Methamphetamine

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Summary sheet: Methamphetamine
Methamphetamine
Molecular structure of Methamphetamine
Methamphetamine.svg
Chemical Nomenclature
Common names Methamphetamine, Meth, Speed, Ice, Glass, Shard, Tina, Crank
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
WARNING: Always start with lower doses due to differences between individual body weight, tolerance, metabolism, and personal sensitivity. See responsible use section.
DISCLAIMER: PW's dosage information is gathered from users and resources for educational purposes only. It is not a recommendation.
This dosage and duration information has been sourced from TripSit
Bioavailability >90%
Threshold < 5 mg
Light 5 - 10 mg
Common 10 - 20 mg
Strong 20 - 60 mg
Heavy 60 mg +
Duration
Total 1 - 3 hours
Onset 0 - 2 minutes
Peak 20 minutes
Offset 1 hour
After effects 2 - 3 hours
Oral
Dosage
Threshold < 5 mg
Light 5 - 15 mg
Common 15 - 30 mg
Strong 30 - 60 mg
Heavy 60 - 150 mg +
Duration
Total 8 - 12 hours
Onset 20 - 45 minutes
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 1 - 3 hours
Onset 0 - 2 minutes
Peak 20 minutes
Offset 1 hour
After effects 6 - 12 hours





Intravenous
Dosage
Threshold < 5 mg
Light 5 - 10 mg
Common 10 - 30 mg
Strong 30 - 40 mg
Heavy 40 - 80 mg +
Duration
Total 4 - 8 hours
Onset 1 - 2 minutes
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.

N-Methylamphetamine (also known as Methamphetamine,[1] Meth,[1] Glass,[1] Ice,[1] Shard,[1] Crank,[1] Tina,[1] Tweak,[1] Yaba,[1] and Crystal[1]) is a highly potent, widely-used synthetic stimulant of the phenethylamine and amphetamine chemical classes that produces powerful and long-lived classical stimulant effects such as stimulation, wakefulness, disinhibition, thought acceleration, and intense states of euphoria when administered.

Methamphetamine hydrochloride is approved by the United States Food and Drug Administration (USFDA) under the trade name "Desoxyn".[2] 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.

Recreationally, methamphetamine is used to lift the mood, increase energy, and increase sexual desire. In low doses, methamphetamine can produce an elevated mood and increased immersion, increased focus, and physical stamina in fatigued individuals. At heavier doses, it can induce states of anxiety & paranoia, delusions, thought disorganization and psychosis, in addition to severe physical injuries such as rhabdomyolysis (kidney damage) and cerebral hemorrhage. It is associated with compulsive redosing, especially when it is vaporized ("smoked") or injected, due to the initial overwhelming euphoric rush it can produce.

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 that are essential in maintaining the proper processing and integration of sensory information, its integration and controlling motor and behavioral output.[citation needed] Additionally, 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.[citation needed]

Due to its potent psychostimulant effects, established toxicity profile, and ability to cause mental and physical dependence and addiction when misused, it is highly advised to use harm reduction practices if choosing to consume this substance.

Pure "shards" of Methamphetamine Hydrochloride, commonly known as "Crystal Meth".

History and culture

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Amphetamine was first synthesized in 1887 in Germany by Romanian chemist Lazăr Edeleanu who named it phenylisopropylamine.[3] Shortly after, methamphetamine was synthesized from ephedrine in 1893 by Japanese chemist Nagai Nagayoshi.[4] 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.[5]

During World War II, amphetamine and methamphetamine were used extensively by both the Allied and Axis forces for their stimulant and performance-enhancing effects.[6][7] Eventually, as the addictive properties of the drugs became known, governments began to place strict controls on the sale of the drugs.[8] For example, during the early 1970s in the United States, amphetamine became a schedule II controlled substance under the Controlled Substances Act.[9]

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.[10][11][12][13]

Due to the large underground market for these drugs, they are frequently illegally synthesized by clandestine chemists, trafficked, and sold on the black market.[14] Based upon drug and drug precursor seizures, illicit amphetamine production and trafficking is much less prevalent than that of methamphetamine.[citation needed]

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. It also acts as a reuptake inhibitor, 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.[15] Other mechanisms by which methamphetamine are known to increase monoamine levels are by:

  • Blocking the reuptake of monoamines (i.e. norepinephrine, dopamine, and serotonin) by inhibiting the activity of their transporters, allowing them to accumulate in the synaptic cleft between neurons in various brain regions.
  • 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, MA 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.[16] All of this results in feelings of reward, euphoria, and stimulation as well as an unpleasant offset.

Subjective effects

The effects listed below are based upon the subjective effects index and personal experiences of PsychonautWiki contributors. The listed effects should be taken with a grain of salt and will rarely (if ever) occur all at once, but heavier doses will increase the chances and are more likely to induce a full range of effects. Likewise, adverse effects become much more likely on higher doses and may include injury or death.

Physical effects
Child.svg

Visual effects
Eye.svg

Cognitive effects
User.svg

After effects
Aftereffects (3).svg

Experience reports

There are currently no anecdotal reports which describe the effects of this compound within our experience index. Additional experience reports can be found here:

Toxicity and harm potential

Unlike amphetamine, methamphetamine is directly neurotoxic to dopamine neurons.[17] Moreover, methamphetamine abuse is associated with an increased risk of Parkinson's disease due to excessive pre-synaptic dopamine autoxidation, a mechanism of neurotoxicity.[18][19][20][21] Similar to the neurotoxic effects on the dopamine system, methamphetamine can also result in neurotoxicity to serotonin neurons.[22] It has been demonstrated that a high core temperature is correlated with an increase in the neurotoxic effects of methamphetamine.[23] 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.[24]

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

Lethal dosage

A methamphetamine overdose may result in a wide range of symptoms and is potentially fatal at heavy dosages.[25] 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.[26] 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.[27][28] Death from fatal methamphetamine poisoning is typically preceded by convulsions and coma.[29]

Tolerance and addiction 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 this compound rapidly develops with prolonged and repeated use.[30][31] 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.[32] 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".[33]

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".[34] 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.[35] 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.[36] Withdrawal symptoms are associated with the degree of dependence (i.e., the extent of abuse).[37] The mental depression associated with methamphetamine withdrawal lasts longer and is more severe than that of cocaine withdrawal.[38]

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).[39] A review on treatment for amphetamine, dextroamphetamine, and methamphetamine abuse-induced psychosis states that about 5–15% of users fail to recover completely.[40][41] The same review asserts that, based upon at least one trial, antipsychotic medications effectively resolve the symptoms of acute amphetamine psychosis.[42] Psychosis very rarely arises from therapeutic use.[43][44]

Dangerous interactions

Although many psychoactive substances are safe on their own, they can become dangerous and even life-threatening when combined with other substances. The list below contains some common potentially dangerous combinations, but may not include all of them. Certain combinations may be safe in low doses of each but still increase the potential risk of death. Independent research should always be done to ensure that a combination of two or more substances is safe before consumption.

Legality

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This legality section is a stub.

As such, it may contain incomplete or wrong information. You can help by expanding it.

The production, distribution, sale, and possession of methamphetamine is restricted or illegal in many jurisdictions.[47][48] Methamphetamine has been placed in Schedule II of the United Nations Convention on Psychotropic Substances treaty.[49]

See also

External links

References

  1. 1.0 1.1 1.2 1.3 1.4 1.5 1.6 1.7 1.8 1.9 Erowid. (1992). Erowid Methamphetamine (Speed, Crank) Vault. Retrieved from https://erowid.org/chemicals/meth/meth.shtml
  2. Desoxyn Label (FDA) | http://www.accessdata.fda.gov/drugsatfda_docs/label/2013/005378s028lbl.pdf
  3. Lazăr Edeleano: Über einige Derivate der Phenylmethacrylsäure und der Phenylisobuttersäure. In: Berichte der Deutschen chemischen Gesellschaft zu Berlin; 20. Jg. (1887), Band 3, S. 616–622. https://doi.org/10.1002/cber.188702001142
  4. Grobler, Sias R.; Chikte, Usuf; Westraat, Jaco (2011). "The pH Levels of Different Methamphetamine Drug Samples on the Street Market in Cape Town". ISRN Dentistry. 2011: 1–4. PMC 3189445 Freely accessible. PMID 21991491. https://doi.org/10.5402/2011/974768
  5. Rasmussen N (July 2006). "Making the first anti-depressant: amphetamine in American medicine, 1929–1950". J. Hist. Med. Allied Sci. 61 (3): 288–323. PMID 16492800. https://doi.org/0.1093/jhmas/jrj039. SKF first packaged it as an inhaler so as to exploit the base's volatility and, after sponsoring some trials by East Coast otolaryngological specialists, began to advertise the Benzedrine Inhaler as a decongestant in late 1933.
  6. Rasmussen N (2011). "Medical science and the military: the Allies' use of amphetamine during World War II". J. Interdiscip. Hist. 42 (2): 205–233. PMID 22073434. https://doi.org/10.1162/JINH_a_00212
  7. Defalque RJ, Wright AJ (April 2011). "Methamphetamine for Hitler's Germany: 1937 to 1945". Bull. Anesth. Hist. 29 (2): 21–4, 32. PMID 22849208. https://doi.org/10.1016/s1522-8649(11)50016-2.
  8. "Historical overview of methamphetamine". Vermont Department of Health. Government of Vermont. Retrieved 29 January 2012.
  9. "Controlled Substances Act". United States Food and Drug Administration. 11 June 2009. Retrieved 4 November 2013.
  10. 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.
  11. Wilson, Andrew (2008). "Mixing the Medicine: The Unintended Consequence of Amphetamine Control on the Northern Soul Scene" (PDF). The Internet Journal of Criminology. SSRN 1339332 Freely accessible.
  12. Hill J (4 June 2004). "Paul Erdos, Mathematical Genius, Human (In That Order)" (PDF). untruth.org. Retrieved 2 November 2013.
  13. Liddle DG, Connor DJ (June 2013). "Nutritional supplements and ergogenic AIDS". Prim. Care. 40 (2): 487–505. PMID 23668655. https://doi.org/10.1016/j.pop.2013.02.009
  14. 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.
  15. Canadian Institutes of Health Research. How Drugs Affect Neurotransmitters. Web 2007. Available from: URL: http://thebrain.mcgill.ca/flash/i/i_03/i_03_m/i_03_m_par/i_03_m_par_cocaine.html#drogues
  16. Barr AM, Panenka WJ, MacEwan GW, Thornton AE, Lang DJ, Honer WG, et al. The need for speed: an update on methamphetamine addiction. Journal of Psychiatry and Neuroscience 2006 Mar 6;31(5):301-13.
  17. Malenka RC, Nestler EJ, Hyman SE (2009). "15". In Sydor A, Brown RY. Molecular Neuropharmacology: A Foundation for Clinical Neuroscience (2nd ed.). New York: McGraw-Hill Medical. p. 370. ISBN 978-0-07-148127-4. "Unlike cocaine and amphetamine, methamphetamine is directly toxic to midbrain dopamine neurons."
  18. A review of the clinical pharmacology of methamphetamine (PubMed.gov / NCBI) | http://www.ncbi.nlm.nih.gov/pubmed/19426289
  19. Methamphetamine-induced neurotoxicity: the road to Parkinson’s disease | http://www.if-pan.krakow.pl/pjp/pdf/2009/6_966.pdf
  20. Intraneuronal dopamine-quinone synthesis: a review (PubMed.gov / NCBI) | http://www.ncbi.nlm.nih.gov/pubmed/12835101
  21. Dopaminergic neuron-specific oxidative stress caused by dopamine itself (PubMed.gov / NCBI) | http://www.ncbi.nlm.nih.gov/pubmed/18596830
  22. Methamphetamine toxicity and messengers of death (PubMed.gov / NCBI) | http://www.ncbi.nlm.nih.gov/pubmed/19328213
  23. Relationship between temperature, dopaminergic neurotoxicity, and plasma drug concentrations in methamphetamine-treated squirrel monkeys (PubMed.gov / NCBI) | http://www.ncbi.nlm.nih.gov/pubmed/16293712
  24. A review of the clinical pharmacology of methamphetamine (PubMed.gov / NCBI) | http://www.ncbi.nlm.nih.gov/pubmed/19426289
  25. "Desoxyn Prescribing Information" | http://www.accessdata.fda.gov/drugsatfda_docs/label/2013/005378s028lbl.pdf
  26. Westfall DP, Westfall TC (2010). "Miscellaneous Sympathomimetic Agonists." In Brunton LL, Chabner BA, Knollmann BC. Goodman & Gilman's Pharmacological Basis of Therapeutics (12th ed.). New York: McGraw-Hill. ISBN 978-0-07-162442-8.
  27. Malenka RC, Nestler EJ, Hyman SE (2009). "15". In Sydor A, Brown RY. Molecular Neuropharmacology: A Foundation for Clinical Neuroscience (2nd ed.). New York: McGraw-Hill Medical. p. 370. ISBN 978-0-07-148127-4. "Unlike cocaine and amphetamine, methamphetamine is directly toxic to midbrain dopamine neurons."
  28. http://www.ncbi.nlm.nih.gov/pubmed/19328213
  29. "Desoxyn Prescribing Information" | http://www.accessdata.fda.gov/drugsatfda_docs/label/2013/005378s028lbl.pdf
  30. Efficacy of psychostimulant drugs for amphetamine abuse or dependence (PubMed.gov / NCBI) | http://www.ncbi.nlm.nih.gov/pubmed/23996457
  31. http://www.merckmanuals.com/home/special_subjects/drug_use_and_abuse/amphetamines.html
  32. Treatment for amphetamine dependence and abuse (PubMed.gov / NCBI) | http://www.ncbi.nlm.nih.gov/pubmed/11687171
  33. Treatment for amphetamine dependence and abuse (PubMed.gov / NCBI) | http://www.ncbi.nlm.nih.gov/pubmed/11687171
  34. Treatment for amwithdrawal (PubMed.gov / NCBI) | http://www.ncbi.nlm.nih.gov/pubmed/19370579
  35. Treatment for amphetamine withdrawal (PubMed.gov / NCBI) | http://www.ncbi.nlm.nih.gov/pubmed/19370579
  36. Treatment for amphetamine withdrawal (PubMed.gov / NCBI) | http://www.ncbi.nlm.nih.gov/pubmed/19370579
  37. Treatment for amphetamine withdrawal (PubMed.gov / NCBI) | http://www.ncbi.nlm.nih.gov/pubmed/19370579
  38. Methamphetamine abuse (PubMed.gov / NCBI) | http://www.ncbi.nlm.nih.gov/pubmed/17990840
  39. Treatment for amphetamine psychosis | 1
  40. Treatment for amphetamine psychosis | 1
  41. Hofmann FG (1983). A Handbook on Drug and Alcohol Abuse: The Biomedical Aspects (2nd ed.). New York: Oxford University Press. p. 329. ISBN 9780195030570.
  42. Treatment for amphetamine psychosis | 1
  43. Stimulant Misuse: Strategies to Manage a Growing Problem | http://www.acha.org/prof_dev/ADHD_docs/ADHD_PDprogram_Article2.pdf
  44. http://www.accessdata.fda.gov/drugsatfda_docs/label/2013/021303s026lbl.pdf
  45. Adderall Prescription info | http://www.accessdata.fda.gov/drugsatfda_docs/label/2013/021303s026lbl.pdf
  46. Gillman, P. K. (2005). Monoamine oxidase inhibitors, opioid analgesics and serotonin toxicity. British Journal of Anaesthesia, 95(4), 434-441. https://doi.org/10.1093/bja/aei210
  47. http://www.unodc.org/pdf/youthnet/ATS.pdf
  48. http://web.archive.org/web/20051205125434/http://www.incb.org/pdf/e/list/green.pdf
  49. http://web.archive.org/web/20051205125434/http://www.incb.org/pdf/e/list/green.pdf