Synonyms Methamphetamine (USAN). Street names: Ice, uppers, crystal
Brand names Desoxyn
IUPAC name

IUPAC name






PDB fields




(Jmol 3D structure)
Mol. mass

149.2328 g/mol

Metamfetamine is a notorious drug of abuse that produces its effects by inducing the release of dopamine, noradrenaline and to a lesser extent serotonin from the synaptic vesicles and inhibiting their reuptake (via activating TAAR1), see this article for an explanation of what this means. This produces profound euphoria, increased alertness, reduced appetite and sleep, improved mood, changes in sexual function (usually increases in impulsivity and sexual activity), followed by withdrawal effects such as depression and anxiety.[1] It is medically used to treat resistant cases of attention-deficit/hyperactivity disorder, obesity and low blood pressure.[1] Like amfetamine it was also used widely in World War II by members of the German air force.

Medical usesEdit

Metamfetamine’s neurotransmitter effects are also the reason why it is used in the U.S. for the treatment of treatment-resistant ADHD, low blood pressure (albeit rarely) and obesity under the brand name Desoxyn, although it is not used for this purpose in many other countries and is hence prohibited in all other countries, except when used for specific research purposes. See ADHD is characterised by reduced dopamine and noradrenaline activity in certain parts of the brain (especially near the front of the brain). It is a schedule 8 drug in Australia (SUSMP, 222) and schedule 2 drug in the U.K. (SI, 2001). Obese patients benefit from metamfetamine because it has appetite-suppressing effects. This action is believed to be mediated in the hypothalamus of the brain, which regulates feeding behaviour. It is usually used for this indication solely in the short-term as long-term data regarding its efficacy is unavailable and long-term use just increases the risk of addiction. Levmetamfetamine, the less stimulating form of metamfetamine, is sometimes used as a nasal decongestant (that is, to dry up runny noses).[1]

Recreational useEdit

The usual dosage range used medically is 5-25 mg, given once or twice daily; whereas 5-30 mg is considered a low-moderate dose for recreational users and >50 mg is sometimes used by recreational users. It is sometimes used recreationally by guys with severe sexual dysfunction as it can help them achieve an erection and keep it. Its use has become popular amongst the nightclub-going gay community and is called “party n’ play” (PNP) which means they use crystal metamfetamine (a very pure form of metamfetamine) to get high and have sex. Its popularity on the street is likely due to its relatively easy synthesis from pseudoephedrine and ephedrine, which are found in some cold and flu medications. Recreationally it is taken orally (that is, by mouth as a tablet/capsule), intravenously (by an injection into a vein), rectally (that is, as a suppository) and via smoking the crystals.[1]

Side effectsEdit

The major adverse effects of metamfetamine are related to its powerful effects on catecholamine release and include:[1][2][3]

  • Nausea
  • Vomiting
  • Sympathetic effects[note 1]
  • Increased risk of strokes, heart attacks, etc.
  • Psychosis[note 2]
  • Dizziness
  • Tolerance
  • Euphoria (a “high”)
  • Dysphoria[note 3]
  • Headache
  • Numbness
  • Dry skin
  • Tremor
  • Hives
  • Acne
  • Twitching
  • Anxiety
  • Paranoia
  • Parasympathetic effects[note 4]
  • Taste changes
  • Dry mouth.
  • Necrotizing angiitis[note 5]
  • Grandiosity[note 6]

Dry mouth, which is a common side effect of metamfetamine, is known to contribute, along with poor dental hygiene which is common amongst metamfetamine addicts, to the dental consequences of metamfetamine abuse, the so called “meth mouth” which is mostly rampant cavities, tooth wear and breaks. Additionally smoking the crystals has been associated with pulmonary oedema (a fancy way of saying the collection of fluid within the lungs), cardiomyopathy, involuntary muscle movements and rhabdomyolysis.[1] Long-term use may also cause permanent brain damage (causing memory, learning, attention, etc. deficits) and Parkinson’s disease. This is probably because drugs that directly induce the synaptic release of dopamine (including other amfetamines) are known to cause neuronal death to dopamine-signalling neurons, or at least in animals.[4][5][6][7][8]

While metamfetamine and other stimulants are known to promote alertness and fight off fatigue if people use it to stay awake for an extended period of time it often causes severe fatigue and depression. Withdrawal syndromes consisting of fatigue, depression, anxiety, etc. also often result from amfetamine abuse. Stimulants can also cause psychosis (hallucinations and delusions) as dopamine release in the MLP is also implicated in the hallucinations experienced by schizophrenics. In children all strong stimulants (which of course, excludes caffeine as it is a fairly weak stimulant) are known to cause growth stunting, likely due to a suppression of growth hormone production in the pituitary gland and of their appetite.[9][5]


Metamfetamine, has a elimination half-life in the body of roughly 10 hours, which means it takes about 10 hours for the levels in the body to be reduced by half, although this rate is heavily influenced by urinary pH, the more alkaline (that is, higher the pH) of your urine, the longer this half-life gets. Metamfetamine can be administered via a number of different routes, although medically it is usually given either by injection (although this is not a licensed use in the U.S.) or orally (that is, via a tablet). It usually comes in hydrochloride salt form, which is freely soluble in water (meaning it takes two millilitres of water to dissolve one gram of it) meaning it can be easily dissolved in water by drug addicts looking to inject the drug for a more intense “rush”. It degrades upon contact with light and air.[10]

Treatment of metamfetamine addictionEdit

Metamfetamine addiction is usually treated solely with psychosocial interventions, like narcotics anonymous and other programmes. It can also be treated with cognitive behavioural therapy (CBT) and contingency therapy (CT).[11]

Despite this a few drugs have shown some activity against metamfetamine addiction; including:[12][13]

One medication that was tried and failed in treating metamfetamine dependence was a drug called topiramate. It failed because it actually seemed to improve the “high” produced by metamfetamine, hence promoting its abuse further.[14]

External linksEdit


  1. Like hypertension, tachycardia, insomnia, restlessness and loss of appetite
  2. Characterized by hallucinations and delusions
  3. The opposite to euphoria
  4. Excessive sweating, constipation, diarrhoea, dry mouth, blurred vision, pupil dilation, difficulty passing urine, etc.
  5. The death of the cells lining the veins into which it is injected
  6. Being full of oneself

Reference listEdit

  1. 1.0 1.1 1.2 1.3 1.4 1.5 Brayfield, A, ed. (30 January 2013). "Metamfetamine Hydrochloride". Martindale: The Complete Drug Reference. London, UK: Pharmaceutical Press. Retrieved 22 May 2014.
  2. Ciccarone, D (March 2011). "Stimulant abuse: pharmacology, cocaine, methamphetamine, treatment, attempts at pharmacotherapy.". Primary Care 38 (1): 41–58, v–vi. doi:10.1016/j.pop.2010.11.004. PMC 3056348. PMID 21356420.
  3. Cruickshank, CC; Dyer, KR (July 2009). "A review of the clinical pharmacology of methamphetamine.". Addiction 104 (7): 1085–99. doi:10.1111/j.1360-0443.2009.02564.x. PMID 19426289.
  4. Ares-Santos, S; Granado, N; Moratalla, R (May 2013). "The role of dopamine receptors in the neurotoxicity of methamphetamine.". Journal of Internal Medicine 273 (5): 437–53. doi:10.1111/joim.12049. PMID 23600399.
  5. 5.0 5.1 Panenka, WJ; Procyshyn, RM; Lecomte, T; MacEwan, GW; Flynn, SW; Honer, WG; Barr, AM (May 2013). "Methamphetamine use: a comprehensive review of molecular, preclinical and clinical findings.". Drug and Alcohol Dependence 129 (3): 167–79. doi:10.1016/j.drugalcdep.2012.11.016. PMID 23273775.
  6. Rusyniak, DE (August 2011). "Neurologic manifestations of chronic methamphetamine abuse.". Neurologic Clinics 29 (3): 641–55. doi:10.1016/j.ncl.2011.05.004. PMC 3148451. PMID 21803215.
  7. Rusyniak, DE (June 2013). "Neurologic manifestations of chronic methamphetamine abuse.". The Psychiatric Clinics of North America 36 (2): 261–75. doi:10.1016/j.psc.2013.02.005. PMC 3764482. PMID 23688691.
  8. Thrash, B; Thiruchelvan, K; Ahuja, M; Suppiramaniam, V; Dhanasekaran, M (November-December 2009). "Methamphetamine-induced neurotoxicity: the road to Parkinson's disease." (PDF). Pharmacological Reports 61 (6): 966–77. PMID 20081231.
  9. Mackey, S; Paulus, M (March 2013). "Are there volumetric brain differences associated with the use of cocaine and amphetamine-type stimulants?". Neuroscience and Biobehavioral Reviews 37 (3): 300–16. doi:10.1016/j.neubiorev.2012.12.003. PMC 3604030. PMID 23253945.
  10. "Methamphetamine". PubChem. National Center for Biotechnology Information, U.S. National Library of Medicine. Retrieved 2 June 2014.
  11. O'Connor, PG, ed. (December 2013). "Amphetamines: Drug Use and Dependence". Merck Manual Professional. Merck Sharp & Dohme Corp. Retrieved 5 June 2014. 
  12. Brensilver, M; Heinzerling, KG; Shoptaw, S (September 2013). "Pharmacotherapy of amphetamine-type stimulant dependence: an update.". Drug and Alcohol Review 32 (5): 449–60. doi:10.1111/dar.12048. PMID 23617468.
  13. Pérez-Mañá, C; Castells, X; Vidal, X; Casas, M; Capellà, D (March 2011). "Efficacy of indirect dopamine agonists for psychostimulant dependence: a systematic review and meta-analysis of randomized controlled trials.". Journal of Substance Abuse Treatment 40 (2): 109–22. doi:10.1016/j.jsat.2010.08.012. PMID 21036508.
  14. Shinn, AK; Greenfield, SF (May 2010). "Topiramate in the treatment of substance-related disorders: a critical review of the literature.". The Journal of Clinical Psychiatry 71 (5): 634–48. doi:10.4088/JCP.08r04062gry. PMC 3736141. PMID 20361908.