Methamphetamine

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Summary sheet: Methamphetamine
Methamphetamine
Methamphetamine.svg
Chemical Nomenclature
Common names Methamphetamine, Meth, Crystal, Desoxyn, Speed, Ma, Ice, Glass, Shard, Tina, T, Tweak, Crank, Shabu, Yaba
Substitutive name N-Methylamphetamine
Systematic name N-Methyl-1-phenylpropan-2-amine
Class Membership
Psychoactive class Stimulant
Chemical class Amphetamine
Routes of Administration

WARNING: Always start with lower doses due to differences between individual body weight, tolerance, metabolism, and personal sensitivity. See responsible use section.


⇣ Smoked
Dosage
Bioavailability >90%
Threshold < 5 mg
Light 5 - 10 mg
Common 10 - 20 mg
Strong 20 - 60 mg
Heavy 60 mg +
Duration
Total 2 - 6 hoursUp to 12h for irregular users.
Onset 7 - 10 seconds
Come up 5 - 10 seconds
Peak 1 - 3 hours
Offset 1 - 3 hours
After effects 2 - 24 hours
⇣ Oral
Dosage
Bioavailability ~70%[1]
Threshold < 5 mg
Light 5 - 10 mg
Common 10 - 25 mg
Strong 25 - 50 mg
Heavy 50 mg +
Duration
Total 8 - 12 hours Up to 24h for irregular users.
Onset 15 - 45 minutes
Come up 1 - 3 hours
Peak 3 - 5 hours
Offset 3 - 4 hours
After effects 12 - 24 hours



⇣ Insufflated
Dosage
Bioavailability >90%
Threshold < 5 mg
Light 5 - 10 mg
Common 10 - 30 mg
Strong 30 - 60 mg
Heavy 60 mg +
Duration
Total 4 - 7 hours Up to 12h for irregular users.
Onset 3 - 5 minutes
Come up 3 - 5 minutes
Peak 1.5 - 3 hours
Offset 2 - 4 hours
After effects 6 - 24 hours
⇣ Rectal
Dosage
Bioavailability ~99%[2]
Threshold < 5 mg
Light 5 - 10 mg
Common 10 - 30 mg
Strong 30 - 40 mg
Heavy 40 mg+
Duration
Total 6 - 10 hours Up to 18h for irregular users.
Onset 5 - 15 minutes
Come up 3 - 5 minutes
Peak 2 - 4 hours
Offset 3 - 5 hours
After effects 12 - 24 hours




⇣ Intravenous
Dosage
Bioavailability ~100%[1]
Threshold < 5 mg
Light 5 - 10 mg
Common 10 - 30 mg
Strong 30 - 40 mg
Heavy 40 mg+
Duration
Total 4 - 8 hours Up to 18h for irregular users.
Onset 15 - 30 seconds
Come up 1 - 2 minutes
Peak 1 - 3 hours
Offset 3 - 4 hours
After effects 12 - 24 hours

DISCLAIMER: PW's dosage information is gathered from users and resources for educational purposes only. It is not a recommendation and should be verified with other sources for accuracy.

Interactions
Alcohol
GHB
GBL
Opioids
Cocaine
Cannabis
Caffeine
Ketamine
Methoxetamine
Psychedelics
DXM
PCP
25x-NBOMe
2C-T-x
5-MeO-xxT
DOx
Tramadol
aMT
MAOIs


N-Methylamphetamine (also known as Methamphetamine, Ma, Meth, Glass, Ice, Shard, Crank, Tina, T, Tweak, Yaba, Shabu, and Crystal[3]) is a classical stimulant substance of the amphetamine class. It is structurally related to amphetamine, however it crosses the blood-brain barrier more rapidly, due to its relatively high lipid solubility.[4] It produces its effects by increasing levels of the neurotransmitters serotonin, dopamine, and norepinephrine in the brain.

Methamphetamine was first synthesized from ephedrine in 1893 by Japanese chemist Nagayoshi Nagai.[5] Along with heroin and cocaine, it has a notorious reputation as a dangerous and highly addictive "street drug".[6]

Subjective effects include motivation enhancement, stamina enhancement, appetite suppression, increased libido, and euphoria. Chronic high-dose use can induce states of anxiety & paranoia, delusions, thought disorganization, psychosis, and violent behavior. It is associated with compulsive redosing, especially when it is vaporized ("smoked") or injected, due to the overwhelming euphoric rush it produces in the user upon initial administration.

Methamphetamine has been shown to have extremely high abuse and addiction potential; it is widely considered to be one of the most addictive substances due to the intense euphoria it produces.[citation needed] Additionally, unlike amphetamine at therapeutic doses, methamphetamine at moderate to heavy recreational doses is considered to be directly neurotoxic to humans, damaging both dopamine and serotonin neurons within the central nervous system. In nonhuman mammals, degeneration of monaminergic terminals and neuronal apoptosis (cell death) has been known to occur.[7] In humans the effects are also neurotoxic.[8] It also displays cardiotoxicity, including increased blood pressure and elevated risk of stroke and heart attack.

It is highly advised to use harm reduction practices if using this substance.

Pure "shards" of Methamphetamine Hydrochloride, commonly known as "crystal meth".

History and culture

Amphetamine was first synthesized in 1887 in Germany by Romanian chemist Lazăr Edeleanu who named it phenylisopropylamine.[9] Shortly after, methamphetamine was synthesized from ephedrine in 1893 by Japanese chemist Nagai Nagayoshi.[10] Neither drug had a pharmacological use until 1934, when Smith, Kline, and French began selling amphetamine as an inhaler under the trade name Benzedrine as a decongestant.[11] During World War II, amphetamine and methamphetamine were used extensively by both the Allied and Axis forces for their stimulant and performance-enhancing effects.[12][13]

Eventually, as the addictive properties of the drugs became known, governments began to place strict controls on the sale of the drugs.[14] For example, in 1970 in the United States, the two drugs methamphetamine and amphetamine became schedule II controlled substances under the Controlled Substances Act.[15]

Despite strict government controls, both amphetamine and methamphetamine have still been used legally or illicitly by individuals from a variety of backgrounds for different purposes.[16][17][18][19] Due to the large underground market for these drugs, they are frequently illegally synthesized by clandestine chemists, trafficked, and sold on the black market.[20] Based upon drug and drug precursor seizures, illicit amphetamine production and trafficking is much less prevalent than that of methamphetamine.[citation needed]

Methamphetamine hydrochloride is approved by the United States Food and Drug Administration (USFDA) under the trade name "Desoxyn".[21] However, it is rarely prescribed due to its abuse potential, typically being reserved for cases of severe obesity or ADHD in which all other treatment options have been exhausted.

Chemistry

Methamphetamine, or N-methylamphetamine, is a synthetic molecule of the amphetamine family. Molecules of the amphetamine class contain a phenethylamine core featuring a phenyl ring bound to an amino (NH2) group through an ethyl chain with an additional methyl substitution at Rα. Amphetamines are alpha-methylated phenethylamines. Methamphetamine contains an additional methyl substitution at RN, a substitution which is shared with MDMA, methcathinone, and mephedrone.

Stereoisomers

Methamphetamine exists as two enantiomers: dextrorotary and levorotary. Dextrorotatory or dextromethamphetamine (also known as d-methamphetamine) is a stronger central nervous system (CNS) stimulant than levomethamphetamine; however, both are considered to be dependence-forming and addictive when misused and capable of producing similar toxicity symptoms at heavy recreational doses.[citation needed]

Pharmacology

Methamphetamine primarily affects the central nervous system (CNS) by acting as a releasing agent for neurotransmitters such as dopamine, norepinephrine, and serotonin.[22] It also acts as a reuptake inhibitor for some transporter neurons, thereby holding neurotransmitters like norepinephrine in the synapse.[23] Meth also acts as reverse transporter for some transporter neurons, increasing levels of monoamines by forcing the neurotransmitters out of their storage vesicles and expelling them into the synaptic gap by making the dopamine transporters work in reverse.[24][25] Other mechanisms by which methamphetamine are known to increase monoamine levels are by:

  • Decreasing the expression of dopamine transporters at the cell surface, which has the same effect as listed above.
  • Increasing cytosolic levels of monoamines by inhibiting the activity of monoamine oxidase (MAO)
  • Increasing the activity and expression of the dopamine-synthesizing enzyme tyrosine hydroxylase (TH)

In addition to releasing potent amounts of monoamines, Methamphetamine has a high lipid solubility which leads to a relatively fast transfer of the drug across the blood-brain barrier and a quick onset in comparison to other stimulants.[4] All of this results in feelings of reward, euphoria, and stimulation as well as an unpleasant offset.

Subjective effects

Disclaimer: The effects listed below cite the Subjective Effect Index (SEI), an open research literature based on anecdotal user reports and the personal analyses of PsychonautWiki contributors. As a result, they should be viewed with a healthy degree of skepticism.

It is also worth noting that these effects will not necessarily occur in a predictable or reliable manner, although higher doses are more liable to induce the full spectrum of effects. Likewise, adverse effects become increasingly likely with higher doses and may include addiction, severe injury, or death ☠.


Physical effects
Child.svg

    • Stimulation - In terms of its effects on the physical energy levels of the user, methamphetamine is usually considered to be extremely energetic and stimulating in a fashion that is identical to that of amphetamine, but stronger than that of modafinil, caffeine, and MDMA. It is similar yet distinct from the stimulation experienced on MDMA, encouraging physical activities such as dancing, socializing, running, or cleaning. The particular style of stimulation which methamphetamine presents can be described as forced. This means that at higher dosages, it becomes difficult or impossible to keep still as jaw clenching, involuntarily bodily shakes and vibrations become present, resulting in extreme shaking of the entire body, unsteadiness of the hands, and a general lack of motor control.
      • Physical euphoria - As a potent stimulant, methamphetamine is capable producing states of intense physical euphoria, especially when it is vaporized or injected. However, the initial rush of euphoria can wear off well before the substance has run its course which can promote compulsive redosing, which can have extremely damaging cumulative effects.
    • Abnormal heartbeat
    • Increased blood pressure
    • Increased heart rate
    • Appetite suppression
    • Body odor alteration - Methamphetamine can potentially leave a very distinct odor within one's urine, sweat and general bodily secretions. Most people would consider it as unpleaseant, but few people do enjoy it and find it a very pleaseant odor.
    • Bronchodilation
    • Dehydration
    • Frequent urination
    • Increased bodily temperature
    • Increased perspiration
    • Muscle contractions
    • Muscle spasms
    • Neurotoxicity -- from long-term use.
    • Stamina enhancement - This effect is more prominent than with any other commonly used stimulant.
    • Tactile enhancement
    • Tactile hallucination - High doses and/or prolonged usage of certain stimulants like methamphetamine and cocaine can lead to hallucinatory sensations of bugs crawling on the surface of or underneath one’s skin. This is typically referred to as delusional parasitosis or more informally as “meth mites”.
    • Teeth grinding
    • Temporary erectile dysfunction
    • Vasoconstriction
    • Pupil dilation
    • Vibrating vision - At high doses or certain routes of administration, a person's eyeballs may begin to spontaneously wiggle back and forth in a rapid motion, causing the vision to become blurry and temporarily out of focus. This is a condition known as nystagmus.
    • Seizure - This is an uncommon effect but can happen in those predisposed to them, especially while in physically taxing conditions such as being dehydrated, fatigued or undernourished, or if miusing the substance for extended periods of time.

Visual effects
Eye.svg

  • The visual effects of methamphetamine are usually less consistent and are only mildly noticeable at higher dosages. They are somewhat comparable to the visuals produced by deliriants and are more frequent in darker areas. Scenarios consisting of severe sleep deprivation caused by wakefulness can lead to more intense visual effects and even hallucinations.

    Suppressions

    Distortions

    • Visual drifting - This effect is usually subtle or barely noticeable and only occurs at higher dosages or when combined with cannabis. It is most prominent when smoked or taken intravenously and is usually delirious in nature. Commonly this, high dosages or prolonged use can cause level 1-2 visual drifting.
    • Brightness alteration

    Hallucinatory states

    • Transformations - This effect occurs very rarely, and typically only when the user has taken high doses, is coming down, or has been awake for unusually long periods. They are usually very mild when they do happen to occur.

Cognitive effects
User.svg

After effects
Aftereffects (3).svg

Experience reports

There are currently 2 experience reports which describe the effects of this substance in our experience index.

Additional experience reports can be found here:

Toxicity and harm potential

Table from the 2010 ISCD study ranking various drugs (legal and illegal) based on statements by drug-harm experts. Methamphetamine was found to be the fourth overall most dangerous drug.[26]

Neurotoxicity

There is evidence that methamphetamine causes brain damage from long-term use in humans; this damage includes adverse changes in brain structure and function, such as reductions in gray matter volume in several brain regions and adverse changes in markers of metabolic integrity.[27]

Unlike amphetamine, methamphetamine is directly neurotoxic to dopamine neurons.[28] Moreover, methamphetamine abuse is associated with an increased risk of Parkinson's disease due to excessive pre-synaptic dopamine autoxidation, a mechanism of neurotoxicity.[29][30][31][32] Similar to the neurotoxic effects on the dopamine system, methamphetamine can also result in neurotoxicity to serotonin neurons.[33] It has been demonstrated that a high core temperature is correlated with an increase in the neurotoxic effects of methamphetamine.[34] As a result of methamphetamine-induced neurotoxicity to dopamine neurons, chronic use may also lead to post acute withdrawals which persist beyond the withdrawal period for months, and even up to a year.[29]

Dependence and abuse potential

As with other stimulants, the chronic use of methamphetamine can be considered extremely addictive with a high potential for abuse and is capable of causing psychological dependence among certain users. When addiction has developed, cravings and withdrawal effects may occur if a person suddenly stops their usage.

Tolerance to the effects of methamphetamine rapidly develops with prolonged and repeated use.[35][36] This results in users having to administer increasingly large doses to achieve the same effects. After that, it takes about 3 - 7 days for the tolerance to be reduced to half and 1 - 2 weeks to be back at baseline (in the absence of further consumption). Methamphetamine presents cross-tolerance with all dopaminergic stimulants, meaning that after the consumption of methamphetamine all stimulants will have a reduced effect.

The evidence on effective treatments for amphetamine and methamphetamine dependence and abuse is limited.[37] In light of this, fluoxetine and imipramine appear to have some limited benefits in treating abuse and addiction, "no treatment has been demonstrated to be effective for the treatment of methamphetamine dependence and abuse".

In highly dependent amphetamine and methamphetamine abusers, "when chronic heavy users abruptly discontinue methamphetamine use, many report a time-limited withdrawal syndrome that occurs within 24 hours of their last dose".[38] Withdrawal symptoms in chronic, high-dose users are frequent, occurring in up to 87.6% of cases, and persist for three to four weeks with a marked "crash" phase occurring during the first week.[38] Methamphetamine withdrawal symptoms can include anxiety, drug craving, dysphoric mood, fatigue, increased appetite, increased movement or decreased movement, lack of motivation, sleeplessness or sleepiness, and vivid or lucid dreams.[38] Withdrawal symptoms are associated with the degree of dependence (i.e., the extent of abuse).[38] The mental depression associated with methamphetamine withdrawal lasts longer and is more severe than that of cocaine withdrawal.[39]

Although it is clear that vaporised methamphetamine is more addictive than oral or insufflated amphetamine, there is debate as to whether the drug itself is inherently more addictive, and if so, how important the difference is. Besides the duration of action, the main difference between the two drugs is that methamphetamine is proportionally more centrally and less peripherally active. One reason is because the increased lipid solubility of the methyl group causes faster central absorption. Another cause is the fact that methamphetamine releases proportionally more dopamine at an equivalent dose. D-methamphetamine releases a dopamine:norepinephrine ratio of ~1:1.3 from synapses versus ~1:2 for d-amphetamine.[40] Their effect on the norepinephrine (NET) and dopamine (DAT) transporters are more alike but there is a slight difference. D-methamphetamine favours NET by a factor of about 4 vs 5 for d-amphetamine. D-methamphetamine is also slightly more serotonergic. This may be a negligible difference, as the ratio of serotonin:norepinephrine release is only 1:60 for d-methamphetamine and 1:80 for d-amphetamine. Neither drug has any appreciable affinity for the serotonin transporter (SERT).

This increased central vs peripheral effect of methamphetamine agrees with the common subjective feeling among stimulant users that the methamphetamine high has less of an inherently 'jittery' quality to it. The downside is that this aversive effect may be helpful as it discourages harmful levels of use. It is unclear what real world impact this difference has. A double-blind but small study of 13 methamphetamine users revealed only a minor preference towards methamphetamine, and this may be explained by the users having a greater familiarity with the drug.[41]

It is strongly recommended that one use harm reduction practices when using this substance.

Psychosis

Main article: Stimulant psychosis

Abuse of methamphetamine can result in a stimulant psychosis that may present with a variety of symptoms (e.g., paranoia, hallucinations, delusions).[38] A review on treatment for amphetamine, dextroamphetamine, and methamphetamine abuse-induced psychosis states that about 5–15% of users fail to recover completely.[38][42] The same review asserts that, based upon at least one trial, antipsychotic medications effectively resolve the symptoms of acute amphetamine psychosis.[38] Psychosis very rarely arises from therapeutic use.[43]

Overdose

A methamphetamine overdose may result in a wide range of symptoms and is potentially fatal at heavy dosages.[44] A moderate overdose of methamphetamine may induce symptoms such as abnormal heart rhythm, confusion, dysuria, high or low blood pressure, hyperthermia, hyperreflexia, myalgia, severe agitation, tachypnea, tremor, urinary hesitancy, and urinary retention.[45] An extremely large overdose may produce symptoms such as adrenergic storm, methamphetamine psychosis, anuria, cardiogenic shock, cerebral hemorrhage, circulatory collapse, hyperpyrexia, pulmonary hypertension, renal failure, rhabdomyolysis, serotonin syndrome, and a form of stereotypy ("tweaking"). A methamphetamine overdose will likely also result in mild brain damage due to dopaminergic and serotonergic neurotoxicity.[28][33] Death from fatal methamphetamine poisoning is typically preceded by convulsions and coma.[46]

Emergency treatment

Acute methamphetamine overdose is largely managed by treating the symptoms, and administration of benzodiazepines relieves symptoms such as agitation, hypertension, tachycardia, and seizure.[47]

Harm reduction

Studies have shown that N-acetylcysteine (NAC) can block the harmful neurotoxic effects of methamphetamine while preventing neurotransmitter depletion in rats[48] and clinical trials in humans to treat methamphetamine dependence are currently underway. NAC may be effective for reducing the cravings and psychological dependence as well.[49] NAC has a short half life and a sustained release formulation may be preferred for harm reduction purposes. Selenium has also been shown to protect the brain against meth induced neurotoxicity.[50] However, it is worth noting that this data is preliminary and may not be applicable to humans.

Dangerous interactions

Warning: Many psychoactive substances that are reasonably safe to use on their own can suddenly become dangerous and even life-threatening when combined with certain other substances. The following list provides some known dangerous interactions (although it is not guaranteed to include all of them).

Always conduct independent research (e.g. Google, DuckDuckGo, PubMed) to ensure that a combination of two or more substances is safe to consume. Some of the listed interactions have been sourced from TripSit.

  • Alcohol - Drinking alcohol on stimulants is considered risky because it reduces the sedative effects of the alcohol that the body uses to gauge drunkenness. This often leads to excessive drinking with greatly reduced inhibitions, increasing the risk of liver damage and increased dehydration. The effects of stimulants will also allow one to drink past a point where they might normally pass out, increasing the risk. If you do decide to do this then you should set a limit of how much you will drink each hour and stick to it, bearing in mind that you will feel the alcohol and the stimulant less.
  • GHB/GBL - Stimulants increase respiration rate allowing a higher dose of sedatives. If the stimulant wears off first then the depressant effects of the GHB/GBL may overcome the user and cause respiratory arrest.
  • Opioids - Stimulants increase respiration rate allowing a higher dose of opiates. If the stimulant wears off first then the opiate may overcome the patient and cause respiratory arrest.
  • Cocaine - The rewarding effects of cocaine are mediated by DAT inhibition, and an increase of exocytosis of dopamine through the cell membrane. Amphetamine reverses the direction of DAT and the direction vesicular transports within the cell by a pH mediated mechanism of displacement, thus excludes the regular mechanism of dopamine release through means of exocytosis because the effects Na+/K+ ATPase are inhibited. You will find cardiac effects with the combination of cocaine and amphetamine due to a SERT mediated mechanism from the subsequent activation of 5-HT2B, which is an effect of serotonin-related valvulopathy. Amphetamines generally cause hypertension in models of abuse, and this combination can increase the chances of syncope due to turbulent blood flow during valve operation. The rewarding mechanisms of cocaine are reversed by administration of amphetamine.[51][52]
  • Cannabis - Stimulants increase anxiety levels and the risk of thought loops and paranoia which can lead to negative experiences.
  • Caffeine - This combination of stimulants is generally considered unnecessary and may increase strain on the heart, as well as potentially causing anxiety and physical discomfort.
  • Tramadol - Tramadol and stimulants both increase the risk of seizures.
  • DXM - Both substances raise heart rate, in extreme cases, panic attacks caused by these substances have led to more serious heart issues.
  • Ketamine - Combining amphetamine and ketamine may result in psychoses that resemble schizophrenia, but not worse than the psychoses produced by either substance alone, but this is debatable. This is due to amphetamines ability to attenuated the disruption of working memory caused by ketamine. Amphetamine alone may result in grandiosity, paranoia, or somatic delusions with little to no effect on negative symptoms. Ketamine, however, will result in thought disorders, disruption of executive functioning, and delusions due to a modification of conception. These mechanisms are due to an increase of dopaminergic activity in the mesolimbic pathway caused by amphetamine due to its pharmacology effecting dopamine, and due to a disruption of dopaminergic functioning in the mesocortical pathways via NMDA antagonism effects of ketamine. Combining the two, you may expect mainly thought disorder along with positive symptoms.[53]
  • PCP - Increases risk of tachycardia, hypertension, and manic states.
  • Methoxetamine - Increases risk of tachycardia, hypertension, and manic states.
  • Psychedelics (e.g. LSD, mescaline, psilocybin) - Increases risk of anxiety, paranoia, and thought loops.
    • 25x-NBOMe - Amphetamines and NBOMes both provide considerable stimulation that when combined they can result in tachycardia, hypertension, vasoconstriction and, in extreme cases, heart failure. The anxiogenic and focusing effects of stimulants are also not good in combination with psychedelics as they can lead to unpleasant thought loops. NBOMes are known to cause seizures and stimulants can increase this risk.
    • 2C-T-x - Suspected of mild MAOI properties. May increase the risk of hypertensive crisis.
    • 5-MeO-xxT - Suspected of mild MAOI properties. May increase the risk of hypertensive crisis.
    • DOx
  • aMT - aMT has MAOI properties which may interact unfavorably with amphetamines.
  • MAOIs - MAO-B inhibitors can increase the potency and duration of phenethylamines unpredictably. MAO-A inhibitors with amphetamine can lead to hypertensive crises.

Legal status

The production, distribution, sale, and possession of methamphetamine is restricted or illegal in many jurisdictions.[54][55] Methamphetamine has been placed in Schedule II of the United Nations Convention on Psychotropic Substances treaty.[56]

  • Australia: Methamphetamine is placed under Schedule 8, meaning that it is available for medical use, but possession, production or supply of it is illegal without authority.[57] Personal quantities under 1.5 grams are decriminalized in the Australian Capital Territory (ACT) as of 28 October 2023.[58]
  • Austria: Methamphetamine is illegal to possess, produce and sell under the SMG (Suchtmittelgesetz Österreich).[59]
  • Brazil: Methamphetamine is a Class F2 prohibited psychoactive substance.[60]
  • Canada: Methamphetamine is listed on the CDSA as a schedule I substance.[61]
  • Czech Republic: Methamphetamine is a Schedule II controlled substance.[62]
  • Germany: Methamphetamine was added to the Opiumgesetz (Opium Act) on July 1, 1941.[63] It is controlled under Anlage II BtMG (Narcotics Act, Schedule II)[64] as of March 1, 2008. Before that, it could be prescribed on a narcotic prescription form because it was in Anlage III (Schedule III).[65] It is illegal to manufacture, possess, import, export, buy, sell, procure or dispense it without a license.[66]
  • Japan: Methamphetamine is prohibited under the "Amphetamines Control Law" of 1954.[67]
  • The Netherlands: Methamphetamine is a List I controlled substance.[68]
  • New Zealand: Methamphetamine is a Class A controlled substance.[69]
  • Poland: Methamphetamine is a Group II-P controlled substance.[70]
  • South Korea: Methamphetamine is prohibited in South Korea in compliance with the United Nations Convention on Psychotropic Substances.[71]
  • Sweden: Methamphetamine is classified as a drug by the United Nations and is included in list P II in the 1971 Psychotropic Convention, as well as in list II in Sweden.[72]
  • Switzerland: Methamphetamine is a controlled substance specifically named under Verzeichnis A.[73]
  • United Kingdom: Methamphetamine is a Class A drug as of 18 January 2007.[74]
  • United States: Methamphetamine is a Schedule II controlled substance in the United States.[75]

See also

External links

References

  1. ↑ 1.0 1.1 Rau, T., Ziemniak, J., Poulsen, D. (4 January 2016). "The neuroprotective potential of low-dose methamphetamine in preclinical models of stroke and traumatic brain injury". Progress in Neuro-Psychopharmacology and Biological Psychiatry. 64: 231–236. doi:10.1016/j.pnpbp.2015.02.013. ISSN 0278-5846. 
  2. ↑ Methamphetamine - City Vision 
  3. ↑ Erowid Methamphetamine (Speed, Crank) Vault 
  4. ↑ 4.0 4.1 Barr, A. M., Panenka, W. J., MacEwan, G. W., Thornton, A. E., Lang, D. J., Honer, W. G., Lecomte, T. (September 2006). "The need for speed: an update on methamphetamine addiction". Journal of Psychiatry and Neuroscience. 31 (5): 301–313. ISSN 1180-4882. 
  5. ↑ Nagai N (1893) Studies on the components of Ephedraceaein herb medicine. Yakugaku Zasshi 139 :901-933
  6. ↑ Galbraith, N. (October 2015). "The methamphetamine problem". BJPsych Bulletin. 39 (5): 218–220. doi:10.1192/pb.bp.115.050930. ISSN 2056-4694. 
  7. ↑ Jayanthi, S., Daiwile, A. P., Cadet, J. L. (October 2021). "Neurotoxicity of methamphetamine: Main effects and mechanisms". Experimental Neurology. 344: 113795. doi:10.1016/j.expneurol.2021.113795. ISSN 0014-4886. 
  8. ↑ Khoshsirat, S., Khoramgah, M. S., Mahmoudiasl, G.-R., Rezaei-Tavirani, M., Abdollahifar, M.-A., Tahmasebinia, F., Darabi, S., Niknazar, S., Abbaszadeh, H. A. (September 2020). "LC3 and ATG5 overexpression and neuronal cell death in the prefrontal cortex of postmortem chronic methamphetamine users". Journal of Chemical Neuroanatomy. 107: 101802. doi:10.1016/j.jchemneu.2020.101802. ISSN 0891-0618. 
  9. ↑ Edeleano, L. (January 1887). "Ueber einige Derivate der Phenylmethacrylsäure und der Phenylisobuttersäure". Berichte der deutschen chemischen Gesellschaft. 20 (1): 616–622. doi:10.1002/cber.188702001142. ISSN 0365-9496. 
  10. ↑ Grobler, S. R., Chikte, U., Westraat, J. (26 June 2011). "The pH Levels of Different Methamphetamine Drug Samples on the Street Market in Cape Town". ISRN Dentistry. 2011: 1–4. doi:10.5402/2011/974768. ISSN 2090-4371. 
  11. ↑ Rasmussen, N. (21 February 2006). "Making the First Anti-Depressant: Amphetamine in American Medicine, 1929-1950". Journal of the History of Medicine and Allied Sciences. 61 (3): 288–323. doi:10.1093/jhmas/jrj039. ISSN 0022-5045. 
  12. ↑ Rasmussen, N. (September 2011). "Medical Science and the Military: The Allies' Use of Amphetamine during World War II". The Journal of Interdisciplinary History. 42 (2): 205–233. doi:10.1162/JINH_a_00212. ISSN 0022-1953. 
  13. ↑ Defalque, R. J., Wright, A. J. (April 2011). "Methamphetamine for Hitler's Germany: 1937 to 1945". Bulletin of Anesthesia History. 29 (2): 21–32. doi:10.1016/S1522-8649(11)50016-2. ISSN 1522-8649. 
  14. ↑ "Historical overview of methamphetamine". Vermont Department of Health. Government of Vermont. Retrieved 29 January 2012.
  15. ↑ "Controlled Substances Act". United States Food and Drug Administration. 11 June 2009. Retrieved 4 November 2013.
  16. ↑ Gyenis A. "Forty Years of On the Road 1957–1997". wordsareimportant.com. DHARMA beat. Archived from the original on 14 February 2008. Retrieved 18 March 2008.
  17. ↑ Wilson, A. (2009), Mixing the Medicine: The Unintended Consequence of Amphetamine Control on the Northern Soul Scene, Social Science Research Network 
  18. ↑ Hill, J. (2004), Paul Erdős – Mathematical Genius, Human (In That Order) 
  19. ↑ Liddle, D. G., Connor, D. J. (June 2013). "Nutritional Supplements and Ergogenic Aids". Primary Care: Clinics in Office Practice. 40 (2): 487–505. doi:10.1016/j.pop.2013.02.009. ISSN 0095-4543. 
  20. ↑ Chawla S, Le Pichon T (2006). "World Drug Report 2006" (PDF). United Nations Office on Drugs and Crime. pp. 128–135. Retrieved 2 November 2013.
  21. ↑ Desoxyn Label (FDA) | http://www.accessdata.fda.gov/drugsatfda_docs/label/2013/005378s028lbl.pdf
  22. ↑ Kish, S. J. (17 June 2008). "Pharmacologic mechanisms of crystal meth". CMAJ : Canadian Medical Association Journal. 178 (13): 1679–1682. doi:10.1503/cmaj.071675. ISSN 0820-3946. 
  23. ↑ Haughey, H. M., Brown, J. M., Wilkins, D. G., Hanson, G. R., Fleckenstein, A. E. (28 April 2000). "Differential effects of methamphetamine on Na(+)/Cl(-)-dependent transporters". Brain Research. 863 (1–2): 59–65. doi:10.1016/s0006-8993(00)02094-1. ISSN 0006-8993. 
  24. ↑ Lin, M., Sambo, D., Khoshbouei, H. (5 October 2016). "Methamphetamine Regulation of Firing Activity of Dopamine Neurons". The Journal of Neuroscience: The Official Journal of the Society for Neuroscience. 36 (40): 10376–10391. doi:10.1523/JNEUROSCI.1392-16.2016. ISSN 1529-2401. 
  25. ↑ How Drugs Affect Neurotransmitters, Canadian Institutes of Health Research, retrieved January 1, 2007 
  26. ↑ Nutt DJ, King LA, Phillips LD (November 2010). "Drug harms in the UK: a multicriteria decision analysis". Lancet. 376 (9752): 1558–1565. CiteSeerX 10.1.1.690.1283 Freely accessible. doi:10.1016/S0140-6736(10)61462-6. PMID 21036393.  Unknown parameter |s2cid= ignored (help)
  27. ↑ Nie, L., Zhao, Z., Wen, X., Luo, W., Ju, T., Ren, A., Wu, B., Li, J. (10 April 2020). "Gray-matter structure in long-term abstinent methamphetamine users". BMC psychiatry. 20 (1): 158. doi:10.1186/s12888-020-02567-3. ISSN 1471-244X. 
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  35. ↑ Pérez-Mañá, C., Castells, X., Torrens, M., Capellà, D., Farre, M. (2 September 2013). "Efficacy of psychostimulant drugs for amphetamine abuse or dependence". The Cochrane Database of Systematic Reviews (9): CD009695. doi:10.1002/14651858.CD009695.pub2. ISSN 1469-493X. 
  36. ↑ http://www.merckmanuals.com/home/special_subjects/drug_use_and_abuse/amphetamines.html
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  38. ↑ 38.0 38.1 38.2 38.3 38.4 38.5 38.6 Shoptaw, S. J., Kao, U., Heinzerling, K., Ling, W. (15 April 2009). "Treatment for amphetamine withdrawal". The Cochrane Database of Systematic Reviews (2): CD003021. doi:10.1002/14651858.CD003021.pub2. ISSN 1469-493X. 
  39. ↑ Winslow, B. T., Voorhees, K. I., Pehl, K. A. (15 October 2007). "Methamphetamine abuse". American Family Physician. 76 (8): 1169–1174. ISSN 0002-838X. 
  40. ↑ https://en.wikipedia.org/wiki/Monoamine_releasing_agent#Activity_profiles
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  48. ↑ Fukami, G., Hashimoto, K., Koike, K., Okamura, N., Shimizu, E., Iyo, M. (July 2004). "Effect of antioxidant N-acetyl-l-cysteine on behavioral changes and neurotoxicity in rats after administration of methamphetamine". Brain Research. 1016 (1): 90–95. doi:10.1016/j.brainres.2004.04.072. ISSN 0006-8993. 
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  60. ↑ https://www.in.gov.br/en/web/dou/-/resolucao-rdc-n-804-de-24-de-julho-de-2023-498447451
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