food and nutrition


Methamphetamine

Question: MeThAmPhEtAmInE!?!?!?!? anything similar to methamphetamine, if so can you give me detailzzzz on everything First off Im writing a paper on this and need to know was there anything chemically similar, obviously you won't be getting the best answer, and yes I have seen the faces of meth and how is Ritalin like it, any info on that?

Answer: Methamphetamine (methylamphetamine or desoxyephedrine), popularly shortened to meth and also nicknamed "ice", is a psychostimulant and sympathomimetic drug. The dextrorotatory isomer dextromethamphetamine can be prescribed to treat attention-deficit hyperactivity disorder, though unmethylated amphetamine is more commonly prescribed. Also, narcolepsy, and obesity can be treated by the aforementioned isomer under the brand name Desoxyn. It is considered a second line of treatment, used when amphetamine and methylphenidate cause the patient too many side effects. It is only recommended for short term use (~6 weeks) in obesity patients because it is thought that the anoretic effects of the drug are short lived and produce tolerance quickly, whereas the effects on CNS stimulation are much less susceptable to tolerance. It is also used illegally for weight loss and to maintain alertness, focus, motivation, and mental clarity for extended periods of time, and for recreational purposes. Methamphetamine enters the brain and triggers a cascading release of norepinephrine, dopamine and serotonin. To a lesser extent Methamphetamine acts as a dopaminergic and adrenergic reuptake inhibitor and in high concentrations as a monamine oxidase inhibitor (MAOI). Since it stimulates the mesolimbic reward pathway, causing euphoria and excitement, it is prone to abuse and addiction. Users may become obsessed or perform repetitive tasks such as cleaning, hand-washing, or assembling and disassembling objects. Withdrawal is characterized by excessive sleeping, eating and depression-like symptoms, often accompanied by anxiety and drug-craving.[2] Users of methamphetamine often take one or more benzodiazepines as a means of "coming down". History Methamphetamine was first synthesized from ephedrine in Japan in 1893 by chemist Nagayoshi Nagai.[3] In 1919, crystallized methamphetamine was synthesized by Akira Ogata via reduction of ephedrine using red phosphorus and iodine. The related compound amphetamine was first synthesized in Germany in 1887 by Lazăr Edeleanu. World War II One of the earliest uses of methamphetamine was during World War II when the German military dispensed it under the trade name Pervitin. [4] It was widely distributed across rank and division, from elite forces to tank crews and aircraft personnel. Chocolates dosed with methamphetamine were known as Fliegerschokolade ("flyer's chocolate") when given to pilots, or Panzerschokolade ("tanker's chocolate") when given to tank crews. From 1942 until his death in 1945, Adolf Hitler was given daily intravenous injections of methamphetamine by his personal physician, Theodor Morell as a treatment for depression and fatigue. It is possible that it was used to treat Hitler's speculated Parkinson's disease, or that his Parkinson-like symptoms which developed from 1940 onwards were related to abuse of methamphetamine.[5] Post war use After World War II, a large supply of amphetamine, formerly stockpiled by the Japanese military, became available in Japan under the street name shabu (also Philopon (pronounced ヒロポン, or Hiropon), its tradename there.[6]) The Japanese Ministry of Health banned it in 1951; and its prohibition is thought to have added to the growing yakuza-activities related to illicit drug production.[7] Today, methamphetamine is still associated with the Japanese underworld, but its usage is discouraged by strong social taboos. In the 1950s there was a rise in the legal prescription of methamphetamine to the American public. According to the 1951 edition of Pharmacology and Therapeutics by Arthur Grollman, it was to be prescribed for "narcolepsy, post-encephalitic Parkinsonism, alcoholism, ... in certain depressive states... and in the treatment of obesity." In the 1960s significant use began of clandestinely manufactured methamphetamine and methamphetamine created in users' own homes for personal use. The recreational use of methamphetamine peaked in the 1980s. The December 2, 1989 edition of The Economist described San Diego, California as the "methamphetamine capital of North America."[citation needed] In 2000, The Economist again described San Diego, California as the methamphetamine capital of North America, and South Gate, California as the second capital city. Legal restriction in the United States In 1983 laws were passed in the United States prohibiting possession of precursors and equipment for methamphetamine 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 drugs. Despite this, or perhaps in part because of this, usage of methamphetamine expanded throughout rural United States, especially through the Midwest and South. Since 1989 five federal laws and dozens of state laws have been imposed in an attempt to curb the production of methamphetamine. Methamphetamine is easily “cooked up” in home laboratories using pseudoephedrine or ephedrine, the active ingredients in over-the-counter drugs such as Sudafed and Contac. However, preventative legal strategies of the past 17 years have steadily increased restrictions to the distribution of pseudoephedrine/ephedrine-containing products. As a result of the Combat Methamphetamine Epidemic Act of 2005, a subsection of the PATRIOT Act, there are restrictions on the amount of pseudoephedrine and ephedrine one may purchase in a specified time period, and further requirements that these products must be stored in order to prevent theft. Methamphetamine is a potent central nervous system stimulant which affects neurochemical mechanisms responsible for regulating heart rate, body temperature, blood pressure, appetite, attention, mood and responses associated with alertness or alarm conditions. The acute effects of the drug 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. The methyl group is responsible for the potentiation of effects as compared to the related compound amphetamine, rendering the substance on the one hand more lipid soluble and easing transport across the blood brain barrier, and on the other hand more stable against enzymatic degradation by MAO. Methamphetamine 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. Methamphetamine 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[9]). Methamphetamine is a potent neurotoxin, shown to cause dopaminergic degeneration.[10][11] High doses of methamphetamine 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 methamphetamine. It has been proposed that dopamine plays a role in methamphetamine induced neurotoxicity because experiments which reduce dopamine production or block the release of dopamine decrease the toxic effects of methamphetamine administration. When dopamine breaks down it produces reactive oxygen species such as hydrogen peroxide. It is likely that the oxidative stress that occurs after taking methamphetamine mediates its neurotoxicity. [12] It has been demonstrated that a high ambient temperature increases the neurotoxic effects of methamphetamine.[13] Recent research published in the Journal of Pharmacology And Experimental Therapeutics (2007) [3], indicates that methamphetamine binds to a group of receptors called TAAR. TAAR is a newly discovered receptor system which seems to be affected by a range of amphetamine-like substances called trace amines. Effects Common immediate effects.:[14] Euphoria Increased energy and attentiveness Diarrhea, nausea Excessive sweating Loss of appetite, insomnia, tremor, jaw-clenching (Bruxism) Agitation, compulsive fascination with repetitive tasks (Punding) Talkativeness, irritability, panic attacks Increased libido Side effects associated with chronic use: Drug craving Weight loss Withdrawal-related depression and anhedonia Rapid tooth decay ("meth mouth") Amphetamine psychosis Side effects associated with overdose: Brain damage/ Meningitis (Neurotoxicity) Formication (sensation of flesh crawling with bugs, with possible associated compulsive picking and infecting sores) Paranoia, delusions, hallucinations, which may trigger a tension headache. Rhabdomyolysis (Muscle breakdown) which leads to Kidney failure Death from overdose is usually due to stroke, heart failure, but can also be caused by cardiac arrest (sudden death) or hyperthermia. Pharmacokinetics The half life of methamphetamine is 9-15 hours. It is excreted by the kidneys and its half life depends on urinary pH. One of the metabolites of methamphetamine is amphetamine. [15] Tolerance As with other amphetamines, tolerance to methamphetamine is not completely understood, but 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 varies widely between individuals, and even within one person it is highly dependent on dosage, duration of use and frequency of administration. Many cases of narcolepsy are treated with methamphetamine for years without escalating doses or any apparent loss of effect. Short term tolerance can be caused by depleted levels of neurotransmitters within the 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 methamphetamine may eventually cause the receptors to downregulate in order to compensate for increased levels of dopamine within the synaptic cleft.[16] To compensate, larger quantities of the drug are needed in order to achieve the same level of effects. Addiction Methamphetamine is addictive[17], especially when injected or smoked.[18] While not life-threatening, withdrawal is often intense and, as with all addictions, relapse is common. To combat relapse, many recovering addicts attend 12 Step meetings, such as Crystal Meth Anonymous. Methamphetamine-induced hyperstimulation of pleasure pathways leads to anhedonia. Former users have noted that they feel stupid or dull when they quit using methamphetamine. 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 method of recovery has not been shown to be consistently effective. It is shown that taking ascorbic acid prior to using methamphetamine 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 methamphetamine dosage had toxicity mediated, yet this will likely be of little avail in solving the serious behavioral problems associated with methamphetamine use that create many of the problems the users experience. To combat addiction, doctors are beginning to use other forms of amphetamine such as dextroamphetamine to break the addiction cycle in a method similar to methadone for heroin addicts. There are no publicly available drugs comparable to naloxone, which blocks opiate receptors and is therefore used in treating opiate dependence, for use with methamphetamine problems.[19] However, experiments with some monoamine reuptake inhibitors such as indatraline have been successful in blocking the action of methamphetamine.[20] There are studies indicating that fluoxetine, bupropion and imipramine may reduce craving and improve adherence to treatment.[21] Research has also suggested that modafinil can help addicts quit methamphetamine use.[22] [23] Since the phenethylamine phentermine is a constitutional isomer of methamphetamine, it has been speculated that it may be effective in treating methamphetamine addiction. Although phenteremine is a central nervous stimulant that acts on dopamine and norepinephrine, it has not been reported to cause the same degree of euphoria that is associated with other amphetamines. Abrupt interruption of chronic methamphetamine use results in the withdrawal syndrome in almost 90% of the cases. Withdrawal of amphetamine often causes a depression which is longer and deeper than even the depression from cocaine withdrawal Meth mouth Main article: Meth mouth Methamphetamine addicts may lose their teeth abnormally quickly, a condition known as "meth mouth". This effect is not caused by any corrosive effects of the drug itself, which is a common myth. According to the American Dental Association, meth mouth "is probably caused by a combination of drug-induced psychological and physiological changes resulting in xerostomia (dry mouth), extended periods of poor oral hygiene, frequent consumption of high calorie, carbonated beverages and tooth grinding and clenching."[25] Similar, though far less severe symptoms have been reported in clinical use of other amphetamines, where effects are not exacerbated by a lack of oral hygiene for extended periods.[26] METH MOUTH Like other substances which stimulate the sympathetic nervous system, methamphetamine causes decreased production of acid-fighting saliva and increased thirst, resulting in increased risk for tooth decay, especially when thirst is quenched by high-sugar drinks Here's a great link for meth


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