this subculture, who are almost entirely made up of male gay male methamphetamine users, will usually meet through internet dating sites and have sex. Due to the powerful stimulatory and aphrodisiac effects and the inhibitory effect on ejaculation, with repeated use, these sexual encounters will sometimes continue for several days. Accidents after the use of methamphetamine in this way are very often severe, with a real hyperomnia (excessive daytime sleepiness). Party and subculture play is prevalent in major US cities such as San Francisco and New York City.
Maps Methamphetamine
Contraindications
Methamphetamine is contraindicated in individuals with a history of substance use disorders, cardiovascular disease, or severe agitation or anxiety, or in individuals currently experiencing arteriosclerosis, glaucoma, hyperthyroidism, or severe hypertension. The FDA states that individuals who have experienced hypersensitivity reactions to other stimulants in the past or are currently using a monoamine oxidase inhibitor should not take methamphetamine. The FDA also advises individuals with bipolar disorder, depression, elevated blood pressure, liver or kidney problems, mania, psychosis, Raynaud's phenomenon, seizures, thyroid problems, tics or Tourette syndrome to monitor their symptoms while taking methamphetamine. Because of the potential for stunted growth, the FDA recommends monitoring the height and weight of growing children and adolescents during treatment.
Side effects
Physical
The physical effects of methamphetamine can include loss of appetite, hyperactivity, dilated pupils, reddened skin, excessive sweating, increased movement, dry mouth and grinding teeth (lead to "meth mouth"), headache, irregular heartbeat (usually like heartbeat accelerated or slowed) heart rate), rapid breathing, high blood pressure, low blood pressure, high body temperature, diarrhea, constipation, blurred vision, dizziness, twitching, numbness, shaking, dry skin, pimples and pale appearance.
Mouth Meth
Methamphetamine users and addicts can lose their teeth quickly, regardless of the route of administration, from a condition that is informally known as meth. This condition is generally the most severe in users who inject drugs, rather than swallowing, smoking, or inhaling. According to the American Dental Association, meth mouth "may be caused by a combination of psychological and physiological changes caused by drugs resulting in xerostomia (dry mouth), long periods of poor oral hygiene, frequent consumption of high-calorie beverages, carbonated and bruxism (grinding teeth and clenching ) ". Because dry mouth is also a common side effect of other stimulants, which are unknown to contribute to severe tooth decay, many researchers argue that methamphetamine-related tooth decay is more caused by other options users. They suggest the side effects have been exaggerated and distilled to create current user stereotypes as a precaution for new ones.
Sexually sexually transmitted infections
Methamphetamine use was found to be associated with a higher frequency of unprotected intercourse in both HIV-positive and unknown couples, a more prominent association in HIV-positive participants. These findings suggest that the use and involvement of methamphetamine in unprotected anal sex is a joint risk behavior, a behavior that potentially increases the risk of HIV transmission among gay and bisexual men. Methamphetamine use allows the users of both sexes to engage in prolonged sexual activity, which can cause genital wounds and abrasive and priapism in men. Methamphetamine can also cause cuts and abrasions in the mouth through bruxism, increasing the risk of sexually transmitted infections.
In addition to sexual transmission of HIV, it can also be transmitted between users sharing common needles. The rate of needle sharing among methamphetamine users is similar to those of other drug injectors.
Psychological
Psychological effects of methamphetamine may include euphoria, dysphoria, libido changes, alertness, fear and concentration, decreased fatigue, insomnia or awakening, self-confidence, social skills, irritability, anxiety, greatness and repetitive and obsessive behavior. Strange for methamphetamine and related stimulants is "punding," a persistent non-goal-directed repetitive activity. Methamphetamine use also has a high association with anxiety, depression, amphetamine psychosis, suicide, and violent behavior.
Neurotoxicity and neuroimmun response
Unlike amphetamines, methamphetamine is directly neurotoxic to dopamine neurons in both laboratory and human animals. In addition, methamphetamine neurotoxicity is associated with an increased risk of Parkinson's disease, an effect that partially arises through excessive cytosolic and synaptic production of reactive oxygen species and dopamine autoxidation. In addition to dopaminergic neurotoxicity, evidence of human evidence also suggests that high-dose methamphetamine use may be neurotoxic for serotonin neurons. It has been shown that high core temperatures are correlated with increased neurotoxic effects of methamphetamine. As a result of methamphetamine-induced neurotoxicity against dopamine neurons, chronic use may also lead to post-acute withdrawals lasting months after a typical withdrawal period.
Studies of magnetic resonance imaging in human methamphetamine users have also found evidence of neurodegeneration, or adverse neuroplastic changes in brain structure and function. Specifically, methamphetamine appears to cause hypertension and white matter hypertrophy, shrinkage marked by hippocampi, and reduce gray matter in the cingulate cortex, limbic cortex, and paralimbic cortex in recreational methamphetamine users. In addition, evidence suggests that adverse changes in the level of biomarker integrity and metabolic synthesis occur in recreational users, such as reduction of N -aceteletpartate and creatine levels and elevated levels of choline and myoinositol.
Methamphetamine has been shown to activate TAAR1 in human astrocytes and produce cAMP as a result. The local astrocyte-TAAR1 activation seems to function as a mechanism by which methamphetamine weakens the level of EAAT2 (SLC1A2) bound to the membrane and functions in these cells.
Methamphetamine binds and activates the subtypes of sigma receptors ,? 1 and? 2 , in the brain. Activation of Sigma receptors by methamphetamine promotes methamphetamine-induced neurotoxicity by facilitating hyperthermia, enhancing the synthesis and release of dopamine, affecting microglial activation, and modulating cascades of apoptotic signals and formation of reactive oxygen species.
Review 2015 concludes that behavior resulting from methamphetamine use may be due in part to the neurotoxic effects of the drug. Excitotoxicity, oxidative stress, metabolic compromise, UPS dysfunction, protein nitration, endoplasmic reticulum stress, p53 expression and other processes contribute to this neurotoxicity.
Overdose
Overdose of methamphetamine can cause various symptoms. Overdose moderate methamphetamine can cause symptoms such as heart rhythm abnormalities, confusion, difficult and/or urination pain, high blood pressure or low, high body temperature, reflexes too active and/or too responsive, muscle pain, severe agitation, rapid breathing, tremors, urinary doubts, and an inability to urinate. Extremely overdose can produce symptoms such as adrenergic storm, methamphetamine psychosis, substantial decrease or no urine output, cardiogenic shock, cerebral hemorrhage, circulatory collapse, hyperpyrexia (ie, high dangerous body temperature), pulmonary hypertension, renal failure, rapid muscle damage, serotonin syndrome, and stereotyped forms ("tweaking"). An overdose of methamphetamine is also likely to cause mild brain damage as a result of dopaminergic and serotonergic neurotoxicity. Deaths due to methamphetamine poisoning are usually preceded by seizures and coma.
Psychosis
Methamphetamine abuse can cause stimulatory psychosis that can arise with various symptoms (eg, paranoia, hallucinations, delirium, and delusions). A Cochrane Collaboration review of treatments for amphetamines, dextroamphetamine, and misuse of methamphetamine abuse psychosis states that about 5-15% of users fail to fully recover. The same review confirms that, based on at least one trial, antipsychotic medications effectively resolve the symptoms of acute amphetamine psychosis. Amphetamine psychosis also sometimes develops as a side effect arising from treatment.
Emergency treatment
Acute methamphetamine intoxication is largely managed by treating symptoms and treatment may initially include the provision of activated charcoal and sedation. There is not enough evidence of hemodialysis or peritoneal dialysis in the case of methamphetamine toxicity to determine its usefulness. Forced acid diuresis (eg, with vitamin C) increases methamphetamine excretion but is not recommended as it may increase the risk of aggravating acidosis, or cause seizures or rhabdomyolysis. Hypertension presents the risk of intracranial hemorrhage (ie, bleeding in the brain) and, if severe, is usually treated with intravenous phentolamine or nitroprusside. Blood pressure often decreases gradually after sufficient sedation with benzodiazepines and provides a soothing environment.
Antipsychotics such as haloperidol are useful for treating agitation and psychosis of methamphetamine overdose. Beta blockers with lipophilic properties and CNS penetration such as metoprolol and labetalol may be useful for treating CNS and cardiovascular toxicity. Labetalol mixture of alpha and beta-blockers is very useful for the treatment of tachycardia and hypertension caused by methamphetamine. The phenomenon of "alpha stimulation without opponents" has not been reported with the use of beta-blockers for the treatment of methamphetamine toxicity.
Dependency
The current addiction model of chronic drug use involves changes in gene expression in certain parts of the brain, especially the nucleus accumbens. The most important transcription factor that produces this change is? FosB, cAMP element binding protein (CREB), and nuclear factor kappa B (NF? B). Fosb plays an important role in the development of drug addiction, because the overexpression of the D1 type middle-spaced neurons in nucleus accumbens is necessary and sufficient for most behavioral and neurological adaptations arising from addiction. Once? FosB is sufficiently expressed, it induces an addictive state that gets progressively worse with a further increase in the FosB expression. It has been implicated in alcoholism, cannabinoids, cocaine, methylphenidate, nicotine, opioids, phencyclidine, propofol, and amphetamine substitutions, among others.
? JunD, transcription factors, and G9a, the histone methyltransferase enzyme, both directly opposed the induction of Fosb in nucleus accumbens (ie, they opposed the increase in expression). Simply over-expressed? JunD in nucleus accumbens with viral vectors can actually block many of the nerve changes and behaviors seen in chronic drug abuse (ie, changes mediated by? FosB). Fosb also plays an important role in regulating behavioral responses to natural rewards, such as good food, sex, and exercise. Because both natural rewards and addictive drugs induce expression? FosB (that is, they cause the brain to produce more), this chronic appreciation can result in the same pathological state of addiction. Fosb is the most significant factor involved in amphetamine-induced and amphetamine-induced sex addiction, which is compulsive sexual behavior resulting from excessive sexual activity and amphetamine use. This sex addiction (ie, drug-induced compulsive sexual behavior) is associated with dopamine dysregulation syndrome that occurs in some patients who use dopaminergic drugs, such as amphetamine or methamphetamine.
Epigenetic factors in methamphetamine addiction
Methamphetamine addiction is persistent for many individuals, with 61% of individuals treated for addiction relapse within one year. About half of those with methamphetamine addiction continue to use over a ten-year period, while the other half reduces use starting about one to four years after initial use.
Persistent persistence suggests that long-lasting changes in gene expression can occur in certain areas of the brain, and may contribute significantly to the phenotype of addiction. Recently important roles have been found for epigenetic mechanisms in driving enduring changes in gene expression in the brain.
A review in 2015 summarizes a number of studies involving the use of chronic methamphetamine in rodents. Epigenetic changes are observed in the brain "reward" areas, including ventral tegmental areas, nucleus accumbens, dorsal striatum, hippocampus, and prefrontal cortex. The use of chronic methamphetamine causes histone-specific acetylation of genes, deacetylations and methylations. DNA-specific methylation of genes in specific areas of the brain is also observed. Various epigenetic changes cause downregulation or upregulations of certain genes that are important in addiction. For example, the use of chronic methamphetamine causes lysine methylation at the 4th position of histone 3 located on the promoter of c-fos and the
In mice addicted to methamphetamine, epigenetic regulation through the reduction of histone acetylation, in striatal brain neurons, leads to decreased transcription of glutamate receptors. Glutamate receptors play an important role in regulating the effects of substance abuse reinforcement.
Care and management
Current cognitive behavioral therapy is the most effective clinical treatment for psychostimulary addiction in general. As of May 2014, there is no effective pharmacotherapy for methamphetamine addiction. Methamphetamine addiction is mostly mediated through increased activation of dopamine receptors and NMDA co-localization receptors
NMDA in nucleus accumbens. Magnesium ions inhibit NMDA receptors by blocking calcium receptor channels.Dependence and tethering
Tolerance is expected to evolve with regular methamphetamine use and, when used recreatively, this tolerance develops rapidly. In the dependent user, withdrawal symptoms are positively correlated with drug tolerance levels. Depression from methamphetamine withdrawal lasts longer and more severe than withdrawal of cocaine.
According to Cochrane's current review of drug addiction and withdrawal to recreational users of methamphetamine, "when chronic heavy users suddenly discontinue use of [methamphetamine], many reports of limited-time withdrawal syndrome occur within 24 hours of their last dose". Chronic withdrawal symptoms, high-dose users are common, occur in up to 87.6% of cases, and persist for three to four weeks with the "stuck" phase marked occurring during the first week. Symptoms of methamphetamine withdrawal may include anxiety, drug craving, dysphoric mood, fatigue, increased appetite, increased movement or decreased movement, lack of motivation, sleeplessness or drowsiness, and clear or clear dreams.
Methamphetamine present in the maternal bloodstream can pass through the placenta to the fetus and secreted into breast milk. Babies born to mothers who abuse methamphetamine may have neonatal withdrawal syndromes, with symptoms involving abnormal sleep patterns, poor food intake, tremors, and hyponemia. The withdrawal syndrome is relatively mild and requires only medical intervention in about 4% of cases.
Interactions
Methamphetamine is metabolized by the liver enzyme CYP2D6, so the CYP2D6 inhibitor will prolong the half-life of methamphetamine elimination. Methamphetamine also interacts with monoamine oxidase inhibitors (MAOIs), as both MAOI and methamphetamine increase plasma catecholamines; Therefore, concurrent use is dangerous. Methamphetamine can decrease the effects of sedatives and depressants and increase the effects of antidepressants and other stimulants as well. Methamphetamine can neutralize the effects of antihypertensives and antipsychotics because of their effect on the cardiovascular system and their cognition. PH gastrointestinal and urine contents affect the absorption and excretion of methamphetamine. In particular, the acidic substances will reduce the absorption of methamphetamine and increase urinary excretion, while alkaline substances do the opposite. Because of the effect of pH on absorption, the proton pump inhibitor, which reduces gastric acid, is known to interact with methamphetamine.
Pharmacology
Pharmacodynamics
Methamphetamine has been identified as a potent agonist of receptors associated with amine 1 (TAAR1), the protein-coupled G (GEP) receptor that regulates the brain catecholamine system. Activation of TAAR1 increases the production of cyclic adenosine monophosphate (cAMP) and either completely inhibits or reverses the transport direction of dopamine transporters (DAT), norepinephrine (NET) transporters, and serotonin transporters (SERT). When methamphetamine binds to TAAR1, it triggers transporter phosphorylation via protein kinase A (PKA) and protein kinase C (PKC) signaling, eventually resulting in internalization or reverse function of the monoamine transporter. Methamphetamine is also known to increase intracellular calcium, an effect associated with DAT phosphorylation through independent dependent Ca 2/calmodulin-dependent kinase (CAMK) dependent signaling, which in turn results in dopamine depletion. TAAR1 has also been shown to reduce the rate of burning of neurons through direct activation of potassium G protein-coupled inwardly-rectifying channels. Activation of TAAR1 by methamphetamine in astrocytes appears to modulate membrane expression and EAAT2 function negatively, a type of glutamate transporter.
In addition to the plasma membrane monoamine transporter, methamphetamine inhibits absorption and induces scattering of neurotransmitters and other substrates in vesicular monoamine transporters, VMAT1 and VMAT2. In neurons, methamphetamine induces the removal of monoamine neurotransmitters through VMAT2, resulting in monoamine outflow from synaptic vesicles into the cytosol (intracellular fluid) of the presinaptic neurone. Other carriers of methamphetamine known to inhibit are SLC22A3 and SLC22A5. SLC22A3 is an extraneuronal monoamine transporter present in astrocytes, and SLC22A5 is a high affinity carnitine transporter.
Methamphetamine is also an alpha-2 adrenergic receptor agonist and sigma receptor with greater affinity for? 1 than? 2 , and inhibits monoamine oxidase A (MAO-A) and monoamine oxidase B (MAO-B). Activation of sigma receptors by methamphetamine facilitates the effects of central nervous system stimulation and increases neurotoxicity in the brain. Methamphetamine is known to inhibit liver enzyme CYP2D6 as well. Dextromethamphetamine is a stronger psychostimulant (about ten times in striatal dopamine), but levomethamphetamine has stronger peripheral effects, longer half-life, and longer effects are felt among addicts. At high doses, both methamphetamine enantiomers can induce similar stereotypy and methamphetamine psychosis, but levomethamphetamine has a shorter psychodynamic effect.
Pharmacokinetics
After oral administration, methamphetamine is well absorbed into the bloodstream, with the highest shabu-shabu concentration reaching about 3.13-6.3 hours after consumption. Methamphetamine is also well absorbed after inhalation and after intranasal administration. Due to the high lipophilicity of methamphetamine, it can easily move through the blood-brain barrier faster than any other stimulant, where it is more resistant to degradation by monoamine oxidase. Peak of amphetamine metabolites at 10-24 hours. Methamphetamine is excreted by the kidneys, with levels of excretion into the urine greatly affected by urinary pH. When taken orally, 30-54% of the dose is excreted in urine as methamphetamine and 10-23% as amphetamine. After the IV dose, about 45% was excreted as methamphetamine and 7% as amphetamine. Methamphetamine half-life varies with a range of 5-30 hours.
CYP2D6, dopamine? -hydroxylase, monooxygenase 3 containing flavin, butyl-CoA ligase, and glycine N-acyltransferase is an enzyme known to metabetize methamphetamine or its metabolites in humans. The major metabolites are amphetamines and 4-hydroxymethamfetamine; Other minor metabolites include: 4-hydroxyamphetamine , 4-hydroxynorephedrine , 4-hydroxyphenylacetone , benzoic acid, hypuratic acid, norephedrine, and phenylacetone, metabolites amphetamines. Among these metabolites, active sympathomimetics are amphetamine, 4-hydroxyamphetamine, 4-hydroxynorephedrine, and norephedrine.
The main metabolic pathway involves aromatic hydroxylation, aliphatic alpha and beta hydroxylation, N-oxidation, N-dealkylation, and deamination. Known metabolic pathways include:
Detection in biological fluid
Methamphetamine and amphetamines are often measured in urine or blood as part of a drug test for exercise, occupation, toxic diagnostics, and forensics. Chiral techniques can be used to help differentiate drug sources to determine whether the drug was obtained illegally or legally through prescription or prodrug. Chiral separation is necessary to assess the levomethamphetamine contribution, which is an active ingredient in some OTC nose decongestants, to a positive test result. Dietary zinc supplements can mask the presence of methamphetamine and other drugs in the urine.
Chemistry
Methamphetamine is a chiral compound with two enantiomers, dextromethamphetamine and levomethamphetamine. At room temperature, the methamphetamine-free base is a clear, colorless liquid with a distinctive odor of geranium leaves. It is soluble in diethyl ether and ethanol and can be soluble with chloroform. In contrast, the methamphetamine hydrochloride salt does not smell with bitterness. It has a melting point between 170 and 175 ° C (338 ° to 347 ° F) and, at room temperature, occurs as a white crystalline or white crystalline powder. The hydrochloride salt is also soluble in ethanol and water.
Degradation
The timing and concentration of bleaching exposure correlates with methamphetamine destruction. Methamphetamine in the soil has been shown to be persistent pollutants. Methamphetamine is mostly degraded within 30 days in bioreactor studies under exposure to light in wastewater.
Synthesis
Racemic methamphetamine can be prepared starting from phenylacetone either by Leuckart or the reductive amination method. In Leuckart's reaction, one phenylacetone equivalent is reacted with two equivalents of N -methylformamide to produce formyl amide from methamphetamine plus carbon dioxide and methylamine as by-products. In this reaction, the iminium cation is formed as an intermediate that is reduced by the second equivalent N -methylformamide . The medium-amide formyl is then hydrolyzed under acidic aqueous conditions to produce methamphetamine as the final product. Alternatively, phenylacetone may be reacted with methylamine under reduction conditions to produce methamphetamine.
History, society and culture
Amphetamine, discovered before methamphetamine, was first synthesized in 1887 in Germany by Romanian chemist Lazor Edeleanu who called it phenylisopropylamine. Shortly after, methamphetamine was synthesized from ephedrine in 1893 by Japanese chemist Nagai Nagayoshi. Three decades later, in 1919, methamphetamine hydrochloride was synthesized by pharmacologist Akira Ogata through the reduction of ephedrine using red and iodine phosphorus.
During World War II, methamphetamine was sold in tablet form under the brand name Pervitin (not to be confused with Perviton , which is a synonym for Phenatine), produced by Berlin-based pharmaceutical company Temmler. It is used extensively by all branches of the combined Wehrmacht armed forces of the Third Reich, and is popular with Luftwaffe pilots in particular, for the stimulant effects that improve performance and to induce an extended extension. Pervitin became the colloquial language known among the German troops as "Stuka-Tablet" ( Stuka-Tabletten ) and "Herman-GÃÆ'¶ring-Pills" ( Hermann-GÃÆ'¶ring-Pillen ). The side effects were so serious that the army quickly reduced its use in 1940. Historian Lukasz Kamienski said, "A soldier who will fight in Pervitin usually finds himself unable to perform effectively for the next day or two.Sick of drugs and looks more like a zombie rather than a great warrior, he must recover from its side effects. "Some soldiers turned very cruel, committed war crimes against civilians; others attack their own officers.
Obetrol, patented by Obetrol Pharmaceuticals in the 1950s and indicated for the treatment of obesity, is one of the first brands of pharmaceutical methamphetamine products. Due to the psychological effects and methamphetamine stimulants, Obetrol became a popular diet pill in America in the 1950s and 1960s. Finally, due to the addictive nature of the drug known, the government began to strictly regulate the production and distribution of methamphetamine. For example, during the early 1970s in the United States, methamphetamine became controlled substance II under the Controlled Substance Act. Currently, methamphetamine is sold under the trade name Desoxyn , a trademark by the Danish pharmaceutical company, Lundbeck. In January 2013, the Desoxyn trademark has been sold to the Italian pharmaceutical company, Recordati.
Legal status
Production, distribution, sales, and ownership of methamphetamine are restricted or illegal in many jurisdictions. Methamphetamine has been placed in Schedule II of the United Nations Convention on the Agreement of Psychotropic Substances.
Australia
Methamphetamine is a Schedule 8 controlled substance in Australia under Standard Poison (July 2016). A schedule controlled substance 8 is one that must be available for use but requires restrictions on manufacture, supply, distribution, ownership and use to reduce abuse, misuse and physical or psychological dependence.
In Western Australia under the Drug Abuse Act 1981 4.0g methamphetamine is the number of illicit drugs that determine the court, 2.0 g is the amount required for the presumption of intent to sell or supply and 28.0 g is the amount required for the purpose of drug trafficking.
Research
It has been suggested, based on animal studies, that Calcitriol, an active vitamin D metabolite, can provide significant protection against the DA-and 5-HT-depleting effects of methamphetamine neurotoxic doses.
See also
Note
- Image legend
Reference notes
References
External links
- Methamphetamine Toxnet entry
- Methamphetamine Poison Information Monograph
- Drug Trafficking: Aryan Brotherhood Methamphetamine Surgery Dismantled, FBI
- Neurologic manifestations of chronic methamphetamine abuse
- Full review of history, pharmacology, and methamphetamine abuse effects, with links to related articles.
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